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.

1. 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

4. MICROBIAL ANTAGONISM

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

6. Plant pathogen

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.

9. BACTERIA AND LEGUMES

10. Animal diseases

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".

12. RUMINANTS AND MICROBES

13. Interaction with human

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

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 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

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

54. Virus and fungi

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

61. Mechanisms of Pathogenicity

62. Portals of Exit
• Respiratory tract
– Coughing, sneezing
• Gastrointestinal tract
– Feces, saliva
• Genitourinary tract
– Urine, vaginal secretions
• Skin
• Blood
– Biting arthropods, needles/syringes