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MICROBIAL INTERACTIONS
LECTURE CONTENTS
1. Types of interaction
  –   Interaction with other
      microbes
  –   Interaction with plants
  –   Interaction with
      animals
  –   Interaction with human
2. Microbes and Disease
3. 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 and
Xanthomonas                head blight in wheat
Gram-negative, yellow-     and barley
pigmented plant
pathogenic 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 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".
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
• Koch's Postulates are
  used to prove the cause
  of an infectious disease.
Koch’s Postulates
• Koch's 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 Disease
1. Contact
  – Direct
     • Requires close association
       between infected and
       susceptible host


  – Indirect
     • Spread by fomites


  – Droplet
     • Transmission via airborne
       droplets
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
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         antibiotics
Gram + 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 anthracis
Portal of entry       ID50

Skin                  10-50 endospores


Inhalation            10,000-20,000
                      endospores

Ingestion             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 disease
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)
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
Exotoxin




Source                              Mostly Gram +
Metabolic product             By-products of growing cell

Chemistry                              Protein
Fever?                                    No
Neutralized by antitoxin                 Yes
LD50                                    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.
Endotoxins



Source                     Gram–
Metabolic product          Present in LPS of outer membrane
Chemistry                  Lipid
Fever?                     Yes
Neutralized by antitoxin   No
LD50                       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

• Parasite's 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

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Microbial interactions

  • 2. LECTURE CONTENTS 1. Types of 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
  • 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
  • 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 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.
  • 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".
  • 14. Normal Microbiota and the Host: • Locations of normal microbiota on and in the human body
  • 15. 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
  • 16. 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.
  • 17. 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
  • 18. Koch’s Postulates • Koch's Postulates are used to prove the cause of an infectious disease.
  • 19. Koch’s Postulates • Koch's Postulates 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 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
  • 24. 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
  • 25. 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)
  • 26. 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
  • 27. The Stages of a 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
  • 29.
  • 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
  • 33.
  • 34. Relative frequency of nosocomial infections
  • 35. Common Causes of Nosocomial 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 study of where and when diseases occur Figure 14.11
  • 39. 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
  • 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 Invading Microbes • 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 of entry ID50 Skin 10-50 endospores Inhalation 10,000-20,000 endospores Ingestion 250,000-1,000,000 endospores
  • 44. 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
  • 45. Mechanisms to cause disease 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
  • 47.
  • 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 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
  • 50. Exotoxins • A-B toxins or 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
  • 55. Cytopathic Effects of Viruses Table 15.4
  • 56. 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
  • 57. Pathogenic Properties of Fungi • Mycotoxins – Ergot toxin • Claviceps – Aflatoxin • Aspergillus – Neurotoxins: Phalloidin, amanitin • Amanita
  • 58. Pathogenic Properties of Protozoa • Presence of protozoa • Protozoan waste products may cause symptoms • Avoid host defenses by – Growing in phagocytes – Antigenic variation
  • 59. Pathogenic Properties of Helminths • Use host tissue • Presence of parasite interferes with host function • Parasite's metabolic waste can cause symptoms
  • 60. Pathogenic Properties of Algae • Neurotoxins produced by dinoflagellates – Saxitoxin • Paralytic shellfish poisoning
  • 62. Portals of Exit • Respiratory tract – Coughing, sneezing • Gastrointestinal tract – Feces, saliva • Genitourinary tract – Urine, vaginal secretions • Skin • Blood – Biting arthropods, needles/syringes

Hinweis der Redaktion

  1. Symbiosisco dependent
  2. TP-syphillis