microbial interactions
TRANSCRIPT
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