BACTE MODULE 1

• Disease

  ➢ alteration or deviation of the normal state of

  the body that disturbs or interrupts the

  proper performance of physiological

  functions
• Infection

  ➢ entry of a living agent into an animal’s body

  and sets up disturbance in body functions
• Causes of diseases

  1. External

  ➢ Bacteria, Protozoa, Viruses, Parasites

  ➢ Trauma, Heat, Cold

  ➢ Vitamin/trace element deficiencies

  ➢ Chemical poisons

  2. Internal

  ➢ Metabolic and endocrine abnormalities,

  ➢ Organ degeneration, neoplasms, genetic

  defects, Autoimmunity
• Sources of Infection

  1. Direct or immediate contact with diseased

  animal

  2. Contact through fomites

  3. Contact with disease carriers (serve as carriers

  of infection)

  4. Infection from the environment

  5. Infection from food and water

  6. Air-borne infections

  7. Infections from blood sucking arthropods

  8. Iatrogenic infections

  9. Nosocomial infections

  10. Endogenous infection
• Portals of Entry

  ❖ Routes or pathways by which pathogens

  enter the body and initiate infection

  ➢ Through cuts and abrasions of the skin

  ➢ Through the mucus membranes of the

  respiratory tract

  ➢ Through the eyes, mouth, gastro-

  intestinal

  tract and genito-urinary tract
• Fates of infecting

  pathogens

  ➢ Destruction of the pathogen by the host’s

  tissues

  ➢ Elimination of the pathogen in the host’s

  secretions and excretions

  ➢ Destruction of the pathogen with the host’s

  carcass

  ➢ Organism and host can reach an impasse
• Virulence (indicates the degree of pathogenicity)

  ➢ Involves a set of morphologic, biochemical and

  functional traits present for a successful disease

  production
• Properties of Pathogenic Bacteria

  
  

  1. Virulence

  2. Ability to propagate in tissues and on body surfaces

  3. Ability to produce other active substances that enhance microbial virulence
• Gene-controlled Virulence

  of bacteria

  ➢ Antibiotic resistance due to the presence of R-factors

  ➢ Heavy metal resistance

  ➢ Toxin production

  ➢ Heat stability

  ➢ Heat-labile enterotoxin production

  ➢ Cell penetration

  ➢ Iron penetration

  ➢ Iron chelation

  ➢ Adhesin production

  ➢ Colonization factor

  ➢ Edema disease toxin

  ➢ Colisin production

  ➢ Hemolysin factor
• Plasmid-related Virulence of

  bacteria

  ➢ Colonizing antigens (fimbriae and capsule)

  • K88 (F4), K99 (F5) of E. coli

  ➢ Enterotoxin production

  • ST (heat-stable), LT (heat-labile) enterotoxins

  ➢ Edema disease toxin

  ➢ Resistance to complement –mediated killing

  ➢ Iron scavenging

  ➢ Hemolysin

  ➢ Anthrax capsule and toxin

  ➢ Tetanus hematoxins and neurotoxins

  ➢ Enteroinvasive ability (Salmonella sp.)

  ➢ Invasive ability (Yersinia sp.)
• Elements for the

  production of infection

  ➢ Organ Colonization

  ➢ Penetration of Host surfaces

  • passage of bacteria between cells

  ➢ Dissemination

  • mediated by enzymes

  ➢ Microbial growth in tissues
• Organ colonization

  ➢ Pathogen attachment to host

  surfaces ( interaction between

  pathogen adhesins and host

  receptors)

  ➢ Attachment of organisms (resist

  being swept away by the natural

  cleansing forces of peristalsis,

  ciliary action and fluid flow)
• manifestation of organ

  colonization

  ➢ Mucosa of the small intestines of swine

  (E. coli K88 and K99 positive strains)

  ➢ Tracheal cilia and bronchi of dogs

  (B. bronchiseptica)

  ➢ Attachment to the bronchial epithelium of

  chickens (Mycoplasma gallisepticum)

  ➢ Attachment to the pharyngeal epithelium of

  horses (Streptococcus equi )

  ➢ Adherence to the epithelial cells of the

  mammary ducts of cows (Staphylococcus

  aureus)
• Bacterial adhesins

  ➢ Fimbrial proteins of E. coli and

  Salmonella sp.

  ➢ P-1 protein of Mycoplasma

  pneumonia

  ➢ Afimbrial surface proteins of

  Streptococci sp.
• Host receptors

  ➢Fibronectin (Streptococci and

  Staphylococci)

  ➢Mannose (E. coli)

  ➢Sialic acid (M. pneumonia)
• Inhibitors of bacterial attachment

  ➢ Bacteriocins

  ➢ Microcins

  ➢ Lysozymes

  ➢ Lactoferrins

  ➢ Organic acids
• Microbial growth in tissues Neutralization of host defenses by a pathogen and initiate relevant adaptations
• Capsule (capsular galactan) Antiphagocytic bacteria

  B. anthracis

  K. pneumonia

  S. equi

  P. aeruginosa
• Membrane protein antiphagocytic bacteria S. equi
• Adenylate cyclase-Inhibits chemotaxis, phagocytosis and immuno-effector cell functions. B. pertussis
• Cytotoxin- Damages alveolar macrophages and polymorphonuclear leukocytes P. hemolytica
• Leukocidin-Damages leukocytes S. aureus
• O-polysaccharide structure-Diminishes activation of complement

  Salmonella sp.
• Serum resistance-Diminishes complement- mediated

  bacterial killing

  E. coli
• Iron capture-Enhances bacterial growth

  E. coli
• Cell wall sulfolipids-Inhibits phagolysosomal fusion

  Mycobacteria

  sp.
• Phospho-lipase-Induces lysis of phagolysosomal membranes

  Rickettsia sp.
• IgA protease-Induces proteolysis of IgA

  Hemophilus sp.

  Neisseria sp.
• Bacteria-related injury to tissues

  ➢Potent toxins circulate in the body

  through the blood (neurotoxin and

  tetanospasmin of C. tetani)

  ➢Release of bacterial enzymes damage cell

  membranes and body components

  (lecithinase and phospholipids)

  ➢Bacterial cell wall components exert a

  cascade of pathological conditions on

  host (endotoxins)
• Biological effects of endotoxins

  ➢Fever

  ➢Hypotension (pooling of blood in the

  splanchnic vasculature)

  ➢Intravascular coagulation (DIC)

  ➢Hemorrhage

  ➢Neutropenia and thrombocytopenia

  ➢Hyperglycemia

  ➢Complement depletion
• Host’s response to infection

  ➢Entry of a pathogen to a susceptible host

  ➢Rapid changes in the local vasculature ➢Fever ➢Immune responses
• ➢Local immune responses

  • Antibody production (Tonsils)

  • Production of macrophages, neutrophils,

  lymphocytes, eosinophils and plasma cells (Trachea

  and bronchi’s lamina propria)

  • Alveolar macrophages (Lungs)

  • IgA production (Cells of the Peyer’s patches of the

  intestines)

  • IgA immobilizes pathogenic protozoa (Neutrophils

  and plasma cells of the female genital tract)

  • Urinary tract produces IgG and IgA

  • IgA is secreted (plasma cells of the Lacrimal glands)

  • Plasma cells (Joints)

  • Neutrophil production (Mammary glands)