CALS Farm and Industry Short Course Program: Farm Microbiology: Archived Lecture Notes

SECTION 6.
Microbial Diseases of Humans, Animals and Plants

PART ONE – BACKGROUND

1. Concepts of host-parasite relationships.
   
   
   1. Parasite.  Simply an organism that grows in or on a host. Not necessarily a pathogen.
      
      
   2. Host.  An organism that harbors a parasite.
      
      
   3. Infectious disease.  Organisms are growing in the host, causing a disease. (Compare meanings of infection and infestation.)
      
      
   4. Pathogenicity.  Ability of a pathogen to do harm to a host.
      
      
   5. Virulence.  Degree of damage done by a pathogen. Also, what degree of diversity of hosts are affected by the pathogen.
      
      
   6. Contagious disease.  Disease spread from one individual to another by various direct or indirect means.
      
      
   7. Epidemic.
      
      
   8. Endemic.
      
      
   9. Host's natural resistance.  Natural ability of a host to resist being harmed by a parasite. Can be due to the natural integrity of the host. Can also be due to being helped by such things as the normal flora.
      
      
   10. Host immunity.  Ability of a host to resist infection.
       
       
2. Koch and his Postulates:
   
   
   1. Who was Koch?
      
      
   2. Koch's Postulates  Proof that a microorganism causes a disease. This can apply to plants as well as animals.
      
      
      1. Infection.  The organism should be constantly present in animals suffering from the disease and should not be present in healthy individuals.
         
         
      2. Isolation.  The organism must be isolated from the animal in pure culture and this isolate should be characterized as fully as required.
         
         
      3. Re-infection.  The pure culture should cause the disease when inoculated into a healthy animal.
         
         
      4. Re-isolation.  The organism should be re-isolated and found to have the same properties (be of the same strain) as noted upon initial isolation.
         
         
3. Pathogenic mechanisms of bacteria.  There are two broad qualities of successful pathogens – ability to invade and ability to produce toxins.
   
   
   1. Invasive qualities.  Ability to enter, grow and spread in the host.
      
      
      1. Easy portals of entry for any potential pathogen.  Urogenital tract, gastrointestinal tract, respiratory tract, eyes. Significant numbers of bacteria not thought of as being pathogens can cause an infection, especially in areas where there are no or few other organisms to crowd them out. These are called "opportunistic pathogens." For example, E. coli can cause infections in the urinary tract and the eye.
         
         
      2. Colonization.  Bacterial surface components: Fimbriae (pili) and capsule help with adherance for the pathogen to get an initial foothold – build up numbers into a real and spreadable infection. Capsule can make cell more difficult to phagocytize.
         
         
      3. Spreading factors.  These are extracellular enzymes which break down specific host cell components. Collagenase breaks down collagen, the framework of muscles; bacteria that cause gangrene use this to facilitate their invasion. Hyaluronidase breaks down hyaluronic acid which binds connective tissue. Cellulase and pectinase break down cellulose and pectin which are important components of plant tissues (cellulose in cell wall and pectin the "cementing" substance between cells).
         
         
      4. Resistance to host defenses.  Invading organisms may be able to "hide" in areas where host defenses would not be activated, as an inflammatory response by the host would trigger phagocytes to action. Antigens which could trigger antibody formation can be "hidden" by surface components such as capsules.
         
         
   2. Toxin production.  Ability to produce a substance which is toxic to host cells or tissues.
      
      
      1. Endotoxins.  Part of the outer cell wall of gram-negative bacteria. ("Endo" actually means "inside" but here means not released away from the cell.)
         
         
      2. Exotoxins.  Some are among the most potent biological poisons known. These are secreted by the cells during exponential growth in the host (e.g., tetanus) or a food later consumed by the host (e.g., Staphylococcus food poisoning).
         
         
      3. Enterotoxins.  Exotoxins which act in the enteric tract.
         
         
4. The Spread of Pathogens.
   
   
   1. Some examples of methods:
      
      
      1. Direct contact with individuals (with active disease or in carrier state)
         
      2. Food
         
      3. Water
         
      4. Soil
         
      5. Fomites (clothing, toys, bedding, tools, implements, etc.)
         
      6. Air
         
      7. Insects
         
      8. Mites & ticks
         
         
   2. Preventing the Spread of Pathogens.
      
      
      1. Control of insects, mites, ticks and protection against them.
         
         
      2. Treatment of sewage.
         
         
      3. Control of human carriers.
         
         
      4. Sanitation/sterilization of foods, water, infected materials.  This can include heating (pasteurization or other applicable heat treatment), disinfection and irradiation.
         
         
      5. Slaughter and disposal of infected animals; destruction of infected plants.
         
         
      6. Ventilation, air purification.
         
         
      7. Adequate treatment of hosts.  Chemotherapy, antibiotics, immune serum, etc.
         
         
      8. Breeding resistant strains or varieties.
         
         
      9. Quarantine.
         
         
5. Host defense against pathogenic microorganisms.
   
   
   1. Natural (constitutive) defense.
      
      
      1. Skin and mucous membranes.  Effective anatomical defenses when intact.
         
         
      2. Microbicidal substances.
         
         
         1. Lysozyme.  Found in serum, saliva, sweat and tears. Lyses bacterial cells by degrading the peptidoglycan in the cell wall.
            
            
         2. Interferon.  Antiviral proteins produced by various types of cells. One type induces fever and contributes to inflammation.
            
            
         3. Complement.  Destroys invading bacteria and foreign cells by disrupting cytoplasmic membranes; also contributes to inflammation.
            
            
      3. Normal flora.  Compete for space with invaders. Can produce substances which act against other organisms – e.g., acid.
         
         
      4. Inflammation and phagocytosis.  Inflammation is tissue response to infection or injury: redness, swelling, heat, pain – some of which may be directly attributed to the invader. Overall effect of inflammation is to get the body's defence mechanisms to the scene where they can work efficiently. Higher temperature and slightly lower pH effected during inflammation can enhance defence mechanisms. Phagocytosis – ingesting organisms whole – is accomplished by specialized cells which act much like some protozoa do.
         
         
   2. Immune (inducible) defense.  Acquired immunity. Directed specifically against an invading pathogen.
      
      
      1. Two types of acquired immunity.
         
         
         1. Active.  This is due to formation of antibodies in the animal in response to antigens on the invading organism or its products.
            
            
         2. Passive.  This is acquiring antibodies from another individual (human or animal) or from tissue culture (monoclonal antibodies).
            
            
      2. Antigens and antibodies.
         
         
         1. Definition of an antigen.  Anything which causes a body to produce antibodies in an effort to neutralize it.
            
            
         2. Examples of antigens.  Proteins, pollens, food substances, viruses, cell wall and flagellar components of microbial cells, microbial toxins.
            
            
         3. Definition of an antibody.  What an animal produces to counteract a specific antigen. It's a protein present in serum or other body fluid.
            
            
         4. How antibodies protect host.  Accomplished by:
            
            
            1. Blocking the colonization of pathogens.
               
               
            2. Neutralization of toxins or viruses.
               
               
            3. Direct killing of bacterial cells (with complement – proteins that help bind the antibody to the antigen).
               
               
            4. Agglutination or precipitation of antigens.
               
               
            5. Making antigens more susceptible to phagocytosis and cell killing by host white blood cells.
               
               
      3. Artificial immunization.
         
         
         1. History of "vaccination."  It was long noted that individuals who contracted smallpox rarely got it again. Ancient Chinese would be inoculated with material from smallpox lesions – an extremely risky practice but successful often enough to continue to be practiced. Toward the end of the 18th century, British physician Edward Jenner noted that milkmaids who contracted cowpox rarely got smallpox. After injecting a small boy with material from a cowpox lesion and then exposing him to pus from a smallpox case, Jenner achieved success when the boy did not contract smallpox.
            
            
         2. Active: vaccine and toxoid.  Antigen or mixture of antigens injected to cause animal or human to produce antibodies. Attenuated or avirulent strains of pathogenic species are generally used. Modified ("detoxified") toxin which is still able to cause the animal or human to produce antibodies against the toxin.
            
            
         3. Passive: antitoxin, antiserum and immunoserum.  These terms refer to serum which contains one or more antibodies. Antitoxin specifically refers to serum which contains antibodies against a particular toxin.
            
            
         4. Current and future vaccination procedures.  Moving toward monoclonal antibodies, purified antigens, possibly DNA, etc.
            

PART TWO – INFECTIOUS DISEASES

1. Human Diseases.
   
   
   1. Examples. (* = in table below)
      
      
      1. Caused by invasive bacteria:  tuberculosis (Mycobacterium tuberculosis), bacterial pneumonia (Klebsiella pneumoniae, Streptococcus pneumoniae), cholera (Vibrio cholerae), Legionnaire's disease*, Lyme disease*, whooping cough (Bordetella pertussis), gonorrhea (Neisseria gonorrheae), meningitis (Neisseria meningitidis), strep throat (Streptococcus pneumoniae), gastric ulcers (Helicobacter pylori), gastrointestinal infections*, typhoid fever*, bubonic/pneumonic plague (Yersinia pestis). Also dental caries, boils, pimples, abscesses.
         
         
      2. Caused by toxigenic bacteria:  anthrax*, tetanus (Clostridium tetani), diphtheria (Corynebacterium diphtheriae), botulism*, staphylococcal food poisoning*, toxic shock syndrome (Staphylococcus aureus), hemolytic-uremic syndrome.*
         
         
      3. Caused by viruses:  common cold, influenza, viral pneumonia, measles, rubella, mumps, chickenpox, smallpox, poliomyelitis, herpes, hepatitis, AIDS, hantavirus pulmonary syndrome.
         
         
      4. Caused by fungi & protozoa (covered earlier):  blastomycosis, histoplasmosis; malaria, trypanosomiasis (sleeping sickness), amoebic dysentery, giardiasis, cryptosporidiosis.
         
         
   2. Some specific human diseases caused by bacteria:
      

   disease	causative agent	bacterial characteristics	transmission	symptoms
   Clostridium perfringens food infection	Clostridium perfringens	gram-positive, strictly anaerobic, endospore-forming rod	food-borne	cramps, diarrhea
   Staphylococcus aureus food poisoning	Staphylococcus aureus	gram-positive, facultatively anaerobic coccus	food-borne toxin	rapid onset of nausea, vomiting and cramping
   Salmonella food infection (gastroenteritis)	many Salmonella serotypes	gram-negative, facultatively anaerobic rod	food-borne	cramps, nausea, vomiting, diarrhea
   Typhoid fever	Salmonella serotype Typhi	gram-negative, facultatively anaerobic rod	food, water
   Shigellosis	Shigella	gram-negative, facultatively anaerobic rod	food, water	dystentery (bloody diarrhea)
   Hemolytic-uremic syndrome	Shiga toxin-producing strains of Shigella and E. coli	gram-negative, facultatively anaerobic rod	food, water	anemia, kidney failure, nervous system injury
   Anthrax	Bacillus anthracis	gram-positive, facultatively anaerobic, endospore-forming rod	food, inhalation, through opening in skin	tissue swelling, hemorrhage, circulatory failure
   Lyme disease	Borrelia burgdorferi	gram-negative, microaerophilic spirochete	ticks (mice and deer are among the animal reservoirs)	stage I: rash, flu-like symptoms with fever & chills, joint pains; stage II: acute effects on heart and nervous system; stage III: chronic arthritis and impairment of the nervous system
   Legionnaire's disease	Legionella	gram-negative rod	water	flu-like symptoms leading to major complications

   
   
2. Animal Diseases.
   
   
   1. Examples. (* = in table below)
      
      
      1. Caused by bacteria:  brucellosis*, mastitis*, tuberculosis*, Johne's disease (Mycobacterium paratuberculosis), anthrax*, Salmonella infections*, actinomycosis (Actinomyces israelii), scours, foot rot.
         
         
      2. Caused by viruses:  foot and mouth disease (covered earlier), hog cholera, Newcastle disease of poultry, rabies, pseudorabies of swine, canine distemper.
         
         
      3. Caused by prions (covered earlier):  mad cow disease, scrapie of sheep.
         
         
   2. Prevention and control.
      
      
      1. Sanitation and confinement.
         
         
      2. Vaccination.
         
         
      3. Antibiotics.
         
         
      4. Quarantine.
         
         
   3. Some specific animal diseases caused by bacteria:
      

   disease	causative agent	bacterial characteristics	transmission	symptoms
   Brucellosis, Bang's disease, undulant fever	species of Brucella	gram-negative rod	directly thru mucous membranes, skin abrasions, ingestion of infected milk	affects cattle, dogs, goats, pigs, humans, bison, elk, moose, caribou & reindeer; affects mammary glands & uterus in animals; in humans causes recurring fevers and may lead to bone infection
   Mastitis	Staphylococcus aureus, Streptococcus agalactiae	gram-positive cocci (S. aureus = fac. anaerobe; Strep. agalactiae = aerotolerant anaerobe)	direct contact	infection of mammary glands
   Tuberculosis (bovine)	Mycobacterium bovis	gram-positive, strictly aerobic, acid-fast rod	ingestion (transmitted to humans in milk)	infection and tissue nodulation in intestinal tract, lymph nodes, bones & joints
   Anthrax	Bacillus anthracis	gram-positive, facultatively anaerobic, endospore-forming rod	as for humans (above table)
   Salmonella diseases of poultry	Salmonella serotypes Pullorum and Gallinarum (would be classified as one serotype, but different biochemical reactions and disease symptoms require separation)	gram-positive, facultatively anaerobic, endospore-forming rod	direct contact and transmission thru eggs/into embryos	pullorum disease: high mortality with white diarrhea in young chicks & poults; fowl typhoid: high mortality with yellow diarrhea in young and adult poultry

   
   
3. Plant Diseases.
   
   
   1. Examples.
      
      
      1. Caused by bacteria:  soft rots (Erwinia) and wilts (Erwinia, Pseudomonas, Burkholderia, Ralstonia, Xanthomonas) of vegetables, galls (Agrobacterium tumefaciens), common potato scab (Streptomyces scabies).
         
         
      2. Caused by viruses and viroids:  mosaic diseases of cucumber, potato and bean; also peach yellows, aster yellows, curly top of sugar beets, potato spindle tuber viroid.
         
         
      3. Caused by fungi:  late blight of potato, powdery mildews, corn smut, Dutch elm disease, cereal rusts, white pine blister rust.
         
         
      4. Caused by abiotic factors:  nutritional deficiencies, mineral toxicities, toxicity due to pollutants (including pesticides).
         
         
   2. Prevention and control.
      
      
      1. Difficulties in controlling bacterial plant diseases.
         
         
         1. Organisms often overwinter in protected places.
            
            
         2. They can spread rapidly through direct contact.
            
            
         3. They can spread in wind.
            
            
         4. They can enter damaged plants fast.
            
            
         5. They can multiply rapidly once in compatible host.
            
            
      2. Sanitation.  Use of clean seed: growing plants for seed in uncontaminated areas (can involve different parts of country); hot-water treatments.
         
         
      3. Crop-rotation.  Alternating different "families" of plants.
         
         
      4. Chemical treatment.  Use of local and systemic fungicides and bactericides.
         
         
      5. Development of resistant varieties.
         
         
      6. Elimination of insect vectors.
         
         
   3. Symptoms of plant diseases caused by bacteria.
      

      
      Generalized Diagram of Plant Diseases.

      1. Rots.  Destruction of tissue, usually by enzymatic digestion of the "cement" between cells followed by the subsequent death of the cells. Pectinase, an extracellular enzyme produced by some species of Erwinia, destroys pectin.
         
         
      2. Wilts.  Invasion of bacteria followed by destruction or blockage of vascular tissue (that which conducts water).
         
         
      3. Leaf spots and blights.  Spots of dead cells sometimes surrounded by destruction of chlorophyll (green yields to yellow; photosynthetic capability of plant is decreased).
         
         
      4. Cankers and blights of woody tissue.  Destruction of woody tissue and subsequent death of distal portions.
         
         
      5. Galls.  Tumor-like proliferation and enlargement of cells, often interfering with water movement.
         

Some internet references:

Mechanisms of Bacterial Pathogenicity
Constitutive Defenses of the Host
Inducible Defenses of the Host
Medically-Important Bacteria
Common names of plant diseases
Plant diseases and damage

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Page last modified on 3/14/05 at 3:45 PM, CST. John Lindquist, Dept. of Bacteriology, University of Wisconsin – Madison