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Microbial interactions
This document discusses microbial interactions, including both positive and negative interactions. It provides examples of symbiotic relationships between microbes and plants, such as lichens and nitrogen-fixing bacteria in legume roots. Microbial interactions with animals are also discussed, including relationships between rumen microbes and ruminant digestion. The document concludes by examining the interaction between the human microbiome and the host.
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Overview of microbial interactions with other microbes, plants, animals, and humans, including pathogenic effects.
Positive and negative interactions; details on microbial antagonism, lichen symbiosis, and plant pathogens.
Focus on animal diseases, specifically how ruminants utilize resident microbes to digest cellulose.
Details of normal microbiota in humans, including transient and permanent colonization and microbial antagonism.
Definitions and principles of disease, including pathology, etiology, infection, and types of diseases. Classifications of infectious diseases based on symptoms, transmission type, and occurrence.
Mechanisms of disease transmission, including direct contact, vectors, and vehicles.Overview of hospital-acquired infections: frequency, causes, and emerging infectious diseases.
Study of disease occurrence, with a focus on CDC reporting, morbidity, and mortality definitions.Mechanisms of pathogenicity, including portals of entry, infection dose, adherence, and toxins.
Properties of toxins and pathogens including bacteria, viruses, fungi, protozoa, and helminths.
Mechanisms of how pathogens exit the host body via various routes like respiratory and gastrointestinal.
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Microbial interactions
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- 2. LECTURE CONTENTS 1. Typesof interaction – Interaction with other microbes – Interaction with plants – Interaction with animals – Interaction with human 2. Microbes and Disease 3. Microbes and the Environment
- 3. • Positive interaction •Negative interaction
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- 5. • 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
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- 7. Plant pathogens F graminearum causes a disease know as ear Tobacco mosaic virus and stalk rot in corn and Xanthomonas head blight in wheat Gram-negative, yellow- and barley pigmented plant pathogenic bacteria
- 8. • Symbiotic NitrogenFixation – 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.
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- 11. • 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 can't 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".
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- 14. Normal Microbiota andthe Host: • Locations of normal microbiota on and in the human body
- 15. Normal Microbiota andthe 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
- 16. Normal Microbiota andthe 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.
- 17. Principles of Diseaseand 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
- 18. Koch’s Postulates • Koch'sPostulates are used to prove the cause of an infectious disease.
- 19. Koch’s Postulates • Koch'sPostulates are used to prove the cause of an infectious disease. Figure 14.3.2
- 20. 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.
- 21. 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.
- 22. 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.
- 23. Severity or Durationof 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
- 24. Extent of HostInvolvement • 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
- 25. Extent of HostInvolvement • 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)
- 26. Predisposing Factors • Makethe body more susceptible to disease – Short urethra in females – Inherited traits such as the sickle-cell gene – Climate and weather – Fatigue – Age – Lifestyle – Chemotherapy
- 27. The Stages ofa Disease
- 28. 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
- 30. Transmission of Disease 1.Contact – Direct • Requires close association between infected and susceptible host – Indirect • Spread by fomites – Droplet • Transmission via airborne droplets
- 31. Transmission of Disease 2.Vehicle Transmission by an inanimate reservoir (food, water) 3. Vectors Arthropods, especially fleas, ticks, and mosquitoes 4. Mechanical Arthropod carries pathogen on feet 5. Biological Pathogen reproduces in vector
- 32. Nosocomial (Hospital-Acquired) Infections • Are acquired as a result of a hospital stay • 5-15% of all hospital patients acquire nosocomial infections
- 34. Relative frequency ofnosocomial infections
- 35. Common Causes ofNosocomial Infections Percentage of Percentage resistant to nosocomial infections antibiotics Gram + cocci 34% 28%-87% Gram – rods 32% 3-34% Clostridium difficile 17% Fungi 10%
- 36. 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
- 37. 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)
- 38. Epidemiology • The studyof where and when diseases occur Figure 14.11
- 39. Centers for DiseaseControl 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
- 40. Microbial Mechanisms of Pathogenicity • Pathogenicity The ability to cause disease • Virulence The extent of pathogenicity
- 41. Portals of Entry •Mucous membranes • Skin • Parenteral route
- 42. Numbers of InvadingMicrobes • ID50: Infectious dose for 50% of the test population • LD50: Lethal dose (of a toxin) for 50% of the test population
- 43. Bacillus anthracis Portal ofentry ID50 Skin 10-50 endospores Inhalation 10,000-20,000 endospores Ingestion 250,000-1,000,000 endospores
- 44. Adherence • Adhesions/ligands bindto receptors on host cells – Glycocalyx Streptococcus mutans – Fimbriae Escherichia coli – M protein Streptococcus pyogenes – Opa protein Neisseria gonorrhoeae – Tapered end Treponema pallidum
- 45. Mechanisms to causedisease Enzymes – Coagulase Coagulate blood – Kinases Digest fibrin clots – Hyaluronidase Hydrolyses hyaluronic acid – Collagenase Hydrolyzes collagen – IgA proteases Destroy IgA antibodies Siderophores Take iron from host iron-binding proteins Antigenic variation Alter surface proteins Toxins Production of toxins (endotoxin; exotoxin)
- 46. Toxins • Toxin Substances that contribute to pathogenicity • Toxigenicity Ability to produce a toxin • Toxemia Presence of toxin the host's blood • Toxoid Inactivated toxin used in a vaccine • Antitoxin Antibodies against a specific toxin
- 48. Exotoxin Source Mostly Gram + Metabolic product By-products of growing cell Chemistry Protein Fever? No Neutralized by antitoxin Yes LD50 Small
- 49. Exotoxins • Superantigens ortype 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
- 50. Exotoxins • A-B toxinsor type III toxins Figure 15.5
- 51. 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.
- 52. Endotoxins Source Gram– Metabolic product Present in LPS of outer membrane Chemistry Lipid Fever? Yes Neutralized by antitoxin No LD50 Relatively large
- 53. Endotoxins Figure 15.6
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- 55. Cytopathic Effects ofViruses Table 15.4
- 56. Pathogenic Properties ofFungi • 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
- 57. Pathogenic Properties ofFungi • Mycotoxins – Ergot toxin • Claviceps – Aflatoxin • Aspergillus – Neurotoxins: Phalloidin, amanitin • Amanita
- 58. Pathogenic Properties ofProtozoa • Presence of protozoa • Protozoan waste products may cause symptoms • Avoid host defenses by – Growing in phagocytes – Antigenic variation
- 59. Pathogenic Properties ofHelminths • Use host tissue • Presence of parasite interferes with host function • Parasite's metabolic waste can cause symptoms
- 60. Pathogenic Properties ofAlgae • Neurotoxins produced by dinoflagellates – Saxitoxin • Paralytic shellfish poisoning
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- 62. Portals of Exit •Respiratory tract – Coughing, sneezing • Gastrointestinal tract – Feces, saliva • Genitourinary tract – Urine, vaginal secretions • Skin • Blood – Biting arthropods, needles/syringes