Animal Health Midterm 2

What three determinants of disease that determine the outcome of an infection?

• Agent: Pathogenicity and virulence (e.g., viruses, bacteria, fungi, parasites)

• Host: Immunity and susceptibility (human or animal)

• Environment: Housing, climate, healthcare settings, travel

What are the components of the host's innate defense system against bacterial infections?

• Physical, physiological, and cellular defenses

• Acute inflammation (neutrophil migration)

• Monocyte-macrophage system

• Normal bacterial flora

• Complement system (activated via LPS and mannose-binding pathways)

What are the components of the host's adaptive defense system against bacterial infections?

• Passive immunity: Transferred through colostrum

• Active immunity: Derived from T and B lymphocytes

What two main capabilities determine a bacterium's pathogenicity?

1. Ability to infect cells: Adhesion, multiplication, colonization, tissue invasion, and circumvention of host defenses.

2. Ability to damage cells: Release of toxins (endotoxins/exotoxins), cytolysis, and invasion of the extracellular matrix.

Flagella — Structure & Primary Function

• Structure: Helical appendage; single = flagellum, plural = flagella.

• Function: Motility (movement toward or away from stimuli) via a rotating motion.

Fimbriae — Structure & Primary Function

• Structure: Short, straight appendages; more numerous than flagella.

• Function: Helps bacteria attach to host cells and other bacterial cells.

• Pathogenicity Example: Salmonella uses fimbriae to attach to host cells and form biofilms with other Salmonella.

Pili — Structure & Primary Functions

• Structure: Longer and less numerous than fimbriae; best seen under electron microscopy when coated with viruses.

• Functions:

  • Attachment to mucosal membranes

  • Gene transfer (conjugation)

  • Twitching motility (gliding via extension and retraction)

  • Viral receptors

What are the major bacterial surface structures mentioned in the lecture?

Flagella, Fimbriae, Pili, Glycocalyx (capsule/slime layer)

How do pili contribute to specific animal diseases like E. coli infections and UTIs?

• Colibacillosis in pigs: E. coli uses pili to attach to the intestinal mucosa.

• Urinary Tract Infections (UTIs): Attachment pili allow bacteria to adhere to mucous membranes and resist the flushing action of urine.

What is bacterial conjugation, and what structure facilitates it?

• Conjugation: The process of gene transfer (bacterial "sexual reproduction").

• Structure: Facilitated by the F-pilus (fertility pilus).

• Significance: Allows the transfer of antibiotic resistance and other virulence genes between bacteria.

Glycocalyx — Definition & Functions

• Definition: An external polysaccharide or protein coating located outside the cell wall.

• Functions: Protects against the immune system (anti-phagocytic), enables attachment, resists drying/desiccation, serves as a nutrient reservoir, and acts as a waste depot.

What is the difference between a Slime Layer and a Capsule?

• Slime Layer: Glycoproteins are loosely associated with the cell wall; primarily protects against dehydration and nutrient loss.

• Capsule: Polysaccharides are firmly attached to the cell wall; has a gummy/sticky consistency that provides protection and attachment to solid surfaces/nutrients.

What are the three forms of mucoid-like glycocalyx structures?

Capsule, Slime layer, Biofilm

Bacterial Cell Wall — Functions

• Maintains cell rigidity and prevents the cell from bursting (osmotic lysis).

• Defines bacterial shape.

• Serves as an environmental barrier.

What are the primary bacterial shapes mentioned in the slides?

• Coccus: Spherical

• Coccobacillus: Oval / intermediate between sphere and rod

• Bacillus: Rod-shaped

• Vibrio: Curved rod / comma-shaped

• Spirillum: Rigid spiral

• Spirochete: Flexible spiral

Peptidoglycan — Composition & Immunological Significance

• Composition: Made up of polysaccharides cross-linked with amino acids.

• Significance: Unique strictly to bacteria (not found in eukaryotes) and acts as a strong stimulant of the host immune system.

How does the cell wall envelope of Gram-negative bacteria differ from Gram-positive bacteria?

Gram-negative bacteria possess an outer cell membrane located outside of their peptidoglycan layer

Internal Bacterial Structures — Key Components & Functions

• Nucleoid: Area containing the coiled bacterial circular DNA.

• Plasmids: Small, extrachromosomal DNA rings that carry non-essential/virulence/resistance genes.

• 70S Ribosomes: Protein synthesis machinery.

• Cytoplasmic Inclusions: Storage deposits for nutrients or reserves.

• Plasma Membrane: Phospholipid bilayer controlling transport into/out of cytoplasm.

What type of bacterial motility involves pili?

Twitching motility — the ability of bacteria to glide along a solid surface through the extension and retraction of the pilus

Why do Salmonella resist cleaning in food processing environments, and what role do surface structures play?

They form biofilms. Salmonella use fimbriae to adhere to surfaces and attach to other Salmonella cells, creating a protective, mucoid glycocalyx matrix (biofilm) that resists cleaning processes.

How do Gram-positive and Gram-negative bacterial cell walls differ structurally?

• Gram-positive: Thick layer of peptidoglycan; contains lipoteichoic acids (LTA); cell wall is less complex and consists almost entirely of a single type of molecule.

• Gram-negative: Complex, multilayered cell wall with a thin layer of peptidoglycan, an outer membrane containing lipopolysaccharides (LPS), and a periplasmic space.

What are the two major groups bacteria are divided into based on their Gram stain reaction?

Gram-positive (Gram +ve) & Gram-negative (Gram -ve)

What is Lipoteichoic Acid (LTA), where is it found, and how does it influence virulence?

• Definition/Location: Important surface antigen found exclusively in Gram-positive bacteria that anchors peptidoglycan to the cytoplasmic membrane.

• Virulence Role: Acts as an important antigen that stimulates the host's immune system.

What is Lipopolysaccharide (LPS), where is it found, and how does it influence virulence?

• Definition/Location: A major surface antigen embedded in the outer membrane of Gram-negative bacteria.

• Virulence Role: Acts as an endotoxin; triggers host complement activation, cytokine release, inflammatory responses, and severe toxic effects (endotoxic shock).

What two structural components make up Lipopolysaccharide (LPS) as shown on cell wall diagrams?

• O antigen (polysaccharide portion extending outward)

• Lipid A (lipid component embedded in the membrane)

What is an endotoxin, and what severe systemic response can large amounts of it cause?

• Endotoxin: Another name for Lipopolysaccharide (LPS).

• Systemic Response: Triggers endotoxic shock, which is characterized by fever and vascular changes.

How does LPS interact with the host's innate immune system, and what clinical symptoms result?

• Immune Activation: Acts as an innate activator of the complement cascade that causes cytokine release and inflammatory cell recruitment.

• Clinical Symptoms: Triggers violent symptoms such as diarrhea, vomiting, and gas production (e.g., during Salmonella spp. and E. coli infections).

What is the structure and function of the outer membrane in Gram-negative bacteria?

• Structure: Phospholipid bilayer carrying a negative charge and embedded with porins and LPS.

• Function: Forms a selective barrier similar to the plasma membrane of eukaryotic cells.

What are porins in Gram-negative bacteria, and what is their eukaryotic equivalent?

• Definition: Transmembrane protein channels located in the outer membrane of Gram-negative bacteria.

• Eukaryotic Equivalent: Function similarly to transmembrane transport proteins in eukaryotic cells.

What is the periplasmic space (periplasm)?

The fluid-filled compartment in Gram-negative bacteria located between the outer membrane and the inner cytoplasmic membrane, containing the thin peptidoglycan layer.

Which pathogenic bacteria lack a cell wall, and how do they maintain membrane integrity?

• Organism: Mycoplasma spp.

• Mechanism: They lack a cell wall entirely but incorporate sterols into their cell membrane for added strength.

What is the structure and primary functions of the bacterial cytoplasmic membrane?

• Structure: Phospholipid bilayer containing integral and peripheral membrane proteins.

• Functions:

  1. Retains cytoplasm

  2. Acts as a selectively permeable barrier with transport proteins

What are the components and functions of the bacterial cytoplasm?

• Cytosol: Thick, transparent fluid that suspends organelles and serves as the site for anaerobic metabolic reactions.

• Organelles/Structures: Holds genetic material (DNA/plasmids) and protein synthesis machinery (ribosomes).

Where is genetic material found within a bacterial cell?

• Chromosomal DNA (located in the nucleoid)

• Plasmid DNA (extrachromosomal rings)

What is bacterial chromosomal DNA, and what function does it serve?

• Location/Structure: Located in the nucleoid region; typically a single, circular double-stranded DNA molecule.

• Function: Encodes essential cellular functions ("housekeeping genes") and proteins required for basic growth and survival.

Key genomic facts of Escherichia coli chromosomal DNA:

• Single, circular double-stranded DNA chromosome

• Contains approximately 4.68 million base pairs

• Contains about 4,300 genes

What is plasmid DNA, and what functions does it serve?

• Structure: Small, circular double-stranded DNA that replicates independently of the bacterial chromosome.

• Function: Codes for protective/accessory characteristics, including virulence determinants and antimicrobial resistance (AMR) genes.

How are plasmids transferred between bacterial cells, and can they integrate into the genome?

• Transfer: Transferred cell-to-cell via conjugation (using pili), even between different species of bacteria.

• Integration: Yes, plasmids can occasionally incorporate directly into the bacterial host chromosome.

What are bacterial ribosomes made of, and what is their function?

• Composition: Complexes of protein and RNA (70S in prokaryotes).

• Function: Sites of mRNA translation into new proteins.

Compare and contrast the cell envelope layers from innermost to outermost for Gram-positive vs. Gram-negative bacteria

• Gram-positive: Cytoplasmic membrane —> Thick Peptidoglycan (with LTA).

• Gram-negative: Cytoplasmic membrane —> Periplasmic space (with thin Peptidoglycan) —> Outer membrane (with LPS & Porins).

Why are epidemiologists much more concerned about finding plasmid-associated antimicrobial resistance (AMR) genes than chromosomal AMR genes?

Because plasmids replicate independently and can be rapidly transferred horizontally between different cells and even different species of bacteria via conjugation (pili), spreading resistance across populations much faster than chromosomal genes passed strictly through cell division.

What is the primary role of lipoproteins in the Gram-negative cell wall?

Lipoproteins anchor the outer membrane to the underlying thin peptidoglycan layer within the periplasmic space.

Which structural component of bacteria is targeted by scientists for bacterial classification?

The cell wall.

How does cytosol facilitate bacterial metabolism?

It acts as the fluid suspension site where anaerobic reactions take place within the cell.

What is virulence in bacterial infections?

Measures how effectively a bacterium can establish an infection, evade the body's defenses, and harm tissues.

What are the four main steps in the bacterial infectious disease process, and how is harm caused to the host?

Enter host, Multiply, Evade host defenses, Harm host

How harm is caused: Harm occurs through both bacteria-mediated pathogenesis (secreted toxins causing somatic cell damage) and host-mediated pathogenesis (prolonged immune and inflammatory responses to bacterial antigens by leukocytes).

What roles do bacterial virulence factors play during an infection?

Virulence factors assist bacteria in:

1. Attachment (e.g., Type 1 fimbriae, H antigen, surface appendages)

2. Invasion and Motility (e.g., Flagellum)

3. Evading the immune system (e.g., Vi capsule antigen inhibiting complement binding; O antigen & H antigen inhibiting phagocyte killing; antiphagocytic proteins)

4. Causing harm (e.g., Cytotoxins, Enterotoxins, Endotoxins)

Compare the fundamental differences in origin and release mechanisms between Exotoxins and Endotoxins.

• Exotoxins: Produced and excreted by both Gram-positive and Gram-negative bacteria as they live, divide, and grow in numbers.

• Endotoxins: Derived exclusively from the outer membrane (LPS layer) of Gram-negative bacteria and are released primarily when the bacteria die and lyse.

What are the three functional categories of exotoxins based on their targets?

• Cytotoxins: Directly damage or lyse host cells.

• Neurotoxins: Disrupt nerve signal transmission and neuromuscular function.

• Enterotoxins: Target gastrointestinal cells and alter fluid/electrolyte transport.

How does the Cytotoxin alpha-toxin from Staphylococcus aureus cause cell death?

• Mechanism: alpha-toxin forms a pore/channel directly in the host cell membrane.

• Effect: causes potassium efflux and loss of essential cellular nutrients, leading directly to cell lysis/death and damage to immune cells.

Describe the mechanism and clinical symptoms of Tetanus toxin (tetanospasmin) from Clostridium tetani.

• Mechanism: Blocks the release of the inhibitory neurotransmitter glycine at the neuromuscular junction (glycine normally inhibits acetylcholine release).

• Effect: Prevents muscle relaxation —> causes continuous stimulation by excitatory transmitters —> leads to spastic paralysis ("lock jaw", stiff-legged gait, elevated tail/ears).

Describe the mechanism and clinical symptoms of Botulinum toxin from Clostridium botulinum.

• Mechanism: Blocks the release of acetylcholine (ACh) from vesicles at the motor end plate of the neuromuscular junction.

• Effect: Blocks nerve stimulation of muscles —> muscles cannot contract —> leads to flaccid paralysis.

Explain the A-B toxin system using Cholera toxin (Vibrio cholerae) as an example.

• B subunit ("The lock picker"): Binds to ganglioside receptors on the cell membrane and facilitates entry of the A subunit into the host cell.

• A subunit ("The bad guy"): Increases adenylate cyclase activity —> increases cyclic AMP (cAMP) —> causes massive loss of sodium, water, chloride, potassium, and bicarbonate —> severe diarrhea and dehydration.

What component of Gram-negative bacteria constitutes an endotoxin, and what common bacterial genera release it upon cell death?

• Component: Lipopolysaccharide (LPS) found in the outer cell membrane.

• Genera: Escherichia coli, Salmonella spp., Pseudomonas spp., Haemophilus, and Bordetella spp.

Describe the step-by-step systemic pathogenesis of Endotoxemia when large amounts of LPS enter the bloodstream.

• LPS causes release of pro-inflammatory cytokines (TNF, IL-1) from macrophages and endothelial cells.

• Activation of the complement cascade (C3a, C5a) releasing endogenous pyrogens.

• Activation of the coagulation cascade and platelets.

• Increased vascular permeability and vasodilation leading to hypotension and shock.

What specific clinical conditions and pathology are triggered by systemic LPS release in animals?

• Fever: Induced by pyrogenic cytokines (TNF, IL-1) acting on host pathways.

• Disseminated Intravascular Coagulation (DIC) & Thrombosis: Clotting cascade activation.

• Hypotension & Shock: Increased vascular permeability and mast cell mediators.

• Hypoglycemia: Liver function alteration.

• Decreased serum iron levels.

Do Gram-positive bacteria produce endotoxins? What molecule in Gram-positive bacteria mimics LPS action?

• No, Gram-positive bacteria do not have LPS/endotoxin.

• Lipoteichoic acid (LTA) (from Gram-positive cell walls, e.g., Staphylococcus aureus) behaves like an endotoxin.

• LTAs act as superantigens, stimulating large numbers of immune cells to cause complement activation, massive inflammation, and tissue damage.

How do Exotoxins and Endotoxins differ in terms of chemical structure and origin?

• Exotoxins: Secreted proteins produced by both Gram-positive and some Gram-negative bacteria.

• Endotoxins: Lipopolysaccharides (LPS) integral to the outer membrane of Gram-negative bacteria, released upon cell lysis.

How do Exotoxins and Endotoxins differ in their mode of action and clinical symptoms?

• Exotoxins: Highly specific; bind to specific host cell receptors causing distinct effects (cytotoxic, enterotoxic, neurotoxic).

• Endotoxins: General, non-specific physiological effects across host systems (fever, diarrhea, vomiting, systemic shock).

Compare the toxicity levels of Exotoxins vs. Endotoxins.

• Exotoxins: Highly toxic, frequently fatal even in minute doses.

• Endotoxins: Weakly toxic per molecule, rarely fatal unless released in large quantities causing endotoxic shock.

Compare the pyrogenicity (fever production) of Exotoxins vs. Endotoxins.

• Exotoxins: Do not inherently produce fever in the host.

• Endotoxins: Highly pyrogenic (reliably induce fever via host cytokine release).

How do Exotoxins and Endotoxins differ in immunogenicity and host neutralization?

• Exotoxins: Highly immunogenic; stimulate the production of specific neutralizing antibodies (antitoxins).

• Endotoxins: Produce an immune response, but the host immune response is unable to neutralize the toxin.

Why do exotoxins make effective vaccines while endotoxins do not?

• Exotoxins: Because they are highly immunogenic protein molecules, they can be inactivated (in the form of toxoids, e.g., Tetanus toxoid) to safely induce protective neutralizing antibodies.

• Endotoxins: The host immune response cannot neutralize LPS toxicity, and the host's own immune hyper-reactivity causes the damage; thus, endotoxins are poor vaccine candidates.

What is the fundamental difference in how damage is caused between Exotoxins and Endotoxins?

• Exotoxins: The toxin itself directly damages the host cells.

• Endotoxins: The host’s own immune system causes the damage due to hyper-activation of inflammatory and complement cascades triggered by the toxin.

Which host immune cells are primarily activated by LPS to release pro-inflammatory cytokines during endotoxemia?

• Macrophages (Mphi)

• Endothelial cells (cells lining blood vessels)

• Polymorphonuclear leukocytes (PMNs) / Granulocytes

What are Strict Aerobes, and what is their relevance to animal health and pathology?

• Definition: Bacteria that require oxygen (O2) to grow.

• Pathology: Only a few strict aerobes are pathogens. They primarily cause skin and burn infections.

What are Facultative Anaerobes, and how common are they among pathogens?

• Definition: Microorganisms that use oxygen if it is available, but can switch to anaerobic methods of energy production when oxygen is absent.

• Prevalence: Includes all fungi, most bacteria, and most pathogens.

What are Microaerophiles? Give a specific bacterial example.

• Definition: Bacteria that require oxygen for energy production, but are harmed by standard atmospheric oxygen concentrations (21% O2).

• Example: Campylobacter spp.

What are Strict Anaerobes, and what bacterial genus is a classic pathogenic example?

• Definition: Bacteria for which oxygen (O2) is toxic.

• Example: Clostridium spp.

What are the primary macronutrients required by bacteria, and what percentage of a bacterial cell is carbon?

• Primary Macronutrients (needed in large amounts): Carbon, Hydrogen (H), Oxygen (O), Nitrogen (N), Phosphorus (P), Magnesium (Mg), Calcium (Ca), Sodium (Na), and Potassium (K).

• Carbon Content: Carbon makes up 50% of a typical bacterial cell. Nitrogen makes up 12%.

What are micronutrients and growth factors in bacterial metabolism, and what is the role of iron?

• Micronutrients (trace amounts): Iron (Fe), which plays a major role in cell respiration.

• Growth Factors: Vitamins, amino acids, purines, and pyrimidines.

How do pathogenic bacteria acquire iron (Fe) inside a host animal?

• In host animals, iron is tightly bound to host proteins.

• Pathogens produce specialized iron-scavenging molecules called siderophores to steal bound iron from the host.

What process do bacterial cells use to replicate?

Binary Fission: A parent cell replicates its genetic material and divides into two identical daughter cells.

What is "Generation Time" (GT) in bacterial growth?

• The time it takes for a population of bacteria to double in number (also known as doubling time).

• It ranges from 20 minutes to several days depending on the bacterial species and environmental conditions.

What occurs during the Lag Phase of the bacterial growth curve?

• Cells are adapting to their new environment and preparing to divide.

• There is no net increase in cell numbers.

• Duration ranges from hours to days.

What occurs during the Log (Exponential) Phase of the bacterial growth curve?

• Bacteria divide at their maximum rate.

• Clinical Significance: Bacteria are most sensitive to antibiotics and radiation during this phase.

What occurs during the Stationary Phase of the bacterial growth curve?

• Growth rate slows down because nutrients become exhausted and toxic wastes accumulate.

• Rate of growth = Rate of death, resulting in a plateau on the growth curve.

What occurs during the Death Phase of the bacterial growth curve?

• Death Rate > Growth Rate.

• The population of viable cells experiences a steady decrease over time.

What is a vegetative bacterial cell?

A bacterial cell that is metabolically active and capable of actively growing and replicating.

What is an Endospore, and which bacterial genera are famous for forming them?

• Definition: A highly resistant, dormant stage produced by certain bacteria that allows them to survive extreme environments.

• Key Genera: Clostridium spp. and Bacillus spp.

What triggers endospore formation, and what are its key characteristics?

• Trigger: Usually brought on by a lack of nutrients (starvation).

• Characteristics:

  • Resistant to heat, UV radiation, chemicals, and drying

  • Not capable of replicating

  • Able to survive/persist in extreme environments for decades

What are Sporulation and Germination?

• Sporulation: The process where a vegetative bacterial cell converts into a dormant endospore when conditions become adverse.

• Germination & Outgrowth: The process where an endospore rapidly returns to an active, growing vegetative state when favorable conditions return.

Summarize the complete Sporulation and Germination cycle.

Vegetative cell —> Sporulation (due to harsh conditions/nutrient loss) —> Lysis of mother cell —> Free Endospore —> Germination and Outgrowth (when favorable conditions return) —> Active Vegetative Cell.

Why do endospores pose significant challenges in animal health and veterinary sanitation?

• Because endospores survive heat, drying, chemical disinfectants, and UV radiation, standard cleaning methods fail to eliminate them from environment/equipment.

• They can persist in soil and animal housing for decades, repeatedly causing infections (e.g., Clostridium infections like tetanus or blackleg) when ingested or introduced into wounds.

What are the key agent characteristics of Mycobacterium spp.?

• Gram-positive, non-motile, non-spore forming rod-shaped bacilli.

• Obligate aerobe (can survive but not grow in anaerobic environments).

• Facultative intracellular organism.

• High cell wall lipid content containing mycolic acid.

Which primary Mycobacterium species affect humans versus bovine hosts?

• Mycobacterium tuberculosis primarily infects human hosts.

• Mycobacterium bovis primarily infects bovine hosts (cattle).

What structural component gives Mycobacterium its acid-fast property and environmental resistance?

Mycolic acid bound to cell wall peptidoglycan creates a waxy, hydrophobic consistency that resists environmental factors, desiccation, and disinfectants. It requires Ziehl-Neelsen (ZN) staining to visualize.

What role does Lipoarabinomannan (LAM) play as a virulence factor?

• LAM has immunoregulatory and anti-inflammatory effects:

  • Inhibits T-cell proliferation.

  • Inhibits macrophage activity.

  • Contributes to granuloma formation.

How does Mycobacterium evade host defenses inside macrophages?

Once phagocytosed, it inhibits the fusion of the phagosome and lysosome, allowing it to survive and replicate inside the macrophage's phagosome.

How is Tuberculosis transmitted into the host?

• Inhalation: Inhaled airborne droplets containing bacteria (<3 bacilli/droplet; ~3,000 droplets per cough/5 min talking).

• Ingestion: Consuming infected raw milk (enters via mesenteric lymph nodes).

What host factors influence the severity of Tuberculosis infection?

Immune status. Immunocompetent hosts mount a protective cell-mediated immune (CMI) response. Immunocompromised or malnourished hosts fail to contain the bacteria, leading to extensive tissue damage, necrosis, and dissemination.

What type of hypersensitivity reaction and immune response drive TB granuloma formation?

A Type IV (delayed-type) hypersensitivity driven by Cell-Mediated Immunity (CMI). Antigen-presenting macrophages activate TH1 cells, which release cytokines (IFN-gamma, TNF) to recruit more macrophages, cytotoxic T cells, and form granulomas.

What are the key cellular components of a TB granuloma?

• Infected, enlarged macrophages and foamy macrophages

• Multinucleated giant cells and epithelioid cells

• Lymphocytes (T_H and T_C cells)

• Surrounding fibrous cuff/fibroblasts

What is caseous necrosis in a TB granuloma, and what happens when it breaks down?

Lytic enzymes from macrophages turn the center of the granuloma into a semi-solid, cheesy mass. Breakdown of the granuloma releases free mycobacteria into airways/tissues, causing active disease spread and coughing.

What is Miliary TB?

Disseminated tuberculosis where bacteria spread via blood, lymphatics, or migrating macrophages, forming many small foci of infection in organs like bones, lymph nodes, lungs, urogenital tract, and mammary glands.

What is the standard diagnostic screening test for bovine TB in cattle?

The Caudal Fold Skin Test (CFT). Tuberculin (purified cell wall protein) is injected intradermally into the caudal fold, and the site is examined 72 hours later for delayed-type hypersensitivity swelling.

Why should you wait 3–6 weeks after suspected exposure before testing cattle for TB?

Mycobacterium grows very slowly, so it takes several weeks for the host to develop a measurable cell-mediated immune response. Early tests may yield false negatives.

What do Test Sensitivity and Test Specificity mean in TB diagnostics?

• Sensitivity: Percentage of true positive cases detected by the test.

• Specificity: Percentage of positive test results that are truly infected.

What is the main wildlife reservoir for Bovine TB in Michigan?

White-tailed deer (particularly in counties like Oscoda County).

How do white-tailed deer transmit bovine TB to domestic cattle herds?

Through shared food and water sources, or living in and sharing the same pasture areas.