lOMoARcPSD|6765175 Motherload of Micro Notes Microbiology for Health Professionals (MacEwan University) StuDocu is not sponsored or endorsed by any college or university Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Microbiology – HLSC 124 BN03 Chapter 1 Microbiology: Study of very small organisms (microbe) Microscopic (Ch. 3) Independent Units (Ch. 2, 4, 5) Complexity (Ch. 4) Rapid Growth Rates (Ch. 6) Omnipresent – almost everywhere (Ch. 6, 7) MIDTERM 1: CHAPTERS 1-7 ABOVE Why Study Microbiology? Knowledge of microorganisms allows us to: 1. Prevent disease occurrence 2. Developed aseptic techniques to prevent contamination and spread of disease 3. Prevent food spoilage Two Kingdoms: 1. PROkaryotes Pro = Pre (Greek) Karyotos = Nucleus Genetic material (genome) free floating chromosome (1 single chromosome), circular = Nucleoid No organelles in cell except ribosomes Cell walls have several layers and very complex to protect themselves, made up of peptidoglycan Cell division: Binary Fission (2 cells) 2 Groups A. Archaea (ancient) bacteria, do not cause disease, never find them in our regions B. Eu-Bacteria, causes disease* 3 EUkaryotes Eu = True (Greek) Karyotos = Nucleus Nucleus contain genetic material, DNA never circular but instead linear and several If continued -> Human cell has 46 chromosomes Several organelles (Ex. ER, Golgi, Mitochondria, Ribosomes) No wall, less complex, instead plasma membrane Mitosis; Meiosis Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Fungi, Algae, Protozoan, Parasites, and biggest which is human cell belong in this group Ribosomes are so important because they generate proteins (protein synthesis) Virsus(es) do not belong in either group HIV (Aids) Influenza Herpes (8 common, 1-5) Hepatitis (A-E) Skin Rash (Measles, Shingles) Golden Age of Microbiology – Who Contributed (1857 - 1914) A. Louis Pasteur (1861): Demonstrated that life did not arise spontaneously from nonliving matter Spontaneous Generation Theory: Life can arise spontaneously from nonliving matter Prove that spontaneous generation is false Experiments: Took a flask and filled with broth, heated, and then sealed one and kept another open, found that broth left open became full of microbes Then took another flash with s-shaped head, microorganisms couldn’t climb up and caught in the neck Conclusions: a. Microorganisms are everywhere b. Devise methods to curve their growth (aseptic techniques ex. heat, plug) in lab and hospital c. Refuted the Theory of Spontaneous Generation and proposed Theory of Biogenesis (life gives life to life) Merchants sent wine and beer and became spoiled on the way AIR NO AIR Bacteria took over wine and Applied just enough heat beer, destroyed alcohol into (Pasteurization Ex. Milk) acidic acid (vinegar) which Destroys bacteria and triggers equals to spoilage yeast (unicellular fungi) to ferment the sugar (fermentation Ex. yogurt, cheese, pickles) to alcohol B. Robert Koch (1876): Established experimental steps for directly linking a specific microbe to a specific disease = Koch’s Postulates (experimental steps) Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Proved that a bacterium causes anthrax: Bacillus anthracis Bacillus = family name/genus (CAPITAL B), anthracis = species name (lower case) Eu-bacteria Koch’s Postulates: a specific microbe causes a specific disease C. Edward Jenner (1798): inoculated a subject with cowpox virus, who was then protected from smallpox (less pathogenic form) Took blister of cowpox and withdrew fluid, then injected it into milkmaid Vaccination is derived from vacca, for cow, the protection is called immunity Pasteur comes 60 years later and called it immunization or vaccination Chapter 2: Chemical Principles Proteins Organic molecules that contain C, H, O, N, ad S Essential in cell structure and function Building Blocks of Proteins 1. Amino Acids (central carbon atom with 4 valence electrons) a. Carboxyl group b. Amino group c. H-Group d. R-Group*: could be an H, or very complex side chains 20 universal amino acids from differentiation of R-Group Amino acids come together to form proteins and peptide bond forms and takes out H2O molecule Peptide = dehydration Up to 300 amino acids make up a protein Primary Structure is a chain of amino acids held together by a peptide bond and loss of water and our genetics determines our proteins Changed into spiral called helical form or pleated form and called secondary structure Tertiary structure is the 3-dimensional structure Quaternary structure is 2 or more tertiary structures coming together 2. Denaturation The unraveling/disruption of the secondary, tertiary or quaternary structures Nucleic Acids DNA Double helical structure Made up of nucleotides Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 RNA 1. Base (GCAT) a. Purine (2 ring structure) Adenine, Guanine b. Pyrimidine (1 ring structure) Thymine, Cytosine Attached by hydrogen bonds 2. Sugar Organic molecule with 5 carbon atoms is called a ribose sugar Removes Oxygen from Carbon 2 therefore called deoxyribose* Deoxyribonucleic acid 3. Phosphates (backbone is made up of sugar and phosphates) Full ribose sugar, no deoxygenation Single stranded molecule Never Thymine in RNA but instead Uracil Involved in protein synthesis mRNA (messenger) rRNA (protein synthesis) tRNA (transfer, brings amino acid) Chapter 3: Observing Through Microscope Staining: bacteria are negatively charged at the pH of 7, bacteria are generally stained with basic stains Simple Stains single basic dye that shows shape/arrangement of organism ex. crystal violet (C.V.) a mordant may be used to hold the stain or coat the specimen to enlarge it ex. iodine Differential Stain (distinguishes between bacteria) a. Gram Stain distinguishes between gram positive or negative) Discovered by H.C. Gram (1888) 1. Primary Stain: crystal violet (C.V.) 1 minute = purple 2. Add Mordant: iodine (I2) 1 minute = color intensified, creates C.V.-I2 complex in peptidoglycan for gram positive, gram negative only has one layer of PG and therefore cannot hold onto the colour and C.V.-I2 seeps out of holes 3. Decolorizing: alcohol acetone, 30 sec max = purple (gram positive), colourless (gram negative) 4. Counter Stain: safranin, 1 min = purple stayed, colourless to red b. Acid-Fast Stain Only done for one species; mycobacterium (T.B. or leprosy) Mycolic acid layer stops other stains 1. Primary Stain: carbolfuchsin, heat for 10-15 min over boiling water = red Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 2. Decolorizing: acid-alcohol, some red, some colourless 3. Counter Stain: methylene blue, some red (acid fast positive bacteria ex. T.B. or leprosy), some blue (acid-fast negative bacteria) Special Stains a. Capsule Stain 1. Acidic Stain: india ink or nigrosin; never absorbed, colors background 2. Decolorizing: wash it off with water 3. Counter Stain: safranin, bacteria absorbs the red, but colorless halo around is the capsule b. Endospore Stain Primary Stain: malachite green, heat for 5 minutes Decolorizing: wash it off with water, green dot in center left Counter Stain: safranin, bacteria absorbs red with green dot in center c. Flagella Stain Carbolfuchsin stain = red Use of red mordant Chapter 4: Functional Anatomy Prokaryotic Cells Shapes: 1. Spiral a. Vibrio C-shaped Flagella Ex. Vibrio cholera, causes cholera b. Spirillum C-shapes together Flagella c. Spirochete Very thin and quick spirals Moves from endoflagella Ex. Treponema pallioum (syphilis) 2. Bacillus (rod or staff) If in pairs, it’s called diplobacilli Streptobacilli = chains Ex. Bacillus anthracis 3. Coccus (spherical or ovoid) If in pairs, it’s called diplococci Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Strepto = chains Staphylo = clusters Streptococcus pyogene causes strep throat Staphylococcus aureus causes skin infections (boil, TSS, food poisoning, etc.) Coccobaccilus (completely different than bacillus and coccus; combination) Pleomorphie (varied in their shape and arrangement) Structure of Prokaryotic Cell 1. Glycocalyx (outside cell wall) Sugar cap – can’t stain (forms halo) Made up of polysaccharides or polysaccharides and polypeptides Secreted by the microbe to protect itself (usually sticky) a. Increase virulence; disease causing ability of organism – they can escape phagocytosis – make surface slippery (ex. streptococcus pneumoniae) b. Allows bacterial cell to attach to human host cells (ex. streptococcus mutans; attach to teeth, dental cavities, dental decay) c. Capsules avoid phagocytosis (avoid being caught); evade our immune system 2. Flagella Made up of filaments that are made up of chains of flagellin (protein molecule) Attached to a protein hook (hook is thicker part where filament sits on bacteria) (hook is made of protein) Anchored to wall and membrane by the basal body Filament -> hook -> basal body (rod and protein rings) One set of rings = Gram-positive Two sets of rings = Gram-negative a. Monotrichous (one hair/wip) b. Amphitrichous (one hair on both end) c. Lophotrichous (tuft/bundle of hairs on one end) (one end = polar) d. Peritrichous (hair all around the cell - most common) (bacteria can move in all directipons) Moving o Very mobile o Run -> tumble -> run o Running is preferred, change direction through tumbling Axial Filaments Endo flagella; inside of cell Found in spirochete (ex. syphilis) Instead of running/tumbling, these will twist like a corkscrew Outer sheath; to protect endo flagella Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 3. Fimbria(e) and Pilus(i) Fimbriae; comes from all corners; for attachment, not movement; way more than flagella, maybe hundreds (ex. Neisseria gonorrhoeae) Pilus; bridge formed between two cells so they can transfer DNA (ex. Escherichia coli) 4. Cell Wall Second layer Peptidoglycan (murein = wall) PG* a. “Peptide” proteins that hold together the wall polypeptides and tetrapeptides tetrapeptides linking NAM’s b. “Glycan”; glucose changes into NAG and NAM NAG; N acetyl glucosamine NAM; N acetyl muramie acid Joins NAG and NAM together by Oxygen Gram-Positive and Gram-Negative Cell Walls Positive: Several layers of peptidoglycan (PG) Teichoic Acid present a. Alcohol and phosphate Complex alcohol called Ribitol, or Glycerol and attach to phosphates b. Wall teichoic acid and Lipoteichoic acid 1. Role of Teichoic Acid Antigenic specificity (can recognize bacteria from the acid) Phosphates attract positive ions into cell Negative: Has only one layer of peptidoglycan (maybe 2) No teichoic acid Has outer membrane a. Phospholipid (main structure) b. Lipoproteins (anchors to peptidoglycan) c. Porin protein (transports) d. Lipopolysaccharide Lip = endotoxin; causes fever, nausea, vomiting, shock Opolysaccharide = recognition capability and antigenic specificity Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 e. Periplasmic space (between outer membrane and peptidoglycan and plasma membrane) Atypical Cell 1. Mycobacterium species (ex. M. tuberculosis, M. leprae) - have cell wall Put layer on top of peptidoglycan wall called mycolic acid which is a waxy lipid layer 2. Mycoplasma species (pneumonia) Lack cell wall so they only have a plasma membrane with sterols 3. Archaea Wall-less or walls of pseudomurein No peptidoglycan Damage to the Cell Wall 1. Lysozyme: in mucus, saliva, tears, breast milk, digests disaccharide in peptidoglycan, attacks both gram-positive and negative Positive: outside thick PG layer, attack glycan of PG and becomes wall-less and dies (protoplast) Negative: one PG layer and outer membrane, removed middle PG which is now called spheroplast and dies a. Protoplast: formed is a wall-less gram-positive cell b. Spheroplast: is formed by the action of lysozyme on a gram-negative cell 2. Penicillin: inhibits peptide bridges in peptidoglycan Attacks peptido of PG Kills gram-positive very fast because there is more PG (strep throat) Hurts gram-negative less because of fewer PG layers (except newer penicillin molecules hurt more) Internal Structures of Cell Plasma Membrane: phospholipid bilayer, selective permeability Cytoplasm: inside plasma membrane, no organelles except ribosomes, contains bacterial chromosome Nucleoid: contains bacterial chromosome Ribosome: freely floating, size of 70S, smaller than human ribosomes (80S) Endospores Formed when water and food are unavailable Called resting cells How? Sporulation: endospore formation 1. Spore septum isolates new DNA 2. Plasma membrane surrounds DNA, cytoplasm, and membrane Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 3. Spore septum surrounds isolated portion, forming forespore 4. PG layer forms between membranes 5. Spore coat forms 6. Endospore is freed from cell Dipicolinic acid: protects cell from extreme heat and chemicals, will disappear when cell returns to og state Germination: return to vegetative state Gram-positive makes endospores 1. Bacillus anthracis (anthrax) 2. Clostridium tetani (tetanus) a. Clostridium botulinum (botulism; food poisoning) b. Clostridium perfringens (gangrene) c. C. difficile (colitis) 3. Only one Gram-negative Coxiella burnetti (pneumonia; pneu-fever) Chapter 5: Microbial Metabolism Metabolism: chemical reactions, the build-up and breakdown of nutrients within a cell to maintain life (catabolism and anabolism make up metabolism) Catabolism: provides/produces energy and building blocks for anabolism a. Degradative (break down into simple component parts b. Hydrolytic reaction (uses water) c. Exergonic (energy released) d. ATP is produced Anabolism: uses energy and building blocks to build large molecules a. Biosynthetic reactions b. Dehydration reaction (takes out water) c. Endergonic (uses energy) d. ATP is used ATP: (A – Ribose – Tri – Phosphate) 3 phosphates unstable bonds because phosphates are negatively charged (3 are repelling each other) lose one phosphate and becomes A – D – P (D for double) + P- + energy saves phosphates, can exchange and used anytime Enzymes 1. Biological Catalyst 2. Speed up reaction/ increase likelihood 3. It is “unharmed” after reaction; never used up Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 4. Made up of proteins a. Can be Simple enzymes (proteins only) b. Complex enzymes Enzymes are made up of: Apoenzyme: protein component Cofactor: inorganic molecules, Fe+, Mg+, etc. forms the active site organic cofactor is called coenzyme (more complex) Coenzymes use the vitamin B’s from food Holoenzyme: both apoenzyme and cofactor Coenzymes (all derived from Vitamin B’s) a. NAD+ (Nicotinamide – Adenine – Dinucleotide) b. NADP+ (Nicotinamide – Adenine – Dinucleotide – Phosphate) c. FAD (Flavin – Adenine – Dinucleotide) d. FMN (Flavin – Mono – Nucleotide) e. Coenzyme A (CoA, CoQ, Ubiquinone) Factors Affecting Enzymatic Action 1. Temperature Rate of reaction increases as temperature increases Rate of reaction decreases if temperature continues to increases because the enzymes denatures (falls apart) Highest rate of reaction happens at 37 degrees 2. pH narrow range of pH (6.5 – 7.5) neutral causes denaturation 3. Substrate Concentration ex. glucose rate of reaction becomes uniform (plateau) when active sites become saturated 4. Inhibitors a. Competitive Inhibitor: inhibits substrate because they fill the active site (ex. PABA (para – amino – benzoic – acid -> folic acid to yield DNA and RNA) is inhibited by sulfanilamide and shutdown enzymatic reaction; no folic acid -> no DNA and RNA -> cell death in bacterium (not human cells, but has side effects, especially for pregnant women and fetal growth, or people with liver problems; jaundice) b. Non-competitive Inhibitor: occupies a site other than the active site called the allosteric site, changing the structure of the active site and shutting down enzymatic reaction, however most of the time it is reversible c. Feedback Inhibition: conserve important reserves without wasting them, enzymes re-changing the structure and allosterically binds to first enzyme and then shut down Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Energy Production 1. Oxidation – Reduction Reactions (Redox) Oxidation = removal of electrons Reduction = gain of electrons Always adds or removes a proton to keep balance which equals a hydrogen atom Dehydrogenation reactions (removes hydrogen) oxidation reaction Hydrogenation (additional hydrogen) reduction reaction Ex. Glucose and NAD+ coenzyme 2. Phosphorylation Added a phosphate group ADP + P to produce ATP Redox Reactions Energy released from transfer of electrons (oxidation) of one compound to another (reduction) to generate ATP in electron transport chain reduced coenzymes -> enter electron transport chain -> releases potential energy stored in hydrogen atom -> adds P to ADP -> produce ATP Substrate Level Phosphorylation Energy from the transfer of a high energy PO4- to ADP, generates ATP Has a P to give away Photophosphorylation Lights causes chlorophyll to give up reactions, energy released from transfer of electrons (oxidation) to generate ATP 3. Glucose Catabolism 1. Glycolysis yields 2 NADH and 2 ATP molecules (net ATP) 10 steps to yield pyruvic acid 2x pyruvic acid (half of what glucose is) 2. Kreb’s Cycle breaks pyruvic bonds and creates 2x Acetyl CoA and produce 2 NADH and brings in CoA enzyme Enters real Kreb’s Cycle and releases CoA 6 NADH + 2 FAHD2 + 2 ATP Total 8 NADH + 2 FADH2 + 2 ATP (net) 3. Electron Transport Chain Produces energy Has 4 complexes Found in cell membrane in bacteria, found in mitochondria in humans Brings 10 NADH, 2 FADH2 into chain Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Releases H is complexes and releases the protons out and electrons transferred to next complex, finally falls back into cytoplasm, absorbs by oxygen and made into water Protons collect on top and make a proton motive force, fall down ATP synthase channel through chemical osmosis, creates ATP from ADP + P Produces most energy, each NADH -> 3 ATP, each FADH2 -> 2 ATP, 1 glucose molecule -> 38 ATP in bacteria (happens in cytoplasm) Total of the 3 cycles: 38 ATP made Respiration in Prokaryote Aerobic Respiration: final electron acceptor is oxygen, 38 produced in bacteria, 36 in humans Anaerobic Respiration: final electron acceptor is not oxygen, any other inorganic molecule other than oxygen (nitrate, bicarbonate, sulfate), less energy than aerobic because part of the Kreb’s Cycle operates under anaerobic conditions, bacteria harmed by oxygen by causing cell death, vary in ATP molecules (Clostridium sp. all fall here) Fermentation: uses an organic molecule as the final electron acceptor, no Kreb’s Cycle or ETC, only Glycolysis, don’t care about oxygen, only 2 ATP, yeast (CO2 and ethanol) and Lactobacillus (lactic acid) Chapter 6 – Microbial Growth Factors what determine growth in prokaryotes: A. Physical Factors 1. Temperature Bell curve diagram GROUP A GROUP C Psychrophiles Can Grow 0 Optimum Cannot Grow Environme nt 15 20 (warm room) Cold GROUP B Psychrotropes (Facultative) 0, but can adapt 25-30 Around 40 Mesophiles Thermophiles 25-35 80-110 (130) Hyperthermop hiles 80-110 (130) 37 Around 50 50-60 Below 45 50-60 Below 45 Cold, present in our regions Average, present in our Hot, not present in our Hot, not present in our regions Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Info True species, Psychro means cold Flexible species, disease, food spoilage regions Most common diseasecausing group regions True species, no health concern No health concern 2. pH Bell curve diagram Most love a neutral pH Enzymes are for growth (last why pH and heat can affect growth) 3. Osmotic Pressure Want equal pressure = isotonic B. Chemical Factors C, H, N, S, P, but, very careful with oxygen Oxygen divides bacteria into 5 large groups Table 6.1 1. Obligate Aerobes Absolutely aerobic, need oxygen ATP=? Final electron acceptor is oxygen Most bacteria belong to this group Grows where oxygen in present in tube = top SOD, catalase 2. Obligate Anaerobes Absolutely cannot use oxygen ATP = varies Harmed by oxygen Final electron acceptor is organic molecule other than oxygen (nitrates, sulfates, etc.) Only glycolysis and part of kreb’s cycle, no electro transport chain Clostridium sp. Are anaerobic (clostridium tetani) Grows at bottom of tube = less oxygen No SOD, no catalase 3. Facultative Anaerobes (flexible) Middle of both When oxygen is available, they prefer it, growth will be fast, ATP will be high in amount When oxygen is unavailable they won’t worry about it, ATP yield reduced and varies If become desperate they can start fermentation Final electron acceptor can be oxygen in aerobic or any other is anaerobic Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Escherichia coli Grow everywhere, more at top with oxygen 4. Aerotolerant Anaerobes All 3 groups above Tolerant oxygen Anaerobes that choose to avoid oxygen Obligate fermenters – uses organic molecule Lactobacillus sp., yeast, ethanol, (lactic acid to ferment) Spread equally in tube, doesn’t want oxygen 5. Microaerophiles Are aerobes, but, in quantities that are much lower Choose to use less oxygen Helicobacter pylori (peptic ulcers, stomach) Campylobacter jejuni (gastroenteritis) Grow in middle in tube with medium oxygen level Small quantities of SOD and catalase Effect of Oxygen on Growth Bacterial Growth in Tube Growth Explanation s Oxygen’s Effects Info Obligate Aerobes Oxygen required Obligate Anaerobes Cannot use and harmed by oxygen Top of tube Bottom of tube High Less or no oxygen level oxygen Facultative/ Flexible Anaerobes Middle of first two groups, if oxygen is available, they prefer it. If oxygen is unavailable, it doesn’t bother them Aerotolerant Anaerobes Combination of the first three groups, tolerates oxygen, but, chooses to avoid Microaerophile s Aerobes that choose to use oxygen in very low quantities Spread equally inn tube Middle of tube Doesn’t want oxygen Medium oxygen level Why Oxygen? – Toxic Oxygen Starts to form singlet oxygen (higher energy state) steals things from other molecules Superoxide free-radical, steals electrons from neighboring molecule and will get more excited and continue stealing Eventually the neighboring cells dies Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 To stop the stealing, we use an enzyme called a superoxide dismutase (SOD) to turn oxygen into H2O2 – hydrogen peroxide Hydrogen peroxide is just as bad, it will break down into O2 negative 2 charge Enzyme catalase takes peroxide and makes H2O plus O2 Then enzyme peroxidase into 2 H2O Hydrogen peroxide will start stealing electrons and become hydroxide freeradical (OH) and cell will die, very bad Why Culture in Tubes Nutrient broth growth culture, helps bacteria grow for analysis, liquid medium Or Solid growth medium in petri dish, nutrient agar which is gelatin Add agar to nutrient broth and get solid medium Heat to 100 degrees for sterilization, them to 45 s to pour which is still a solid medium Remains solid at 37 degrees Cannot be eaten away by bacteria Pure cultures from streak plate method First steak is very crowded Second streak has clump of colonies Third streak will have small colonies Media Types 1. Selective Media Suppress unwanted microbes and encourage desired microbes Ex. Bismuth sulfite Agar to grow Salmonella typhus, causes: Typhoid fever 2. Differential Media Makes is easy to distinguish colonies Ex. Blood Agar to grow Streptococcus pyogenes, causes: Strep throat Hemolysis of RBC (death) 3. Selective and Differential Media Suppress unwanted microbes and make it easy to distinguish colonies Ex. Mannitol Salt Agar to grow Staphylococcus aureus, causes: TSS Yellow zone = mannitol as organism changes pH Colonies Appear from Binary Fission One bacteria will elongate and splits in the middle (no mitosis) Phases of Growth: 4 Phases 1. Lag Phase Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Preparing, can take minutes, hours, or days 2. Log Phase * Binary fission is at its max, patient is very sick Generation time (one binary fission) is always constant Generation time = 60 min x hours / number of generations 2^0 > 2^1> 2^2 = the generations Most susceptible time to attack because they are growing so fast (radiation, antibiotics, chemicals) 3. Stationary Phase: Not much growth New cells form and balanced by old cells dying, equilibrium 4. Death Phase Very little organisms left Chapter 7 – The Control of Microbial Growth Sterilization: Removing all microbial life Disinfection: refers to the destruction of vegetative (non-endospore forming) pathogens, which is not the same as complete sterility Actions of Microbial Control Agents Alteration of membrane permeability Damage to proteins Impairment of nucleic acids 1.Heat Moist Heat: denatures proteins a. Boiling: kills everything except viruses and endospores (not complete sterilization) b. Autoclaving: (removes all microbial life - sterilization) steam will raise temperature to 121 degrees for 15 minutes, under pressure of 15 PSI, complete removal of all microbial organisms (instruments, etc.) pressure cooker at home c. Pasteurization: spoilage organisms and increase the shelf life i. Classic Method (Batch): 63 degrees for 30 minutes ii. HTST Method (Hash): 72 degrees for 15 seconds iii. UHT Method: 140 degrees for 4 seconds Dry Heat: kills by oxidation Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Flaming Loop: reducing microbial life Incineration: no sharp things allowed, safety first Hot-Air Sterilization: complete removal of all microbial organisms, 170 degrees for 2 hours Field: ex. Anthrax 2. Filtration (if heat sensitive) a. Vaccine, enzyme solutions, antibiotics b. Mask c. Units: O.R., Burn, all have filtered air through HEPA filters 3.Radiation a. Ionizing Radiation: Damages DNA, ionizes water to release OH - OH radical damages DNA - x-rays, gamma rays, electron beams (dental supplies, medical supplies, pharmaceuticals) - spices, meat, and veggies can goes through this to elongate shelf life b. Non-Ionizing Radiation: damages DNA - hits thymine’s in DNA and starts forming abnormal bonds between them (thymine dimers) and damages DNA - UV (260 nm) - hospital O.R., hospital nurseries, hospitals cafeteria Chemical Methods 1.Phenol and Phenolics a. Phenol: destroys cell membranes, unpleasant odor, skin irritation b. Phenolic: simple addition makes it good, clean surfaces with ex. Lysol, good to clean organic matter (vomit, etc.) 2.Halogens a. Iodine: skin irritation and stains everything b. Iodophor: add organic molecule, takes away staining, denatures by attaching to amino acid Tyrosine, making di-iodo-tyrosine, bacteria will die from this c. Chlorine: adds water and make HOCL, redox reaction and kills everything 3.Alcohols a. Ethanol: too expensive, volatile, not readily available, never be 100% (70%) b. Isopropanol: adding organic molecule makes this from ethanol, denatures proteins and dissolves lipids (ex. Swab) 4.Surface-Active Agents (QUATS) a. quaternary (4) ammonium compounds (detergents) NH4+ b. degerming: bactericidal, denature proteins, disrupt plasma membrane 5.Gaseous Chemosterilizers Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 a. Ethylene Oxide: volatile gas, carcinogen, highly penetrating, denatures proteins by causing alkylation, kills all microbes and endospores, used on machines (respirators, mattresses, etc.) Chapter 8: Microbial Genetics Central DOGMA: all organisms use DNA to make RNA to make proteins for cellular function DNA: made up of nucleotides, (is a polynucleotide molecule), double helical structure Gene: a segment of DNA that codes for a functional product that generally is an mRNA molecule, alternatively produce rRNA or tRNA, eventually will make a functional protein Genome: entire genetic complement of an organism Complimentary base pairs (AT, GC) held together by hydrogen bonds Antiparallel Nature: says that one strands of double helix is upside down, relative to the other sugar is upside down C5 is where you find the phosphate group prepares 2 strands (leading strand is 5 to 3 and lagging strand is 3 to 5) this creates stability 5’ ----------- 3’ 3’ ----------- 5’ Semi-Conservative Replication: one strand is new and one is old, anabolic reaction Enzyme DNA helicase unzips DNA (separates leading strand from lagging strand) Enzyme DNA gyrase relieves tension and keeps them uncoiled (DNA wants to coil back so you have to stabilize it and keep the unzipped portion open) slide 7 Forms a replication fork (place where new nucleotides can meet up) Leading strand: DNA polymerase (enzyme) picks up new nucleotides from cytoplasm, proof reads and attaches complimentary bases, making new strand (old and new) Lagging strand: DNA polymerase cannot identify because its upside down, so enzyme RNA polymerase forms a short strand of RNA primer, now DNA polymerase comes and adds new nucleotides by removing RNA primer and RNA polymerase (called exonuclease activity), and replaces it with DNA, but adds nucleotides in short fragments called Okazaki fragments (few to thousand nucleotides long), leaving gaps, DNA ligase joins gaps, now have 2 strands (old and new) DNA Replication in Bacteria Ring structure, one region called origin of replication Two replications going in opposite directions and meet at termination replication point Two new rings created (one old and one new) Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Transcription Copying of a gene Makes RNA (mRNA, rRNA, tRNA) mRNA = new, tRNA and rRNA are recycled Always assume mRNA is made, most common RNA polymerase copies gene and creates one strand (RNA is one strand) Happens is cytoplasm in prokaryotic cell and nucleus in eukaryotic cell In eukaryotic cells protein synthesis happens in the cytoplasm and RNA needs to be spliced so it can get out of the nucleus RNA Splicing: Bad ones are called introns and good ones are called exons, introns get cut out and exons join together and wiggle out of nucleus Translation RNA will be translated to make proteins mRNA: carries the code/ language, copy of one strand of DNA, formed in triplet sequences called codons (start codon = AUG, stop codon = UAG, UGA, UAA) there are other codons for this rRNA: forms ribosomal unit where decoding happens (kind of in-between) tRNA: has 3 arms (longest one called acceptor arm) that has 3 nucleotides called anticodon (complementary to codon on mRNA) and carries amino acid (one at a time) 20 amino acids universally used so about 20 tRNA’s also Methionine (a-amino acid) will be left from tRNA from AUG start codon, and dehydration reaction At the end the ribosomal unit will fall apart and released polypeptide forms a new protein Role of Genetic Code Relates to: 1. relate to nucleotide sequence in DNA molecule = to gene in DNA 2. relate to mRNA sequence 3. relate to amino acid sequence in new protein - Making 3 positions on codon (1st, 2nd, 3rd) from 4x4x4 = 64 combinations - degeneracy of genetic code = several amino acids have more than one codon Order Helicase - unwinds Gyrase – keeps them unwinded, replication fork DNA polymerase - proof reader and adds complimentary bases RNA polymerase – adds primer RNA primer – DNA polymerase can now read DNA polymerase – only makes fragments Okazaki fragment – holes in DNA Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 DNA ligase - fills fragments Chapter 11: Bacterial Groups Eubacteria (true bacteria = health implications) The Gram-Negative Bacteria A. Proteobacteria ALPHA Category Shape Info Spread Causes Effects Ricksettia ricksettia Obligate parasite Coccobacilli or bacillus Aerobic Insect or tick bites Spotted fever (may cause heart infection) Attacks and damages cardiovascular system by changing permeability of blood vessels BETA Sub-Divisions Category Shape Info Spread Causes Effects Bordetella pertussis GAMMA SubDivisions Category Pseudomonadales Shape Info Spread Aerobic Bacillus Capsule N. gonorrhoeae Aerobic Coccus Capsule, fimbriae Whooping cough Gonorrhoeae Pseudomonas aeruginosa Best psychrotrophs Moraxella lacunata Aerobic Neisseria N. meningitis Aerobic Coccus Capsule Meningitis Legionellales Legionella pneumophila Endospore Bacillus, mono or Coccobacilli Bacillus lophotrichous flagella Produce blue/green pigment called pyocyanin Challenge in Contaminated water Downloaded by Kleina Mash (kleina_mash@yahoo.ca) Coxiella burnetti Aerobic parasite Bacillus Only gramnegative that produces endospores Harbored in Vibrionales Vibrio cholerae Facultative anaerobic Bacillus, monotrichous flagella Aerobic because they can still use oxygen lOMoARcPSD|6765175 Causes GAMMA SubDivisions Category Shape Info Spread Causes Effects hospitals because they love carbon, ex. antibiotics, antiseptics, QUATS, pharmaceuticals Blue/green pus on burn patients and forms abscesses, UTI’s, pink eye, conjunctivitis droplets, ex. Water supply lines, AC units, etc. cannot spread through humans Pink eye, Pneumonia in 2 conjunctiviti forms s 1. Pontiac fever (mild, no hospitalization) 2. Legionnaires disease (fatal) Enteriobacteriales domesticated animals like cattle and spread through unpasteurized milk and aerosols Q-fever (type of Rice Water pneumonia) Stools (diarrhea) Pasteurellales Escherichia coli Salmonella typhus Shigella dysenteriae Hemophilus influenza Facultative anaerobes Bacillus, peritrichous flagella, fimbriae, form pili 5 different sub types, also called coliform bacteria, lab pet because it grows easily, water supplies will be tested Food borne illness ex. ground beef Severe travellers’ diarrhea, 75% of UTI cases Kills everything in intestinal tract (enterics) because they produce bacteriocins (protein molecules) which kill and destroy all other bacteria Facultative anaerobes Bacillus, peritrichous flagella, fimbriae, form pili Selective media can separate from Salmonella enterica, which is always a food source Facultative anaerobes Bacillus, peritrichous flagella, fimbriae, form pili Produce powerful toxin called Shiga toxin Always a human carrier Severe gastrointestinal infection Kills everything in intestinal tract because they produce bacteriocins (protein molecules) which kill and destroy all other bacteria Scarring and abscesses in large intestine from toxin Kills everything in intestinal tract because they produce bacteriocins (protein molecules) which kill and destroy all other bacteria Downloaded by Kleina Mash (kleina_mash@yahoo.ca) Aerobic Coccobacilli with capsule Needs blood to grow because its missing coenzyme NAD (NADP) for aerobic respiration and redox reactions (V-factor = NAD, X-factor = cytochrome from iron) Can grow in chocolate agar (so dense with blood) Meningitis, pneumonia, otitis media (middle ear infections) lOMoARcPSD|6765175 DELTA No hospital pathogens, all plant pathogens EPSILON Category Shape Info Spread Causes Effects Helicobacter pylori Microaerophilic Vibrio (curved rod) Peritrichous flagella Campylobacter jejuni Microaerophilic Vibrio (curved rod) Monotrichous flagella Peptic ulcers, severe gastric ulcers Whole gastroenteritis b. Non-Proteobacteria Chlamydiae Aerobic, obligate parasites Coccobacilli Bacteriodetes Bacteroides Bacillus Info Life cycle: Elementary body; infectious part and Reticulate body; binary fission Anaerobic Causes Trachoma (blindness), 2 STD’s Non-Gonococcal Urethritis and LymphoGranuloma Venereum, pneumonia Pus formation in urethra (urethritis) and attacks lymph nodes (venereum) Gingivitis, peritonitis (bowel infection) Category Shape Effects Fusobacteria Fusobacterium Bacillus with pointed edges (spindle shaped) Anaerobic Gingivitis Spirochetes Endoflagella/axial filaments Cannot be grown in vitro, only in live body, genome also completely mapped (vaccine possible) Treponema pallidum (syphilis) Pus formation in bowel 2. Gram Positive Bacteria A. Firmicutes (low G+C ratio: guanine and cytosine) Clostridiale Clostridium tetani Clostridium difficile Clostridium Downloaded by Kleina Mash (kleina_mash@yahoo.ca) Clostridium lOMoARcPSD|6765175 s Shape Info Spread Causes Bacillales Category Shape Info Spread Causes Effects Bacillus Produce endospores, lollipop rods because endospore on end Soil Tetanus Bacillus Produce endospores, lollipop rods because endospore on end botulinum Bacillus Produce endospores, lollipop rods because endospore on end perfringens Bacillus Produce endospores, lollipop rods because endospore on end Soil Colitis Soil Botulism Soil Food Poisoning Bacillus anthracis Facultative anaerobic (still aerobe) Bacillus, endospore with central position Can be biological weapon Soil Anthrax Lactobacillale Lactobacill s us Example Staphylococcus aureus Facultative anaerobe (still aerobe) Grape clusters Gold coloured (aureus) Skin infections, TSS, found poisoning Staphylococcus saprophyticus causes UTI’s Staphylococcus epidermidis not disease causing, good but potential causes infection Streptococcus Streptococc us pyogenes Category Fermenters, aerotolerant anaerobes Aerotolerant Shape Bacillus Chains, no capsule, instead Mprotein Info Good probiotics, pregnancy, first contact of newborn is with lactobacillus ; protective Streptococc us mutans Streptococcus pneumoniae Capsule Diplococcus (breaks name rule), capsule Give them sucrose agar and they will thrive can grow in blood agar but no clear zone, instead green zone called alphahemolytic because it Downloaded by Kleina Mash (kleina_mash@yahoo.ca) Listeria Listeria monocytogen es Enterococc us Enterococcu s faecalis Enterococcu s faecium Facultative anaerobic Food organisms, psychrotrophs , facultative anaerobic Bacillus Coccus growth happens in monocytes, immune system cells Hardiest microbes known to man, survive in air, bedding, hands, nosocomial lOMoARcPSD|6765175 mechanism changes hemoglobin into methemoglobi n Spread Puberty; increase in vaginal region Causes Strep Throat, Tooth decay/ Pneumonia can cause dental caries scarlet fever after strep throat, Rheumatic fever, skin infections Keep sterile, Grows in pH changes blood agar, because of produces fermentation clear zone glycogen because from eating blood estrogen cells called betahemolysis Effects Mycoplasmatale s Category Shape Info Spread Causes Effects infection: got infection in hospital Food; cold cuts, premade salads, soft cheese Deadly meningitis Fecal matter, intestinal region Severe catheters infections, UTI’s, wounds Very dangerous for pregnant women, babies will die after birth, deadly to low immune system Mycoplasma pneumoniae Atypical? fried egg appearance lacks cell wall, no shape so we call them pleomorphic (vary in appearance), has plasma/cell membrane, has sterols in plasma membrane, need sterols in culture or cannot grow smallest genome, very flexible, can squeeze and can contaminate anything, ex. nutrient rich things in lab or hospital Lung infections treatment changes; cannot treat that kill cell wall ex. penicillin; needs to go deep into cell membrane called tetracycline B. Actinobacteria (high G+C) (3 different) Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Mycobacteriu m Sub-Category General Information Corynebacterium Propionibacterium T.B. and Leprosy Corynebacterium diphtheria Propionibacterium acnes Category Shape Aerobic Rods Anaerobic Bacillus Info Long term treatment (9 months long), acid fast stain, fastest methods, mycolic acid resistance to drying and desiccation, antiseptics, antibiotics nutrients enter cell very slowly, won’t see colonies for weeks, very slow, 4-6 weeks, long lag phase Facultative Anaerobic Bacillus, pleomorphic, picket fence (palisade) rods or Chinese letters Full of granules that emit light called meta-chromatic granules that store phosphorous Diphtheria (upper respiratory tract), DTP vaccine for this Acne Spread Causes Can be fermenters, Swiss cheese (flavour due to propionic acid Chapter 13: Viruses Parasite Virions: complete developed viral/infectious particle (IP/mm3) Has own genetic material/genome Contain DNA or RNA (try to fool us with RNA ex. HIV) Has viral protein coat (capsid) and enclosed by an envelope (some have spikes) Protein Coats Capsomeres of capsid can be arranged in different ways Coat is for protection, transmission, and attachment Can be used to recognize virus Envelope Made up of proteins, and phospholipid bilayer, and carbohydrates Extra layer of protection Spikes Made up of proteins and carbohydrates (GP: glycoproteins), (when this changes it is a new strain) Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Triangular spike: 500 per virion (per infectious particle), Hemagglutionation (HA spike) kills blood cells and penetrate the cell, but can be used to recognize the virus Bulb spike: 100 per virion, Neuraminidase spike (NA spike), separate cell from infected cell Ex. H1N1, H3N1, etc. = small mutations in spikes give for names, for each mutation made HIV – Human Immunodeficiency Virus Called retrovirus: has reverse transcriptase enzyme (virus RNA DNA) (SS) single stranded DNA and used in host cell, now uses enzyme again to recopy and create a (DS) double stranded DNA and becomes parasite in our cell (called provirus stage of infection) Has RNA, capsid, envelope, and spikes Uses 2 copies of RNA (one for backup) RNA is single stranded Also has enzyme reverse transcriptase GP41 and GP120 are well studied spikes HIV1 is most common in western hemisphere and Europe HIV2 is prevalent in west Africa (original virus) AIDS Not a disease but a syndrome Capability of producing new viral particles from provirus Latent stage of provirus means its hiding and once it emerges, cycle continues Converts T-helper cell into cancer cell (Kaposi’s sarcoma) Attacks CD4 cells/T-Helper cells Stages of Aids (created by CDC) Stage A T-helper/CD4 cell count has fallen (500/mm3) normal is 1000 or higher Body will react with swollen lymph nodes called lymphadenopathy Stage B T-helper/CD4 cell count is 200-499/mm3 Lymphadenopathy Persistent fever, diarrhea, possibly shingles (herpes virus #3), precancerous growth on female cervical region Hairy oral leukoplakia (Herpes #4) Fungal growth Stage C – Clinical AIDS T-helper/CD4 cells under 200/mm3 Fungus from oral into throat region and lungs Pneumonia, tuberculosis, Kaposi sarcoma, brain degeneration, confusion Effective Drugs Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Antiretroviral drugs because it attacks the retrovirus that does reverse transcription Reduction of viral load, reducing number of new virions On a cocktail of drugs to avoid immunity Zidovudine ® (AZT) Lamivudine ® (3-TC) Transmission Blood: 10-1000 virions (IP/mm3) Semen: 10 -50 IP/mL Cytopathic Effects: 1. Lytic/Acute Infection Ex. cold virus Causes lysis of cells, cannot live with dead cell so they move out 2. Persistent Infection Continues for months, years until death No death of cell Ex. measles, which can cause brain degeneration, eventually death 3. Latent Infection Hiding in cells, then emerge Ex. Human Herpes #3, hides and emerges causing shingles Herpes #1 and causes cold sores 4. Host Cell Becomes Cancer Cell Ex. Herpes #4, converts cells in jaw into tumour called Burkett’s lymphoma, and nasopharyngeal cancer Chapter 14: Principles of Disease Pathogenesis: manner of development of a disease Infection: the process of infecting or the state of being infected Disease: a disorder of structure of function Normal flora/Transient flora: bacteria found in our bodies/bacteria found on skin Opportunistic organisms: bacteria that takes advantage of certain opportunities to cause disease Etiology (Etiological agent): the cause, set of causes, or manner of causation of a disease or condition Symptoms: a physical or mental feature that is regarded as indicating a condition of disease Signs: any objective evidence of disease Communicable disease: an infectious disease transmissible by direct contact or by indirect means Non-communicable disease: disease that is not caused by infectious agents Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Frequency of Occurrence of disease Sporadic disease: occurring occasionally, singly, scattered instances Endemic disease: characteristic of a particular population, environment, or region Epidemic disease: rapid spread of infectious disease to a large number of people in a given population Pandemic disease: disease prevalent over a whole country or the world Severity or Duration of disease An acute disease: lasts a short time, comes on rapidly with distinct symptoms A chronic disease: lasts 3 months or more, cannot be cured A subacute disease: between acute and chronic A latent disease: present but not visible, remains inactive or hidden phase Extent of Host Involvement A local infection: disease that originates in and is confined to one organ system A systemic infection: affecting entire body A focal infection: bacteria localized in some region Fomite: objects that are likely to carry infection Nosocomial infection: hospital acquired infection Chapter 15: Mechanisms of Pathogenicity Understand spread and treatment Pathogenicity: ability to cause disease Virulence: the extent of pathogenicity Entry Points (3 main ones): 1. Mucous Membrane (most frequently invaded) a. Respiratory (easiest); ex. pneumonia, T.B, influenza b. Gastrointestinal Tract; ex. Salmonella, Hepatitis A, E. coli c. Genitourinary Tract; ex. STD’s, HIV, syphilis d. Conjunctiva; eye area, ex. Conjunctivitis, pink eye 2. Skin S. Aureus, fungal (athletes foot, nail infection) 3. Parenteral Route Punctured the skin and goes into the tissue Ex. Injection/immunization sites, insect bite, catheter, surgery, puncture wound (tetanus) Adherence Necessary to attach upon entry 1. Establishment of organism in our body 2. Invasion Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Pathogen and host must form a bond: Pathogen Host Adhesion/ligand Receptor Glycoprotein or Lipoprotein Complex sugar molecules Ex. Mannose, fucose Can be: capsules, on cell wall, fimbriae, flagella Always on plasma membrane 1. Streptococcus mutans (teeth) - attaches by capsule - invade using its own enzyme called glucosyltransferase - breaks down dietary sugar (sucrose) present on teeth, into glucose and fructose - enzyme glucosyltransferase breaks glucose into glucan/dextran, end resulting in plaque which can result in dental caries (tooth decay) - enzyme glucosyltransferase breaks fructose into organic acids and results in degeneration and loosening of tooth 2. E. coli - uses fimbriae to attach 3. Streptococcus pyogenes - M-protein is an acid and heat resistant molecule (no other strep uses m-protein) - uses to evade phagocytosis and found on top of cell wall on little fibrils 4. M. tuberculosis - attaches by mycolic acid Invasion Exoenzymes are secreted by bacteria 1. Coagulase - Coagulates blood - conversion of fibrinogen into fibrin threads (makes up clot) - ex. S. aureus, coagulase + - ex. few Streptococcus 2. Kinases - digests fibrin clot - ex. S. pyogenes, streptokinase bacteria (can be used to break clot) - ex. some Staphylococcus produce 3. Hyaluronidase - hydrolyzes hyaluronic acid (HA) breaks down - present in connective and muscle tissue - blackening of the overlying skin when acid is broken down - facilitates spread of infection Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 eating - ex. Clostridium perfringens (gangrene) and Streptococcus pyogenes (flesh disease) 4. Collagenase - hydrolyzes collagen (breaks down) - ex. Clostridium perfringens and some Streptococcus pyogenes Toxin: substances that contribute to pathogenicity Toxigenic: ability to produce a toxin Toxemia: presence of toxin in host’s blood Toxoid: inactivated toxin used in a vaccine Antitoxin: antibodies against a specific toxin Toxins Endotoxins (inside): Produced by only gram-negative bacterial cell walls (outer membrane) Lipid molecules Lipid A (L-part) from lipopolysaccharides (LPS) Lipid A causes fever (nausea, vomiting, diarrhea, dysentery) and more seriously septic shock (end of infection) Cannot neutralize them by antitoxins (body does not form antibodies) Pyrogenic response = Fever or shock Fever: starts when monocyte and enter gram-negative bacteria and ingests it. Lysosomes start to degrade the bacteria, Lipid A released and goes back into macrophage and triggers it to release Interleukin-1 (IL-1), it then travels through blood to hypothalamus and starts fever. Hypothalamus secretes prostaglandins which tell brain to reset body’s thermostat to a higher temp degree causing fever a. Chills Stage: abundance of IL-1 in blood, shivering (give blankets) b. Crisis Stage: IL-1 decreasing, sweating In general fever is a good thing – body’s way of fighting off bad bacteria Septic Shock: any life-threatening change in blood pressure, gramnegative, monocyte gets Lipid A and releases Cachein (Tumor Necrosis Factor; TNF), travels in blood to vital organs (G.I. Tract and kidneys), changes permeability of blood vessels in these organs and causes shock (nausea, vomiting, kidney failure, turning pale, breathing heavy) Shock is never good! Exotoxins (outside) (3 classes): Produced by few gram-negative but mostly gram-positive Protein molecules Produced as a part of metabolism (not on cell wall) Are always protein molecules Soluble in body fluids Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Always produce specific signs and symptoms (ex. Tetanospasmin) Can be neutralized, body produces Ig molecules, antitoxins Use: chemically changed called toxoids and can be used as vaccines (ex. DTP vaccine – Diphtheria & Tetanus are exotoxins) 1. Classic A&B exotoxins: - always have two polypeptide chains (A and B) - B used for entry, binds to host cell, brings A into cell, A cause damage cell, is the active part - ex. Diphtheriotoxin (high G + C group), B binds and A inhibits protein synthesis cell death, forms a pseudomembrane and could die of suffocation, blocks respiratory tract - ex. Tetanospasmin (low G + C), B binds and A becomes a neurotoxin, shuts down relaxation pathway in neuromuscular junction, inhibits the release of GABA and causes severe spasms/inability for pt to contract some muscles (lockjaw; early, then opisthosomas (end stage of tetanus); back spasms, could cause spinal fracture) death occurs if attacks cardiovascular or respiratory systems - ex. Botulinum, B binds and A comes in as a neurotoxin, inhibits release of acetylcholine in neuromuscular junction, no action potential or nerve movement, muscles freeze causing flaccid paralysis, C.V. or respiratory system paralysis will cause death - ex. Vibriotoxin, B binds to intestinal cells and A converts the cells into little pumps (second cyclic AMP system), pumping out water, causing watery diarrhea (rice water stools) 2. Membrane-disrupting: - disrupt plasma membrane, forms holes in membrane - ex. Hemolysis (Blood Agar – clear zone), disrupts rbcs - ex. Leucocidin disrupts white blood cells - ex. Erythrogenic toxin disrupts membrane of skin and blood vessels (red skin rash) called Scarlet fever, also S. pyogenes 3. Superantigens: - provoke an intense immune response - T-cells are released and secrete cytokines which circulate in the blood to various parts of the body (vital organs), especially the G.I. tract - results in nausea, vomiting, diarrhea, and later effect: super antigenic shock (may result in death) - ex. S. aureus = TSS in females (tampons, surgery, childbirth) and food poisoning Chapter 20: Antimicrobial Agents Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Spectrum: how many bacteria can they kill? Narrow spectrum = only kill one group (ex. gram – only), extended spectrum = could kill more (ex. gram – and +) Mechanisms of Action to kill the microbe: 1. Attack the Cell Wall a. Penicillin - destroys the peptidoglycan (PG), penicillin breaks peptido part of PG cell death recovery - nucleus is called the beta lactam ring (active part) - 50 species of penicillin - difference comes from side chain (R) - natural penicillin called PenG (O group differs from PenB, oral), needs injection, IV, gram-positive, (staph, streptococcus) - penicillinase can destroy beta lactam ring - semisynthetic is resist to penicillinase produced by gram-positive - methicillin MRSA strain (resistant) - oxacillin resistant - ampicillin can attack few gram-negative Adverse Effects Allergies b. Cephalosporin - cephalosporin attacks PG protein, destroys P part of PG cell falls apart cell death recovery - beta lactam ring - resistant to penicillinase, natural, but problem is lab purification makes it more expensive - semisynthetic forms created: no names, called by generation (1st, 2nd, 3rd, 4th) each generation gets a broader and broader spectrum Adverse Effects Use for meningitis, STD’s Mild abdominal discomfort Might cause a mild fever 2. Attack the Protein Synthesis a. Chloramphenicol - inhibits peptide bond formation - simple structure helps to penetrate tissues well and blood brain barrier (BBB) - natural, can synthesis molecule in lab - less expensive - can treat meningitis Adverse Effects - rare, but, fatal aplastic anemia (suppressing white and red blood cells) Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 - stops translation by attaching to 50S ribosomal unit preventing peptide bond formation - grey baby syndrome b. Erythromycin (Macrolides) - big ring structure (macrocyclic lactone ring) - safer to use, can prepared as flavoured syrup - binds to and attacks 50S subunit, preventing ribosome from moving along mRNA (translocation) causes incomplete protein - if someone is allergic to penicillin use this drug! - used for legionnaires disease, skin diseases Adverse Effectsc - mild GI tract discomfort, nausea, mild diarrhea c. Streptomycin - attach to 30S subunit and changes its shape, causing mRNA to be read incorrectly, unread or dismantled – always causes a misread protein - aminoglycoside sugar - used for T.B. but not anymore because of resistance Adverse Effects - very toxic to kidneys (can cause kidney failiure), and deafness (destroys auditory nerve) d. Tetracycline - can have pure or semisynthetic (semisynthetic better – more resistant, longer retention time in our bodies) - broadest spectrum of activity - attacks 30S subunit of ribosome, mRNA cannot be read, blocking docking site of tRNA (when blocked, none of the codons can be read, no protein can be made) - gram-positive and negative - drug of choice for mycoplasma (lack of cell wall) uses sterols - in animal feed Adverse Effects Has a lot of adverse effects Most dangerous Severe diarrhea, killing microbes in G.I. tract causing super infections from fungus Candida fungus Avoided in pregnancy (fetal abnormalities, deformed skull, cause brown teeth [tetracycline binds to Ca+], inhibition of bone growth) and liver and kidney dysfunction in mother, increased photosensitivity 3. Attack Nucleic Acid a. Rifamycin (Rifampin) - for T.B. - oral drug Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 - attacks RNA polymerase so inhibits RNA transcription Adverse Effect - in high doses can cause liver damage - reduce dose and give with other agents like streptomycin - absolutely avoided during pregnancy b. Quinolones and Fluoroquinolones - Q was first one discovered, FluroQ is superior one, all they did was add a fluro - Cipro ® - drug of choice for legionnaires disease & UTI’s - attacks/inhibits DNA gyrase (stop replication fork) Adverse Effects - Affects cartilage development bad for growing children and young adults to age 25, and elderly - Avoid during pregnancy 4. Attack Plasma (Cell) Membrane a. Polymyxin B - drug of choice for pseudomonas infections (blue/green pus) - only topical use (ointment) - breaks plasma membrane and phospholipid bilayer - cellular contents leak out causing cell death Adverse Effects can’t give in oral dose, it is toxic to kidneys (nephrotoxicity) 5. Inhibit Metabolisms a. Sulfa Drug (Sulfanilamide) - competitive inhibitors of enzymatic action of folic acid Adverse Effects - cannot give in pregnancy, especially 3rd trimester (mental retardation) - jaundice, anemia, and allergies b. Trimethoprim - competitive inhibitors of enzymatic action of folic acid (PABA eventually turns into folic acid, one enzyme attacks early on, the other attacks later) – commonly used for UTIs PABA - 1 attack - 2 attack Folic Acid Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Adverse Effects Less bad jaundice, mild anemia, and allergies Mechanism of Action of Antivirals generally, are nucleosides which become false nucleotides (base + sugar + synthetic phosphate) and shut down DNA/RNA replication and transcription reduce viral load on the exam: what is a nucleotide? It is a base plus sugar and phosphate what is a nucleoside? It is a base plus a sugar minus the phosphate examples of false nucleotides/nucleosides: Name: Analog: Acyclovir Guanine Ganciclovir Guanine Ribavirin Zidovudine (ZDV) Lamivudine Guanine Thymine Use: HSV-2 (Herpes Simple) HSV-3 (Chicken Pox) HSV -5 (Eye Infections) Hep C HIV Cytosine HIV and Hep B Chapter 21: Microbial Diseases of the Skin and Eyes Staphylococcus Skin Infections: (can use penicillin) Staphylococcus aureus 1. Direct invasion, attach to and infect hair follicle (folliculitis) Infection Symptoms Info Sty Folliculitis of an eyelash Furuncle Pus formation (red, swollen, pain, pus) Carbuncle Inflammation of tissue under the skin (pus, Surgical removal/drainage of pus systemic; various organs) and start use of antibiotics Impetigo (often Yellowish crusting pus sores of bacteria No exotoxin, is a pyoderma, may newborn) growth on epidermis, local inflammation enter lymph nodes Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Staphylococcus Scalded Skin Syndrome (SSSS): in children and elderly, skin starts to develop general redness (20-100% of skin and genitals), irritation, rash, NO pus, blisters that fill with clear fluid (48-72 hrs), blisters break and skin starts to peel off in scalded looking sheets, this leaves skin vulnerable to secondary infections like Strep, Pseudomonas, so isolate patient, antibiotics (penicillin) and clean fomites Why does SSSS happen? Exfoliative exotoxin (destroys skin cells by breaking up ester bonds), skin goes through massive desquamation Toxic Shock Syndrome: females with tampon use, after child birth, after surgery, symptoms are: fever, headaches, muscle aches, confusion, sunburn rash (could become SSSS), nausea, bloodshot eyes, vomiting, diarrhea, kidneys failure, shock, death (happens < 3% of the time) Why does this happen? 1. Super antigenic response due to TSS exotoxins (TSS Toxin-1 or TSST-2) 2. Absorbency of tampon has reached max, nutrient rich, breeding ground for exotoxins 3. material of tampon scrapes vaginal epithelium, depletion of Mg+ ion in vagina Preventative Measures: handwashing before and after, look at absorbency level & following - frequent changing of tampon, avoid wearing tampon at night (recommend pad), cautious of abrasion Streptococcal Skin Infections S. pyogenes 1. Direct Invasion M–proteins; Group A strep, beta hemolytic Impetigo (children): yellowish crusting pus sores of bacteria growth on epidermis, no exotoxin, is a pyoderma, inflammation, may enter lymph nodes Erysipelas: infection of the dermal regions (deeper), reddish patches, raised margins, can become full blown septicemia, treatable with penicillin and cephalosporin Necrotizing Fasciitis: enters through breaks in the skin, secretes collagenase, hyaluronidase, and Exotoxin A and can spread to several organs, 50% mortality rate from organ/system failures, amputation Pseudomonas Infections P. aeruginosa - gram-negative, pyocyanin (blue/green pus) Dermatitis: self-limiting (will go away by itself) skin rash, can be caused by water (pools, hot tub that hasn’t been cleaned), can last 2 weeks Otitis Externa: middle ear infection, bad if infects the eardrum, can be caused by water (natural waters) Opportunistic infections: blue/green pus. can enter hospital through flower vases, mop water Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 a. post burn victims, can lead to prolonged treatment/hospital stay and possible fatality b. Immunosuppressed, ex. cancer patients (radiation, chemo) c. Cystic Fibrosis infected lungs Viral Diseases of the Skin 1. Warts Disease Cause Warts Human Papillomaviruses (HPV) - 50 species (species 16/18, associated with cancers, especially cervical) Spread Interpersonal contact (hand contact), fomites (towel, clothing), sexual contact, moist areas, spread quickly 2. Human Herpes Simplex Virus (HHSV) Spread Reoccurrence Facts HHSV-1 Oral and Latent in Transfer between 1 and 2 (cold sores, respiratory trigeminal nerve can only happen between fever route (near eye) oral sex blisters) Spread HHSV-2 (genital sores) HHSV-3 (chicken pox) Varicella HHSV-3 (Shingles) Zoster Sexual contact Reoccurrenc e Latent in sacral nerve Spread Starting point is respiratory tract blood skin Extra Info Others forms; herpetic whitlow (finger), ocular infections (eye) Treatment Facts Extra Info Acyclovir (travels towards brain; encephalitis; 70% mortality) Transfer between 1 and 2 can only happen between oral sex Others forms; herpetic whitlow (finger), ocular infections (eye) Reoccurrence Latent in dorsal root ganglion (spinal nerve) and reappears as shingles Location Girdle area of body (abdomen ish area) Treatment Liquid nitrogen (cryotherapy), electrodessication, salicylic acid (24% [ ] min.), laser Facts Appear as a “crop”, dots on skin called macule papule vesicle (fluid) pustule (pus, full blown, scratching; causes secondary infections) crust (healing) scar Treatment Acyclovir to lessen viral load and symptoms Extra Info Immunization available, Incubation time of 14-21 days, called “exanthema” - start and end in different places Facts Not itchy, but painful and lasting weeks Downloaded by Kleina Mash (kleina_mash@yahoo.ca) Extra Info Vaccine for 50+ years old “Exanthema” – lOMoARcPSD|6765175 (girdle/belt) start & end in diff places 3. Measles Symptoms Rubeola (red) -Macular red rash -Normal cold/fever/flu symptoms (runny nose) -Koplik’s spots (oral lining with white dots) Spread Just appears all over body Can become middle ear infection, pneumonia Concern In pregnant women can cause low birth weight, still born, spontaneous miscarriage Vaccine MMR vaccine (combined) , no antivirals Brain encephalitis, and subacute sclerosing pan encephalitis (persistent brain infection) Rubella (german) Pink rash (3-day duration) Can cause babies to be born with severe mental defects, cataracts, deaf Microbial Diseases of the Eye 1. Conjunctivitis: Disease Conjunctivitis - Pink eye/Red eye Pathogen Bacteria and viruses (ex. Rubeola virus) Spread Unsanitary contact lens; especially pseudomonas Symptoms Inflammation of the eye, red, swollen, teary, highly sensitive, discomfort with pus (pus more common with bacteria than viruses) Treatmen Antibiotics for bacteria t 2. Trachoma: Disease Trachoma Pathogen Chlamydia trachomatis Symptoms Starts as conjunctivitis of eyelids (eyelids turn inward), abrading the cornea causing Trichiasis (abrasion) loss of eye sight resulting in blindness Info Leading cause of blindness Treatmen Tetracycline or erythromycin, penicillin t Chapter 22: Diseases of the Nervous System Downloaded by Kleina Mash (kleina_mash@yahoo.ca) MMR vaccine (combined) , no antivirals lOMoARcPSD|6765175 A. Caused by Bacteria Bacterial Meningitis: inflammation of the meninges, with accumulation of WBC’s causing swelling Symptoms: Initial severe headache, nausea, violent vomiting stiff neck* (neck for adults, Kernig’s sign stiffness of hamstring for children), convulsions (coma), possible death in 24 hours rapid diagnosis Diagnosis: lumbar puncture CSF simple gram stain quick treatment plan serology test IG molecules prepared (antibodies) culture CSF Treatment: third generation of cephalosporin’s (safe drug) 3 Main Causes: a. Hemophilus influenza: - 6 months to 4 years old - 6 strains A-F (most common is B, 95% of cases) - prevention Hib Vaccine b. Neisseria meningitidis: - up to age 5 and young adults, prisoners (close together) - 5 strains A, B, C. W135, Y (C most common) - throbbing headache with sore throat - spread into blood tissue destruction - petechiae bluish spots of dead tissue amputation, paralysis or deafness c. Streptococcus pneumoniae - up to age 5 (30%) and elderly (80%) - 82 strains (serology used) - Entry Points: sinusitis, otitis media, head/neck surgery or trauma d. Listeria monocytogenes - Listeriosis - spread by food - immunosuppressed (cancer) - older males who smoke and drink are more prone - pregnant women and transferred to fetus - very ill baby (60-65% death in first year) - stillborn - miscarriage e. Escherichia coli - birth canal Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Tetanus: Clostridium tetani A and B exotoxin Spasms, starts with general restlessness, irritability Stiff neck, lockjaw, and back spasms (opisthotonus) CV/respiratory death Inhibits GABA Endospores grows in deep wounds Botulism: Clostridium botulinum Strains A, B, E. F will affect humans (A worst) lethal form of food poisoning 12-36 hours to develop A and B exotoxins Causes flaccid paralysis Inhibits acetylcholine Canned food (except tomatoes because they are so acidic) Starts with dry mouth, abdominal discomfort, diarrhea (constipation in children), blurred vision*, CV/respiratory system death B: Caused by Viruses Poliomyelitis: infantile paralysis (1%) Fecal-oral route (H2O/food) India has worked nationwide and irradiated polio in 2012 (vaccination) Initial symptoms are sore throat and nausea enter lymph nodes and blood stream Viremia (virus in blood) a. Transient Form: immune system beats it, no clinical symptoms and gets better b. Persistent Form: immune system weak and virus moves in CNS and attacks motor neurons (kills them) paralysis 2 vaccines available (1954: Jonas Salk and 1963: Albert Sabin) Salk killed virus and made IPV (inactivated polio vaccine) form of vaccine safe to take but have to take boosters Sabin weakened the virus and made OPV (oral polio vaccine) form of vaccine less expensive, easy to administer, one dose (1 in a million may actually develop it) Chapter 23: Microbial Diseases of the Cardiovascular Systems 1. Caused by Bacteria a. Septicemia: “blood poisoning” can become Sepsis Septic shock Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 33% (1/3) cases in hospital (nosocomial; S. pyogenes, Staph., Pseudomonas) wound, uti, e-coli, Symptoms: fever, chills, laboured breathing, anxiety, Lymphangitis* (inflamed lymph vessel through arm or leg) Puerperal Sepsis: Childbirth fever from S. pyogenes Progress from uterine tissue to abdominal region Becomes sepsis b. Rheumatic Fever: inflammation of heart valves c. Anthrax: Bacillus anthracis Robert Koch (disease of animals, G.I. form), burned carcasses G.I. Form: from undercooked food, nausea, hemorrhages in G.I. tract, septicemia (50% death) Cutaneous Form: enters though minor cuts, causes crust lesions called Eschar septicemia (20% death) Sept. 2001 Erin O’Connor Pulmonary Form: inhaled endospores germination chest pain, breathing difficulty, septicemia (100% death), survivors become disabled Ciprofloxacin, penicillin, and erythromycin Vaccine has 6 doses over 18 months Produces 3 Exotoxins a. Protective toxin: binds, entry and phagocytic death b. Lethal toxin: binds, entry and phagocytic death c. Edema toxin: cause swelling d. Gangrene: necrotic tissue from cut off blood supply Clostridium perfringens Endospore germination, deep cleaning can reduce spores Abrupt pain, swelling, ooze blood tainted fluid from ruptured vessels, blackening of tissue Swelling from gas production H+ and CO2, snap, crackle, pop noises and foul odour X-Toxin attacks blood vessels, RBC and WBC, lecithin of cell membrane e. Spotted Fever: Ricksetti ricksetti Make its way to heart – destroy valves Only one that occurs on white parts of our bodies (soles of feet, hands) Cause fever, rash (on white parts) 2. Caused by Viruses Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 a. Burkitt’s Lymphoma: HHSV-4 or Epstein-Barr Virus (couldn’t find cause of virus) Fast growing tumor of jaw Not latent in Herpes virus Latent in B. lymphocytes Productive infection not latent Non-productive infection latent Infectious Mononucleosis: spread through saliva, B. lymphocytes nonproductive, starts with fever, sore throat, pus, EB in saliva for 18 months, 1.8 million college students, extreme fatigue Nasopharyngeal Carcinoma: cancer of nose and throat, B. lymphocytes Chronic Fatigue Syndrome: yuppie flu, extreme muscle fatigue, memory loss, swollen lymph nodes, rare death in ruptured spleen 3. Caused by Protozoa Malaria: plasmodium vivax 2 hosts (definitive; mosquito and intermediate; human) Causes fever, vomiting (?), severe headaches, pain in muscles Fever Phase: (paroxysm; cycle) cold phase, hot phase, wet phase (drenched) Life Cycle: Mosquito bite Sporozoite form through CV system to liver releases mature asexual merozoite in blood attacks RBC’s form ring stage will produce more merozoites cycle continues RBC’s dies and releases merozoites merozoites can become male/female gametes which cannot mature (won’t spread at this point) mosquito meal zygote formation and new sporozoites Severe anemia, enlarged spleen and liver Quinine drug as effective drug Chapter 24: Microbial Diseases of the Respiratory Tract Bacterial Diseases 1. Upper Respiratory Tract a. Streptococcal pharyngitis (Strep Throat): red, swollen, painful, yellow discharge (not in any virus) - possible otitis media - no fever unless leave untreated develop Scarlet Fever - streptococcus pyogenes - m protein - contagious - penicillin or erythromycin Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 b. Scarlet Fever: fever, red skin rash, deep red colored tongue, cheeks on children are deep red - produce family of exotoxins (streptococcal pyrogenic exotoxin – SPE or Erythrogenic exotoxin) - changes permeability of RBC’s membranes - contagious - penicillin or erythromycin c. Otitis media: middle ear infection - can occur from nasopharyngeal infection (nose and throat), strep throat, cold, contaminated water (pool) - streptococcus pneumoniae (35%) - extreme pain, may lead to vomited, pain due to pus formation d. Diphtheria: membrane on tonsils - diphtheria exotoxin produced, A and B exotoxin stop protein synthesis - kills cells of upper respiratory tract, pseudo membrane forms (whitish/gray) - mild fever, dramatic swelling of neck, fatigue, mild sore throat, oozing fluid and thickens forming false membrane blocking throat causing suffocation death or quick tracheostomy - antibiotics at beginning, later has to be scraped or surgically removed - prevented by DTaP vaccine Cutaneous Diphtheria: infected skin wound leading to slow-healing ulcer 2. Lower Respiratory Tract a. Pertussis: whooping cough - capsule attaches to tracheal cells - exotoxin called tracheal cytotoxin and releases endotoxin releases nitrous oxide death of ciliated tracheal cells (kills immune response) mucous accumulation extreme coughing - can result in broken ribs, bloodshot eyes, brain hemorrhages may later on lead to seizures - DTaP vaccine Stage 1: Catarrhal Stage - common cold Stage 2: Paroxysmal Stage – violent coughing sieges Stage 3: Convalescence Stage – get better, very long stage b. Tuberculosis: - mycobacterium 1. Healthy Individuals infection arrested by macrophages, immune system on high infection is present but, no symptoms 2. Partial Failure macrophages didn’t arrest infection forms a tubercle becomes calcified called GHON complex Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 3. Total Failure tubercle ruptures miliary T.B. throughout lungs - coughing blood, extreme weight loss, loss of vigour and fatigue - prolonged treatment with multiple antibiotics - Isoniazid: blocks mycolic acid formation (liver toxicity) - Ethambutol: blocks from going into cell wall (weak) - Rifampin, Pyrazinamide, Streptomycin - BCG vaccine - Mantoux Test: purified version, injected in forearm, can form red swelling if there is ongoing infection Bacterial Pneumonias Inflammation of the lungs, alveoli fill with fluid 1/3 cases are nosocomial 2 Types a. Typical: Streptococcus pneumoniae (capsule – 82 or more strains) - susceptible to COPD patients, diabetes, kidney disease, alcohol consumption, asthma - symptoms: HIGH fever*, breathing difficulty, chest pain, rust colored sputum - can invade bloodstream (septicemia), pleural cavity, and meninges b. Atypical: any other cause then streptococcus (virus, bacteria, fungal, protozoa) - slower onset, less fever and chest pain A. H. influenza pneumonia: Bacteria - slow onset, can grow in chocolate agar (blood) - susceptible to alcohol consumption B. Mycoplasma pneumoniae: Bacteria - walking pneumonia - gram-stain, grow to see its completely different than others - college students susceptible - mild disease - can develop otitis media (15%), and extreme fatigue C. Legionella pneumophila: Bacteria - Pontiac fever (mild form), slow onset - Legionnaires disease (fatal form), CNS, G.I. tract, kidneys, liver - can give erythromycin, and rifampin D. Q-Fever: Bacteria - Coxiella burnetti, endospore - slow onset Viral Atypical Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 E. RSV: Virus (respiratory syncytial virus) - Syncytial form giant cells in bronchioles, impedes air flow (wheezing) give oxygen - very young (1-3) and elderly - contagious - Houdini virus, hides from immune system, and grows in lungs F. Viral Influenza: Virus - flu - chills, fever, headache, muscle aches (no intestinal symptoms) * - Antigenic Drift: N and H spikes mutate slightly each year (annual breakouts of flu) - Antigenic Shift: complete genetic change of N and H spikes Chapter 25: Microbial Diseases of the Digestive System Bacterial Diseases of the Mouth: 1. Dental Caries: tooth decay, streptococcus mutans - attaches to tooth by capsule, causing plaque formation - roughness on tooth, yellowish discoloring, sensitive, tooth may break into pieces 2. Periodontal Disease a. Gingivitis: if dental caries is not maintained - plaque between gum tissues, bleeding gums - S. mutans, gram-negative bacteriodetes and fusobacterium b. Periodontitis: if gingivitis is not maintained - pockets in gums, gums receding, pus formation - porphyromonas gingivitis are bacteriodetes in gums (produce exotoxin and releases endotoxins), degeneration of tooth structures - loosens tooth loss of tooth - root canals Bacterial Diseases of the Digestive System: Infection: bacteria through food or water, grow in stomach (incubation period) Intoxication: already growing in food, so instead you get the toxins Gastroenteritis: can affect stomach, intestine, and causes inflammation Oral Rehydration Therapy (ORT): first step in treatment, cleans G.I. tract, after antibiotics General Symptoms: nausea, vomiting, diarrhea, dysentery (intestinal infection) constipation and fever? (in some) Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 1. Staphylococcal Food Poisoning: Food Disease Food Poisoning Pathogen Staphylococcus aureus Spread Chicken, ham, creamy foods Symptoms Nausea, vomiting, diarrhea Intoxicatio Intoxication, super antigenic n Diagnosis Abrupt, violent, immediately after eating the toxin contaminated food (1-6 hrs) Treatment ORT, possible antibiotics 2. Shigellosis: Infection Toxin Disease Shigellosis Pathogen Shigella dysenteriae Info Incubation period of 12-36 hrs, small intestine and moves to large Symptoms Severe bowel movements, dysentery, dehydration, slight fever Intoxicatio Infection of Shiga exotoxin inhibits protein synthesis in large n intestinal cells and destroying them completely (leaves scar) Diagnosis Isolation of bacteria Treatment ORT, quinolones 3. Salmonellosis: Food Sources Disease Salmonellosis Pathogen Salmonella enterica Spread Food sources; beef, poultry, spinach, cantaloupe, raw eggs Symptoms Nausea and diarrhea Intoxicatio Infection of endotoxin n Diagnosis Isolation of bacteria; serotyping Treatment ORT 4. Cholera Disease Pathogen Info Symptoms Intoxicatio n Treatment Cholera Vibrio cholerae Lose 12-20L of fluid per day very dehydrated Diarrhea, dehydration, shock, kidney failure, collapse, loss of body weight (50%) A and B toxin turns intestinal cells into little pumps rice water stools ORT (water only) and then antibiotics (tetracycline) Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 5. Helicobacter pylori: Peptic Ulcer Disease Disease Peptic Ulcer Disease (Small Intestines) Pathogen Helicobacter pylori Info Flagella, produce exotoxin, attach to stomach region, phagocytosis, and produce enzyme urease Symptoms Ulcer, pain, belching (constant) Intoxicatio Infection of exotoxin; inhibits acid production in stomach, enzyme n urease; converts proteins in stomach to urea ammonia alkaline pH* Diagnosis Urea breath analysis (radioactive urea), bacterial culture (95% of cases) Treatment Antimicrobial drugs; metronidazole 6. Clostridium difficile: Colitis Disease Colitis Pathogen Clostridium difficile Spread Endospore*, can occur with continued use of antibiotics stop all antibiotics reassess and start with new kind Symptoms Severe diarrhea (life threatening), abdominal pain Intoxicatio A and B exotoxin causing pseudomembranous colitis (membrane n of colon starts to fall off) Info Kills all normal organisms in stomach and intestines, elderly (mortality high) and young children susceptible Treatment ORT, metronidazole 7. Escherichia coli Form Entero-toxigenic (ETEC) Entero-aggregative (EAEC) Entero-invasive (EIEC) Entero-pathogenic (EPEC) Entero-hemorrhagic (EHEC) Symptoms Travellers’ diarrhea (severe) Diarrhea Severe invasion, dysentery (shigellosis) Severe chronic diarrhea Severe stomach problems Info Attaches to small intestine (65% of cases) Newer form (35% 0f cases), forms brick like arrangement, treat with ORT Attaches to large intestine Common in newborns Source is beef, RBC and kidney hemorrhages causing Hemolytic Uremic Syndrome (HUS) Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Viral Diseases of the Digestive System 1. Mumps: Disease Mumps; to mumble Enters Respiratory route and settles in salivary glands Incubatio 2-3 weeks n Info Very contagious, can spread into blood and can discharge through urine or fecal matter (good for diagnosis) Symptoms Swelling of parotid glands (salivary), inability to chew or talk, mild fever, anorexia, headaches, can go into CNS/brain and cause meningitis or deafness Other Males: enlargement/inflammation of penis (orchitis) Females: pelvic pain, ovaries enlarged Diagnosis Urine and fecal samples Treatment MMR vaccine for prevention (mumps, measles, rubella) 2. Hepatitis: Inflammation of Liver Disease Transmissio Chronic Vaccine n ? Hep A: Infectious Fecal-oral No Inactivated virus Form Hep B: Serum Form Parenteral, Yes Recombinant (Blood) STI, drug use (genetically engineered yeast), Lamivudine or 3-TC Hep C (Non-A-B) Parenteral, Yes None, Ribavirin + transfusion Interferon Hep D (Defective) Parenteral, Yes HBV Vaccine coinfection with Hep B Hep E Fecal-oral No HAV Vaccine Facts Causes jaundice, no deaths 85% cases recover from acute, 15% Dane Particle doesn’t leave 80-85% cases are chronic, 15% liver disease Defective because its missing capsule High mortality rate in pregnant women (20%) 3. Cytomegalovirus Infections: CMV Disease Cytomegalovirus Infections: CMV Pathogen HHSV-5 (Human Herpes) Spread Saliva, semen, vaginal secretion’s (G.I. Tract and STI), congenital transfer: babies have severe mental defects Symptoms Lymph nodes become enlarged 2-3x and called Owl’s Eyes Reoccurrenc Latent in T-cells (cardiovascular system) e Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 Treatment Info Ganciclovir (reduce viral load) Chronic retinitis (ex. in HIV Chapter 26: Microbial Diseases of the Urinary and Reproductive Systems Bacterial Diseases of the Urinary System: 1. Cystitis: inflammation of the bladder (UTI) - common in females (10-25%), because of shorter urethra, 33% Honey Moon cystitis, contraceptives - symptoms: dysuria (dysfunctional urination), pyuria (pus and WBC’s in urine) - 75% is E. coli, 25% is S. saprophyticus - treatment: trimethoprim-sulfamethoxazole or quinolones - if not treated, develops into pyelonephritis 2. Pyelonephritis: inflammation of one or both kidneys - severe pelvic pain, fever, chills, nausea, tenderness in back, sweating, scarring of tissue, kidney failure treatment: cephalosporin Bacterial Diseases of the Reproductive System 1. Gonorrhea: - Neisseria gonorrhea - 90% chance - capsule and fimbriae - painful urination, irritation - males: external, “the drip” pus discharge, can go into testes (sterility), Proctitis (anal gonorrhea) - female: internal, burning sensation, can become PID Oral Form: oral sex, pus Congenital Form: through birth canal, severe eye infection in newborn 2. Pelvic Inflammatory Disease (PID) - affect ovaries - ectopic pregnancy (tube) - sterility 3. Nongonococcal Urethritis (NGU) - Chlamydia trachomatis - inflammation of urethra - can have all 3 diseases above at the same time - also develop into PID 4. Syphilis - Treponema pallidum (spirochetes) 4 Stages 1. Primary Downloaded by Kleina Mash (kleina_mash@yahoo.ca) lOMoARcPSD|6765175 stops this - males: lesion (chancre) with discharge with bacteria - females: on cervix - spread: CV/lymph to rest of body, very contagious this stage 2. Secondary - skin rash, weakness, hair loss, lesions everywhere in body (oral, vaginal, etc.) - non-sexual transmission 3. Latent - 1-10 yrs. - dangers: congenital transmission (severe neurological damage) 4. Tertiary - re-emerges - “Gumma’s” are severe lesions, mass of tissues become deformed (can be oral, cardiovascular or external) modern antibiotics stage - treat with Benzathine Penicillin Viral Diseases 1. Genital Warts 2. Genital Herpes 3. AIDS Downloaded by Kleina Mash (kleina_mash@yahoo.ca)
