Livestock Immune Response

Immune Response Against Pathogens

The lecture focuses on the immune response against various pathogens in livestock, including bacteria, viruses, fungi, protozoa, and helminths.

Major Pathogens of Concern

  • Viral: African swine fever, Foot and Mouth Disease, deformed wing virus, lumpy skin disease, rotavirus.
  • Fungal: Nissima, Bacterochromatorium dendriticobatus, Pseudogemoniaecious destructus (white nose syndrome).
  • Bacterial: Foot rot (Dichelobacter nodosus), mastitis (polybacterial), American foulbrood, canine pyoderma.
  • Helminths: Haemonchus contortus, Teladorsagia circumcincta, Fasciola hepatica.
  • Protozoa: Theileria, Babesia, and Neospora.

Size of Pathogens

Pathogen size affects the immune response; larger pathogens like parasites trigger different responses compared to smaller bacteria or viruses.

Two Arms of the Immune Response

  • Innate Immune Response: The body's first line of defense, providing immediate but nonspecific protection through physical barriers like skin and immune cells.
  • Adaptive Immune Response: More specialized, taking longer to develop, involving T cells and B cells targeting specific pathogens and creating memory for future responses.

Innate Immune Response Against Viruses

Model: Rotavirus (A, B, C).

  • Rotavirus binds to intestinal lining, triggering an innate response.
  • The mucosal layer inhibits binding, and secretions like mucus act as barriers.
  • Enzymes and defensins neutralize pathogens; defensins are antimicrobial peptides.
  • Polyreactive immunoglobulins (natural antibodies) provide broad defense.
  • Innate immune cells: gamma delta T cells, macrophages, dendritic cells, and natural killer cells.
  • Infected cells express interferon alpha and interferon beta, signaling neighboring cells.
  • Infected cells present antigens through MHC class one and class two molecules.

Induction of Adaptive Immune Responses to Viruses

  • Antigen-presenting cells (APCs) sample viral antigens and migrate to lymph nodes.
  • APCs activate naive and memory T cells.
  • Th1 cells activate cytotoxic T cells, IgG-producing B cells, and natural killer cells.
  • Th2 cells activate IgA-producing B cells.

Antiviral Effector Mechanisms

  • Cytolysis: Cytotoxic T cells and natural killer cells directly kill virus-infected cells.
  • Antibodies: Prevent receptor binding, increase phagocytosis of free virus.
  • Complement Dependent Lysis: The complement system lysis virus-infected cells.
  • Treg Cells: Modulate the immune response.

Bacterial Pathogens

Model: E. coli and Salmonella.
E. coli shiga toxin causes edema disease via toxin binding, leading to increased fluid loss and high mortality.

Innate Immune Response to Bacterial Pathogens:

Enzymes, defensins, and polyreactive immunoglobulins, microbiome competes with pathogens.

Induction of Antibacterial Immune Responses:

Intestinal responses are predominantly Th2, occurring in draining lymph nodes.

Effective Molecules:

  • Antibodies block adhesion, bind toxins, aggregate, and lyse bacteria.
  • Complement system leads to complement-dependent lysis.
  • Activated macrophages become more phagocytotic.

Helminths

Model: Haemonchus contortus (barber pole worm).

Innate Immune Responses to Helminths:

  • Mucosal layer inhibits feeding and aids expulsion.
  • Mucus, enzymes, galectins, defensins, and polyreactive immunoglobulins.

Galectins

Proteins that bind carbohydrates, probing/blocking pathogen adhesion or directly binding to pathogens.

Immune Responses Mediated to Intestinal Nematodes:

  • Driven by Th2 response involving IgE antibodies and mast cells, reducing parasite establishment and survival.
  • IgA and eosinophils reduce nematode fecundity.

Protozoa

Vector-borne (Babesia, Leishmania, Trypanosomes) or intestinal (Cryptosporidium, Giardia).

Leishmania

Immune responses in dogs: resistant (Th1) vs. susceptible (Th2).

In resistant dogs, Th1 cells activate B cells and macrophages, leading to complement-mediated lysis and phagocytosis.

Fungal Infections

Canine aspergillosis caused by Aspergillus fumigatus.
Antigen-presenting cells activate Th1 and Th17 responses, leading to phagocytosis of fungal spores. Antibody-dependent cellular cytotoxicity and complement-dependent cytotoxic pathways are also involved.

Summary of Immune Responses

  • Innate: Similar across pathogens, involving mucus, enzymes, defensins, and polyreactive immunoglobulins.
  • Adaptive:
    • Bacteria/Viruses: Th2 response, antibodies block receptor binding.
    • Fungal: Th1 and Th17.
    • Protozoa: Th1.