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100 Cards in this Set

  • Front
  • Back
diarrhea in cattle (by age)
1. calves
a) neonatal calf diarrhea
b) colisepticaemia
c) salmonellosis
2. young cattle
a) ostertagiosis
c) coccidiosis
3. adult cattle
a) johne's disease
b) winter diarrhea
c) renal amyloidosis
colisepticaemia (key points)
+particular serotypes of E. coli
+acute onset of disease
+affected animals generally hypogammaglobulinaemic
colisepticaemia (definition)
+condition of agammaglobulinaemic or severely hypogammaglobulinaemic calves < 1 wk old
+sudden onset and affected calves almost invariably die
colisepticaemia (clinical signs)
+sudden death - calf seemed well when last observed
+dull, stiff & reluctant to rise and feed
+pyrexia (40.5 deg C; 105 deg F) - temp drops rapidly to sub-normal as calf collapses
+diarrhea, if at all, is scanty and a terminal event
+enlarged, puffy joint casules
+CNS disturbances due to meningitis (occasionally)
+death within 12 hr of onset of clinical signs
+if survive: joint ill, pyaemic abscesses in viscera, umbilicus & CNS
colisepticaemia (pathogenesis)
+colostrum deprived calves < 4 days old
+entry thru GIT or respiratory
+endotoxin: endothelial cell damage; activates platelets, phagocyte & complement system
+septic shock --> DIC & vascular collapse
colisepticaemia (pathology)
+widespread petechial haemorrhages of lungs, trachea, myocardium, thymus, spleen & subendocardium
+enlargement of spleen & distention of joint capsule with serofibrinous material
colisepticaemia (epidemiology)
+classic condition of calf that has been deprived of colostrum or has not absorbed colostran Ig
+IgM is most important
+calves older than 1wk are usually resistant
colisepticaemia (control)
increase concentration of passively acquired Ig in serum of newborn calves
colisepticaemia (diagnosis)
+sudden death in calves < 1wk + evidence of hypogammaglobulinaemia or poor hygiene
+culture from blood, spleen or liver
colisepticaemia (treatment)
usually ineffective due to rapid onset & death of affected animals
joint ill (key points)
+infectious polyarthritis
+often assoc. with "navel ill"
+usually in calves born indoors
+colostrum & environmental hygiene important
+occurs in young calves but can become a chronic condition
joint ill (definition)
+infectious polyarthritis of young calves
+often assoc. with umbilical infxn
joint ill (pathogenesis)
+polyarthritis from haematogonenous spread of omphalophlebitis (navel ill)
+passes either thru urachus to bladder or via umbilical venis to liver
+may occur via oral route, passing through tonsil, lung or GIT
joint ill (pathology)
+usually carpal, hock, stifle & fetlock (less commonly shoulder, elbow or hip)
+soft tissue swelling, acute synovitis, free fibrin & pus, ersosion of cartilage
+often a moist, necrotic & purulent umbilical cord or umbilical abcess
joint ill (clinical signs)
+joints are swollen, hot & painful
+incr. synovial fluid volume that is turbid w/ fibrin or pus
+lameness is progressive w/ chronic synovitis, pannus, progressive joint distruction and periarticular granulation/fibrosis
+joints rarely discharge of ankylose
+calves are dull, pyrexic, anorexic & become unwilling to stand
joint ill (diagnosis)
+lesions in 2 or more joints of calf < 1 month (esp. if umbilical infection)
+isolation of streptococci & coliforms from joint fluid
joint ill (treatment)
+broad spectrum antibiotic for several days
+effectiveness depends on ability of drug to penetrate joint capsule (relates to pH of septic joint fluid & pharmacokinetics)
joint ill (control)
+adequate colostrum
+hygiene (esp. bedding)
+disinfect umbilicus w/in 1hr of birth (repeat on day 2 & 3 where previous problems)
+uncommon in calves born outside
neonatal calf diarrhea (aetiology)
+E. coli (enterotoxigenic - ETEC): F5 or K99 fimbrae - calves < 10d
+E. coli (enteropahtogenic - EPEC)
+Rotavirus: in faeces of calves 5-15 days old
+Coronavirus: in faeces of calves 5-15 days old
neonatal calf diarrhea (incidence)
+mortality rates of 2-8%
+approx. 50% of neonatal calf mortality due to GI conditions
+approx. 2.5% of all purchased calves die within 1 month of purchase
neonatal calf diarrhea (clinical signs)
+ETEC: very young calves (usually < 5d & frequently as young as 24h), very sudden
+others: 2nd or 3rd wk of life
+profuse watery diarrhea (brownish-yellow)
+loss of up to 15% of BW in 24h
+dull, lethargic, dehydrated, eventually recumbent
+terminal stage: hyperpnoea, bradycardia, cardiac arrythmias, poor volume pulse, sunken eyes
+high mortality
neonatal calf diarrhea (pathology)
+ETEC: lesion in SI (middle to distal third); bacteria adherent to brush border of absorptive villus epithelial cells
+EPEC: adherence as ETEC + villi stunted & thickened with incr. inflamm. cells in lamina propria
+Rotavirus: stunting & thickening of vill in proximal & middle SI; may be slight crypt hyperplasia & secondary infxn
+Coronavirus: middle/lower SI & colon; SI villi shortened & low cuboidal cells replace normal tall columnar epithelial cells
+Cryptosporidium: mainly ileum with some in lower jejunum, caecum & colon; stunting & fusion of villi, flattening of epithelial cells, marked loss of microvillous surface area
neonatal calf diarrhea (pathogenesis)
+ETEC: enterotoxin alters fluid & electrolyte transport in SI that results in net secretion of Na, Cl & K producing H20 loss into distal SI
+EPEC: damage to villus epithelial cells resulgin in excess cell loss, villus stunting & severe inflammation
+Rota/Coronavirus: colonize absorptive cells of SI & cause stunting/thickening of villi w/ decr. in absorptive capacity of electrolytes & H20
+CoD: severe depletion of fluid & electrolytes from diarrhea
neonatal calf diarrhea (epidemiology)
+colostrum deprivation
+bucket fed > suckling
+calves born in byres > born in yards, boxes or fields
+mortality highest in 1st wk then declines exponentially
+mortality in particular calf house directly proportional to length of time building has been occupied by young calves
+mortality highest from Jan - April
+larger herds > smaller herds
neonatal calf diarrhea (zinc turbidity test - ZST)
+rapid test for immunoglobulins
+ZST=0 (little of no Ig): often die during neonatal period (many from colisepticaemia, rest from diarrhea)
+ZST>10: no colisepticaemia but deaths from diarrhea common
+ZST>30: diarrhea can occur but calves rarely die
neonatal calf diarrhea (dagnosis)
+ELISA (must rule out salmonellosis)
+ETEC: correlated with fimbrial antigens (F5/K99) confirmed by slide agglutination from faecal cultures
+Cryptosporidium: giemsa stained faecal smears, ZN stained faecal smears
neonatal calf diarrhea (treatment)
+antibiotics (not effective vs crypto):
few indications for antibiotics unless caused by salmonella or E. coli
+fluid therapy for hypovolaemia (often acidosis as well)
+food withdrawl for no more than 24hr (if at all)
neonatal calf diarrhea (control)
+colostrum (well trained stockman to observe and take early action if necessary)
+small,self-contained groups if possible
+vaccination (eg. Rotavec K99)
+Crypto: halofuginone lactate (Halocur) as prophylactic (not as treatment) + good hygiene/colostrum mgmt
neonatal calf diarrhea (key points)
+common problem
+generally in calves < 1 month old
+bacterial, viral & parasitic aetiologies
+colostrum an important preventative factor
+major economic importance
salmonellosis (key points)
+affects calves & adults
+diarrhea (dysentery)
+carrier animals important in spread
salmonellosis (definition)
+serotypes of Salmonells enterica (usually)
+fever, diarrhea (frequently with dysentery), death in both calves & adults
+occasionally abortion may be only clinical sign
+disease in cattle source of infection in man (zoonosis)
salmonellosis (aetiology)
+S. dublin & S. typinmurium are most common serotypes
+S. dublin has increased while S. typhimurium has decreased in prevalence - S. dublin now most important
+S. typhimurium highly resistant to antibiotics - S. dublin largely sensitive
salmonellosis (clinical signs - adults)
+rapid onset of dullness & pyrexia (40-41C; 104-106.5F) with inappetence & dramatic drop in milk yeild
+severe watery diarrhea +/- blood, mucus & shreds or casts of necrotic bowel epithelium
+abdominal pain, collapse, recumbency
+abortion (may be only clinical sign with S. dublin)
+severe: death in 4-7d after onset of clinical signs
+diarrhea persists for 14d and full recovery up to 2 months (high mortality if not treated)
salmonellosis (clinical signs - calves)
+most frequent from 2-8 weeks
+dull, lethargic, inappetent
+pyrexia (up to 41.5C; 106.5F) and profuse evil smelling diarrhea +/- dysentery
+rapid loss of condition, weakness, rucumbency
+death within 2-3 days after onset clinical signs (mortality 30%+)
+diarrhea persists up to 2wk in untreated survivors
+can get gangrene-like lesions & osteitis of extremities with sloughing of ear edges, tip of tail and distal extremities of limbs
salmonellosis (pathogenesis)
+faecal-oral (usually)
+invades GIT mucosa --> acute inlammatory rxn (diarrhea)
+multiply in lamina propria and enters systemic circulation (possibly via Peyer's patches) --> septicaemia
+may become localized in joints, foetus (abortion), gall bladder
+excrete virus for few months after recovery
salmonellosis (pathology)
+enteritis: often severe & haemorrhagic with necrosis & ulceration of intestinal mucosa
+mesenteric LNs may be enlarged & congested
+if septicaemia: splenomegaly, swollen pale liver, enlarged, oedematous or hameorrhagic LNs
salmonellosis (epidemiology)
+host range: S. dublin occurs in other species but mostly cattle; S. typhimurium infects wide variety of species (cross species spread)
+S. dublin more important
+from other cattle excreting virus (bought in or cow to calf)
+from contaminated food or water
+can survive up to 30wk in winter slurry and 24wk in soil (store slurry at least 4wk before spreading & don't graze for another 4wk after)
+from other domestic animals (and man)
+from wild animals (esp. rats)
salmonellosis (carrier animals)
+S. dublin excreted for years after recovery (if not life)
+S. typhimurium excreted for several weeks after recovery
salmonellosis (diagnosis)
+age of onset (3-4wk in calves)
+symptoms (fever, depression, diarrhea +/- blood)
+history of recent purchase through markets
+confirm with isolation of organism (culture from faeces, gut, feed & slurry samples) + phage typing
salmonellosis (treatment)
+antibiotics (both oral & parenteral routes - same class of drugs for both)
+drugs (in order of preference): ampicillin, amoxycillin, enrofloxacin, TMP/sulphonamide, neomycin
+S. typhimurium widespread resistance; S. dublin largely sensitive
+adults become carriers after treatment (not calves)
+nursing: heat lamps, turn regularly, feed several times per day
salmonellosis (control)
+source from salmonella free herds if possible
+prophylactic antibiotics not advised
+vaccinate at risk animals such as pregnant cows (both humoral & cellular immune mechanisms so live vax best)
+isolation of clinical cases (continue for at least 2wk after recovery)
+cull recovered cases of S. dublin (life long carriers)
+hygiene & biosecurity
ostergagiosis (key points)
+usually group condition
+2 disease syndromes: Type I & Type II in calves/young cattle
+Type I: diarrhea, weight loss in calves during the 1st summer grazing
+Type II: weight loss, anaemia +/- diarrhea in yearlings during post-grazing housing
+control based on grazing mgmt &/or strategic prophylactic anthelmintic dosing during grazing or at housing
ostertagiosis (definition)
+Ostertagia osteragi is the most common cause of PGE in temperate areas
+characterized by weight loss & diarrhea, typically affecting young cattle during or following their 1st grazing season
+sporadic cases in adult cattle
ostertagiosis (aetiology)
+direct life cycle (21d): eggs passed in faeces develop into infective L3 on grass, L3 in abomasal glands before emerging on day 18 to become sexually mature on mucosal surface
+L3 may inhibit at early 4th larval stage (EL4) for up to 6 months
+clinical signs maximal when emerge from gastric glands
ostertagiosis (pathogenesis)
+damage to parietal cells & replace with undifferentiated cells --> thickened hyperplastic gastric mucosa
+leakage of pesinogen & loss of plasma proteins into gut lumen leading to hypoalbumaemia
+rise in abomasal pH (loss of parietal cells) causing loss of bactericidal activity (overgrowth) & loss of pepsinogen activation (impaired protein digestion)
ostertagiosis (epidemiology - dairy herds)
+L3 survive winter on pasture & infect calves at level that cause patent subclinical infection (subsequent eggs contaminate pasture for rest of season)
+many eggs deposited April through June and become infective from mid-July to October --> Type I disease
+if infective L3 ingested late in season, will become inhibited (EL4) --> Type II when reactivates (eg. at housing)
+primarily young cattle but can affect older if no previous exposure; immunity slow to develop & require boosting by repeated challenge
+high mortality for overwintered L3 so pasture safe if not grazed in spring
ostertagiosis (epidemiology - beef herds)
+spring calving herds: not common (little egg production b/c immune adults - overwintered L3s die before weaning)
+autumn/winter calving herds: similar to dairy calves; whether Type I or Type II depends on grazing management
ostertagiosis (clinical signs - Type I)
+calves grazed intensively during 1st grazing season from ingestion large # of larvae 3-4wk previously (from mid-July on)
+diarrhea: profuse (with green color)
+weight loss
+morbidity high/mortality low
ostertagiosis (clinical signs - Type II)
+yearlings in late winter or spring following their 1st grazing season; from maturation of larvae ingested during previous autumn & subsequently inhibited (EL4)
+diarrhea: intermittent with anorexia & thirst
+weight loss
+hypoalbumaemia (submandibular oedema) & moderate anaemia
+morbidity low/mortality high
ostertagiosis (pathology)
+raised nodules in abomasum (may coalesce to produce "morocco leather")
+oedema & hyperaemia of abomasal folds +/- necrosis & sloughing of mucosal surface
+regional LNs enlarged & reactive
ostertagiosis (diagnosis - calves)
+inappetence, weight loss, diarrhea
+grazing (Type I): set stocked in 1 area for several months
+grazing (Type II): in previous year grazed on 1 field from spring to mid-summer, moved and then moved back to original pasture in autumn
+plasma pepsinogen levels (less reliable in cattle > 2yr)
+FECs: only useful in Type I (>1000 epg)
+PM findings (nodules)
ostertagiosis (diagnosis - older animals)
+clinical signs & history similar to younger animals
+FEC & plasma pepsinogen levels are less reliable
ostertagiosis (treatment & prognosis - Type I)
+responds well to anthelmintics that are effective against developing larvae & adults
+following treatment, calves should be moved to pasture which has not been grazed by cattle in the same yr
+field with outbreak may be grazed by sheep or immune adult cattle or rested until the following June
ostertagiosis (treatment & prognosis - Type II)
+must use anthelmintics that are effective against inhibited larvae as well as developing larvae & adult stages
+by the time Type II is diagnosed, there may be serious damage to the abomasal mucosa & recover, if at all, may be slow
ostertagiosis (prevention & control)
+traditionally: routine anthelmintic treatment of young cattle over period of peak disease (1 or 2 tx from July to Sept) + treat at housing
+currently: control by limiting exposure (enough to stimulate immunity but not cause productivity losses):
1. prophylactic anthelmintics to limit pasture contamination during periods when climate is optimal for larval development (2 or 3 doses from spring to July)
2. pasture rested or grazed with another host (eg. sheep) which are not susceptible to O. ostertagi until most of existing L3 have died out
3. combo of 1 & 2: dose in early July & move to another pasture (eg. silage or hay aftermath)
PGE (other nematodes)
+Cooperia oncophora: SI (little pathogenicity)
+Trichostrongylus axei: early spring, abomasum, "thumb print" lesion
+Nematodirus helvetianus: mid-summer (spring born calves)
fascioliasis (key points)
+group condition, mostly young cattle in fluke areas
+mainly chronic disease
+weight loss, marked anaemia, sub-mandibular oedema in severe cases
+diarrhea if combined fascioliasis/ostertagiosis (F/O) complex
+several anthelmintics available incl. combination products for F/O complex
+fluke forecasts
fascioliasis (definition)
+wetter western areas of country after very wet years
+less severe in cattle than sheep (cattle develop some resistance)
+chronic dx of calves or yearlings which have spent their 1st autum on infected pasture
fascioliasis (clinical signs)
+loss of condition
+marked anaemia
+submandibular oedema (severe cases)
+oesinophilia, hypoalbumaemia & raised blood gamma GT levels
+similar to chronic fascioliasis in sheep
fascioliasis (pathology)
+fibrosis of liver (esp. ventral lobe)
+scarring of hepatic parenchyma
+bile duct distention, fibrosis & calcification ('pipe stem' lesion)
+compensatory hyperplasia of dorsal (right) lobe
fascioliasis (diagnosis)
+clinical signs
+eggs in faeces
fascioliasis (treatment)
+triclabendazole (Fasinex), nitroxynil (Trodax), oxyclozanide (Zanil - avail. in combo with lavamisole)
+most flukicides not for lactating cattle (48hr withdrawl minimum)
+F/O complex: combo of ivermectin & clorsulon (Ivomec super) - not for lactating animals
fascioliasis (control)
+prophylactic dose in December & January with drug effective against adult stages
+triclabendazole is only drug effective against most of migratory stages in liver (drug of choice at housing)
+wet springs: 2nd dose given to outwintered stock in May to remove infections acquired during winter & to minimize pasture contamination
+keep cattle away from IMH by fencing off wet pasture
+meteorological info (esp. rainfall & temp) can be used to forecast fluke
coccidiosis (key points)
+group condition in young calves < 6 months
+watery diarrhea +/- blood +/- tenesmus
+associated with mgmt and hygiene
+treat with sulphadmidine, sulphamethoxypyridazine or decoquinate
coccidiosis (definition)
+calves < 6mo kept in crowded unhygienic conditions
+water & sometimes blood-stained diarrhea
+important in USA
coccidiosis (clinical signs)
+21 days after initial infection with oocysts
+mild: faeces are watery with no blood
+severe: blood
+tenesmus, dehydration, loss of condition
+presents as sudden oubreak of dysentery among calves in crowded unhygienic conditions (eg. in loose boxes)
coccidiosis (pathology)
+1st stage schizonts in epithelial cells of SI
+2nd stage schizonts in LI
+clinical disease when epithelium in glands of caecum & colon is infected by 2nd gen schizonts & gametocytes
+loss of epithelium of LI with fibrinous exudate, diptheritic membranes +/- erosions or deeper ulceration due to loss of mucosa
+mild: oedema & congestion of LI only
coccidiosis (diagnosis)
+clinical signs
+high faecal oocyst counts
coccidiosis (treatment & control)
+treat 3-5d with sulphadimidine, sulphamethoxypyridazine or decoquinate
+premises thoroughly cleaned & disinfected; bedding kept dry
+alternate grazing if acquired at pasture (avoid pasture for at least 1yr)
+move & clean feed troughs regularly
johne's disease (key points)
+usually animals > 2 years old, but infection acquired when young
+Mycobacterium avium ss paratuberculosis
+chronic thickening of intestinal mucosa by Type IV hypersensitivity reaction ("cobblestone" appearance)
+weight loss despite good appetite
+homogeneous diarrhea
+no effective treatment
johne's disease (deifinition)
Johne's disease is an infectious disease of ruminants, characterized by a long incubation period and clinically by diarrhea and weight loss. The disease is of economic importance only in cattle and sheep, with weight loss being the major clinical sign in sheep.
johne's disease (aetiology)
+Mycobacterium avium subsp. paratuberculosis
+acid-alcohol fast organism
+staining with ZN: uniformly staining thin rods
johne's disease (prevalence)
+slaughterhouse surveys say 11% are infected
+incidence of clinical cases much lower: <0.2% though may be as high as 5% in infected herds
+sporadic disease: 1-2 cows lost per year in infected herd
+incidence reduced by cull for low milk yield
johne's disease (clinical signs)
+older cows (>2yr) often following period of stress (eg. calving or peak lactation)
+initially diarrhea (homogeneous) is intermittent with slight weight loss & slightly reduced milk yield (several weeks)
+diarrhea becomes more persistent with weight loss (esp. hind quarters) & milk decline becoming dramatic
+remains bright & eats well despite disease until near end
+submandibular oedema (occasionally) but disappears when diarrhea becomes persistent
+bradycardia in later stages
johne's disease (haematology & blood chemistry)
+low grade non-regenerative anaemia: PCV around 25%
+hypoalbumaemia: albumen = 10-15 g/L (normal = 21-34 g/L)
johne's disease (pathogenesis)
+ingestion of contaminated H20/feed
+transplacental infection possible
+infection in 1st few months of life - multiplies in intestinal mucosa
+Type IV (delayed type) hypersensitivy: thickening of intestinal wall due to infiltration of macrophages, giant cells, plasma cells & lymphocytes
+15 months to several years to develop clinical signs (some animals clear infection)
+loss of intestinal surface area & malabsorption
+high epithelial cell turnover causes increased permeability: loss of plasma protein (protein losing enteropathy)
+essential proteins maintained at expense of skeletal muscle loss
johne's disease (pathology)
+lesions in terminal ileum, caecum & 1st few feet of colon
+thickening & granularity of intestinal wall - linear corrugations fail to disappear on stretching
+emaciated carcass (slightly wet & sets poorly)
+enlarged mesenteric LNs
+histo: infiltration of lamina propria with macrophages, giant cells, plasma cells & lymphocytes
johne's disease (epidemiology)
+shed in faeces & can survive for at least 1yr
+calves <6mo most susceptible esp. if suckling johne's cow (adults normally resistant)
+onset of clinical signs: 15mo to 3yr or more (peak incidence 4-6yr)
+control difficult b/c shedding long before clinical signs
+possible rabbit resevoir
johne's disease (diagnosis)
+clinical signs
+faeces exam (ZN method)
+faecal culture: difficult
+cell mediated immunity reactions
+serology: little value
+complement fixation test
+ELISA test for serum antibody: very specific & quite sensitive clinical cases, less sensitive in subclinical cases
johne's disease (treatment)
There is no effective treatment.
johne's disease (control)
+limited diagnostics for subclinical infections
+slaughter of clinical cases
+ once johne's is in the herd, cull on dropped milk yield or weight loss before diarrhea becomes evident
+separate calves from adults after initial post-partum mgmt & do not allow grazing of contaminated pastures (not possible in suckler herds)
+ensure last calves of clinical cases are fattened for slaughter rather than kept for breeding
+vaccination of calves reduces incidence of clinical disease & number of organisms shed but does not eliminate infection
+vaccine interferes with tuberculin testing so only allowed if losses warrant
winter diarrhea (key points)
+probably caused by a coronavirus
+profuse, homogenous diarrhea
+occurs in the colder months
+often occurs as an "epidemic" in herd
+most animals recover without intervention
winter diarrhea (definition)
Winter Diarrhea is a highly contagious disease characterized by a brief attack of severe diarrhea, and sometimes dysentery, that occurs during the colder months of the year.
winter diarrhea (prevalence)
+can cause serious economic loss in dairy herds as a result of reduced milk production and loss of body condition
winter diarrhea (clinical signs)
+most serious in adult milking cows (esp. if recently calved)
+young stock only mild but diarrhea can be present in calves as well as adults
+diarrhea is profuse, watery, homogeneous & dark green to black (no mucus or epithelial shreds but dysentery in up to 10%)
+marked drop in milk yield for up to 1wk
+faeces return to normal in 2-3 days
+rarely persistent or death
winter diarrhea (pathology)
+main changes in LI (esp. spiral colon): mucosal erosions or haemorrhages
+hyperaemia of abomasal mucosa & inflammation of SI
winter diarrhea (epidemiology)
+housed cattle in late autumn & winter (esp. 2-3 weeks after housing)
+young, newly-calved heifers or heifers in late pregnancy most severely affected
+older animals less affected & young stock rarely affected
+majority become ill within 7-10 days of index case & subsided completely in 2-3 weeks
+usually from recently acquired infected cattle, visitors or fomites via contaminated H20/food (3-7d incubation)
winter diarrhea (diagnosis)
based on:
1. epidemic during colder months when housed
2. rapid spread from animal to animal
3. no consistent rise in temp during diarrhea phase
4. recovery of majority within 1wk
5. no fatalities
6. coronavirus in faeces
winter diarrhea (treatment)
+most recover without intervention
+occasional fluid replacement if severe dehydration
winter diarrhea (control)
+little can be done to control
+immunity lasting 6mo after attack but outbreaks seldom recur in same herd with 2-3yr
renal amyloidosis (key points)
+amyloid proteins accumulate in kidney & intestine
+formation of amyloid predisposed by chronic disease or noplasm
+polydypsia with nephrotic syndrome
+enlarged kidney can be palpated per rectum
+rectal mucosa often friable
+no effective treatment
+usually dairy cattle, very rare
renal amyloidosis (definition)
Bovine renal amyloidosis is a condition of adult cattle in which deposition of amyloid (an inert, proteinaceous material) ni the renal glomeruli results in a disease characterized clinically by profuse diarrhea, subcutaneous oedema & renal enlarment.
renal amyloidosis (aetilology)
+poorly understood
+abnormal breakdown of proteins, esp. acute phase protein serum amyloid A (SAA) or, less frequently, immunoglobulin light chains
renal amyloidosis (prevalence)
+sporadic disease of middle-aged to old cows (>5y)
+most frequently in dairy cows, becoming clinically evident after calving
renal amyloidosis (clinical signs)
+due to renal dysfunction with development of a nephrotic syndrome
+profuse homogeneous diarrhea +/- considerable mucus
+subcutaneous eodema in submandibular, presternal & ventral abdominal wall area
+renal enlargement readily detected by palpation of left kidney per rectum
+thin but bright & afebrile with good appetite until near end
+amyloid also deposited in GIT & can make rectal mucosa very friable (rectal palpation may cause severe bleeding)
+marked depression of milk yield & progressive weight loss
+increased H20 consumption: 30-50+ L/day (normal non-lactating adult = up to 25 L/day)
+death usually in 1-2wk (up to 1mo)
renal amyloidosis (pathogenesis)
+amyloid is a pathological, extracellular, proteinaceous material deposited in the walls of small BVs & other tissues, often along basement membranes. 2 main types:
1. secondary
a) chronic infections (suppurative pneumonia, osteomyelitis)
b) chronic inflammatory disease (arthritis)
c) neoplasms (myeloma, renal carcinoma)
2. primary: in absence of predisposing factor
+BOTH: any organ esp. kidney along mesangium & GBM --> protein leak into urine causing hypoalbumaemia & oedema (nephrotic syndrome)
+eventually capillary lumina are obliterated followed by renal fibrosis
+terminally: severe glomerular capillary shut down with uraemia
+diarrhea from combo of intestinal eodema from nephrotic syndrome & intestinal amyloid deposition interfering with fluid absorption
renal amyloidosis (pathology)
+carcasses thin with widespread subcutaneous oedema of intermandibular space, brisket & ventral abdomen
+both kidneys 2-3x larger than normal & are pale, granular, yellowish-brown with a way appearance
+kidneys: firm to cut & glomeruli often visible on cut surface
+intestine: subepithelial oedema with distortion of villus architecture
renal amyloidosis (haematology & biochemistry)
+urine: marked proteinuria often (>300 mg/100mL)
a) severe hypoalbumaemia <10g/L (normal = 25g/L)
b) globulin levels normal
c) uraemia present terminally >30mmol/L (normal = 0-8.3mmol/L)
renal amyloidosis (diagnosis)
+clinical signs sufficiently characteristic
+PM exam to confirm
renal amyloidosis (treatment)
+no effective treatment
+effected animal should be slaughtered