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caseous lymphadenitis
chronic contagious disease of sheep and goats that effects lymph nodes and lymphatic tissue resulting in significant economic losses to producers
caseous lymphadenitis etiology
gram + intracellular bacteria that releases an endotoxin that damages the cell wall of the host. two biotypes exist, one infecting sheep/goats and another infecting horses
caseous lymphadenitis resistance and zoonotic
live on surfaces for 2 mo and soil up to 8 mo. highly resistant. zoonotic
caseous lymphadenitis enter host
trough damaged skin or via mucous membranes. once in host bacteria invades lymph nodes or other internal organs
caseous lymphadenitis incubation
1-3 mo. internal and external abceses develop and drain
external caseous lymphadenitis symptoms
draining lymph nodes! draining abscess heal w scar tissue but purulent material contaminates env.
common lymph nodes for caseous lymphadenitis
submandibular, prescapular, parotic, prefemoral
internal caseous lymphadenitis symptoms
chronic weight loss, failure to thrive, variable due to what organ is involved
caseous lymphadenitis diagnosis
clinical signs, culture and sensitivity of purulent material, extensive workup to diagnose internal
caseous lymphadenitis treatment
aimed at limiting transmission, recurrence is common. antibiotic therapy if cull is not an option. draining abscess and isolation
biosecurity for caseous lymphadenitis
isolation, disinfection, cull infected once draining abscess heals, vaccinate, pasteurize milk
lamb body temp normal
102.2-104 F
mild hypothermia in lamb
98.6-102.2
severe hypothermia in lamb
less than 98.6
risk factors for hypothermia
increased body surface, small lambs, thin coat, drafty env, poor mothering
prevent hypothermia
indoor lambing, observation, short lambing season, excellent maternal nutrition to improve lamb birthweight, ensure colostrum intake
brown fat stores
lamb uses them to generate energy to maintain body temp (initiated by oxygen and colostrum intake. brown fat is laid down in pregnancy. poor ewe nutrition means small lamb with little brown fat reserves. a small weak lamb will be slow to nurse and so no start of brown fat metabolization. once brown fat is utilized, lamb must get energy from milk to provide heat.
hypothermia timeline
brown fat used within 5-12 hr post birth. if lamb doesn’t get energy from milk, then risk for hypothermia and hypoglycemia
hypoglycemia
low blood glucose
clinical signs of hypothermia/hypoglycemia
weakness, lethargy, decreased or absent suckle reflex, seizures from hypoglycemia from decreased glucose delivery to the brain
treatment for hypothermia/hypoglycemia
provide warmth and nutrition. tube feed colostrum if can swallow. if lamb cant swallow, warm first and glucose via injection before tube feeding. warm with circulating air
orogastric intubation
proper training necessary before attempting procedure. ensure in stomach not lungs
diabetes mellitus
disease associated w absolute or relative insulin deficiency in both dogs and cats. due to destruction of islet of Langerhan cells in pancreas
diabetes mellitus predisposing factors
glucocorticoid admin, pregnancy in dogs, obesity
pancrease
near duodenum. endocrine component contained in clumps of cells called pancreatic islets or islets of langerhans. alpha cells produce glucagon, beta cells produce insulin
insulin
essential for life. causes absorption of glucose, AA, fatty acids into cells. overall effect is to lower blood glucose levels.
hyperglycemia
results from insulin deficiency. insulin decreases blood glucose by increasing cellular uptake of glucose and storage in the form of glycogen and fat. when no insulin, body cannot use glucose so it breaks down fat or protein
diabetes mellitus etiology
occurs when pancreas cant produce sufficient amounts of insulin or when the cells are resistant to insulin
type i
insulin dependant
type ii
non insulin dependent. results from resistance of tissue to the activation of insulin
diabetes mellitus clinical signs
polyuria, polydipsia, polyphagia, weight loss, diabetic ketoacidosis if left untreated
diabetic ketoacidosis
life threatening emergency. if cells can’t use glucose, they begin fat metabolism. ketones are byproduct
diabetes mellitus diagnosis
persistent hyperglycemia and glucosuria, fructosamine
diabetes mellitus treatment
dietary management, insulin therapy (multiple types and twice daily dosing)
diabetes mellitus dietary management in dogs
high fiber diet
diabetes mellitus dietary management in cats
high protein low carb
insulin types
must be given parentally usually SQ. types: long acting, intermediate acting, short acting. concentration is measured in units of insulin per mL
use of insulin products
must be refrigerated, given at time fed, site rotation to prevent scar tissue, roll don’t shake bottle, twice daily, only use insulin syringes twice, owner edu, too much insulin can cause hypoglycemia
hyperthyroid
due to excessive secretion of thyroid hormone from the thyroid gland, results in increased metabolic rate, primarily a disease of cats
thyroid gland
two lobes on either side. produce thyroid hormone after stimulation by TSH from pituitary gland and produces calcitonin
thyroid hormone
helps regulate the body’s metabolic rate, growth and development, body temp, skin conditions, etc. T4 is circulating reservoir converted to T3 in peripheral tissues and is active form in body.
calcitonin
helps lower blood calcium levels
hyperthyroid clinical signs
weight loss, increased appetite, unthrifty appearance, polyuria, polydipsia, palpably enlarged thyroid gland, tachycardia, hypertension, vomiting and diarrhea
hyperthyroid diagnosis
high circulating thyroid hormone levels in blood - free T4 is most common
hyperthyroid treatment
radioactive iodine (of choice), thyroidectomy has potential to damage parathyroid gland and can lead to hypothyroidism, antithyroid meds need lifelong treatment and can effect WBCs
hypothyroidism
primarily a disease of dogs but can be seen in cats. due to destruction of thyroid gland. results in overall decrease of metabolic rate. (in cats usually secondary to treatment for hyperthyroidism)
hypothyroidism clinical signs
lethargy, weight gain without increase in appetite, exercise intolerance, alterations in haircoat like dry skin and alopecia
hypothyroidism diagnosis
measuring T4, free T4, and or TSH. commonly over diagnosed. non thyroid issues can lower thyroid hormones and mimic (such as euthyroid sick syndrome)
hypothyroidism treatment
treated by supplementation w thyroid hormone. easily treated but requires lifelong therapy. levothyroxine sodium is treatment of choice
cushing’s syndrome
any disease causing increased cortisol concentrations in the blood
cushings disease
elevated cortisol due to pituitary dependent hyperadrenocorticism or adrenal dependent hyperadrenocorticism. PDH is most common cause due to an adenoma of pituitary gland
adrenal gland
small gland lives adjacent to kidneys. cortex produced cortisol, aldosterone, and androgens. medulla produced epinephrine and norepinephrine. controlled by ACTH which is produced by pituitary gland
adrenal cortex
develops from glandular tissue. outer gland. produces steroid hormones stimulated by ACTH from anterior pituitary
glucocorticoid hormones
includes cortisol and corticosterone. hyperglycemic effect. catabolism of proteins and lipids, breakdown products converted to glucose in liver. help maintain BP and help body resist the effects of stress
hyperadrenocorticism
common endocrine disease of dogs caused by excessive circulating cortisol. two types (pituitary dependent and adrenal dependent)
pituitary dependent hyperadrenocorticism
benign tumor of the pituitary gland causes gland to produce too much ACTH resulting in excess cortisol
adrenal dependent hyperadrenocorticism
tumor of one of the AGs and it produces a large amount of cortisol
cortisol
function to help body prepare for fight or flight
hyperadrenocorticism signs
polyuria, polydipsia, polyphagia, muscle wasting, poor skin condition, pendulous abdomen, chronic infection
hyperadrenocorticism treatment
meds available to decrease amount of cortisol from adrenal gland. meds vary depending on if patient has PDH or ADH. requires lifelong therapy and regular monitoring
hypoadrenocorticism
addison’s disease. due to insufficient aldosterone production by adrenal gland. these dogs usually present as an emergency case, in shock, but they can present w chronic GI symptoms, anorexia, PU/PD, hypoglycemic
mineralocorticoid hormones
aldosterone. regulates levels of some important electrolytes. target organ is the kidney where it causes Na ions to be reabsorbed from urine in exchange for K and H ions. water accompanies Na back into bloodstream
hypoadrenocorticism symptoms
dehydration, sodium depletion, potassium excess
heartworm disease etiology
dirofilaria immitis nematode parasite transmitted by mosquitoes
heartworm lifecycle
microfilaria are ingested by mosquitoes - molt several times in mosquito to L3 stage - L3 larvae enter tissues of host when mosquito bites - L3 mature to L4 in tissues of host in 3-12 d - L4 develop into immature adults about 50-70 days - immature adults migrate to heart and develop to sexually mature worms about 70-120 d - mature worms produce microfilaria about 6 mo post infection
heartworm pathogenesis
adult worms live in pulmonary vasculature. symptoms result from inflammation in the lungs, increased blood pressure, and R heart failure
wolbachia pipiens
intracellular endosymbiotic bacteria who lives within the heartworm. releases endotoxins and worsens symptoms of disease. bacteria appears to be necessary for normal maturation and repro of worm
heartworm clinical signs in dogs
cough, decreased activity, unthrifty appearance, dyspnea, cyanosis, syncope, collapse, ascites
heartworm clinical signs in cats
cough, dyspnea, vomiting, diarrhea, weight loss. associated w respiratory disease w asthma like symptoms from a secondary allergic response to the worm
heartworm diagnosis in dogs
ELISA antigen test detects infection 5-6 mo post infection. tests for a protein from mature female worm. microfilaria test in blood test like smear. radiographs to determine stage of disease
heartworm diagnosis in cats
harder to diagnose bc small worm burdens and male only infections. symptoms, radiographs, ultrasounds. antigen tests have high false negatives, antibody tests indicate exposure but not a definitive test
heartworm treatment in dogs
curative treatment w injectable meds. treatment of 3 injections over 2 mo period, each followed by strict exercise restriction for 30 days. antibody therapy to remove wolbachia. staging is performed prior to therapy to determine safest approach.
heartworm treatment in cats
no curative treatment. symptomatic for clinical signs
heartworm prevention
year round prevention recommended for cats and dogs regardless of housing
heartworm prevention macrocyclic lactones
ivermectin, moxidectin, milbemycin oxime, selemectin, also target GI nematodes