microbial interactions

MICROBIAL INTERACTIONS

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

• 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 and stalk rot in corn and head blight in wheat and barley

Xanthomonas Gram-negative, yellow-pigmented plant pathogenic bacteria

Tobacco mosaic virus

• 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 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. VectorsArthropods, especially fleas, ticks, and

mosquitoes

4. MechanicalArthropod carries pathogen on feet

5. BiologicalPathogen 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 nosocomial infections

Percentage resistant to 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 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 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

LD50Small

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

• A-B toxins or type III toxins

Exotoxins

Figure 15.5

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.

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