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96 Cards in this Set
- Front
- Back
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year round calving- overall performance measures
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100 day in calf rate- typical 53, achievable 64
200d not in calf rate- typical 12, achievable 7 |
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why is repro performance imporant
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maintain fresh herd with maximum number in most productive phase of lactational curve
need heifers for culling, expansion, surplus maintain FCR |
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investigating repro performance
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calving interval- 1 year good
conception rates- typical 49 (55) % 1st inseminations resulting in pregnancy 80d submission rates- typical 66 (77) % cows receiving at least one insemination by 80d post calving- heat detection, management- time for 1 more cycle before 100d in calf pregnancy rate % of eligable cows that concieve in a 21d period of time if 45% of cows are in heat and are inseminated, if 30% concieve the PR is .45x.30x100= 13.5% accounts for heat detection and conception rate |
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female factors
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ovulatory functions
conception rates implantation early embryonic death and abortion |
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signs of poor repro performance
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poor milk yeild despite good nutrition
poor preg test rates not enough heifers long calving intercal increased returns to services poor submission rates overt signs- vag DC, aborted foetus |
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most common repro problems
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anoestrus
heat detection poor conception rates abortion |
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management factrs for repro
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nutrition
stress heat detection record keeping/calving system insemination techniques/ skill |
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THings to consider in hx in case of abortion
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age
previous abortion- neospora likel to abort again dogs/foxes baseline cases fertiliser use- nitrate new introductions- new bulls vacc hx- eg lepto PT rates age nd stage of gestation |
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Causes of abortion and stage of gestation
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trichomoniasis- 2-4
vibriosis (c. fetus) 5-6m lepto 6m+ salmonella- any neospora- 5-7 BVDV/pesti early septicaemia listeriosis akabane (late) IBR nitrate aspergillus iatrogenic causes of severe anaemiaor hypoxia- theileriosis |
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samples for abortion investigation
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cow
blood, vag swab, membraes FOETUS_ can send whole body in esky otherwise sample EVERYTHING bull- preputial swab |
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most common abortive infections
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L. hardjo, L pomona
c.fetus- vibrio BVDV neospora caninum |
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mainifestations of fetal loss
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early embryonic death
-repeat breeders return to servie think venereal dz- tri, camp, myco abortion- before 260d think infectious/toxic stillbirth- 260 or after think cow probs- dystocia, malntriion |
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stage of gestation vs likely agent
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1st half gest- trichomonas
mid- campylobacter 2nd half- lepto brucella IBR, mycotic, akabane any time- isteria, neospora |
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lesions indicative of agent
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cerebellar hypoplasia- BVDV
cotyledon necrosis- brucella, campylobacter, listeria arthrogryposis, hydrancephaly- akabane fungal dermatitis mutlifocal hepatitis- listeria or neoplasia |
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how would you sample for abortion
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bacteriology samples in separate formalin container- placenta, liver, stomach contents, lung
serology of thoracic/abdo fluid in red top tube all other tissues for PCR/virology can be pooled as long as 1:10 formalin |
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infectious causes of abortion with carrier state
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lepto
IBR BVD salmonella (brucella) |
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infectious venereally transmissable causes of abortion
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trichomonas
campylobacter mycoplasma |
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infectious causes of abortion with vertical spred
infectious causes from environment |
neospora
BVD neospora listeria lepto fungi |
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control of main infectious causes
Lepto campylobacter- BVD IBR neospora listeria fungal trichomonas |
Lepto- inactivated vacc, Ab in bull, env. test new animals. serology 2 weeks apart
campylobacter- AI or vacc, test new bull, cull old bull BVD- inactivated vacc for pre-gest Ab. only import from seronegative herds. cull PI animals IBR- inactivated vacc- but may cause latency neospora- no dogs listeria- poor silage fungal storage of grain trichomonas cull bulls akabane- insect repellant, control movement of naive animals |
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3 main dog ticks
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ixodes holocyclus- legs 2,3 paler, complete anal groove
rhipicephalus sanguineus- brown dog tick- anterior legs bigger than posterior legs haemaphysalis longicornis- bush tick. large. reddish browh legs, first set close to hypostome |
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chemicals in tick saliva that affect the host
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anticoagulants
esterases prostaglandins histamine binding proteins holocytotoxin (ixodes)- interfere with presynaptic release of ACh at NMJ- ascending flaccid paralysis |
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Rhipicephalus sanguineus as a vector
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1. babesia canis
2. Ehrlichia canis |
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tick prevention
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daily tick search during tick season (August to Jan)
permethrin spray or spot on fortngithyl fipronil spot on or spray proban kiltix or new scalibor collar- 14w against paralysis tick |
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normal skin flora
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coag neg staphs
alpha haem streps micrococcus corynebacterium propionibacterium actinetobacter sp malassezia pachydermatis |
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tx of sarcoptes
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ML- moxidectin, selamectin
anti seborrheic shampoo to remove crust- pyohex |
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Pathogenesis of otodectes
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surface mite living in external ear canal. Movement of mites stimulates excess wax production and predisposes to secondary bacterial or yeasr infection
black ear discharge and very itchy ears |
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main aspects of development of drench resistance
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1. contribution of genes for resistnance- heritability
2. refugia - spatial, temporal 3. management issues 4. drench failure |
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parasite population models- input parameters
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1. flock- size, age, sex, initial worm burden, breed
2. pasture- number and size of paddocks, initial contamination 3. management- paddick moves, treatments 4. worm genetics- genes for R and gene frequency |
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parasite population omdels- outputs
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larvae on pasture
eggs in faeces worms in sheep death frequemcy of drug resistance alleles |
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Control of trich burdens
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1. nutrition
supp feed weaner and hogget sheep with protein to increase BW and immunity 2. grazing management prepare safe pastures for weaners and hoggets- use smart grazing, spelling or cross grazing with cattle (or dry shep over 3yo), or cropping wiht cereals and hay 3. stock management supplement tail end of mob cull animals with low host resistance- high FEC, CARLA 4. Effective use of Anthelmentics - right drench at right time quarantine drench-BZ/LEv/ML 'QDrench'- drench and hold before mixing with flock - drench rotation, drench combinations, drench and test, refugia control |
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nitromec actives and indications
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nitroxynil, clorsulon, ivermectin
flukicidal Autumn drench (kill burden) Spring drench (prevent pasture build up) |
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non chemical control of worms
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somatic vaccs-
barbervac novel vaccs- tickguard- target cells of the tick gut- need boosters since animal is not being exposed to the antigen and therefore will not produce own Abs irradiated larvae- dilute refugia cu supplementation selection- carla, FEC, pasture fungi (not aus) GM plants supp feeding |
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endogenous and exogenous pyrogens
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prostaglandin release from hypothalamus
bacteria fungi viruses bile salts neoplasia toxins cytokines- alarmins |
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processes encouraging neoplasia
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failure of tumour suppressor genes
oncogene activation failure of apoptosis failure to recognise DNA damage failure to repair DNA damage |
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define hyperthermia
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Any elevation in core body temperatrure abpve accepted reference values for that species. Results from a loss of equilibriumin the heat balance equation such that heat is produced or stored in the body at a rate in excess of heat lost.
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Define fever
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Fever occurs when an anumal is hyperthermic due to an alteration to the homeostatic set point by the anterior hypothalamus in response to endogenous and exogenous pyrogens
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Exogenous pyrogens
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act on monmocytes, lymphocytes and neutrophils to produce endogenous pyrogens
baceria virus fungi bile acids neoplasia toxins and drugs |
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Endogenous pyrogens
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mainly IL1 but over 11 other cytokines. travel to ANterior pituitary and stimulate prostaglandin release- changes set point by increasing muscular activity.
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sequelae of prolonged fever
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dehydration
tissue damage (>41.1) anorexia increased metabolic demands depression |
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treatment of fever
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must first identify underlying cause- fever is a protective adaptive response
treat if over 40.5 regardless of cause NSAIDS antagonist prostaglandin release treatment may reduce pain and discomfort |
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Aetiology factors- gingivitis
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- amount and type of bacteria in ginigival sulcus
- variation in virulence of strains - abberations in host defence - level of dental hygiene - opportunistic pathogens |
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lassifications of periodontal disease
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Feline juvenille gingivitis- prior to teething, minimal plaque. Overactive immune system to teething process
Juvenile onset periodontitis- usually just before of at time of teething. large amounts of plaque and calculus rapidly forming. gingival recession, bone loss and periodontal break down adult onset periodonitits- 70% of cats over 3. anaerobic gram negatives causing tissue damage due to virulence factors and chronic immune response Gingivo-stomatitis- pharyngitis complex non spec reaction to a number of disease agents. Feline osteoclastic resorptive lesions- |
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Gingivo-stomatitis -pharyngitis complex
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all ages, ulceroproliferative changes- concurrent periodontitis may or may not also be present. Elevated serum globulins- submucosa infiltrate of plasma cells lymphos macros and neutrophils
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FEline osteoclastic resorptive lesions
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subgingival dental resorptive lesions at or below cenetoenamal junction. Mainly buccal surfaces or premolars and molars. Pain, reluctance to eat if extends to dental pulp. Areas of granulation tissue extending into the crown surface of the tooth
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Main concepts with Adult onset periodontal disease
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usually begins as gingivitis which progresses to irreversible periodontitis characterised by periodontal damage and alveolar bone loss due to gram negative bacteria virulence factors and chronic inflammation. The extent of disease may vary between each tooth, as each forms its own microcosm.
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Dx and Tx CFA
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palpate the area for pain or small scabs
Drain Debride lavage ABs |
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likely CFA bacteria
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P. multocida
streps anaerobes |
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causes of poor healing or recurrent s/c abscesses
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residual foci of infection
resistant to AB therapy insufficient drainage |
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famciclovir
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anti-herpetic nucleoside analogue
well tolerated and effective at high doses (as opposed to aciclovir) |
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Systemic anti FHV treatments
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famciclovir- antiherpetic nucleoside analogue
L-lysine- decreases availability of arginine that is required for FHV protein synthesis |
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treatment for CPV
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1. fluids
2. antiemetics 3. AB therapy for secondary infection 4. Antivirals- fresh frozen plasma or interferon (recombinant omega interferon) 5. trickle feeding |
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diagnosis of M.haemofelis
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CS, smear from ear vein (wright), real time PCR, retest 1 month after completed tx
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Pathogenesis of m.haemofelis
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attaches to the external surface of the RBC by fine fibrils. This causes direct membrane damage- increases osmotic fragility, shortens lifespan of RBC and may stimulate antierythrocyte antibodies by revealing hidden antigens or altering surface antigens
Predominately causes extravascular, splenic haemolysis but can cause intravasc haemolysis to a lesser extent |
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treatment m.haemofelis
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- Doxycycline or Marbofloxacin at least 6 weeks
-supportive therapy fluids, oxygen therapy and potentially a typed blood transfusion |
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prevalence and transmission of bartonella in cats
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fastidious, gram-negative, intraerythrocytic, arthropod-transmitted bacteria
Cat fleas are considered the main vector of B. henselae in cats asymptomatic infection common- 40 to 70% have seropositivity and 9 to 90% are bacteraemia |
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Tx, Mx bartonella
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- flea control
- ABs rarely eliminate bacteraemia - used at higher than normal doses - because of the difficulty in eliminating bacteraemia, antibiotic therapy is only recommended for those cats that have confirmed Bartonella-associated disease or those in contact with immunosuppressed owners |
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Value of antivirals
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Cost can be prohibitive
Uncertain efficacy in animals Extrapolating from human diseases has not always been successful Need to be specific for the viral replication d t ifi f th h t ll agents? process and not specific for the host cell Some antiviral drugs only effect replicating viruses not ones that are latent eg herpes Diagnosis of viral infections are often only made after viral replication phase In some viral diseases, the immune response is doing most of the damage |
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Acyclovir uses
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Anti-herpetic eye ointment- response not as good as in humans
need to start early before damage to cornea is severe. treat for at least 1 week beyond resolution o f lesions not good bioavailability in cats and poor in vitro efficacy against FHV1- not used systemically |
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Famciclovir uses
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Revolutionised treatment of FHV1
appears safe at high doses effective systemically against FHV1 dose starts at 62.5mg/cat (about 12mg/kg) but can use 30-40mg per cat as it is more effective and still safe available from BOVA |
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L-lysine uses
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limits availability of arginine which is required for herpes protein synthesis.
Safe but no general consensus on its efficacy some evidence that it reduces conjunctivits, ocular shedding in latent infection best used to minimise severity of recrudescent infection when given before a stressful event like boarding |
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treatment for canine papilloma
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azithromycin
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Treatments that have shown improvement in cats with FIP
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20% with dry form improved with polyprenyl immunostimulant
some improvement of survival time, QOL demonstrated in older cats with wet form FIP when treated with recombinant feline omega interferon and tapering dose of pred |
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Different forms of toxo
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oocytes in the intestines and faeces of actively shedding cats
cysts/ bradyzoites in tissues of infected individuals invasive tachyzoites which are responsible for acute toxo infection |
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Diseases caused by toxo infection
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Most severe disease in kittens infected transplacentally or lactationally- inflammation in liver, lung, CNS, may be sudden death
Adult cats- can be self limiting D+ due to enteroepithelial replication most commonly clinically silent acute infection- spead of tachyzoites chronic- reactivation of latent bradyzoites to release tachyzoites- usuallkyt due to immunosuppression- most comm tissues- lung, liver, CNS, pancreas, heart, eyes. Ocular and neuro signs can develop without concurrent signs |
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Diagnosis of toxo
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cirumstatntial evidence provided by biochem and haematology- non regen anaemia, liver enzymes, AST/CK if muscle affected
Cytology- rarely in CSF, FNA, blood- more common in peritoneal or pleural fluid so always send for cyto serology (30% cats seropositive) high IgM- active infection IgG- previous infection- 4x increase then active chronic Some cats may not develop IgG titres for 4 weeks and 20% of cats don’t develop IgM –faecal exam- oocysts- actively shedding |
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Dx FIP
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1. serology- ANY CORONA VIRUS- UNINTERPRETABLE especially if from multicat household. Different test methods can produce different titres. Cats from multicat households have high titres despite health
2. IHC- FIPV in tissue mactophages in context with surrounding pathology. Ony detects macrophages with sufficiently high number of virus 3. Histopath- pyogranulomatous inflamm, serositis, vasculitits, systemic involvement 4. Direct immunofluorescence of effusions- Fluoroscein conjugated antibody to FIPV finds virus within cytoplasm of macrophages – 100% specificity, 72% sensitivity – pleural, abdominal, pericardial, CSF 5. Supportive evidence Cytology – High protein (>35g/L) – Low cellularity <20,000 cells/ml – mainly neutrophils and macrophage/monocyte • Albumin/globulin ratio – < 0.4 is >90% probability of FIP NOT V HELPFUL non regen anaemia mild neutrophilia, lymphopaenia Nucleic acid amplification – blood, CSF, effusion- not enough research into FECV persistence in tissues and fluids |
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What is FIP amd what is its pathogenesis
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Fatal systemic inflammatory disease induced by Feline Infectious Peritonitis virus (FIPV) (mutant forms of Feline Coronavirus)
- Serositis, vasculitis, pyogranulomatous inflammation in usually several body organs - dysregulation of immune system leading to profound T cell depletion and hypergammaglobilinaemia |
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rotavirus structure, path and dx
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non enveloped RNA
replicate in mature enterocytes, causing mild to mod villus atrophy and D+. More severe in young animals. Can predispose to bacterial infections. ELISA (ag) |
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CAV1 structure patho and dx
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non enveloped DNA
lymphoid rep, viraemia, dissemination- liver, kidney, eye, GIT fever, abdo pain, vomiting, D, coagulopathy jaundice, hepatomeg, corneal oedema PCR, histopath- inclusions, lymphopaenia |
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clinical signs CDV
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biphasic fever
lethargy catarrhal inflamm of the larynx, bronchi, tonsils, nasal passages conjunctivitis GIT CNS Severe leucopaenia |
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dx CDV
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clinical signs
IFA o'n discharge biopsy footpads, conjunctiva, bladder, skin immunohistochem reat time pcr |
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ETECS
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attach and are translocated into enterocytes. Produce enterotoxins- inhibit Na and Cl uptake incease HCO3 and Cl secretion- osmotic effect. Hypersecretory diarrhoea. Functional rather than structural effect. D will continue despite fasting
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EPECs
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enteropathogenic e coli
attach to enterocytes and cause atrophy and destruction of miicrovilli maldigestion and osmotic diarrhea |
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EIECs
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enteroinvasive
invae mucosa- inflammation- produce prostaglandins to cause hypersecretory D+- slouging of mucosa to form dysentry |
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EHECs
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enterohaemorrhagic
adhere to and colonise intestinal mucosa exotoxins are elaborated results in vascular damage and manifests as oedema, haemorrhave and thrombosis |
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dx giardia
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CS- smelly fatty D+ young animals
faecal float but shedding intermittent 3 samples over 10 days If fresh diarrhoea on warm microscope, can see trophozoite stage by movements of flagella. Otherwise a faecal smear stained with iodie to see cyst stage. Presence of cysts not diagnostic of giardiosis because parasite is so common. Age & management history also imp. Elisa/SNAP-detection of parasite Ag in faeces (coproantigen). |
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drugs for pig diarrhoea
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TS- salmonella,
lincomycin- PE, SD neomicin- in water for piglet collibacillosis anti-pili vacc for sows enterisol ileitis- live vacc against PE treatment of coccidia- tolturazil |
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important Salmonella serotypes in cattle
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typhimurium and Dubin
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big causes of scouring in calves under 6w of age
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Enterotoxigenic E coli (<4d)
Rotavirus (4 -14 days) but can occur in older and younger calves Coronavirus (4 -30 days) Cryptosoridium parvum (5 -30d) Salmonella (any age but typically 7-28 days) |
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preventing neonatal D+ in ruminants
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1Ensure adequate colostral intake (Time, Volume & Quality)
2.Provide adequate nutrition 3. Provide a clean and comfortable environment 4.Boost specific immunity 5.Minimise pathogen exposure |
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preventing disease in calves
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regular rotation of calving paddocks- free from effluent withgood drainage
isolation of animals with diarrhoea remove from adult cattel as soon as possible avoid overcrowding maternal vaccinations- E. coli K99, salmonella- increase Ab in colostrum calf hutches removal and disposal of faeces nutrition colostrum |
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Cause of abortion
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- Infections
1 Brucella abortus 2 Leptospira (hardjo-bovis & Pomona) 3 Listeria 4 Neospora caninum 5 Trichomonas fetus 6 Campylobacter fetus ssp. Venerealis 7 Mycoplasma 8. Mycotic 9. BVDV - Iatrogenic 10 Live vaccines 11 GCS 12 Prostaglandins - Toxicity 13 Nitrates 14Mycotoxins 15 Estrogenic plants - Other 16 Genetic 17 Multiple fetuses 18 Stress or disease of the dam |
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pattern recognising abortion by stage of gestation
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- Early embryonic death
o “repeat breeders” o <1 month, before implantation These will often be venereal diseases: Trichomonas, Mycoplasma - Abortion (after implantation, < 260) o Think about infections & toxic causes - Stillbirths o > 260 days o Think about problems w the cow (dystocia, malnutrition, stressors) |
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Principles of controling FMD outbreak in Aus
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Objective:
• to eradicate infection ASAP and return to freedom without ongoing vaccination, whilst minimising the economic impact Principles: • preventing exposure of susceptible animals to FMD virus • decreasing virus production by infected animals • increasing resistance of susceptible animals |
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Inital response to potential FMD
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An initial response would include:
• Identification and lab diagnosis of suspected premises • Preventing further spread: – National livestock standstill for at least 72 hours – Movement restrictions on livestock and products within declared disease control areas – Quarantine of suspected, infected and high-risk farms – Valuation, destruction and disposal of livestock on infected farms – Vaccination (depending on the circumstances) • Assessing the potential extent of infection: – conducting surveillance to identify further cases – tracing movements of livestock, products and fomites • Industry support and communication • Informing the OIE and trading partners |
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soil conditions needed for anthrax spore survival
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alkaline, high water content, calcium nitrate rich- limited areas where these conditions exist- athrax belt includes western plains of nsw and extending into Vic
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Types of effusion
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blood
chyle exudate- septic and non septic pure transudate modified transudate urine |
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test for FPT
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Glutaraldehyde Coagulation Test- precipitation of antibody
<4- failure 4-8 partial failure >8 normal |
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testing for campylobacter (Abortion)
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foetal stomach contents
uterine secretions preputial swabs vaginal mucus agglutination test |
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trichomonas testing
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males asymptomatic carriers- preputial swab, test and treat or cull
foetal stomach contents uterine secretions- wet prep smear and culture |
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LIsteria testing
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culture from foetal stomach and systemic organisms
multifocal hepatic lesions |
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vaccinstions for common causes of abortion
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lepto- serovar specific- need to be aware of serovars in the area. OHS issue
IBR- would only vacc if there is a problem- protection against diz., but vaccinates may still shed virus; Campylobacter- can control infection and disease. Check vacc and mating hx with farmer- new bull? BVD- Inactivated vaccine now registered in Australia; prevent infection of foetus by mounting protective antibody. strain variation may cause failure Akabane • vaccine not yet in Australia Neospora •Vaccine (killed) low efficacy, not yet in Australia |
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Abortion caused by environmental contamination
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Neospora
•Mostly vertical transmission; •feed contamination? •ingestion of aborted foetal membranes? Listeria •poor quality silage; •ingestion of aborted foetal membranes. Fungal abortion •tend to be sporadic; •generally feed contamination. |
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hoe to achieve eliminaion of IBR from a herd
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Elimination from a herd/region/country is achievable, by:
–No vaccination –Imports must be seronegative –Regular testing to ID infected ans. –Cull positives. |
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transmission and control of BVDV
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vertical transmission significant;
•horizontal transmission also; •serology used to ID infected herds; •ID carriers (PI) by virus isolation/antigen detection; •cull PI animals; •Vaccination (strain variation?) •imports only from serologically negative herds. Control: infectious causes |
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control of lepto. prevent carriers
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Annual vaccination;
•AB treatment?? to eliminate carrier state in bulls; •Control of spread within the herd (environmental control) •Serology on introduced animals (2 samples, 2 weeks apart). |
