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Microbial interactions
 

Microbial interactions

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Microbial interactions Microbial interactions Presentation Transcript

  • MICROBIAL INTERACTIONS
  • LECTURE CONTENTS1. Types of interaction – Interaction with other microbes – Interaction with plants – Interaction with animals – Interaction with human2. Microbes and Disease3. Microbes and the Environment
  • • Positive interaction• Negative interaction
  • MICROBIAL ANTAGONISM
  • • Lichen symbiosis – Lichens are associations of fungus (host) with photosynthetic alga or cyanobacteria (symbiont). – Fungus (ectosymbiont) provides minerals by releasing lichen acids that dissolve substrate, release small amounts of P, S, other minerals, and obtains water from air. – The endosymbiont carries out photosynthesis, converts CO2 to organic matter to feed itself and fungus host. – Resulting symbiotic organisms can grow attached to rocks, tree trunks, other unlikely habitats
  • Plant pathogen
  • Plant pathogens F graminearum causes a disease know as ear Tobacco mosaic virus and stalk rot in corn andXanthomonas head blight in wheatGram-negative, yellow- and barleypigmented plantpathogenic bacteria
  • • Symbiotic Nitrogen Fixation – symbiosis between bacteria (Rhizobium species) and roots of leguminous plants (alfalfa, clover, vetch, peas, beans, etc.) --> root nodules – Bacteria provide ammonia by nitrogen fixation. Plants provide nutrients and shelter and anaerobic microenvironments – Allows growth in nitrogen-poor soils – Note: there are non-symbiotic nitrogen- fixing bacteria, e.g. Azotobacter. Also other types of symbionts, e.g. Frankia that live in Alder roots, create nodules.
  • BACTERIA AND LEGUMES
  • Animal diseases
  • • Ruminants & Resident microbes – Ruminants (R) are herbivorous animals with four-chambered stomach = rumen. – R eat grasses containing mainly cellulose, but lack enzymes to digest cellulose. – Bacteria and Protists in rumen produce cellulases, hydrolyze cellulose to sugar which is then fermented. – Products include: methane (from methanogens); organic acids (acetate, propionate, butyrate). – Acids are adsorbed by R into bloodstream, provide source of energy. – Methane must be released by belching, ~2 liters/min. Disease "bloat" when cows cant belch. – Microbial population totally anaerobic, achieves highest density of bacteria (up to 1012 cells/ml). – Cellulose digestion is slow process. Animals regurgitate rumen contents back to mouth to facilitate breakdown, "chewing cud".
  • RUMINANTS AND MICROBES
  • Interaction with human
  • Normal Microbiota and the Host:• Locations of normal microbiota on and in the human body
  • Normal Microbiota and the Host• Transient microbiota may be present for days, weeks, or months• Normal microbiota permanently colonize the host• Symbiosis is the relationship between normal microbiota and the host
  • Normal Microbiota and the Host:• Microbial antagonism is competition between microbes.• Normal microbiota protect the host by: – occupying niches that pathogens might occupy – producing acids – producing bacteriocins• Probiotics are live microbes applied to or ingested into the body, intended to exert a beneficial effect.
  • Principles of Disease and Epidemiology• Pathology Study of disease• Etiology Study of the cause of a disease• Pathogenesis Development of disease• Infection Colonization of the body by pathogens• Disease An abnormal state in which the body is not functionally normally
  • Koch’s Postulates• Kochs Postulates are used to prove the cause of an infectious disease.
  • Koch’s Postulates• Kochs Postulates are used to prove the cause of an infectious disease. Figure 14.3.2
  • Classifying Infectious Diseases• Symptom A change in body function that is felt by a patient as a result of disease• Sign A change in a body that can be measured or observed as a result of disease.• Syndrome A specific group of signs and symptoms that accompany a disease.
  • Classifying Infectious Diseases• Communicable disease – A disease that is easily spread from one host to another.• Contagious disease – A disease that is easily spread from one host to another.• Non-communicable disease – A disease that is not transmitted from one host to another.
  • Occurrence of Disease• Incidence Fraction of a population that contracts a disease during a specific time.• Prevalence Fraction of a population having a specific disease at a given time.• Sporadic disease Disease that occurs occasionally in a population.• Endemic disease Disease constantly present in a population.• Epidemic disease Disease acquired by many hosts in a given area in a short time.• Pandemic disease Worldwide epidemic.• Herd immunity Immunity of a population.
  • Severity or Duration of a Disease• Acute disease Symptoms develop rapidly• Chronic disease Disease develops slowly• Subacute disease Symptoms between acute and chronic• Latent disease Disease with a period of no symptoms
  • Extent of Host Involvement• Local infection Pathogens limited to a small area of the body• Systemic infection An infection throughout the body• Focal infection Systemic infection that began as a local infection• Bacteremia Bacteria in the blood• Septicemia Growth of bacteria in the blood
  • Extent of Host Involvement• Toxemia Toxins in the blood• Viremia Viruses in the blood• Primary infection Acute infection that causes the initial illness• Secondary infection Opportunistic infection after a primary (predisposing) infection• Subclinical disease No noticeable signs or symptoms (inapparent infection)
  • Predisposing Factors• Make the body more susceptible to disease – Short urethra in females – Inherited traits such as the sickle-cell gene – Climate and weather – Fatigue – Age – Lifestyle – Chemotherapy
  • The Stages of a Disease
  • Reservoirs of Infection• Reservoirs of infection are continual sources of infection. – Human — AIDS, gonorrhea • Carriers may have inapparent infections or latent diseases – Animal — Rabies, Lyme disease • Some zoonoses may be transmitted to humans – Nonliving — Botulism, tetanus • Soil
  • Transmission of Disease1. Contact – Direct • Requires close association between infected and susceptible host – Indirect • Spread by fomites – Droplet • Transmission via airborne droplets
  • Transmission of Disease2. Vehicle Transmission by an inanimate reservoir (food, water)3. Vectors Arthropods, especially fleas, ticks, and mosquitoes4. Mechanical Arthropod carries pathogen on feet5. Biological Pathogen reproduces in vector
  • Nosocomial (Hospital-Acquired) Infections• Are acquired as a result of a hospital stay• 5-15% of all hospital patients acquire nosocomial infections
  • Relative frequency of nosocomial infections
  • Common Causes of Nosocomial Infections Percentage of Percentage resistant to nosocomial infections antibioticsGram + cocci 34% 28%-87%Gram – rods 32% 3-34%Clostridium difficile 17%Fungi 10%
  • Emerging Infectious Diseases• Diseases that are new, increasing in incidence, or showing a potential to increase in the near future.• Contributing factors: – Evolution of new strains • V. cholerae O139 – Inappropriate use of antibiotics and pesticides • Antibiotic resistant strains – Changes in weather patterns • Hantavirus
  • Emerging Infectious Diseases• Contributing factors: – Modern transportation • West Nile virus – Ecological disaster, war, expanding human settlement • Coccidioidomycosis (Coccidioides immitis ) – Animal control measures • Lyme disease – Public Health failure • Diphtheria (Corynebacterium diphtheriae)
  • Epidemiology• The study of where and when diseases occur Figure 14.11
  • Centers for Disease Control and Prevention (CDC)• Collects and analyzes epidemiological information in the U.S.• Publishes Morbidity and Mortality Weekly Report (MMWR) www.cdc.gov• Morbidity: incidence of a specific notifiable disease• Mortality: deaths from notifiable diseases• Morbidity rate = number of people affected/total population in a given time period• Mortality rate - number of deaths from a disease/total population in a given time
  • Microbial Mechanisms of Pathogenicity• Pathogenicity The ability to cause disease• Virulence The extent of pathogenicity
  • Portals of Entry• Mucous membranes• Skin• Parenteral route
  • Numbers of Invading Microbes• ID50: Infectious dose for 50% of the test population• LD50: Lethal dose (of a toxin) for 50% of the test population
  • Bacillus anthracisPortal of entry ID50Skin 10-50 endosporesInhalation 10,000-20,000 endosporesIngestion 250,000-1,000,000 endospores
  • Adherence• Adhesions/ligands bind to receptors on host cells – Glycocalyx Streptococcus mutans – Fimbriae Escherichia coli – M protein Streptococcus pyogenes – Opa protein Neisseria gonorrhoeae – Tapered end Treponema pallidum
  • Mechanisms to cause diseaseEnzymes– Coagulase Coagulate blood– Kinases Digest fibrin clots– Hyaluronidase Hydrolyses hyaluronic acid– Collagenase Hydrolyzes collagen– IgA proteases Destroy IgA antibodiesSiderophores Take iron from host iron-binding proteinsAntigenic variation Alter surface proteinsToxins Production of toxins (endotoxin; exotoxin)
  • Toxins• Toxin Substances that contribute to pathogenicity• Toxigenicity Ability to produce a toxin• Toxemia Presence of toxin the hosts blood• Toxoid Inactivated toxin used in a vaccine• Antitoxin Antibodies against a specific toxin
  • ExotoxinSource Mostly Gram +Metabolic product By-products of growing cellChemistry ProteinFever? NoNeutralized by antitoxin YesLD50 Small
  • Exotoxins• Superantigens or type I toxins – Cause an intense immune response due to release of cytokines from host cells – Fever, nausea, vomiting, diarrhea, shock, death• Membrane-disrupting toxins or type II toxins – Lyse host’s cells by: • Making protein channels in the plasma membrane (e.g., leukocidins, hemolysins) • Disrupting phospholipid bilayer
  • Exotoxins• A-B toxins or type III toxins Figure 15.5
  • Exotoxins Lysogenic Exotoxin conversion A-B toxin. Inhibits protein• Corynebacterium diphtheriae + synthesis. Membrane-disrupting.• Streptococcus pyogenes + Erythrogenic.• Clostridium botulinum A-B toxin. Neurotoxin +• C. tetani A-B toxin. Neurotoxin• Vibrio cholerae A-B toxin. Enterotoxin +• Staphylococcus aureus Superantigen. Enterotoxin.
  • EndotoxinsSource Gram–Metabolic product Present in LPS of outer membraneChemistry LipidFever? YesNeutralized by antitoxin NoLD50 Relatively large
  • Endotoxins Figure 15.6
  • Virus and fungi
  • Cytopathic Effects of Viruses Table 15.4
  • Pathogenic Properties of Fungi• Fungal waste products may cause symptoms• Chronic infections provoke an allergic response• Tichothecene toxins inhibit protein synthesis – Fusarium• Proteases – Candida, Trichophyton• Capsule prevents phagocytosis – Cryptococcus
  • Pathogenic Properties of Fungi• Mycotoxins – Ergot toxin • Claviceps – Aflatoxin • Aspergillus – Neurotoxins: Phalloidin, amanitin • Amanita
  • Pathogenic Properties of Protozoa• Presence of protozoa• Protozoan waste products may cause symptoms• Avoid host defenses by – Growing in phagocytes – Antigenic variation
  • Pathogenic Properties of Helminths• Use host tissue• Presence of parasite interferes with host function• Parasites metabolic waste can cause symptoms
  • Pathogenic Properties of Algae• Neurotoxins produced by dinoflagellates – Saxitoxin • Paralytic shellfish poisoning
  • Mechanisms of Pathogenicity
  • Portals of Exit• Respiratory tract – Coughing, sneezing• Gastrointestinal tract – Feces, saliva• Genitourinary tract – Urine, vaginal secretions• Skin• Blood – Biting arthropods, needles/syringes