Parasitology

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Mastitis

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Primarily a disease of dairy cattle but may occur in beef cattle, sheep, goats, pigs and horses, small animals and humans;

Most common and costly disease in dairy cattle

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Define Mastitis

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the inflammation of one or more quarters of the udder, producing an increase in somatic cells

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Causes of Inflammation from Mastitis

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Chemical;

Thermal;

Bacteria and;

Mechanical injury

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Impact of Mastitis in Dairy animals

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May result in...

Reduced milk production;

Loss of functional quarter or udder;

Possible death/culling of cow

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Somatic Cells

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Cells from the cow- predominantly WBCs- that are normally present in milk;

The number of somatic cells present in the udder increases to help the cow fight the infection causing mastitis (Monitored by Somatic Cell Count)

Important n the identification and management of mastitis

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Subclinical Mastitis

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Hugely significant, 97% of mastitis cases are subclinical;

No changes to udder;

No visible change in milk;

Difficult to detect, manage, and treat (comes with economical penalties)

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Clinical Mastitis

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Still significant but manageable;

See clinical signs- noticeable changes to udder

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Main Categories to help Identify, Manage, and Treat Mastitis

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Environmental pathogens;

Contagious pathogens

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Contagious Pathogen Transmission

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Cow to cow;

Farmer to cow;

Equipment to cow;

Generally at time of milking

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Contagious Mastitis Pathogens

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Staph. aureus;

Strep. agalactiae;

Mycoplasma bovis

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Staph. aureus

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Located on the skin and teat canal;

May spread cow-cow by horn flies;

Opportunistic pathogen in teat lesions;

Mostly subclinical;

Produces variable somatic cell counts;

Rarely causes somatic cell counts;

Impossible to eradicate;

Very challenging to treat/manage;

Vaccine exists- variable efficacy

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Strep. agalactiae

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Pathogen can only live in mammary gland;

Often subclinical;

May produce high somatic cell counts;

Rarely causes systemic illness

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Mycoplasma bovis

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Less commonly seen than Staph or Strep infections;

Spread by aerosol transmission;

History includes: recent introduction of new animals, previous outbreak of respiratory disease, previous outbreak of cattle with swollen joints, clinical mastitis not responding to treatment, and mastitis affecting more than one quarter at a time;

No effective treatment

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Environmental Pathogens Causing Mastitis

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Transmitted between milkings from the environment;

Found in manure, bedding, feedstuffs, dust, dirt, and water;

Includes: Strep. uberis, Strep. dysgalactiae, environmental coliforms- Escherichia coli, Klebsiella spp., Enterobacter aerogenes

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Escherichia coli, Klebsiella spp. and Enterobacter aerogenes

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Release toxin upon death- primary cause of clinical signs;

Vaccine- decreases severity of symptoms but doesn't prevent infection

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Strep. uberis

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Often found in manure and straw bedding;

Less commonly seen than coliforms;

Responds well to antibiotic therapy;

Easily controlled;

Vaccine being developed

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Nocardia asteroides

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Acute onset, pyrexia, anorexia, rapid wasting, swollen udder;

Usually culled;

Filamentous gram positive bacteria

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Arcanobacterium (Actinomyces) pyogenes

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Profuse, foul-smelling, purulent discharge;

Usually culled

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Pseudomonas aeruginosa

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Symptoms vary in severity;

Usually culled

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Yeast Infections

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Symptoms vary in severity;

If suspected, stop antibiotics

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Monitoring Individual Cows Mastitis

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Production;

General health;

Udder health

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Bulk Tank Test Samples

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At time of shipment;

Testing for mastitis

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Strip Cup Test

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"strip" small sample from teat into cup;

Observe for physical changes to milk- flakes, chunks, pus, blood;

Rudimentary visual inspection of milk- may not diagnose subclinical mastitis (false negative)

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CMT

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California Mastitis Test;

Detects WBC and blood proteins in milk;

Tests each quarter of udder;

Mastitic milk gels, or becomes chunky when using CMT;

Degree of gelling indicates severity of mastitis

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Mastitis Therapy While Lactating

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AKA wet cow therapy;

Have to consider milk contamination issues;

Milk withdrawal time;

Either no treatment, antibiotics, NSAIDS, supportive therapy, euthansia, withdrawal notices on drugs

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Mastitis Therapy While Not Lactating

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AKA dry cow therapy;

Not concerned with drug residues;

Consider withdrawal times vs. due date;

Treatment- intramammary infusions of antibiotics given at end of lactation period and often more effective in eliminating infections than treatment while lactating

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Drug Residues In Milk

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Why we pasteurize milk;

Livestock must have been withdrawn from the medication for the specified period of time prior to consumption of their milk;

There are penalties for farmers

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Human Concern if Drug Residues in Milk

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Allergy potential;

Passing of antibiotic resistant bacteria from livestock to people (also through meat consumption)

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Testing for Drug Residues in Milk

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Beta Lactam Test kit for the presence of antibiotics in milk;

Used on pasteurized or unpasteurized milk;

Uses Snap Technology;

Bulk tank milk is always tested for drug residues

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Immune System

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Resist and control entry into body;

Removal of altered or damaged cells;

Constant "surveillance"

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First Responders

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Non-specific;

Often effective enough to prevent or control infection;

Removal of damaged cells;

Success = recover and restoration to normal homeostasis

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Non-Specific Immune Responses

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Are innate- present at birth;

Barriers- skin/MM;

Soluble mediators;

Phagocytic cells;

Failure of innate response;

Require antigen specific acquired immune responses

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Acquired Immune Response

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Lymphocytes;

Special recognition of foreign material (antigen);

Present at birth but are naive-once exposed result in replications;

Improved response on repeated exposure

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Types of Lymphocytes

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Helper T Cells: produce lymphokines, help improve specific and non specific immunity;

Cytotoxic T Cells: removal of altered host cells;

B Cells: antibody production (immunoglobulins)

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Specific Response

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Improves recovery- resistance on re-exposure termed anamnesis improved;

Natural or vaccine induced

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Innate Resistance

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Physical barrier- skin;

Movement- c/s/v/d;

Soluble mediators-contained in tears, saliva (lysozyme);

Phagocytosis

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Neutrophils

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(polymorphonuclear cell PMNs);

short lived;

quick to site;

can only eat so much;

pus

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Macrophages

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Slower than neuts to site of action;

in blood= monocytes;

in tissue= macrophages;

long lived;

can just keep eating;

also important to specific immunity

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Thrombocytes

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AKA Megakaryocytes;

Avian very important for phagocytosis;

Resposible for 70% of phagocytic cells

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Eosinophils and Basophils

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Small role only

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Stages of Phagocytosis

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Chemotaxis- microbes, factors from damaged cells etc.;

Adherence;

Injestion;

Digestion

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Cytotoxic Cells

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Natural killer cells- cytotoxic lymphocytes, spontaneously kill altered host cells- virus infected, neoplastic, May kill some bacteria/fungi, Very quick to respond, surveillance, macrophages

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Antigens

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Substances bound by specific receptors on lymphocytes

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Factors Determining Immunogenicity

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Size: larger= more likely to stimulate immune response;

Structure;

Stability;

Non-eukaryotic (foreign material)

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Specific Immunity

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Response by lymphocytes- found in circulating blood, LNs, Spleen, and thymus;

Surface receptors recognize antigens very specifically

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B Cells

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Bone marrow is site of B cells maturation in most mammals- Ruminants in ileal Peyers Patche, and Immunoglobulin present on cell surface (bings antigen);

B cells mature to plasma cells- secrete antibody, and responsible for antibody mediated (humoral) immunity

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T Cells

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Thymus is site of T cell maturation in all species;

As maturation occurs begins to express antigen;

Mature T cells only recognize specific antigen presented by other cells;

Responsible for cell mediated immunity

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First Exposure

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10-14 days before antibodies/specific lymphocytes detectable in circulation;

Gradual increase, peaks and begins to decline as antigen removed;

Lymphocytes have "memory" for re-exposure to antigen

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Second Exposure

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AKA subsequent exosure;

Anamnestic response detected within 24-48 hours;

Manymore lymphocytes to respond, occurs much more quickly;

Antibodies/lymphocytes detectable in blood for longer period

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Antigen Specific Immune Response

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Typically anamnestic response controls infection- no clinical signs, infection but no disease;

One lymphocyte specific for one antigen- thousands of antigenic receptors on one cell but all identical;

Clonal selection

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Antigen Specific Immunity Adults vs, Young

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Adults: most circulating lymphocytes by clonal proliferation;

Young: most circulating lymphocytes naive

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Humoral Immunity

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AKA Antibody Mediated Immunity;

Each plasma cell produces antibody specific single antigen;

Identical to first responding B cell;

Plasma cells may only live 3-6 days but are antibody production machines;

Antibodies are what confers immunity

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Antibody

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A molecule produced by animals in response to an antigen;

Has the particular property of combining specifically with the antigen that induced its formation;

Four main classes- IgG, IgM, IgA, and IgE (each isotype has evolved to act at different sites within the body)

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IgG

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Main immunoglobulin found in internal body fluids;

Combats microbes as well as their toxins;

Made on repeated exposure to an antigen;

Only one to cross placenta of primates providing newborn with immune protection

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IgM

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Large macroglobulin confined largely to blood circulation- only enters tissue if vascular damage;

Made up of five immunoglobulin units;

Prominent in early (primary) immune responses;

First Ig produced;

Very good at activating complement and binding antigens because has potential of five times the activity of an IgG molecule

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IgA

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Made up of two basic units which are help together by two extra chains known as the "J" chain and the secretory piece;

Provides primary defense against many local infections owing to its abundance in saliva, tears, bronchial secretions, nasal mucosa, prostatic fluid, vaginal secretions and mucous secretions of small intestine;

Found in very low concentration in serum;

Major function is to prevent adherence to epithelial surfaces

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IgA Action

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Found at raised levels in serum in parasitic infections and in allergy- typically serum levels very low;

Binds to mast cells (and basophils) causing release of proteins important in allergy

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Antibody Function

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Act by impairing normal function of organisms and facilitate removal;

Neutralization- block active site of toxin;

Opsonization- Enhanced attachment to phagocytes;

Complement activation;

Antibody dependent cell mediated cytotoxicity (ADCC): bind cytotoxic cells to antigen bearing target cells to mediate lysis or target cell;

Sensitization of mast cells and basophils

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Complement Activation

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Very complex;

Involves various enzymes/protein found within serum and other bodily fluids;

Ultimately results in death or destruction of offending organisms

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Passive Immunity

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Provided immunoglobulins from source of immune serum to non-immune individual;

Provides immediate protection for as long as present;

Does not form "memory" cells- no residual immunity;

Occurs naturally from dam to offspring or may be induced (tetanus antitoxin);

Allows neonates to develop own active immune resonse

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Mode of Transfer of Passive Immunity

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Primates- IgG crosses placenta and is present in circulation at birth;

Ruminants- no placental transfer, IgG in colostru absorbed in first 24 hrs;

Carnivorous mammals- small amount crosses placenta, remainder in colostrum

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Fetal Immunity

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Immune system present by end of first trimester;

Remain less capable of producing appropriate immune response than adult;

Go through process of 'tolerance'- a state of unresponsiveness of immune system

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Neonatal Immunity

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Most domestic animals fully immune competent at birth;

More susceptible to infection since immune system not primed- has not been previously exposed;

Passive transfer very important- if not critical- "failure to thrive" syndrom

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Passive Transfer

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Transfer of immunity from dam to offspring via placenta or colostrum;

Amount of passive transfer varies with type of placentation;

Dogs, cats: 5-10% of passive transfer via placenta;

Ruminants, pigs, horses: No placental transfer of IgG- rely entirely on colostrum at birth;

Humans, primates, GPs, rabbits- larger aount of IgG transfer;

Colostral IgG absorbed across GIT within first 24-36 hrs- best absorption within first 6 hrs

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Failure of Passive Immunity

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Occurs in all Species;

Recognized most frequently in those neonates that did not nurse immediately after birth;

May be due to- weakness, defect, bad mom, dead mom, too many babies, colostrum leakage prior to birth, and premature birth

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Lactogenic Immunity

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Immunoglobulin also present in milk;

1/10 that of colostrum;

Some species change from IgG to IgA;

Milk Ig protects against local infections (GIT);

Action of suckling important to distribute milk Ig throughout upper GIT and respiratory tract

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Protective Immunity

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Infection much more common than clinical disease- allows infection but prevents disease;

To block infection, must have mechanisms to prevent at site of entry- Mucosal site: IgA, Skin: IgG,and Blood: IgM;

To have antibody present must have had previous exposure- natural exposure or vaccination

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Completely Block Infection Through Protective Immunity

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Rare;

Typically infection rapidly controlled via anamnestic response;

Inhibits replication;

Prevents spread from site;

Type of antigen influences specific immune response employed

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Immunoprophylaxis

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Prevention of disease by induction of active or passive immune responses;

Prevention preferable to treatment- tx unavailable, side effects, cost, performance loss

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Methods of Preventing Diseases

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Management- nutrition, housing, hygiene;

Breeding for resistance;

Prophylactic drug administration;

Immunoprophylaxis

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Vaccination

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Produces active immune response;

Requires lag period where no protection;

If infection during lag time, may result in disease;

Not related to vaccine failure;

Similarly if incubation of disease prior to vaccination

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Immunopathology

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How the immune system contributes to disease;

Hypersensitivity;

Autoimmunity;

Immunodeficiency

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Hypersensitivity

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An immune response which leads to cell tissue damage;

Involves normal immune mechanisms but is at an abnormal level against foreign proteins

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Type 1 Hypersensitivity

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Immediate- anaphylactic;

IgE mediated, mast cell degranulation

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Type 2 Hypersensitivity

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Cytotoxic;

IgM or IgG mediated, affects organs/tissues, minute to hours for occurence- drug induced hemolytic anemia

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Type 3 Hypersensitivity

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Immune Complex;

Complexes may lodge in organs- glomerulonephritis, lupus erythematosus

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Type 4 Hypersensitivity

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Delayed;

> 24 hrs after exposure- tuberculin test

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Autoimmunity

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The reaction of the immune system against self proteins (antibodies or T cells);

Not clear why the immune system starts to react to self proteins;

May be organ specific- against an antigen unique to an organ or a gland;

Ex: IMHA- immune mediated hemolytic anemia in dogs;

May be non-organ-specific- against a broad range of target antigens and involving a number of tissues;

Ex: SLE- systemic lupus erythematosus in horses, cats, and dogs

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Immunodeficiency

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May be primary: due to congenital (inherited) defects in the immune system;

May be secondary due to acquired defects in the immune system (HIV, FIV, FeLV)

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Inflammation

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Clinical signs of inflammation often due to immune permeability;

Edema and pain may be due to increased vascular permeability- allows immune factors to invade site- antibodies and WBCs, phagocytosis may result in sme extracellular degradation products- lysozyme in tissue

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Serology

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Humoral immunity- production of antibodies;

Serological tests classified as primary, secondary, and tertiary binding assays;

Primary binding assays- most common, measures actual binding of antigen-antibody, incl FA, Elisa

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Secondary Binding Assay

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Detects byproducts of antibody-antigen binding;

Less sensitive test;

Incl precipitation, agglutination, virus neutralization

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Tertiary Binding Assays

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No longer in use;

Involved use of live animals

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Titres

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Determines change in antibody level;

Mix dilution of antibody with fixed amount of antigen;

Highest dilution of antibody that leads to agglutination/precipitation of antigen;

Increase in titre greater than or equal to 2 dilutions considered relevant seroconversion;

If no paris serum samples available may compare effected vs. non affected animals

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Measurement of Titres

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Able to confirm causative disease agent via measurement of titres;

If first exposure, naive animal would have low/no antibody to specific antigen and would rise with infection;

If has been exposed, titre will rise from resting level with infection

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Acute and Convalescent Titre Samples

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Acute= blood sample taken ASAP in disease;

Convalescent= sample taken 1 days later

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Evaluation of Serological Tests

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Will determine usefulness of test;

Sensitivity-

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Serological Test Sensitivity

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The number of test positives: decrease frequency of false negative tests and able to detect small amounts of reactant

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Serological Test Specificity

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The number of test negatives divided by the number of true negatives;

Decrease frequency of false positive results;

Tests ability to detect antibodies reacting with antigen of interest (no cross rectivity)

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Serological Test Predictive Value

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Confidence in test result;

Influenced by sensitivity and specificity;

Of most importance clinically

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Serological Test False Positives

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Cross reactivity;

Presence of maternal antibodies

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Serological Test False Negatives

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Too early in immune response;

Immune suppression