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MIC 401 Exam 2

by: Christinee

MIC 401 Exam 2 MIC 401

GPA 3.4

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Lecture notes for exam 2
Biomedical Microbiology
Dr. Amy Jacobs
MIC401, Mic 401, Biomedical microbiology, Christian Ahearn, Amanda Bloom, Terry Connell, Darlene Dombroski, Vicki Evancho, Amy Jacobs, Nicole Luke-Marshall, Khan Umaer
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This 25 page Bundle was uploaded by Christinee on Thursday March 3, 2016. The Bundle belongs to MIC 401 at University at Buffalo taught by Dr. Amy Jacobs in Spring 2016. Since its upload, it has received 210 views. For similar materials see Biomedical Microbiology in Microbiology at University at Buffalo.

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Date Created: 03/03/16
LECTURE 1 – STAPH Staphylococcus Family: Micrococcaceae Genus: Staphylococcus – cluster of grapes arrangement Species: Staphylococcus aureus – true pathogen of the genus – responsible for 90% of diseases caused by genus staph Staphylococcus epidermidis - part of normal flora – OPPORTUNISTIC/NOSOCOMIAL Staphylococcus saprophyticus – part of normal flora – OPPORTUNISTIC/NOSOCOMIAL *nosocomial – hospital infections Microscopic Morphological Appearance Gram positive cocci arrangement – irregular clusters (log phase of growth) non-spore formers non-motile usually no capsule – STAPH AUREUS HAS CAPSULE Virulence Factors I. Extracellular Products A. Protein toxins – produced by bacteria when they grow Hemolysin – lyses red blood cells by disrupting cell membrane (STAPH AUREUS:classified as hemolytic vs. non hemolytic) Leukocidin – lyses white blood cells by disrupting cell membrane – incapacitate host defense Enterotoxin – food poisoning – entero: gut; gut associated toxin Toxic Shock Syndrome (TSST-1) – stimulates production of interleukin (IL-1) by macrophages resulting in fever induction – FEVER SPIKE B. Enzymes – produced by bacteria during growth Coagulase – plasma clotting protein; converts fibrinogen to fibrin****** a. coats bacteria with fibrin and prevents phagocytosis b. aids in attachment **fibrinogen – coagulase – fibrin; forms a fibrin clot that actually coats exterior surface of the bacteria, making it sticky - ATTACHMENT/ANTIPHAGOCYTIC Fibrinolysin – digests fibrinogen (fibrin clots) Hyaluronidase (“spreading factor”) – digests hyaluronic acid around host cells promotes invasion; break apart cement surrounding bricks and allow infection to spread from its focal point Lipase – degrades lipids – allows bacteria to colonize oily skin Penicillinase – hydrolyzes penicillin (beta lactam ring); drug resistance Catalase – degrades H O –2a2toxic aerobic metabolic end product Exfoliatin or epidermolytic toxin – protease that causes peeling of superficial skin layers by dissolving intracellular bridges II. Structural Surface Component Protein A – surface component linked to peptidoglycan layer of cell wall; inhibits antibody-mediated clearance of bacteria by binding to IgG. *only associated with staph aureus; decreases antibody immunity – does this by non competitive binding interactions with IgG Lipoteichoic acid – binds to tissue components; CELL ADHESION – acidic polysaccharide found in gram positive cell wall Staphylococcus aureus – major pathogen of genus – MOST RESISTANT BACTERIA OF ALL NON SPORE FORMERS Carriage location – anterior nares, nasopharynx and skin (normal flora) Carriage rate – 30 to 50% of healthy adults Virulence Factors/Species Identification of Staphylococcus aureus coagulase positive – fibrin clot – attachment/phagocytic hemolysin (alpha toxin) leukocidin protein A capsule Toxins of Staphylococcus aureus I. Blood cell toxins hemolysins leukocidin II. Intestinal toxins enterotoxins III. Epithelial toxins exfoliatin or epidermolytic toxin Infectious Diseases caused by Staphylococcus aureus I. Superficial infections – localized cutaneous infections II. Toxigenic infections A. Staphylococcal Scalded Skin Syndrome (SSSS) B. Toxic Shock Syndrome (TSS) C. Gastrointestinal Disease – extracellular toxin III. Systemic Infections Localized infection Bacteria enter blood stream (bacteremia)/lymphatic system  infect other organs systemic or multi system disease Bacteremia: bacteria in blood stream and actively dividing Localized: primary infection one focal point Systemic: enters blood stream or lymphatic system – any organ can be infected I. Superficial Cutaneous Infections (minor infections) Pyodermic infections – pimples, boils, carbuncles and impetigo Characteristic symptom – pus formation – Staphylococcus – pyogenic cocci ** Both genus staph and streptococci (gram +) – pyogenic cocci: pus producers ** Staph aureus - PIMPLE Mode of infection  Staphylococci invade skin at: a. sebaceous gland opening (skin gland) b. hair follicle c. wound  Infection site – abscess (bacteria, plasma, WBC’s)  Primary infection sites – face, back of neck, buttocks Symptoms – edema, erythema, pain, pus Risk groups – elderly and young children with poor personal hygiene  **As bacteria grow fibrin clot formation (exterior surface of bacteria; inflammatory barrier) pus formed  boils, carbuncles, impetigo (superficial cutaneous infections caused by staph aureus)  Boil: edema, raised, pus at the center  Carbuncles: skin eroding from infection site itself (diabetics have trouble with healing)  Impetigo: primarily a disease of children, on face area – boil that itches and fluid comes out and dries to a yellow crusty appearance Treatment – minor lesions self resolve surgical incision and drainage chemotherapy – topical antibiotics – not oral – it has barrier, oral antibiotic can’t get through that barrier to kill the bacteria* II. Toxigenic Infections (production of toxin as end product) A. Staphylococcal Scalded Skin Syndrome (SSSS) Virulent feature: exfolatin or epidermolytic toxin separates epidermal layer from the dermis blistering and peeling of the skin exposes red under layer general appearance – burned skin *warm to the touch and elevated to an extent; large sheets of exposed skin *redness due to local inflammatory reaction Mode of infection  syndrome begins as an erythema around the mouth and nose  spreads rapidly to infect skin of the neck, trunk and extremities Risk group – infants and young children < 4 years (neonatal infection) Primary infected sites – umbilical cord and eyes – low mortality rate Death – secondary infection of the denuded skin by other bacterial pathogens Treatment – topical antibiotic – mupirocin B. Toxic Shock Syndrome (TSS) Incidence of Infection – usage of super absorbent vaginal tampons Virulent feature – toxic shock syndrome toxin -1 (TSST-1) Mode of infection  super absorbent brands strongly bind Mg ++ ions  low concentration of Mg++ triggers TSST-1 production which is absorbed into the bloodstream  TSST-1 (superantigen) that stimulates T-lymphocytes to produce cytokines intravascularly resulting in endothelial cell damage – shock and multisystem organ failure  Ultra absorbent tampons bind to Mg++  [low Mg] = triggers growth of staph aureus  TSST-1 Toxin  stimulate T lymphocytes  cytokines  endothelial cell damange  All based on concentration of Mg at the site Initial symptoms - high fever, vomiting, diarrhea and muscle cramps (myalgia) Ten days later – hands and soles of feet develop a sunburn-like rash which results in a peeling of the skin, strawberry tongue, sunburn like rash Severe symptoms – shock and multi-organ failure Death – 2 – 5% respiratory failure High risk group/high risk factor menstruating women – usage high absorbancy tampons non-menstruating groups – postpartum women with surgical wound infections (hysterectomies) nasal surgery and packing Prevention/Control - removal of cellulose based superabsorbent tampons from market in 1980 CDC recommends that tampons are not used continuously during a menstrual cycle Treatment – fluid replacement and chemotherapy C. Toxigenic Gastrointestinal Disease – Food poisoning (food intoxication) Ingest toxin* Source contamination – food handler Staphylococcal lesions of skin (hands and nasopharyngeal carriers) contaminate food food unrefrigerated room temperature growth of Staphylococcus aureus production of enterotoxin (exotoxin) -> disrupts GI Virulent feature – enterotoxin (exotoxin) heat stable - not inactivated by digestive enzymes - toxin production does not alter food taste or smell Action of enterotoxin - disrupts gastrointestinal lining Symptoms – start in 4 – 6 hours – vomiting, cramps, diarrhea, nausea Recovery – self-limited – 24 – 48 hours III. Systemic Infection/deeper infection Bacteremia – dangerous because the microbes are carried to all body sites Bacteria reach site via: (somehow the bacteria is displaced)  focus of infection  extensive surgery  traumatic injuries Systemic infections osteomyelitis (inflammation of bone) pneumonia (lung) endocarditis (inflammation of endocardium) meningitis (inflammation of the membrane surrounding the brain and spinal column), and pyoarthritis (infection of joints) Risk factor involved in acquiring a systemic infection Pre-condition in an individual: diabetes, burn wounds, extensive surgery, cystic fibrosis, cirrhosis of liver or those immunosuppressed or immunodefective in phagocytic properties Treatment prolonged combination antibiotic therapy ************************************************************************************* Coagulase Negative Staphylococcus Staphylococcus epidermidis Staphylococcus saprophyticus Staphylococcus epidermidis – normal flora - common inhabitant – human skin, respiratory tract and mucous membrane Route of infection Infections related to surgical procedures that involve the insertion of foreign bodies – artificial heart valves, catheters, prosthetic hips and atrioventricular shunts *IATROGENIC INFECTIONS: caused by physicians Opportunistic Infection Mode of infection  attachment of bacteria to foreign body  multiplication/colonization Staphylococcus epidermidis infections include: endocarditis, urinary tract infections and wound infections Staphylococcus saprophyticus – normal flora Common inhabitant – lower intestinal tract and vagina Primary infection – urinary tract infections (UTI), dysuria (pain during urination), pyuria (pus in urine) and high numbers of the bacteria in the urine Differentiate Coagulase Negative Staphylococcus Staphylococcus epidermidis vs. Staphylococcus saprophyticus Bacterial sensitivity or resistance to the antibiotic novobiocin Staphylococcus epidermidis – sensitive Staphylococcus saphrophyticus – resistant Prevention of Staphylococcal Infections - No vaccine is available 1. Minimize opportunity for infection  hygiene (hand washing)  adequate cleansing of wounds; change bandages frequently  attention to indwelling devices (catheters and needles)  treat surfaces with disinfectants Laboratory Diagnosis 1. clinical presentation of the patient 2. isolation and demonstration of the bacterium from clinical specimens (skin scrapings, blood, pus) a. Gram stain b. inoculation of media Blood agar – enriched medium a. hemolytic pattern b. colony color Mannitol salt agar - selective medium – additive 7.5% NaCl - differential medium – fermentation of mannitol; monitor Δ pH 3. Biochemical tests catalase test, coagulase test ********************************************************************************* *** Nosocomial Infections (Hospital acquired) l. neonates 2. surgical patients Secondary transmission from “carriers” in hospital Carrier rate (Staphylococcus aureus) hospital personnel 70 – 80% general population 30% *Emerging superbug MRSA – Methicillin resistant Staphylococcus aureus or multiple resistant I. MRSA A. HA-MRSA – health care associated (hospitals, nursing homes and dialysis center) Increased risk factors  older adults  weakened immune system  burns, surgical wounds  hospital stays of 10 days  invasive devices – dialysis (catherterized) or feeding tubes  living in a long-term facility  recent antibiotic use B. CA-MRSA – community associated Increased risk factors daycare settings NFL/NBA players/wrestlers dorm residents prisons military training camps gay men These settings have 5 C’s that make it easier for MRSA to spread crowding frequent skin-to-skin contact compromised skin contaminated items lack of cleanliness LECTURE 3 – CLOSTRIDIUM CLOSTRIDIUM   Genus:Clostridium (natural habitat – soil, skin, GI tract animals/humans)   Species: Clostridium perfringens – causative agent of gas gangrene and food poisoning   Clostridium difficile –  antibiotic associated co    s Clostridium tetani ­ tetanus   Clostridium botulinum – food borne botulism   **Non invasive genus – don’t have a specific virulent factor with them; just a variety of toxins and enzymes produced when the bacteria grows ** these infections of this genus are not communicable – unable to be transferred from one person to another **SPORES are the route of entry – can enter through the skin, ingested, germinate (toxin ingested) Microscopic Morphological Appearance Gram positive bacilli Spore formers Most are obligate anaerobes Most are motile Growth Conditions Thioglycollate broth – anaerobic growth (butt of the tube – 0% oxygen) Litmus milk – stormy fermentation – reaction noted in the tube of the curd formation and the amount of gas produced “cottage cheese” Blood agar – double zone of hemolysis (perfringens) Egg yolk agar – β­lecithinase – (α­toxin) (perfringens) – white opaque zone Pathogenic Clostridia   I. Histotoxic Clostridia (tissue infections or infections of muscle) C. perfringens II. Enterotoxigenic Clostridia (food poisoning or more severe disorders) C. perfringens          C. difficile III. Clostridium tetani (tetanus) IV. Clostridium botulinum (food poisoning)’ *NOTE: C. PERFRINGENS: both histotoxic and enterotoxigenic I. Histotoxic Clostridia ­ (gas gangrene)           Causative agent ­ C. perfringens  type A * Most of the time found in soil – high association with car crashes, motorcyclists    Opportunistic pathogens that require a special environment to initiate growth 1.  traumatized tissue – crush wound  2.  vascular damage – impaired blood supply 3.  necrotic tissue – poor aeration  4.  decreased oxygen – spores in this area, they favor low decrease in oxygen * Produces a large variety of exotoxins and enzymes C. perfringens produces a large number of exotoxins and extracellular enzymes such as: 1. collagenase – break down muscle and tissue components 2. proteinase 3. deoxyribonuclease 4. ­toxin­(phospholipase C) – lecithinase ** MOST PATHOGENIC, actually disrupts the membranes of the host cells 5. ­toxin­ hemolysin Clostridial wound infections   A. Anaerobic myonecrosis (gas gangrene) **MOST SEVERE, focal infection at necrotic site but can spread to healthy tissue B. Anaerobic cellulitis *MINOR, infection of necrotic tissue only A.  Anaerobic myonecrosis   Ever widening expansion of necrotic lesion to adjacent healthy muscle tissues. Symptoms   1. local edema/swelling (attributable to the alpha toxin) 2. gas production ­ H  2nd CO  (2ue to fermentation of necrotic tissue) 3. change of skin color to black (due to vascular damage, decrease oxygen supply) 4. generalized fever 5. pain in infected tissue Risk Group Factors   1. traumatic injuries (car injuries, wars) 2. surgical procedures in close proximity to intestinal microflora ­ bowel surgery, abortions (perfringens – part of normal flora in intestine) 3. elderly (impaired vascular flow) Convalescence/Immunity   NO host defense Phagocytic cells useless – due to vascular damage Repeated infections do not produce immunity Treatment   1. removal of dead tissue (debridement) 2. application of antiserum (polyvalent antitoxin) 3. broad spectrum antibiotic ­ penicillin or tetracycline 4. hyperbaric O  2hamber A. Anaerobic Cellulitis   Localized infection of necrotic muscle tissue only Symptoms ­ similar to anaerobic myonecrosis but of a lesser severity *CREPITATION – moving of bunnies limbs to hear a crackling or rattling sound due to gas       ************************************************************************************* II .A. Enterotoxigenic Clostridia ­ (food poisoning)    Causative agent ­ C. perfringens type A Mode of Infection   1. Ingestion of viable vegetative cells 2. Synthesis of enterotoxin in small intestine 3. Enterotoxin produced which breaks down intestinal mucosa  leakage of  plasma membrane  disruption of osmotic equilibrium Symptoms   watery diarrhea, abdominal cramps Convalescence/Immunity   NO immunity ­ repeat attacks Control and Prevention   cook food thoroughly initially ­ destroys spores food refrigeration after preparation ­ prevents enterotoxin production reheating food ­ destroys toxin   *ingested by food, usually in a meat product *spores in food – R.T. germination – ingest cells – (+) enterotoxin sm. Intestine – disrupts osmotic equilibrium ( flux of electrolytes and water aka diarrhea) *second most common form of food poisoning world wide  *SPORES – 121 degrees *BACTERIA – 100 degrees *TOXINS – 80 degrees   II.B. Enterotoxigenic Clostridia ­ (antibiotic­associated colitis aka infection of the gut) Causative agent ­ C. difficile ­ drug resistant normal flora of intestine – endogenous bacteria (normal flora)   Antibiotic therapy ­ disrupts normal flora of intestine allowing a superinfection or secondary infection with C. difficile   Mode of Infection ­ (pseudomembranous colitis)   1. Antibiotic therapy 2. Colonization of intestine by C. difficile 3. Toxins produced ­ injure intestinal lining by inhibiting protein synthesis;  produces hemorrhagic necrosis 4. Leukocyte infiltration into colon due to toxin production 5. Pseudomembrane ­ (white patch on colon) ­ mixture of fibrin, mucus, leukocytes and  necrotic epithelial cells   Symptoms   abdominal pain, watery diarrhea , nausea   Risk group   patients receiving antibiotic therapy ­ primarily a disease of antibiotic induced colitis hospitalized patients   Treatment   discontinue antibiotics maintain fluid/electrolyte balance administer  vancomycin *C. difficile growth – (+) toxin – inhibits protein synthesis (necrosis) *white patches on colon due to action of the toxin – pseudomembrane ­ fibrin mucous WBCs and necrotic cells        ************************************************************************************ III. Clostridium tetani ­ (tetanus)   * always a POLYMICROBIC infection; not found alone, NON INVASIVE, facultative aerobe “puncture wound” A. Generalized tetanus ­ initial involvement of neck and jaw muscles with progression to          large muscle  groups B.    Neonatal tetanus   ­ initial infection of umbilical stump            ­ progression to generalized tetanus Conditions for  infection (favor spore germination) 1.  small puncture wounds 2.  necrotic tissue at wound site 3.  decreased oxygen (polymicrobic infection) * NEURAL TISSUE + GLYCINE (neuroinhibitor) ­> prevents muscle contraction Variety of toxins produced 1.  Neurotoxin ­ tetanospasmin or spasmogenic toxin ­ toxin of primary importance      accounts for classic symptoms *NEURAL TISSUE + TETANOSPASMIN ­> blocks glycine ­> continual contraction (tetany)      Site of action ­ target neurons in the spinal column Function of Toxin  Toxin binds to gangliosides in neural tissue  blocks release of neuroinhibitor glycine   continual contraction of muscles (tetany) Initial Symptoms Cramping and twitching of muscle around wound EXAM INFO:  Tetani & botulinum both produce neurotoxins  Need to know what they are  What they block the release of  What the end product is  Tetani: contraction  Botulinum: flaccid paralysis Later Symptoms sweating pain around wound area lockjaw or trismus ­ clenching of the jaw, muscle stiffness neck and jaw muscles risus sardonicus ­ sarcastic grin opithotonos – arching of the back Extreme Symptoms Progression to other muscle groups Violent spasms trunk and back  bone fractures Risk Groups 1. elderly 2. intravenous drug abusers 3. infants ­ neonatal tetanus (tetanus neonatorum) Death ­ paralysis of respiratory muscles Convalescence/Immunity No innate immunity Repeated infections do not produce immunity 1 1.  small amount of toxin in the circulation                       2.   toxins strong affinity for neural tissue Convalescence ­ no permanent damage to muscles Treatment 1. debridement of necrotic tissue 2. anti­toxin 3. unimmunized ­  human tetanus immune globulin (TIGH) ­ passive immunization immunized    ­   received DPT series, may require a booster shot of tetanus toxoid   4. Antibiotics ­ metronidazole or penicillin 5. Anti­spasmatic drugs or muscle relaxants ­ phenobarbital or chlorpromazine Control/Prevention Active immunization ­ DPT series (tetanus toxoid) Tetanus – world’s most preventable disease EXAM INFO  what’s infected first: neck and jaw  neurotoxin  continual contraction of muscle  neuro inhibitor glycine is blocked      ********************************************************************************** IV. Clostridium botulinum ­ (botulism) (food poisoning – botulin toxin conjugated with hemagglutinin) Neurotoxins A, B, E and F ­ human disease Neurotoxin A­ (Neurotoxin ­ hemagglutinin) – important with toxin’s actions  Function of hemagglutinin ­ prevents deactivation of neurotoxin by gastric enzymes and                 lowered pH of stomach Three Types of Botulism     1.  Food­borne botulism   2.  Infant botulism   3.  Wound botulism 1. Food­Borne Botulism (food poisoning or food intoxication) toxigenic food poisioning Mode of Infection 1. Ingestion of poorly preserved food containing Botulin (Botulinum toxin) a.   Spores not killed b.   Improper food preservation created ideal environment for spores to germinate. 1. anaerobic environment 2 2. storage ­ room temperature 3          3. alkaline foods (beans low acid concentration facilitate growth of bacteria)   c. Botulin (Botulinum toxin) product of metabolism   most potent toxin ­ lethal dose 1 ug. 2. Gastrointestinal tract toxin absorption  lymphatics and circulation  neuromuscular junction of skeletal muscle (site of toxin action) Normal response for muscle contraction: neural tissue + ACH = muscle contraction Action of Toxin Toxin binds to receptor sites at neuromuscular junction  blocks release acetyl­choline  (transmitter)  prevents muscle contraction (flaccid paralysis) Early Symptoms Gastrointestinal disturbance Neuromuscular Symptoms first affect the muscles of the head blurred or double vision (diplopia) slurred speech (dipphonia) difficulty swallowing (dysphagia) Critical symptoms  descending paralysis with involvement of respiratory system Convalescence/Immunity Repeated infections do not produce immunity; 1.  small amount toxin in the circulation 2.  toxins strong affinity for neural tissue Treatment Polyvalent antitoxin therapy Stomach lavage and enemas Control/Prevention Adequate food preservation ­ kill spores  o Heat all canned food ­ toxin inactivated at 80 C for 20 minutes 2.   Infant Botulism (flaccid paralysis or "floppy head baby syndrome") Ingestion of spores ­ dietary supplement honey Multiplies in colon due to the immature state of neonatal intestine and flora Indicators of Illness  Suck and gag reflexes decrease, drooling, head control lost Treatment Antibiotic therapy Control/Prevention Vaccinate pregnant females        3. Wound Botulism ­ rare neuroparalytic disease spores enter a puncture wound  in vitro toxin produced Symptoms similar to food­borne botulism Risk group intravenous drug abusers *************************************************************************************** Clostridium botulinum   Clostridium tetani KNOW BOTH                 neurotoxin neurotoxin                            botulin              tetanospasmin blocks neurotransmitter             blocks neuroinhibitor                                     ACH                    glycine   no muscle contraction         continual contraction        flaccid   paralysis tetany **************************************************************************************** LECTURE 4 – LISTERIA CORNYE BACILLUS LISTERIA MONOCYTOGENES  Slide 5 o (SALINE) Flagella – independent motion o Stab agar, grows out of the area where stabbed due to the fact that it has flagella (motile) o Present in milk – get rid of it by pasteurization  Slide 6 o zoonosis: infections humans acquire from animals o Organism that colonizes animals that when humans contract it it caused a human disease o Strongly associated with milk and milk products o 20% mortality rate – very high death rate  Slide 7 o Survives gastric acidity o Macrophages ingests them – however they can live/grow inside these cells – way to survive o LISTERIOLYSIN– hemolytic toxin secreted  Slide 11 o Penicillin – AMPLICILLIN (particular kind of penicillin) o If allergic trimethoprim C. DIPTHERIAE  Slide 17 o Somewhat difficult to grow o Diptheria toxin o Bacteriophage  Slide 22 o Causes localized disease o Doesn’t spread o Illness itself is a systemic disease – the TOXIN can be disseminated throughout the body o Classic binary toxin  Slide 24 o pseudomembrane: why it’s named diptheria o Leathery like collection of cells o Attached to back of the throat o If becomes detachhed can be inhaled and suffocated  Slide 27 o Know target organs and mechanisms*  Slide 28 o Best way to protect is to immunize o Vaccine is a toxoid o Don’t need to know about treatment BACILLUS  Anthrax  Slide 33 o Profound toxic mediated properties o Plasmid that codes for 3 separate factors o Protective antigen o Lethal factor LECTURE 5 – SALMONELLA & SHIGELLA SALMONELLA  Slide 5 o Single species with 5 groups o Mouse typhoid fever (humans can get this) o Swine gastroenteritis (death of piglets) o Enteritidis typhi and paratyphi - humans  Slide 9 o Non lactose fermenter & reduces sulfur o Bile salts – can inhibit all the gram positive cells in your gut o Acid detector – pink indicates acid o Salmonella - no pink because it doesn’t use lactose  Slide 12 o Can classify by different phenotypes o Flagellated  Slide 13 o Flagellar proteins are antigenically diverse o Antibodies that recognize one type of flagella won’t recognize another o serotypes  slide 14 o Gram negative – has LPS in outer membrane o O polysaccharide side chain: antigenically diverse o O serotypes  Slide 15 o >2400 O serotypes (lipopolysaccharides) o > 119 H Serotypes (flagellum) o Can classify using a combination of both serotypes together  Slide 17 o Where do we get this from? It circulates in the environment o Wild animals contain it (turtles, reptiles) o Chickens & Turkeys – can even pass onto eggs  Slide 21 o Rarely fatal o Eating or drinking contaminated substances – oral infection o Remains in GI tract o INVASIVE – adhere to gut cells cross membrane and enter gut cells (great place to hide from antibodies)  Slide 22 o How do they invade? o Pathogen exploits own cell’s metabolism o Bind to the cells – cause actin cytoskeleton of eukaryotic cell to directly change o Change by forming these “envelopes” that actually circle the bacterial cell and brings it into the eukaryotic cell aka RUFFLING o Ruffling invasion phenotype  Slide 23 o - Why does it cause diarrhea? Grows in gut and produces new progeny & need to get out and infect new people  slide 25 o Different from enteritidis – actually leaves intestine and becomes systemic – enter everywhere and come back in the gut and cause ulcerative lesions o Bloody diarrhea o Typhoid mary – incarcerated  Slide 26 o Small red spots also caused by neisseria meningitidis – bacterial meningitis which can kill you in 24 hours  Slide 27 o - N: ulcer formed by salmonella typhi that disrupted the tissue; ulceration can continue all the way down the entire length of the gut  slide 28 o How does it get in there? o Attack gut epithelium but it doesn’t attack all epithelial cells o Attack M CELLS which were actually designed to take up materials from your gut and sampling environment; making sure we don’t make immuno responses to things we don’t have too o Salmonella typhi bind to M cells and stimulate them to pick them up and drop them into the gut lining  Slide 29 o Both invade o Ruffling of surface and taken in a membrane bound vacuole o Salmonella remains in vacuole and replicates inside of it o Enteritidis just stays in the gut o Typhi disseminates – travels through – gets released into basil part of the gut where macrophages actually take them up again o They do not kill them macrophages travel everywhere and spreads typhi systemically and comes back to the gut  Slide 31 o In many cases, virulent genes end up being clustered in chromosome – ISLANDS o Salmonella has 2 island genes: all the genes involved in pathogenesis  Slide 33 o - We can make mutations in any of these genes and knock out virulence or severely decrease virulence  slide 34 o Many of these genes on this pathogenesis island is involved in TYPE 3 SECRETION SYSTEM  Slide 35 o -cholera toxin (type 2)  slide 36 o Secretion system is encoded by a set of genes o And the proteins that they secrete into the cells are in another section – known as SIP & SSP proteins  Slide 37 o How does it work? o Works by type 3 secretion system o Encodes proteins that make INJECTOSOME (hyperdermic syringe) o Pierce membrane of eukaryotic cell & injects proteins produced by bacterium into eukaryotic cell  Slide 38 o Exploit own metabolisms - must have a way of parasitizing those pathways o Effector proteins take advantage of certain parts of the cell o 1 island had genes for entry inside of the cell o 2 ndisland have genes meant for survival inside of the cell o Effector proteins are injected inside of the cell to protect the cell from killing it  Slide 39 o SPI1 & SIPs  Cause inflammation  Diarrhea  Cytoskeletal rearrangements that allow the cell to be taken up  Invasion into the cell o SPI2 & SSEs  Avoid antimicrobial activities of the cell  Modify cell trafficking to get them to move throughout the cell  Overall survival and replication o Salmonella typhi – important to survive in macrophages SHIGELLA  Shigella is also a gut pathogen  Bacillary dysentery: CAN lead to death  Slide 42 o boydii: don’t see very often o Dysenteriae: severe – potentially lethal  Slide 43 o Like salmonella – evolved to grow just in humans o Highly infectious o Salmonella typhi: 10^5/1-^7 bacteria required for infection – that’s about a tiny colony on a plate o Shigella is only 5-50  Slide 46 o How do we tell the difference? o Lactose, sucrose, salicin – all carbohydrate components  Slide 47 o How do we tell the difference between the species of shigella? o LPS – large variation  Slide 48 o 47 o antigen o Not that many so name them as serotype 1 etc. all based from the side chains  Slide 49 o Submucosal cells – gets to the 2 nd layer of cells o Causes a lot of damage in the gut o Breaks blood cells  Slide 50 o In shigella, a lot of the virulence genes are on the chromosome o Plasmid extremely essential in causing disease, without it can’t cause disease o 30,000 base pair region – encodes INVASION region phenotype (IPA – invasion plasmid antigen) o Type 3 secretion, effectors  Slide 51 o Shigella invades M cells o Vacuole o Type 3 secretion – IPA C triggers actin polymerization/depolymerization which allows the cell to take up shigella into the cell o Unlike salmonella (replicates inside vacuole and stays there) o IPA B is injected through membrane of vacuole and that causes a LYSIS of the vacuole o As a result, the bacteria spills right into the cytoplasm – “nutrient soup” o Replicate inside cell o Shiga toxin – sloughing of intestinal cells, can destroy kidneys  Slide 52 o Shigella has no flagella kind of non motile? o Protein called IPA C – involved in actin polymerization o There’s another protein that occurs right at the polar regions of Shigella  It can stimulate actin polymerization  Actin exist as monomers in cytoplasm – “monomer reservoir”  Cell can get it to polymerize to make long filaments when it needs it  Protein starts activating polymerization which creates a filament there, it will then get larger and it’s going to push  It provides a mode of force called ROCKET PROPULSION  Actually has enough force that the bacteria can be pushed against dual membrane and into the next cell  It’s then in another vacuole but can lyse the vacuole  It can move from cell to cell without jumping out of the cell and back inside  USEFUL to avoid IGA antibodies  Slide 53 o Invaginate by type 3 secretion o Inside vacuole o Lyse vacuole o Replicate in cytoplasm o Polymerize actin o Push around the cell o Push into another cell o Lyse the vacuole and do the same thing Lecture 6 – vibrio campy ecoli VIBRIO  Slide 8 o Flagella – motile o Able to swim in the gut  Slide 9 o - Endemic; can exist in an area for a very very long period of time  slide 12 o - Gut contents are early on are just fluids and mucous – “rice water stool”  slide 13 o Has two life forms o Environment (not pathogenic) vs. gut (pathogenic) o Low oxygen o Secretes a capsule  Slide 14 o >138 O serotypes o Different types of changes and vibrio that’s causing people to get sick  Slide 15 o TCBS AGAR – SELECTIVE AGAR o High pH o Sulfur compound - thiosulfate  Slide 16 o Major determinant is cholera toxin o There’s also a coregulated pilus- seems to only be expressed when cholera toxin exists o Hemagglutinin protease – helps bacteria get induce into the gut o Iron uptake mechanisms o Neuraminidase; makes its own receptor  Slide 17 o - HA protease cleaves the pilus and releases vibrio into the fluids of the gut  slide 19 o Multi subunit toxin that gets secreted into the gut o Binds to GM1 – many other different types o cAMP: secondary messenger for lots of different metabolisms o It regulates K and Na channels o Turning on a “faucet”  Slide 20 o Cholera toxin is actually part of a bacteriophage o Unless vibrio is infected by vibriophage – vibrio isn’t virulent – cholera toxin isn’t being expressed o When its taken into gut, signal in gut that act on promoters and express cholera toxin CAMPYLOBACTER  Similar to salmonella  Undercooked meats  Chease from raw milk  Slide 25 o Unlike other bacteria, does NOT FERMENT SUGARS o Can grow in the presence of a little oxygen but requires CO2  Slide 27 o Various types of species that cause different types of disease o C. Jejuni – common o C. coli / C. fetus: agriculturally – spontaneous abortions  Slide 29 o One of the problems; just being studied o Attachment factors o 2 motile flagellae o Invade inside plasmid cells o Infected – symptoms are a lot like shigella o MONOCYTES – different from shigella o At risk for Guillain Barre Syndrome: paralysis and neurological damage – autoimmune disease  What happens is you get infected by jejuni – there are certain polysaccharides that look a lot like polysaccharides expressed on neuronal cells  Antibodies against yourself ECOLI  Slide 35 o However there are non commensal e. coli that exist – those that cause disease in many different parts of the body o Almost half that occur in the gut are caused by e. coli  MEMORIZE SLIDE 39 and 40  Slide 41 o Enter the cell by forming a PEDICLE – causes actin rearrangements (polymerization/depolymerization) which are caused by effectors (type 3 secretions) o Pedicle is like a column that lifts up underneath the bacterium and ultimately will engulf it and bring it in o EFFACEMENT – changing the face on the surface of the epithelial cell  Slide 42 o Make both heat stable toxin (Sta) and heat labile enterotoxin (LT – like cholera toxin) o STa can boil for an hour and still toxic – doesn’t unfold rapidly but when it does it refolds promptly  Slide 45 o Has a virulence plasmid – if it lacks this plasmid lacks a lot of virulence factors  Slide 46 o Does have a plasmid that contains invasion genes o Pathogens can either involve in the same direction or virulence can be passed horizontally – selective pressure  Slide 47 o Symptomatic o One or two will bind and just form a stacked brick o Bundle forming pilli – pilli aggregate together – helps aggregative form o Intestinal hemorrhage  Slide 48 o Many express type I fimbriae o Women get UTI more because uretha closer to GI tract – easier to cross colonize o UTI in males is limited to uretha in bladda o Women can ascend and cause serious infections  Slide 49 o Adheres to gut lining invasive into cells o Associated with Chron’s disease o Chronic disease LECTURE 7 – BORDETELLA & HAEMOPHILUS BORDETELLA  Slide 4 o Necrotic rhinitis: snout gets deteriorated & infected o URT = upper respiratory tract infection o Bordetella pertussis: obligate pathogen o Vaccine against pertussis doesn’t protect against parapertusis  Slide 5 o bordet gengou agar o Mainly effects ciliated respiratory epithelium  Slide 7 o Culturing bacteria – very slow and not always successful o Pertussis can also enter a VBNC stage – viable but non culturable – in throat and perfectly healthy and growing but when you streak it on agar there’s nothing there – it’s because they shifted their metabolism o Also, can’t use cotton swabs (gentle/cheap) – fatty acids kill pertussis o How else do we detect? Antibodies recognize pertussis proteins using immunofluorescence assay on secretions – the problem is is that they’re expensive, need to have a certain microscope o You can also do agglutination reactions – causes bacteria to fall out of solution because they’ve been cross linked by antibodies – the problem with this is you need A LOT of bacteria o So what do we rely on? Simple clinical diagnosis – (lymphocytosis: infection on local WBCs)  Slide 8 o - Vaccines are selective pressures – there’s been a rise of strains resistant to vaccine  slide 13 o To bind to ciliated epithelium – has many different kinds of adhesins o Filamentous, pertactin, and fimbriae ALL are included in acellular vaccine o Capsule – hard to get a vaccine for o Pili – too divergent  Slide 14 o Vibrio cholera (cholera toxin), diptheria (diptheria toxin), shigella (shiga toxin) o Bordetella pertussis: MULTIPLE TOXINS o Pertussis toxin o A1-B5 class, similar to cholera toxin o Does cause a rise in cAMP – sort of like vibrio, but vibrio is attacking gut epithelial cells these are infecting respiratory epithelial cells o Tracheal cytotoxin o Unlike the other toxins which are proteins, these are a fragment of the cell wall o Actively breaks down own cell wall to make these little toxic fragments which really destroy the ciliated epithelial cells o Adenylate cyclase toxin o Lymphocytosis promoting toxin o Dermonecrotic toxin – not sure weather or not it can effect humans o LPS o Pertusis and tracheal are the main two in causing disease  Slide 15 o Once you get past incubation stage you start showing symptoms o Malaise (tired) Rhinorrhea (nose running) lacrimation (watery eyes) – seems like a cold  Slide 16 o This stage is when things get serious o Respiratory escalator – whatever we’re breathing in goes through the cilia in our nose, but whatever doesn’t go through our noses - what happens is the mucous gets swept upwards until it reaches your throat – we end up swallowing it o If we kill all the cilia – we don’t have the cilia beating the mucous and beating it up o Mucous ends up being still there – so we end up coughing to try to get it out o Erythromycin – end up continuing coughing. Why? It kills the pertussis. But it takes 7-14 days for the basement cells in URT to differentiate into epithelial cells – until the epithelial cells have grown, you’re still coughing – no way to get the mucous out o Convalescence – 3-4 weeks, takes a long time for those epithelial cells to really grow back HAEMOPHILUS  Slide 21 o This stage is when things get serious o Respiratory escalator – whatever we’re breathing in goes through the cilia in our nose, but whatever doesn’t go through our noses - what happens is the mucous gets swept upwards until it reaches your throat – we end up swallowing it o If we kill all the cilia – we don’t have the cilia beating the mucous and beating it up o Mucous ends up being still there – so we end up coughing to try to get it out o Erythromycin – end up continuing coughing. Why? It kills the pertussis. But it takes 7-14 days for the basement cells in URT to differentiate into epithelial cells – until the epithelial cells have grown, you’re still coughing – no way to get the mucous out o Convalescence – 3-4 weeks, takes a long time for those epithelial cells to really grow back  Slide 22 o capsule: India ink stain o HAP protein – pilius attaches to the cell – provides a more intimiate adherence to cell o IgA protease inactivates the immunoglobulin by proteolytic cleavage – it’s produced by plasma cells in blood – it cleaves IGA antibody  Slide 23 o Antigenically different in capsules – K ANTIGENS o Serotype a, b, c o 6 different types  slide 24 o The problem is, after we used it for a decade – most infections caused by unencapsulated strains o Can’t serotype them based on K antigens o NTHI – non typeable – most predominant form causing disease in US  Slide 25 o Emerged as a prominent cause of otits media since the advent of the Hib vaccine o Otitis media – inflammatory and high fever – can lead to meningitis


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