Animal Health Flashcards
health
a state of complete well-being
disease
any state other than complete health
normal function of the body or its parts is disturbed
symptoms
noticeable differences from normal
- indicators of disease
- fever, weight loss, water feces, labored movement or breathing
lesion
change in an organ
-size, color, abscess, tumor
etiology
study of factors that cause a disease
many interactions
-pathogen - host - environment interaction
disease diagnosis
detection of symptoms
formulation of hypothesis for disease cause
development and execution of treatment plan
detection of symptoms
isolated animal? or her mates too?
clinical examination
-visual, auditory, olfactory, palpation
boy fluid or tissue analysis
formulation of hypothesis for disease cause
based on training/ experience of diagnostician
development and execution of treatment plan
individual medicine
herd medicine
nutrition, environment (housing), vaccination etc.
describing disease
clinical vs. sub-clinical
acute vs. chronic
clinical
disease symptoms are clearly present ie clinical mastitis -reddish, hot, swelling of udder -off color or clots in milk -systemic (whole body) fever
sub-clinical
disease carriers no clear outward signs ie. sub clinical mastitis -bacteria present in gland -but no clear symptoms
acute
often intense but short lived (ie days)
chronic
may last the life of the animal
more moderate symptoms w/ occasional flare ups
DAMNIT
Scheme for disease diagnosis Degenerative Allergenic Metabolic Nutrition, neoplasia Infectious, inflammation Trauma, toxins
idiopathic
unknown cause
degenerative
ex. canine hip dysplasia genetic component -often polygenic so difficult to pinpoint cause environmental effects -obesity, excessive exercise of pups
allergic
allergies to food, fleas, pollens, mold, etc
symptoms include scratching, hair loss, skin lesion
IgE antibodies to allergenic particles
-stimulate release of histamine
-some relief by use of anti-histamines
metabolic
affect body's metabolism -often hormonal -often nutritional link diabetes mellitus -hyperglycemia -glucoseuria (glucose in urine) --> polyurea (frequent urination) and poly dypsia (thirst) increased appetite inc. weight loss
metabolic diseases milk fever
calcium is required for muscle contraction
loss of Ca in milk
inability to mobilize Ca stores
lack of coordination, collapse, death
nutritional disorders
obesity-imbalance between energy intake and energy expenditure
nutritional deficiencies: minerals, vitamins, amino acids, essential fatty acids
mineral deficiencies
calcium - osteomalacia (rickets), milk fever
iron - anemia
iodine - hypothyroid (goiter)
copper - hair loss, immune system
selenium - impaired immune function
zinc - loss of dermal integrity (skin condition, parakeratosis in pigs)
vitamin deficiencies
A - vision, bone growth B complex - growth, anemia C - scurvy D - bone growth E - immune function
neoplasia
cancerous growth of cells
treatments: surgery, radiation, chemotherapy
infectious
infection - caused by living organisms - pathogens
fungi - many skin infections, ring worm
nematodes - round worm, heart worm
cestodes - tapeworm
protozoa - unicellular parasite (malaria)
bacteria - staphylococcus sp., salmonella sp.
virus - HIV, H1N1, influenza rabies (living?)
prion - mad cow disease, aka bovine spongiform encephalitis (living?)
inflammatory immune-mediated
ex. rheumatoid arthritis
autoimmune hemolytic anemia
-antibodies to red cells causing them to burst
- treat w/ immunosupressive drugs
trauma
wounds, broken bones, torn ligaments, sprained tendons, burns (chemical, solar radiation)
ligament
connects bone to bone
tendon
connects muscle to bone
toxins
antifreeze -ethylene glycol (sweet) -metabolites cause kidney failure rodenticides - warfarin -interferes w/ production of vit K dependent blood clotting factors lead poisoning - paint -interferes w/ RBC matuation
natural defenses against disease
behavioral or environmental adaptations
proper nutrition
barriers to pathogens: skin, stomach acid, coughing
immnity (non specific + specific (both active and passive))
genetic resistance
non-specific defenses against disease
innate immunity
skin mucous membranes, stomach acid
-protective barriers
antimicrobial proteins
-enzymes that kill bacteria (lysozyme in tears)
phagocytic cells
-macrophages and neutrophils ingest and kill organisms
inflammatory responses
-chemicals released by host that cause inflammation
- recruit phagocytes to site of injury
-elevate temperature and cause swelling
phagocytic cells
neutrophils and macrophages
neutrophils
circulate in blood waiting to be called to site of infection
- engulf pathogens
- “garbage can”
macrophages
reside in tissues
fewer that neutrophils but much greater capacity also ingest dead cells, cellular debris etc.
-“garbage truck”
inflammatory response
redness, heat: inc. blood flow
swelling: leaky blood vessels allow clotting factors and phagocytes to reach site of infection
specific immunity
acquired immunity
2 major divisions
1. Humoral
2. Cell Mediated acquired immunity
Humoral Acquired Immunity
antibodies in body fluids -immunoglobulins (Ig) -IgM, IgG most abundant specialized forms -IgA: secreted (intestine, saliva) -IgE: rare, associated w/ allergies
Antibodies
produced by “B” cells in blood
2 major effects
1. bind specific parts of molecules and neutralize them
-ie. tetanus toxin
2. Bind specific pathogens and aid in recognition by phagocytes
-opsonization
how antibodies are acquired
acquired by:
active immunization and passive immunization
active immunization
endogeneous production of antibodies following
- exposure to the pathogen
- vaccination w/ disabled pathogen or pathogen component (ie. tetanus toxin)
passive immunization
acquired from dam via placenta or colostrum
or given by intravenous injection as a treatment
vaccination
term derived from vacca for cow pox
- Edward Jenner (1769)
- Successfully vacinated boy against smallpox using pus from milkmaids hands from cowpox
Vaccine stimulates
-antibody production
-production of memory B cells that quickly mount a response to subsequent exposure to the pathogen
cell mediated immunity
cytotoxic T cells
- can recognize and destroy body cells that are:
- infected (ie. viral infection)
- concerous
recognition of virally infected cells
infected cell “display” pieces of viral proteins on its surface
cytotoxic T cells “recognize” the viral protein as foreign and kill the cell to prevent the spread of the virus
active antibodies
produced by the body
natural - exposure to infectious agent
artificial - immunization
passive antibodies
ready-made antibodies
natural - maternal antibodies
artificial - antibodies from another source
parasite
receive nutrition from the host rarely kill the host but generally reduce biological fitness -benefits at the expense of the host internal: protozoa, various worms external: fungi, insects (fleas, mosquitos), arachnids (ticks, mites)
fungal infections
often skin diseases ringworm (caused by dermatophytes) esp. young animals (usually "runs its course") older animals generally resistant spread primarily by direct contract
multicellular parasites
- nematode - roundworm, heart worm
-generally thread like - cestodes (tapeworm)
-generally flattened body
common in domestic animals
primary host
definitive host
host in which the parasite reaches maturity and reproduces sexually
heart worm in dogs
secondary host
intermediate host
host that harbors the parasite only for a short transition period, during which some developmental stage is complete
-heart worm in mosquito
vector
an organism that facilitates movement of parasite from one host to another
-mosquito w/ malaria
-deer tick w/ lyme disease
often same as secondary host
heart worm
dirofilaria - a nematode
spread by mosquito btwn infected and healthy animals
treatment to kill worms requires dog to be kept “quite” for weeks to enable phagocytosis
primary host: dog
secondary host (and vector): mosquito
tapeworm
cestode resides in intestine of primary host (dog) eggs shed in feces flea ingest worm eggs (secondary host) dog ingests infected flea while grooming
protozoal parasites
single celled, nucleus, organelles numerous diseases -coccidiosis -toxoplasmosis -malaria prevention and treatment: clean feed and water, insect control, vaccination (difficult for many of these)
transmission vectors for some parasites
insect vectors for: nematodes -heart worm (mosquito bite) cestodes -dog tapeworm (flea ingestion) bacteria -lyme diesase (borrelia sp.) (ticks) protozoa
bacteria
no nucleus or organelles
most have a cell wall covering the cell
bacterial diseases
destruction of the cell wall causes the bacteria to burst
cell wall disruption is site of action of many antibiotics
mastitis, enteritis, metritis, etc.
vaccines may not protect against many types of bacteria
ie. previous exposure does not always lessen risk of new infection
bacterial pathogenesis
generation of disease
- toxins
- indirect damage by host’s own immune response
bacterial toxins
2 types: exotoxins and endotoxins
bacterial exotoxins
secreted proteins that damage host cells
- cholera toxin - sever diarrhea
- tetanus toxin - muscle contraction
bacterial endotoxin
part of the bacterial cell
-lipopolysccharide (LPS)
recognized by host leading to an immune reaction
indirect damage by host immune response
sepsis, hypovolemic shock -fluid moves out of circulation into tissue -less fluid for heart to pump -reduced blood pressure leads to organ failure -kidney failure -heart failure
relative sizes of microorganisms
viruses 20-200nm
bacteria 1um
RBC 6-8 um
viruses
protein coat w/ viral genes inside
DNA or RNA
obligate intracellular parastes - no free living form
not controlled by antibiotics
drugs attack ability to replicate (AZT for HIV)
viral diseases
bovine viral diarrhea distemper - dogs cats -respiratory infection, watery eyes, breathing problems new castle disease - chickens -respiratory disease rabies - most mammals west nile virus - horses from mosquitos from birds foot and mouth disease
treatment/ prevention of viral diseases
vaccine are often effective but new ones are needed to keep up w/ viral mutations
-ie. influenza
antiviral drugs are hard to design b/c the virus uses the host machinery for metabolism
- ie. blocking host metabolism will also kill the host
- AZT for treating AIDs blocks RNA reverse transcriptase
interferon - a natural mammalian cytokine protein helps prevent viral replication
prions
transmissible spongiform enecephalopathies
mad cow disease - BSE (cattle)
kuru (humans cannibalism new guinea)
degenerative neurologial disease
consumption of prion protein from brain tissue
-mutant protein causes formation of more abnormal proteins
-causes holes (sponge-like) appearance of brain
ectoparasites
found on external skin surface cause rashes, hair loss, anemia, etc. fleas, ticks mites: demodectic mange demodex canis -young dogs w/ immature immune systems sacoptic mange -highly transmissible
prevention of disease
natural defenses
behavioral or environmental defenses
proper nutrition
barriers to pathogens: skin, stomach acid, coughing
immunity (nonspecific and specific (active and passive)
“genetic” resistance
