Path- Mammary gland (mastitis) 1

untimely's version from 2015-05-02 20:47


Question Answer
what are the two broad defense mechanisms of the mammary gland?(1) Innate immunity -non-specific defense mechanisms (2) Immune-mediated defense mechanisms –specific defense mechanisms
what are three types of innate immunity (non-immune mediated defenses) the mammary gland has?(1) Teat end sphincter (acts as a mechanical barrier) (2) Teat canal -keratin lined teat canal (more on diff card) (3) Removal of bacteria at milking/nursing
explain how having a keratin-lined teat canal can be an innate immunity/explain the innate immunities within this (3)(1) there is regular sloughing (2) there are bactericidal esterified and non-esterified fatty acids (myristic acid, palmitoleic acid and linoleic acid) within lipids overlying keratin (3) Cationic proteins within the keratin lining teat canal (bacteriostatic and bactericidal) (cause leaky cell wall--> osmotic lysis) (also in long notes, mentions that Bacteria are trapped in the keratin which hinders their migration up into the mammary gland)
what are 4 soluble factors within the mammary gland which contribute to innate (non-immune mediated) immunity?(1) lysozyme (in body secretions including milk) (2) lactoferrin (3) Lactoperoxidase-thiocyanate-hydrogen peroxide system (4) Complement cascade
innate (non-immune mediated) immunity--> why is lysozyme beneficial?lysis of peptidoglycan (part of cell wall of bact!)
innate (non-immune mediated) immunity--> why is lactoferrin beneficial?bacteriostatic/bactericical- binds iron(sequestration inhibits growth/replication)/disrupts cell wall
innate (non-immune mediated) immunity--> explain the Lactoperoxidase-thiocyanate-hydrogen peroxide system, how it plays a role in innate immunitylactoperoxidase is in the mammary tissue (catalyst), thiocyanate is in green feeds(source of reactive product), and hydrogen peroxide (normally not in milk, but bact make this and it activates the lactoperoxidase to catalyze the thiocyanate) combine. The thiocyanite is oxidized via the other two compounds, and this produces hypothiocyanate, a reactive metabolite which releases FREE RADICALS which are bacteristatic for G+ and G- bact
Immune-mediated Defense Mechanisms--> cell mediated--> Lymphocytes, plasma cells, neutrophils are located where to protect the mammary gland?lamina propriaof teat canal and rosette of Furstenberg.
what is a NORMAL amount of phagocytic cells within mammary secretions? (uninfected mammary gland)50,000 to 200,000 phagocytes/ml of milk in normal uninfected mammary gland. Most are macrophages
how many phagocytic cells would you see in mammary secretions in a SUBCLINICAL infection? CLINICAL MASTITIS?SUBCLINICAL: Over 500,000/ml. CLINICAL MASTITIS: over 1,000,000/ml
what is the Rosette of Furstenburg?located in the internal streak canal of the teat. It radiates upward into the teat cistern. It often is considered a barrier for pathogens
what kinda role does the neutrophil play for innate immunity of the mammary gland?play major role in clearing invading bacteria. Phagocytosis following opsonization (compliment that makes things sticky)
are neutrophils more or less effective in milk? explainLESS. They have impaired chemotaxis, decreased superoxide anion production, decreased phagocytosis, and less antibody-dependent cell-mediated cytoxicity
what are Ab concentrations like in milk? colostrum? (say numbers)low in normal milk (below 1mg/ml) but in colostrum OR MASTITIS they are closer to 50mg/ml~
what is the major Ab in milk?IgG1
IgG1--> where does this Ab come from/whats up with it?serum derived, major one in milk
IgG2--> where does this Ab come from?both serum and mammary gland derived
IgA + IgM--> where do these Abs come from?produced locally
IgG + IgM--> what do these Abs do?they opsonize (the process by which a pathogen is marked for ingestion and eliminated by a phagocyte)
IgA--> what does this Ab do?does not opsonize but may prevent adherence of bacteria to epithelium

Mastitis in cows

Question Answer
Bacterial pathogens causing bovine mastitis can be grouped into two main groups:(1) Contagious mastitis (bacteria transferred from infected mammary gland into healthy mammary gland at milking) (2) environmental mastitis (bacteria from the environment that contaminate the mammary gland)
what are the 4 major agents that cause Contagious Bovine Mastitis?(1) Streptococcus agalactiae (2) Streptococcus dysgalactiae (3) Staphylococcus aureus (4) Mycoplasma spp. (bovis)
General Sequence of Events and Pathogenesis of Mammary Infections?entry into the mammary gland via the teat orifice and teat duct--> multiply within the teat duct and the streak canal--> spreads deeper into the mammary tissue into the lactiferous sinus, collecting ducts and alveoli of the mammary lobules--> pathogen localizes. Inflammatory cells are attracted via chemotaxis and the area becomes inflamed and edematous--> Damage to the gland results in loss of mammary tissue and mammary gland fibrosis both of which will result in decreased milk production--> Bacterium can gain entry to the systemic circulation resulting in a septicemia
Streptococcal Mastitis--> Streptococcus agalactiae: (pathogenesis) how does it start? what is the initial sign of this? how does is progress?infects teat/gland, and multiplies in waves, invading the primary mammary tissue. It initially shows as edema with neutrophils, then macrophages come in, and eventually Fibrosis/granulation tissue causes stagnation of milk, premature involution of that part of gland. Progresses.
Streptococcus agalactiae--> does this usually involve one or multiple quarters?usually MORE than 1 quarter involved
how does acute infection with Streptococcus agalactiae present?hyperemia/edema, strands and flecks of debris in milk, pus in more severe cases
how does chronic infection with Streptococcus agalactiae present?obstructed areas may resemble small abscesses. Thickened ducts and sinus mucosa.
why does milk yield drop in a strep agalactiae infection?due to damage to acinar tissue and epithelium of lactiferous ducts, plus fibrosis
which is more severe and more common-- Strep agalactiae or Strep dysgalactiae?agalactiae is more severe/common
how does in infection with step dysgalactiae present early on? in clinical mastitis?Low grade mastitis with flakes and clots (can see in glass tube you put milk in) in forestrippings early on in subclinical mastitis. Swollen, warm edematous quarter (s) in clinical mastitis
Staphylococcal Mastitis--> Staphylococcus aureus--> how bad is this infection/what does severity depend on?Apathogenic to highly pathogenic isolates! Virulence depends upon the virulence factors possessed/produced by the isolate of Staphylococcus aureus involved
name 6 virulence factors that staph aureus may possess to make mastitis even more horrible(1) Alpha toxin (2) Protein A (3) Lipoteichoicacid (4) Panton-Valentine leukocidin (5) Staphyloxanthin (6) Extracellular enzymes
what produces alpha toxin, and what does this toxin do?some strains of staph aureus can make this. It causes vasoconstriction, leukocidal, red cell lysis
what is Protein A, where does it come from, what does it do?it is a virulence factor produced by staph aureus. It is antiphagocytic, and can do complement inactivation
what is Lipoteichoic acid?virulence factor produced by staph aureus
what is Panton-Valentine leukocidin? where does it from what and what does it do?a virulence factor produced by staph aureus, it is toxic to neutrophils
what is Staphyloxanthin? what does it do/where does it come from?virulence factor produced by staph aureus, it is a bacterial antioxidant protects S. aureus from reactive free radicals produced by granulocytes
what are some examples of extracellular enzymes which Staph aureus can produce to increase it's virulence? what do these enzymes do overall? (7)catalase, coagulase, staphylokinase, protease, nuclease, lipase, hyalurondiase..adversely affect the immune response and result in damage to mammary tissue.
which type is the most severe Staphylococcal Mastitis, and when does it usually happen? how does it start/progress?gangrenous, usually around calving. Starts as severe acute inflammation and progresses to gangrene.
how does less severe (not gangrenous) staphylococcal mastitis (S. aureus) usually present?similar to Streptococcal mastitis with acute inflammation followed by chronic inflammation and fibrosis. Small to coalescing abscesses
Staphylococcus aureus is USUALLY observed how and when?The disease is most often observed as a subclinical infection during most of the lactation period
Repeated bouts of clinical and subclinical mastitis throughout the lactation period are a common presentation for what kinda mastitis?S. aureus mastitis
Mycoplasma Mastitis--> most common agent?mycoplasma bovis
Mycoplasma Mastitis--> what are two situations where you usually see this form of mastitis?(1) Herds where other forms of mastitis have been controlled (2) Introduction of infected herds into clean herd.
how much of the mammary is usually affected by mycoplasma bovis? how does the infection often present grossly?One or all quarters of gland. Nodules (abscesses) within parenchyma
how does acute mycoplasma mastitis present?purulent exudate, abscessation
how does chronic mycoplasma mastitis present?more mononuclear inflammatory cells and fibrosis of gland parenchyma
(long notes) two main ways mycoplasma invades into the mammary gland?(1) Hematogenous spread (2) contamination of the teat orifice
what are the 4 main types/agents of environmental mastitis?(1) Coliform mastitis (2) Streptococcus uberis (3) Coagulase-negative staphylococci (4) Trueperella pyogenes
is coliform mastitis contageous or environmental?environmental
Coliform mastitis--> what are the 4 main causative agents of coliform mastitis?E. coli, Enterobacter aerogenes, Klebsiella pneumoniae, Citrobacter spp. (highlighted most common-- all G+)
how is it that in coliform mastitis, the immune system of the cow might be doing more harm than good?Influx of large numbers of neutrophils which phagocytose and kill bacteria –release of endotoxin
explain pathogenesis of endotoxic shock from coliform mastitis (said this in class)macrophage sees endotoxins-- they produce a bunch of interleukins which make a bunch of other reactions in the body. if it stays locally, thats good. but NOT good if it's all over your body (systemic inflammation) so they get endotoxic shock
what is important in controlling coliform mastitis?Environmental sanitation and milking machine hygiene are important in controlling coliform mastitis
(long notes) Coliform mastitis frequently occurs....shortly following calving.
endotoxins from coliform mastitis usually affect where?vasculature
do endotoxins from coliform mastitis more severely affect a lactating or non-lactating mammary gland?more severely affect a lactating gland
what are the initial lesions of coliform mastitis? what can it progress to?Initial lesions include hyperemia, hemorrhage and edema. Can progress to gangrenous mastitis and endotoxic shock
Streptococcus uberis (and other strep spp)--> what kinda pathogen? where do they live and how are they spread? what can make this worse?a G+ bact which is Ubiquitous in dairy environments. It is Spread to udder during milking (lack of proper hygiene with udder preparation and milk machine cleanliness), and Injuries to teats and chapped teats increase colonization
when does mastitis due to strep uberis usually happen? how is the mastitis characterized?usually occurs Early in lactation or late in the dry period. The udder is swollen, edematous, firm and you can see Clots and flecks in the milk
Coagulase-negative Staphylococcus--> what are three examples of this?STAPH. xylosis, S. warneri, S simulans (the staff (warners) thought xylazine was a stimulant for the environement of school)
where do Coagulase-negative Staphylococcus usually live? how do they infect the mammary gland?(STAPH. xylosis, S. warneri, S simulans) these Bacteria are normal flora of the udder and teat skin. So, Damage to skin leads to increased colonization –more bacteria.
how does a astitis with coagulase-negative staphylococcus usually present?Subclinical mastitis at most anytime, Decreased milk production and increased numbers of somatic cells and inflammatory cells.
what causes Summer mastitis (dry cow mastitis)?Trueperella pyogenes
summer mastitis/trueparella pyogenes affects the udder when?Can affect lactating, or non-lactating, or immature udder!
where does trueparella pyogenes like to live? what does it commonly cause?Common bacteria in bovine environments and common cause of bovine abscesses
If trueparella invades the udder, what does it like to do in there?likes to make abscesses in large and small lactiferous ducts
what does a severe vs a mild trueparrella case look like?Diffuse necrosis in severe cases, Fibrosis in milder chronic cases
(long notes) other causes of bovine mastitis in include some fungi (4), other bact (3), and algae (1)FUNGI: Candida sp., Aspergillus spp., Cryptococcus neoformans, Trichophyton beigelii. OTHER BACT: Nocardia sp., Corynebacterium bovis, Clostridium perfringens type A. ALGAE: Prototheca spp