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MICROBIAL INTERACTIONS

Microbial interactions

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Page 1: Microbial interactions

MICROBIAL INTERACTIONS

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LECTURE CONTENTS

1. Types of interaction– Interaction with other

microbes– Interaction with plants– Interaction with

animals– Interaction with human

2. Microbes and Disease3. Microbes and the

Environment

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• Positive interaction• Negative interaction

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MICROBIAL ANTAGONISM

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• 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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Plant pathogen

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Plant pathogens

F graminearum causes a disease know as ear and stalk rot in corn and head blight in wheat and barley

Xanthomonas Gram-negative, yellow-pigmented plant pathogenic bacteria

Tobacco mosaic virus

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• 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.

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BACTERIA AND LEGUMES

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Animal diseases

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• 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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RUMINANTS AND MICROBES

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Interaction with human

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Normal Microbiota and the Host:

• Locations of normal microbiota on and in the human body

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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

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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.

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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

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Koch’s Postulates

• Koch's Postulates are used to prove the cause of an infectious disease.

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Koch’s Postulates

• Koch's Postulates are used to prove the cause of an infectious disease.

Figure 14.3.2

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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.

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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.

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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.

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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

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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

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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)

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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

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The Stages of a Disease

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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

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Transmission of Disease1. Contact

– Direct• Requires close association

between infected and susceptible host

– Indirect• Spread by fomites

– Droplet• Transmission via airborne

droplets

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Transmission of Disease2. Vehicle

Transmission by an inanimate reservoir (food, water)

3. VectorsArthropods, especially fleas, ticks, and

mosquitoes

4. MechanicalArthropod carries pathogen on feet

5. BiologicalPathogen reproduces in vector

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Nosocomial (Hospital-Acquired) Infections

• Are acquired as a result of a hospital stay• 5-15% of all hospital patients acquire

nosocomial infections

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Relative frequency of nosocomial infections

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Common Causes of Nosocomial Infections

Percentage of nosocomial infections

Percentage resistant to antibiotics

Gram + cocci 34% 28%-87%

Gram – rods 32% 3-34%

Clostridium difficile 17%

Fungi 10%

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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

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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)

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Epidemiology

• The study of where and when diseases occur

Figure 14.11

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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

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Microbial Mechanisms of Pathogenicity

• Pathogenicity The ability to cause disease

• Virulence The extent of pathogenicity

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Portals of Entry

• Mucous membranes

• Skin

• Parenteral route

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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

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Bacillus anthracis

Portal of entry ID50

Skin 10-50 endospores

Inhalation 10,000-20,000 endospores

Ingestion 250,000-1,000,000 endospores

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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

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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)

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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

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Exotoxin

Source Mostly Gram +

Metabolic product By-products of growing cell

Chemistry Protein

Fever? No

Neutralized by antitoxin Yes

LD50Small

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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

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• A-B toxins or type III toxins

Exotoxins

Figure 15.5

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ExotoxinsExotoxin Lysogenic

conversion

• Corynebacterium diphtheriae A-B toxin. Inhibits protein synthesis. +

• Streptococcus pyogenes Membrane-disrupting. Erythrogenic. +

• Clostridium botulinum A-B toxin. Neurotoxin +

• C. tetani A-B toxin. Neurotoxin

• Vibrio cholerae A-B toxin. Enterotoxin +

• Staphylococcus aureus Superantigen. Enterotoxin.

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Endotoxins

Source Gram–

Metabolic product Present in LPS of outer membrane

Chemistry Lipid

Fever? Yes

Neutralized by antitoxin No

LD50 Relatively large

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Endotoxins

Figure 15.6

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Virus and fungi

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Cytopathic Effects of Viruses

Table 15.4

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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

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Pathogenic Properties of Fungi

• Mycotoxins– Ergot toxin

• Claviceps

– Aflatoxin• Aspergillus

– Neurotoxins: Phalloidin, amanitin• Amanita

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Pathogenic Properties of Protozoa

• Presence of protozoa

• Protozoan waste products may cause symptoms

• Avoid host defenses by– Growing in phagocytes– Antigenic variation

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Pathogenic Properties of Helminths

• Use host tissue

• Presence of parasite interferes with host function

• Parasite's metabolic waste can cause symptoms

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Pathogenic Properties of Algae

• Neurotoxins produced by dinoflagellates– Saxitoxin

• Paralytic shellfish poisoning

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Mechanisms of Pathogenicity

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Portals of Exit• Respiratory tract

– Coughing, sneezing

• Gastrointestinal tract– Feces, saliva

• Genitourinary tract– Urine, vaginal secretions

• Skin

• Blood– Biting arthropods, needles/syringes