Flashcards in Bovine Deck (459)
How does Traumatic reticulitis occur?
Following ingestion of sharp metal objects and there localisation in the reticular wall.
What are the clinical signs of traumatic reticulitis?
Rectal temperature is 39-39.5, sudden onset anorexia, dramatic fall in milk production, animal stands with an arched back and moves reluctantly, last to enter milking parlour, complete ruminal atony, initial distension then becomes tucked up and guant, refusal to turn sharp corners, ears back, fixed glazed stare, constipated, defecation and urination frequently accompanied by a grunt. Clinical signs only observed when FB is in contact with peritoneal lining of abdominal cavity.
What test can confirm traumatic reticulitis?
A pain response is elicited when back is dipped behind withers or pressure applied slowly behind the xiphersternum with a pole then suddenly released.
How can your diagnosis of traumatic reticulitis be confirmed?
Ultrasonography will identify excess peritoneal fluid and exudate/fibrinous reaction surrounding the penetrating FB.
What will peritoneal sampling reveal with traumatic reticulitis?
High protein and cell count comprised mainly of neutrophils and presence of bacteria, indicates septic peritonitis.
How can traumatic reticulitis be treated?
High left flank laporotomy under distal paravertebral analgesia. Remove foreign body via rumen and pass hand along rumen floor upwards and forward into reticulum. Recovery is slow.
What are the differentials for traumatic peritonitis after the initial 2-3 days of classical clinical signs?
Peritonitis of differing aetiology, liver abscessation endocarditis, chronic suppurative pneumonia/caudal vena cava thrombosis, pleural abscess, septic pericarditis.
When is an LDA most commonly seen?
Occurs during the winter housing period in dairy cows most commonly but not exclusively in the month following calving. Some association with hypocalcamiea, twinning, endometritis and high concentrate low fibre rations. Increasingly, LDA is seen in recently calved heifers and during the summer months. Never seen in suckler cows or intensively fattened cattle.
What are the clinical signs associated with an LDA?
Clinical signs are most severe when an LDA occurs in conjunction with acute metritis in the 5-7 days after calving. The cow is often febrile, depressed, toxaemic, anorexic, with a reduced milk yield. Such cases may also have already suffered a number of bouts of hypocalcaemia. There is profuse, often foetid diarrhoea.
What will be detected on clinical exam of an animal with an LDA?
auscultation and succussion reveals high pitched tinkling sounds - the distended abomasum occupies the cranio dorsal area of the left side f the abdominal cavity.
What would paracentesis of the displaced abomasum contents reveal in an LDA?
Fluid containing no protozoa and a pH of 2.
What are the pros and cons of rolling the cow for LDA treatment?
Rolling the cow takes time, requires three people and may only be 40% effective at best. there is risk of inhalation of rumen contents when the cow is in dorsal recumbency especially if she has been heavily sedated.
What is the preferred treatment for LDA?
Surgical correction. Right flank omentopexy is preferred method.
Describe the right flank approach for treatment of LDA?
Administer IV NSAIDS. Surgery is performed in the standing cow under distal paravertebral analgesia. A right laparotomy incision is made and the abomasum deflated using a 14 guage needle connected to a flutter valve or suction pump. An omentopexy is performed by talking 4cm bites of the omentum or pylorus and then suture continued to close the peritoneum and internal oblique muscle. Oral fluids used to distend shrunken rumen.
What are the potential differential diagnosis for a case with an LDA?
Rumen void syndrome, gas cap in rumen, vagus indigestion, pneumoperitoneum.
How is toggling of the abomasum performed?
Toggling of the abomasum through the ventral abdominal wall overlying the tympanitic abomasum has been described as a more cost effective procedure than right flank omentopexy. The cow is cast into dorsal recumbency and the abomasum located in the midline by percussion. two toggles with nylon sutures are introduced into the abomasum through wide bore trochlars, then the nylon sutures are tied together.
What is the aetiology of a right sided displacement of the abomasum?
Occurs occasionally in dairy cows 3-6 weeks following calving. Less common than LDA. Probably due to a primary distension of the abomasum due to atony caused by high concentrate intake and secondary fermentation. Accumulation of fluid and gas leads to distension and dorsal displacement on the RHS of the abdomen.
What are the clinical signs associated with RDA?
History of poor milk yield, inappetance and weight loss. Auscultation reveals high pitched tympanic sounds, just cranial to the right sublumbar fossa. Torsion of the abomasum may occasionally result.
What is the treatment recommended for RDA?
Reported treatments include 400mls 40% calcium borogluconate iv and substitute concentrates with hay for 3-5 days, plus oral and i/v fluids as necessary. Hyoscine has been reported to be useful but little supporting evidence. Right omentopexy may relieve the problem but why this is succesful is uncertain.
What complications can occur with abomasal ulcers in calves?
Likely to be complicated by secondary fungal infection of the ulcer as such cases have often received prolonged oral antibiotic treatment by the farmer. Oral electrolytes will maintain the calf but prognosis is poor for those cases that will not suck.
What are the clinical signs of abomasal ulcers in adult dairy cows?
Clinical signs include poor milk production in the early PP period, weight loss and melena. Very low pcv.
How may abomasal impaction occur?
Recognised during the winter months in beef cattle fed poor quality diets of wheat straw and liquid urea supplements only.
What are the clinical signs of abomasal impaction?
Poor coat condition, slow dull with a long dry winter coat, abdomen is often pear shaped, normal temperature, very scant hard balls of faeces with copious mucus in rectum. Very sluggish rumen. The rumen can easily be pitted with a clenched fist through the flank.
What is the treatment of abomasal impaction?
Initially 250g sodium chloride in 25-50l of water by stomach tube. Multivitamins can be given iv. repeat treatment day 2 if necessary. 5-10 litres mineral oil or liquid paraffin have been used. Avoid feeding sub maintenance rations to suckler cows and store cattle.
What is the aetiology of caecal dilation and torsion?
Occurs in dairy cows fed restricted roughage and high levels of concentrates. Also may occur following a change of pasture. Incompletely fermented carbohydrate reaching the caecum is fermented and the resultant volatile fatty acids produced cae caecal atony. Decreased motility leads to dilation, impaction and possible torsion.
What are the clinical signs of caecal dilatation and torsion?
Drop in milk yield over several days and poor appetite. The animal shows tenesmus but there are scant faeces in the rectum. rumen activity is normal but the cow is drawn in.
What is the treatment of caecal dilation and torsion?
Remission of the caecal dilation has been recorded following transportation to surgery facility. ACcess is achieved through a right flank laparotomy under distal paravertebral anaesthesia. Exteriorisation and drainage through an incision made in the blind end of the caecum is a simple procedure. Recovery of previous milk yield may take several weeks.
What are the clinical signs of infected patent urachus?
Affected calves are poorly grown, intermittently febrile and may show pain on urination. Urinalysis is helpful in the diagnosis. A corded structure up to 2cm in diameter may be felt on deep palpation extending form the umbilicus to the apex of the bladder but this is not always easy especially if there is considerable painful umbilical reaction.
What age can you use rubber rings on calves lambs and goat kids?
Up to 7 days old without anaesthetic.
What age are you required to use anaesthetic in calves for castration?
How is local anaesthetic used for castration?
Inject 3-5ml proacine under the scrotal skin and into the testicle. General anaesthetic is only considered for mature bulls or complicated cases e.g partially retained testicles, inguinal hernia etc when standing surgery is not possible.
What complications are seen in surgical castration?
Haemorrhage - when vascular portion of cord is snapped off close to the testes. These calves often develop a large scrotal haematoma.
Gut tie is rare complication of surgical castration of older calves - the remnant of the ruptured spermatic cord/ductus deferens recoils into the abdomen and can become adherent to abdominal wall or viscera causing a slow onset mechanical obstruction of the bowel.
What should you do if you are presented with a rig calf?
Crypotorchid calves should not be unilaterally castrated as the remaining testicle may descend at a later date and the bull calf become fertile. Cryptorchid calves should be left entire and reared as bulls.
How is bloodless castration done with burdizzo?
Should be carried out before 2 months of age otherwise local anaesthetic is required. Pull down on testicles to get access to the neck of the scrotum. the burdizzo clamp is applied twice across each side of the spermatic cord taking care to stagger the position of the crushing. The clamps cause crushing of the spermatic vessels which leads to ischaemic necrosis of the testicles over the following weeks.
Describe vasectomy technique in rams?
Ram is positioned on its hindquarters or in dorsal recumbency following sedation and local anaesthesia or preferably lumbosacral epidural anaesthetic. Incision is made in the skin over the spermatic cord a tthe level of the accessory teats. The spermatic cord is exteriorised following blunt dissection with finger or forceps and the vas deferens localised. The vas deferens is ligated twice and section between the sutures removed. During closure the ligated ends are incorporated in different fascial planes to further reduce the possibility of re canalisation.
At what age can you disbud a calf without anaesthetic?
chemical paste can be applied
What nerve block should be used for disbudding in cattle?
Cornual nerve block using 2-4 ml procaine each side. A useful tip when dehorning large beef calves is to add 3-4ml of 2% xylazine injection to a bottle of 100ml local anaesthetic, gives mild sedation which aids in restraint and calms the cattle.
What complications can occur following dehorning?
Haemorrhage form the nose is often seen immediately after dehorning and is simply due to blood running through the sinuses and draining into the nasal cavity. Rarely, fatal haemorrhage form the cornual artery bleeding can occur following dehorning of large calves so calves should always be checked for arteries spurting. Sinusitis is occasionally seen in older cattle after dehorning. Cattle may appear dull and reluctant to feed at barriers . Tx by flushing with dilute iodine and systemic antibiotics.
What are the differences in disbudding goat kids compared to cattle?
Goat kids have a much larger area of horn bud relative to calves and the horn grows rapidly necessitating early disbudding. Ideally a short acting general anaesthetic is given which can be supplemented by local anaesthetic. Maximum 1ml 2% lignocaine pe kid to prevent toxicity. Skull is much thinner than calves and overheating can cause brain damage so iron must only be applied with gentle pressure for short periods only.
How are bulls nose ringed?
All mature stock bulls should have nose rings inserted to aid handling. light sedation with xylazine may be required. Local is injected with a fine needle into septum. The septum is punctured just cranial to the cartilaginous septum using a leather punch or trocar before pushing the sharp end of the open ring through the defect.
What are the most common serovars of leptospira in the UK?
Leotpspira borgpetersenii serovar hardjo.
Leptospira interrogans serovar hardjo.
Rarely infection with leptospira pomona or leptospira icterohaemorrhaghica occurs in cattle giving a severe often fatal septicaemia associated with pyrexia, jaundice, haemoglobinuria etc.
How does infection with leptospirosis occur?
Infection follows bacterial penetration of mucous membranes/skin. In non immune lactating or pregnant animals rapid multiplication in uterus or udder is followed by bacteraemia. BActeraemia persists for 6-9 days unutil humoral antibodies appear in blood. Leptospira organisms can persist after initial bacteraemia in CNS, reproductive tract and kidneys.
How is leptospirosis shed?
Renal shedding of leptospires in urine occurs after about 14 days and may persist for months or intermittent shedding may occur for years.
What is the route of transmission of leptospirosis?
Infection arises from contact with infected urine or from water/pasture contaminated with urine. Products of abortion are also sources of infection. Most spread probably occurs in spring/summer at pasture. Venereal transmission is possible from bulls carrying lepto in accessory sex glands etc.
Which other animals carry leptospira hardjo?
Leptospira hardjo are not carried by vermin/wildlife. Sheep can also carry and excrete leptospira therefore farms with mixed grazing are more at risk.
What are the clinical syndromes seen in leptospirosis infection in cattle?
Milk drop - occurs 2-7 days after initial infection of a non immune cow. Get a sudden reduction or cessation of yield. May get t hick colostrum like, blood tinged milk in all quarters. Udder goes soft and flabby.
Abortion may occur 3-12 weeks following infection . Most abortions occur in last trimester. May also get weak /premature calves born.
Infertility - circumstantial evidence of infertility caused by lepto in reprotract.
How is diagnosis of leptospirosis made?
Microscopic agglutination test used to detect antibodies to lepto hardjo in serum and more recently this is being replaced by an ELISA. Big variation in individual antibody response and duration of MAT titres. Carrier animals may have negative MAT titres. Paired serum samples taken 3-4 weeks apart will normally demonstrate seroconversion.
What tests can be performed on aborted foetus' to diagnose leptospirosis?
Antibodies in foetal fluids - may indicate exposure to lepto in utero after period of immunocompetence >4mths. Foetus may die before mounting an immune response.
Fluorescent antibody test - to detect lepto antigen in foetal tissues eg kidney li& liver. Delay in submitting samples may lead to pm decomposition of lepto.
How can the herd be screened for leptospirosis?
Need to screen about 25% of herd. A milk elisa is available for bulk milk screening. If only a few seropositive animals with low tites then may indicate historical exposure of older cows. If several cows seropositive with some high titres then may indicate active infection in herd.
What is the treatment of leptospirosis?
Streptomycin/dihydrostreptomycin single dose im will probably eliminate infection in most cases. Oxytetracycline or amoxycillin also likely to be effective.
How can leptospirosis be controlled/prevented?
Control of lepto in cattle herds relies on a combination of management decisions, antibiotic treatment and vaccination. Two killed adjuvanted vaccines are available in the uk, leptavoid-H and spirovac. Vaccination should prevent urine shedding and will protect against milk drop and abortion
What control strategies can be used for a closed herd to prevent leptospirosis ?
Avoid mixed grazing with sheep and fields with shared water courses, ay additions to breeding herd including bulls should be isolated for 3 weeks and treated with streptomycin twice days 10-14 days apart before entry.
What control measures should be used for a herd experiencing acute infection with leptospirosis for the first time?
Consider whole herd antibiotic treatment to reduce risk of spread of infection and zoonotic risk. Start vaccination programme for whole herd. Bought in replacements should be vaccinated before entry.
What control measures can be used for a herd with evidence of endemic infection with leptospirosis from herd screening or abortion serology?
Decision must be made whether vaccination worthwhile. If herd vaccination started - should continue annual booster for whole herd. heifers should complete vaccination course before first mating.
What is the most common source of infection of leptospirosis?
Purchase or hire of an infected animal or contact with infected animals on common grazing. Vermin or other wildlife species play no part in spreading L hardjo infection.
What is the cause of malignant catarrhal fever?
Ovine herpes virus 2.
How does MCF occur?
Relatively rare sporadic disease in the uk affecting cattle and deer. Unusual to see more than one case on a single period of time but outbreaks can occur. contact with sheep or goats seems to be necessary for transmission of the disease. Cases of MCF may occur months after contact with sheep suggesting prolonged incubation or latent infection possible. Cattle are dead end hosts and dont transmit MCF.
What are the clinical signs of MCF?
Intense scleral congestion, bilateral keratitis, depression, anorexia, pyrexia, erosive stomatitis of buccal mucosa and muzzle, profuse muco purulent oculo nasal discharge, superficial ln enlargement, nervous signs may include hyperaesthesia and tremors, diarrrhoea.
How is diagnosis of MCF made?
CNS signs are rare with any other mucosal disease - history of sheep contact and characteristic clinical signs. Characteristic pm and histopathological findings. Serological test available but may not be positive at time of clinical signs initially presenting.
What is the treatment for MCF?
No treatment indicated - mortality is close to 100%. High doses of corticosteroids given systemically may give temporary improvement. Euthanasia should be recommended. Occasionally one case survives but may become chronic.
What is the cause of sporadic bovine leukosis?
Cause is unknown and affected cattle are seronegative for the EBL virus.
What clinical signs are seen in the juvenile form of sporadic bovine leukosis?
occurs in calves 2weeks -6months, characterised by generalised enlargement of all lymph nodes. superficial LNs are visinble form a distance and gradual weight loss, depression and other signs related to tumour masses in thorax and abdomen.
What clinical signs are seen in the thymic form of sporadic bovine leukosis?
Occurs in older cattle typically 1-2 years of age. characterised by massive enlargement of the thymus and local LNs. thymic mass causes jugular engorgement, oedema of brisket extending to submandibular region and chronic bloat due to oesophageal compression.
What type of virus is BVD?
A pestivirus closely related to viruses causing border disease in sheep and classical swine fever in pigs.
What are the two types of BVD virus?
Non cytopathic virus.
There is also two pathogenic genotypes type 1 and 2 BVDV, BVD-2 mainly is present in the USA.
How is BVD virus shed?
Viraemic animals shed virus in nasopharyngeal secretions, urine and aerosol droplets. Faeces is not a major source of virus excretion. Sheep and deer can also act as vectors of the virus, causing infection of cattle but this is low risk. Virus can also be transmitted in fresh or frozen semen of infected bulls and via embryos.
When does acute BVDV infection occur?
Seen when a previously unexposed antibody negative animal becomes exposed to non cytopathic BVD virus. Following transient viraemia the animal seroconverts within 3-4 weeks and may remain antibody positive for years. Many infections are subclinical.
What are the clinical signs of acute BVDV infection?
Many are subclinical. Signs include pyrexia, leucopaenia, dullness, oral nasal eroions which quickly heal, transient scour, milk drop. most affected animals recover uneventfully. May temporarily lower immunity to other infectious diseases e.g salmonella, ibr, rsv, coccidia.
What are the sequelae to acute bvdv infection in a pregnant animal?
Acute BVD infection during pregnancy in a naive cow/heifer can cause various problems associated with transplacental infection of the foetus in utero. Depending on stage of pregnancy can get embryonic death, feotal abortion /death, mummification, congenital defect of CNS/eye, weak/premature calves, live persistently viraemic calves or live normal seropositive calves.
What is the sequelae when a cow is infected with BVD when
May lead to the birth of a live persistently infected calf. this is caused by failure of the foetus to recognise virus as foreign due to immune system not being fully functional
What is the sequelae when a cow is infected around 90-150 days of gestation?
May lead to congenital abnormalities forming cataracts, retinal dysplasia, cerebellar hypoplasia, CNS dysmyelination, cerebral cavitation. These calves are normally antibody positive if sampled before sucking colostrum.
What happens if a cow is infected with BVD >150 days of gestation?
Often gives live seropositive calves born at full term. Abortion can occur following infection at any stage of pregnancy but is not common.
when do maternally derived antibodies normally dissapear?
They normally disappear in calves by 6 months but can persist for as long as one year.
How does mucosal disease occur in calves?
Can only occur in animals which have been born persistently viraemic following in utero exposure to Nvp BVD in early pregnancy. Mucosal disease occurs when a PI animal becomes superinfected with CpBVD virus. This can occur from genetic assortment within PI animal or from a new strain or assortment of a heterologous strain to the NCP BVD strain. Most cases occur in 6 months to 2 year age group which may coincide with the waning of passive immunity. Most PI animals die within the first two years of life but a few can survive until much older.
What are the clinical signs of mucosal disease?
Acute onset depression, pyrexia, anorexia. Salivation around muzzle, widespread oral/nasal erosions/ulcers especially on the hard palate, gums, dental pad. Often muco purulent nasal discharge. Profuse diarrhoea/dysentry with shreds of gut mucosa/blood present in terminal stages.
How can acute BVD infection be diagnosed?
Paired acute/ convalescent sera 3-4 weeks apart to demonstrate rising titre (ELISA) hard to interpret in calves
How can mucosal disease be diagnosed?
Characteristic PM findings - virus isolation from pm tissues. Take blood sample and test for antibody/antigen. Normally antibody negative, antigen positive on ELISA test. May be low antibody titre along with virus positive due to persistent maternally derived antibodies.
How can PI calves be diagnosed?
can often be clinically normal before developing mucosal disease but may commonly be presented as chronic ill thriven or stunted calves. Can confirm PI status by testing tissue (ear notch) or blood for persistent viraemia. Ear notch testing can be done at any age. IDEXX BVDV serum antigen test used by some labs appears to accurately detect PI calves from 1 month of age in the presence of maternal antibodies. Take two samples 3-4 weeks apart to confirm persistent virus positive status.
What is the treatment for BVD?
In acute BVD- symptomatic supportive treatment for enteritis.
Mucosal disease - no effective treatment, will invariably die.
Persistent infection - should be disposed of as act as a source of infection.
How can vaccination be used for BVD?
Initial vaccine 2 doses 3-4 weeks apart before first service followed by boosters at 6 or 12 month intervals depending on the vaccine used. if all breeding females are vaccinated then this should control disease by preventing acute BVD and production of PI calves.
How can BVD be eradicated?
By whole herd blood testing and elimination of PI carrier animals. Strict biosecurity measures must be maintained to prevent reintroduction of disease as herd will soon become naive.
What age group of calves is necrotic enteritis most commonly seen in?
Spring born suckled calves and normally affects calves 2-4 months old. Most cases are seen at pasture in june/july.
What are the clinical signs of necrotic enteritis?
Depression and pyrexia in acute stages, diarrhoea often profuse and haemorrhagic then progressing to more scant muco haemorrhagic faeces, tenesmus, abdominal pain, pale mm membranes, occasional oral and nasal ulcers. death in 7-10 days.
What clinical chemistry findings would be present in a calf with necrotic enteritis?
anaemia, leucopaenia caused by a severe non regenerative neutropaenia. Cases exhibiting profound neutropenia carry a poor prognosis.
What gross pathology is seen in calves with necrotic enteritis?
Crusting of nasal mucosa with oral ulceration occasionally seen. Ulcers are often overlaid by necrotic debri and secondary fungal infection. Ileum, caecum and colon are areas most commonly affected with lesions sometimes extending as far as the rectum. The ulcerative lesions vary from small discrete punctate lesions to large linear diptheritic placques overlying peyers patches.
What is the treatment for necrotic enteritis?
No specific aetiological agent has been identified so the treatment is symptomatic - sulphonamides, IV or oral fluid therapy, multivitamins.
What are the most common types of salmonella serovars that infect UK cattle?
S typhimurium and S dublin. S typhimurium is a zoontoic risk.
How is salmonellosis spread?
Faecal oral infection is the most common route of infection. S dublin infection normally arises form exposure to infected puchased animal or from carrier animals in herd. In infected herds cows can become symptomless carriers and excrete at times of stress. S typhimurium infection also normally arises due to contact with infected purchased animals, or via contaminated feedstuffs, pasture or water courses.
When do most outbreaks of salmonellosis occur?
during the winter months
What are the clinical signs of salmonellosis in calves?
Often 2-6 week old calves affected, can be acute septicaemia and death with either serotype, S dublin may cause pneumonia, commonly dull, anorexic, pyrexic and have pasty faeces with blood present, develop more watery foul smelling diarrhoea with shreds of gut lining passed. Progressive dehydration with tucked up abdomen.
What are the clinical signs of salmonella in adult cattle?
salmonella infection causes enteritis and septicaemia often with abortion if infection occurs in late pregnancy or shedding of the causative organism into milk. S dublin can cause abortion with no signs of enteritis/septicaemia. most severe in stressed groups of animals eg newly calved dairy cows, cows in poor body condition, cows in late pregnancy etc. Main clinical signs include acute enteritis, pyrexia, acute milk drop if lactating, depression, septicaemia, abortion followed by septic metritis in some cases.
How is salmonellosis diagnosed?
Easily isolated from faeces. lab will inform defra who will inform public health.
What are the main differential diagnosis when considering salmonella?
BVD, mucosal disease, winter dysentery, indigestion
What is the treatment of salmonellosis?
Isolate affected animals if possible to limit spread. Systemic antibiotics may prolong excretion if used at insufficient doses. Efficacy dubious in adult cattle. prompt treatment of calves during outbreak may prevent septicaemia and sequelae. Supportive treatment may also be needed - NSAIDS, oral iv fluids, nursing. Recovery can be prolonged.
How is the salmonella vaccine used?
two doses 3-4 weeks apart to stimulate immunity, vaccinating in late pregnancy will improve colostral antibody levels for calves. May be worthwhile using to help protect high risk groups of cattle on farm following outbreak.
How can salmonella be prevented on farm?
Avoid introducing infected animals, quarantine introduced stock for 4 weeks, source new stock form other farms not dealers, avoid shared bulls and communal grazing, use dedicated isolation boxes, clean and disinfecte buildings between occupancies, maintain good fences to prevent access of neighbouring stock, protect feed stores from vermin, including birds, avoid contamination of water sources, only spread slurry on arable land, leave grazing land at least 3 weeks after spreading slurry.
What is the suspected cause of winter dysentery?
Bovine coronavirus - has been demonstrated in the faeces and colonic epithelium of affected cattle and the disease has been reproduced experimentally in susceptible adult cows by exposure to coronavirus isolated from calves.
What are the clinical signs of winter dysentery?
acute explosive watery diarrhoea, often dark brown with flecks of blood and malodorous. usually not pyrexic, partial anorexia, depression and milk drop if lactating, cows may show colic symptoms. may be mild respiratory signs, coughing, naso lacrimal discharge. Quickly spreads in herd but outbreak over within 2 weeks.
What is the cause of johnes disease?
a chronic granulomatous enteritis of adult ruminants caused by mycobacterium avium subspecies paratuberculosis.
How is Johnes disease transmitted?
By ingestion of the organism in faeces from infected animals, contaminating food, water or teats. infection mainly occurs in neonatal animals up to a few months old but occasionally older animals also become infected.
When does clinical disease with johnes show symptoms?
usually a long incubation period and clinical disease is not usually apparent until 3-5 years of age although younger cases are possible with a high challenge.
What host factors encourage disease?
Parturition, transport, poor nutrition, concurrent disease, breed susceptibilities.
What is the pathogenesis of Johnes disease?
After ingestion the organism localises in the ileum and gut associated LNs. it is phagocytosed by macrophages and may multiply intracellularly. Depending on the host pathogen balance the animal may become resistant, intermediate (infection partially controlled, shedder) or clinical.
What are the clinical signs of johnes?
usually appear age 2-6 years with onset often linked to recent calving. progressive weight loss and emaciation are the major signs and may also have submandibular oedema and coat depigmentation, fall in milk yield. there is no fever or toxaemia. rumenal activity is normal. Cattle have soft thick diarrhoea with no blood mucus and tenesmus.
Which faecal examination tests can be used to diagnose Johnes?
1- microscopic examination for clumps of acid fast organisms with a ZN stain. Detects heavy shedders but may miss intermittent light shedders.
2- culture of faeces on mycobactin containing media. Grows v slowly up to 3 months.
3- PCR techniques to detect DNA small quantities in faeces,
Which serological tests can be used to diagnose Johnes?
Complement fixation test - not good specificity/sensitivity in subclinical cases.
Agar gel immunodiffusion test - poor at detecting subclinical.
ELISA - best option though still relatively low sensitivity in subclinical animals.
How can Johnes be controlled?
Control is difficult because of the long incubation period, shedding by subclinically infected animals and the imperfect diagnostic techniques. eradication requires a substantial commitment. Serology or faecal pcr may be done every 6-12 months with slaughter of positive cases. Two consecutive negative whole herd tests may indicate eradication. Minimise faecal contamination of food, water and pasture by raising feed and water troughs, strip grazing, use of piped rather than pond water, avoid spreading yard manure on pasture, maintain good hygiene, separate new born calves from dams at birth and rear by bucket.
What are the clinical signs of Johnes in sheep?
Progressive weight loss, sometimes with wool shedding. The faeces usually remains as firm pellets but soft faeces and diarrhoea may deevelop in some advanced clinical case. As with cattle the disease is fatal once signs occur.
How long is the gestation in a cow?
What type of placenta do cows have?
cotyledonary syndesmochorial. Placental cotyledons attach to maternal caruncles to form placentomes. 120 in total. Arranged in 4 longitudnal rows in each horn.
When does the foetus begin to lie in anterior presentation?
at the end of 6 months, the length of the foetus is > the width of the amnion so that foetus lies in the anterior presentation from then onwards.
What is the source of progesterone in pregnancy?
Until day 150 is the CL. Beyond day 150 the CL isnt the sole source of progesterone which is produced by t he ovarian stroma, the placenta and the adrenals.
What can be used to terminate a pregnancy?
Prostaglandin alone up to 150 days,
Beyond day 150+ need combination of Progesterone and corticosteroid injection.
What can you induce parturition with in a cow?
close to gestation - corticosteroid or PGF2a - parturition within 48-72 hours. Cow between 250-270 days of gestation - PGF2a alone will not reliable cause abortion at this stage of pregnancy, best option is a combination of dexamethasone and PGF2a. abortion should occur in 5 days.
How long should you wait after a misalliance pregnancy to terminate?
atleast 7 days to ensure responsive CL is present.
When are most pregnancies lost?
Early embryonic mortality before day 19. When loss occurs before day 19 then maternal recognition of pregnancy does not occur and the cow will then return to oestrus 18-24 days later, therefore no abnormal interoestrus interval will be observed.
By what point must the cow recognise the pregnancy to prevent luteolysis?
How does the cow recognise the pregnancy?
Interferon - tau is secreted from the blastocyst >15mm diameter normally by day 15 until around day 20.
How does interferon - tau work?
It has anti luteolytic properties as it inhibits oxytocin receptor expression in the endometrium which prevents prostaglandin production by the endometrium and prevents luteolysis.
When does mummification occur?
Mummification can only take place when the foetus dies well before the time of expulsion or removal. There is a foetal death in utero, persistence of the CL, cervix remains closed and uterine contractions are absent. Either papyraceous (all fluids reabsorbed) or haematic (blood degenerates into a viscous brown material)
How is a diagnosis of mummification made?
Usually made beyond term, time of calving approaches and no imminent signs are seen, general health of dam is unaffected, small hard uterus via rectal exam, no placentomes, no foetal fluids, no fremitus. Blood sample for oestrone sulphate or pregnancy specific protein B will confirm absence of viable foetus.
When does maceration occur?
If luteal regression occurs and cervix dilates but mummy remains in utero maceration follows. Corpus luteum regresses, parturient process begins but fails to run complete course, bacteria enter the partially dilated cervix and by putrifaction and autolysis the soft tissues regress until a compact mass of bones remain.
How is mummification treated?
Injection with PFG2a can be tried to lyse CL and cause expulsion of mummy. not always effective. in most cases mummified calf may be pushed into cervix/ vagina but require manual assistance to remove. Corticosteroids are ineffective when a dead foetus is present.
How is maceration treated?
Rarely attempted because it is rarely effective. Uterus may be manually emptied of bones but smaller ones usually remain and are invariably attached to or embedded within the endometrium where they cause residual chronic inflammation and stop contraception.
How does pre partum metritis and emphysema occur?
Most commonly encountered in the peri partum period, most notably in cases of neglected dystocia. Uterine infection by gas producing bacteria which usually gain access via the cervix. the uterine contents provide an ideal medium for bacterial growth. Bacteraemia renders the dam acutely ill and the conition may be rapidly fatal.
What is hydramnios?
Gradual accumulation of excess volume of amniotic fluid around mid- late trimester, caused by foetal abnormality impairing ability to swallow fluids. Most cases go to term. induction of calving/abortion rarely required.
What is hydrallantois?
The most common cause of dropsy in the foetal membranes, seen in in last trimester, caused by abnormal placental function and normally the foetus is normal. Sudden onset severe abdominal distension in last trimester associated with massive voluume of allantoic fluid up to 250 litres, cow has distended pear shaped abdomen. Fluid accumulation can lead to rupture of pre pubic tendon and compression of abdominal organs. twin pregnancy is main ddx.
What is foetal anasarca and how does it occur?
A grossly oversized foetus may be aborted - up to 3x normal birth weight, it has excessive subcutaneous fluid grossly distorting whole body and will cause dystocia problems. Quite rare. caused by an autosomal recessive gene. Mild hydrallantois and oedema of the foetal membranes may accompany foetal anasarca.
How does a schistosoma reflexus calf present?
Foetus is presented with 4 feet or intestines at vagina of dam and may require partial embryotomy or caesarean section to deliver.
What are the predisposing factors to a prolapse of the vagina/+- the cervix?
Multifactorial but probably a combination of overcondition, abnormal relaxation of pelvic ligaments associated with increased oestrogen levels and other unknown factors.
describe how to replace a prolapse?
Give caudal epidural analgesia 5-8ml lignocaine, clean perineum and prolapsed tissue, lubricate and replace prolapse by steady manual pressure, drainage of urine via a needle catheter by puncturing the vaginal wall may help in some cases, check replacement correct and no damage done during replacement, give antibiotic and NSAID cover if vaginitis present, select method for retaining prolapse.
What methods are there for retaining prolapses?
trusses and harnesses - not really used in cows
Sutures - most common method. Buhners suture is the best suture technique, least traumatic and doesnt induce straining. Sutures MUST BE REMOVED AT START OF PARTURITION.
When do cows usually resume cyclicity after calving?
90% of dairy cows resume cyclicity by 50 days, 70% of beef cows by 50 days.
How is ovulation inhibited during pregnancy?
Waves of follicles develop and become atretic in the ovaries - ovulation is inhibited by high progesterone levels during pregnancy giving negative feedback on the hypothalamus. Following parturition FSH induced waves of follicular growth are soon accompanied by ovulation and return of regular cyclicity.
When can the first dominant follicle be detected after calving?
7-20 days pp in dairy and beef cows.
What controls the time of the first pp ovulation?
FSH present in sufficient amounts to stimulate waves of follicular growth by 10-20 days but ovulation of dominant follicle requires sufficient LH pulse frequency. LH pulse frequency controlled via gnRH pulse generator in hypothalamus. Delay in pp ovulation in beef cows c/f dairy cows due to delay in sufficient lH pulse frequency rather than FSH problem.
How do nutritional effects cause extended anoestrus?
Inadequate energy in late pregnancy early post partum period can cause extended anoestrus due to suppression of LH pulse frequency. NEB in early pp period affects levels of circulating insulin and growth hormone and oocyte quality.
How can suckling extend anoestrus?
Greater impact from natural suckling than milking therefore more effect in beef cows. Frequency and duration of suckling affects LH via opiod release interfering with gnRH output in hypothalamus.
How does the season affect pp anoestrus?
first dominant follicle appears - 20 days pp in spring, 7 days pp in autumn.
What factors cause delayed uterine involution which can influence anoestrus?
Assisted calvings, RFM, metritis etc can cause delayed involution which may delay resumption of cyclicity.
What other conditions may lead to extended anoestrus?
Cystic ovarian disease - cysts form due to failure of ovulation of early dominant follicles and this can delay the next wave of follicular development. persistent corpus luteum - usually found along with uterine infection/pyometra as this can lead to failure of endometrial PGF2a release. Treat with PG injection.
How can nutritional anoestrus be diagnosed?
Palpate two small hard ovaries with no CL or large follicles with similar rectal findings in 10-14 days. or have two low progesterone values in milk or blood recoded 10 days apart.
How can nutritional anoestrus be treated?
sort out management and nutrition.
Progesterone releasing devices for 9-12 days to mimic luteal phase then ovulation within 2-3 days of implant removal.
GNRH injection - single dose of 5ml receptal given >55days pp will give oestrus in most acylic cows within 23 days.
What is the minimum period after pp that cows should be bred?
42 days - before this the pregnancy rates will be poor. (40-60 days).
Which hormone treatments can be given to improve fertilisation rates?
GNRH on day of service. GnRH injection induces an LH surge ensuring ovulation occurs synchronous with the insemination.
GNRH at day 11-12 post service. GnRH causes LH release > luteinisation of large 2nd wave follicles _ ovulation and formation of accessory CLs. This reduces oestradiol secretion from 2nd wave follicles and reduces chance of early luteolysis if embryo is late to produce BTP1..
Describe the OVSYNCH/intercept regime?
A combination of GnRH and prostaglandin can be used to synchronise dairy cows for fixed time AI.
Day 0 - GNRH
Day 7 - prostaglandin
Day 9 - GnRH
Day 10 - AI 72 hours post PG
What is the cause of repeat breeders?
Undiagnosed pathology and failure of fertilisation - hostile uterine environment for sperm, blocked oviduct/salpingitis, delayed ovulation, bursal adhesions, cervical non patency, hostile uterine environment for embryo which dies on entry to uterus.
Failure of sufficient btp-1 production from embryo leading to failure of maternal recognition of pregnancy.
What may cause uterine tears?
Normally associated with dystocia and excessive traction, large calves.
What are the causes of a uterine prolapse?
Normally associated with the delivery of a large calf, prolonged parturition and straining. Hypocalcaemia is often present. Usually occurs within hours of a calf being delivered. most common in multiparous cows.
How can uterine prolapses be treated?
give i/v calcium borogluconate if hypocalcaemia sever.e If cow down, place in sternal recumbency with hind legs pulled back. Give caudal epidural anaesthetic. Clean uterus and remove placenta is possible. Replace using firm manual pressure starting at cervical portion. If very swollen oedematous can reduce oedema using firm pressure with arms around mass before replacing. Ensure uterus is fully inverted to tip of horn when replacing to reduce risk of recurrence. Insert antibiotic pessaries and give antibiotic cover for 3-4 days. Oxytocin may hasten uterine involution.
What factors affect the normal involution of the uterus?
2. Retained placenta
3. Uterine infection
6. Selenium deficiency
7. Suckling frequency
9. Climate - heat stress
What is post partum vaginal discharge called?
normal for 7-10 days due to sloughing of surface tissue from uterine caruncles. Usually reddish brown and odourless. It is derived from the remains of the foetal fluids, bloods, shreds of foetal membranes but mainly from sloughed surfaces of caruncles. Complete regeneration of caruncular epithelium normally achieved by 25 days pp. Caruncles gradually shrink as involution progresses.
What are the most common bacteria isolated from the uterus?
actinomyces pyogenes, e coli, fusibacterium necrophorum, staph, streps. 90% of uteri swabbed within 15 days post calving have bacterial contamination but this is reduce to around 9% by 46-60 days pp.
Why may bacteria fail to be eliminated from the uterus?
Due to overwhelming degree of bacterial contamination or impaired natural uterine defence mechanisms.
What is puerperal metritis?
Puerperal metritis should be defined as an animal with an abnormally enlarged uterus and a fetid watery red brown uterine discharge, associated with signs of systemic illness and fever >39.5C, within 21 days after parturition. often associated with RFM?
What is the treatment for puerperal metritis?
Systemic broad spectrum antibiotics eg cephalosporins. If toxic shock present give i/v fluids and flunixin.
Why may removal of RFM be contraindicated in puerperal metritis?
Increases uterine trauma and toxin absorbtion, prostaglandin injection may be beneficial when calved 10-14 days.
What is metritis?
Animals that are not systemically ill but have an abnormally enlarged uterus and a purulent uterine discharge detectable in the vagina, within 21 days post partum may be classified as having clinical metritis.
What is clinical endometritis?
Characterised by the presence of purulent uterine discharge detectable in the vagina 21 days or more after parturition. No systemic illness.
What are the predisposing factors associated with endometritis?
Dirty calving environment
Premature calving - twins induced calving
Delay in return of pp cyclicity.
Over fat at calving/fatty liver syndrome
Nutritional deficiency eg selenium
what are the consequences with clinical endometritis?
Extending calving - conception interval in affected cows due to delay in return to cyclicity or deliberate delay in re breeding plus reduced conception rates due to hostile uterine environment causing semen/embryo death.
How Can endometritis be diagnosed?
Evident at three to four weeks post calving by persistent purulent vulval discharge, often evidence of tacky discharge stuck to tail below vulva. May be seen following oestrus when cervix opens. Rectal palpation normally reveals one or both uterine horns enlarged but may be little palpable abnormality in mild chronic cases. Ultrasound is useful to aid diagnosis with distension of the horn and purulent fluid being evident.
What is the treatment of endometritis?
Prostaglandin injection - treatmnet of choice. requires responsive CL for optimum effect.
Intrauterine antibiotics - pessaries of dubious efficacy due to insufficient concentrations of antibiotic administered, metricure washout preferable, can try 12-24 hours after AI in repeat breeder cows if suspect low grade endometritis.
Antiseptic wash out - irritant to endometrium and cause PGF2a release which may have curative effect.
How can endometritis be Prevented?
Environment - general calving hygiene and minimise dystocia problems.
Host immunity - physical barriers, acquired immunity, innate immunity
Pathogens - coli, a pyogenes, anaerobes,
Avoid over fat cows
ensure adequate mineral/vitamin supplementation.
What is a pyometra?
Defined as the accumulation of purulent material within the uterine lumen, in the presence of a persistent corpus luteum and a closed cervix. Will palpate distended uterine horn which must be distinguished from pregnancy as could develop after service. With pyometria uterine wall is often thicker and no membrane slip or cotyledons palpable. Can confirm using ultrasound.
What is the treatment for pyometra?
Injection with PGF2a with luteolysis being followed by return to oestrus and evacuation of the uterus.
What is retained foetal membranes?
Partial or complete retention of foetal membranes beyond 12 hours post partum. effectively this means failure of normal 3rd stage labour. Failure of normal separation of foetal cotyledonary vili from maternal caruncles or primary uterine intertia. Phsyiological processes controlling separation of placenta begin weeks pre partum.
What factors predispose to RFM?
Premature parturition - immature placentomes not physiologically prepared for separation eg twin births, late abortions, induced births.
Oedema of chorionic villie caused by trauma eg dystocia, caesarian, uterine torsion.
Pathological inflammation eg placentitis caused by abortion agent such as bacillus licheniformis.
Uterine inertia due to hypocalcaemia, hyposelenaemia, hydrops, twins.
What are the clinical signs of RFM?
Putrif placenta hanging out from the vulva, but may be retained in the cervix/vagina and not obvious from outside. May be straining in attempt to pass the placenta. Usually no systemic illness unless puerperal metritis develops.
How can RFM be treated?
Manual removal probably contraindicated unless comes away with gentle manual traction. Best time to attempt manual removal is 3-5 days pp. Definetly contraindicated if associated with metritis as causes trauma to endometrium which may increase toxin absorption and decrease phagocytic function. If puerperal metritis is present appropriate systemic antibiotics will be needed.
When do most ovarian cysts develop?
20-60 days pp often in 2nd and 3rd lactation high yielding cows.
What is the definition of an ovarian cyst?
Fluid filled structure >2.5cm diameter present for >ten days on one or both ovaries in the absence of a CL.
What are the two types of ovarian cyst?
Follicular - thin walled, non progesterone producing
Luteal - thicker walled, progesterone producing.
Why do ovarian cysts form?
Cysts form due to failure in LH surge around the time of ovulation, or failure of follicle to respond to LH. Folicle fails to ovulate and instead of becoming atretic continues to grow and forms cysts. Cystic follicles initially produce oestradiol which suppresses further follicular development and then they may enter oestrogen inactive phase during which time the cyst can persist for many weeks.
What are the possible reasons for the failure of LH surge to cause an ovarian cyst?
Sterss - cortisol can interfere with lh surge. eg energy stress, movement, change of diet.
Metritis - also causes cortisol release.
What are the clinical signs of a follicular cyst?
Anoestrus or occasionally nymphomaniacal behaviour i.e irregular or recurrent oestrus behaviour
Luteinised cysts: anoestrus
Most cysts cause anoestrus and are detected on routine pp checks .
How can you diagnose ovarian cysts on milk progesterone?
follicular cysts have low milk progesterone 2ng/ml.
What is the treatment for ovarian cysts?
Progesterone - PRId for 10-12 days. Causes atresia of cyst by suppression of LH and FSH through progesterone negative feedback.
PGF2a - can use alone if luteal cyst.
If positive it is a luteal cyst - use PG
if positive it is a follicular cyst use a PRID/CIDR for 10-12 days or GnRH injection.
If unsure of cyst type use GnRH + PG in 7-14 days if not seen in oestrus or insert prid for 10-12 days with injection of PG at removal.
What is the definition of abortion?
The expulsion of a dead or non viable calf before 260 days gestation.
At what rate should an abortion problem be investigated?
Most herds experience 1 or 2 percent of cows aborting. if 5 percent or more abort a thorough investigation is warranted.
Which samples should be submitted for testing?
The whole foetus, placenta with cotyledons, lesions and normal tissue and possibly a maternal blood sample. if the whole foetus cannot be submitted, fresh samples should be taken including foetal stomach contents, pleural or peritoneal fluid, liver, lung, thymus and blood.
What is freemartinism?
Hormones, blood cells and other cells cross the placental anastomoses, leading to chimerism. Testosterone or male clels lead to masculinisation of female twin. clinical signs may include an enlarged clitoris with tuft of hair, vagina less than normal lenngth and blind, gonads hypoplastic, uterus difficult to palpate, epididymides and vasa deferentia seen on ultrasound.
What is the difference between primary and secondary infectious infertility?
Primary - acting directly on the reproductive tract, placenta, foetus. Secondary - systemic diseases, secondary effect on conception/pregnancy.
List all the infectious agents that cause abortion commonly?
Bovine viral diarrhoea BVD
Bovine herpes virus BHV1 (IBR)
Transmissible viral papillomatosis
Bovine herpes virus 4
Epizootic bovine abortion (chlamydophila abortus)
Trochomonas foetus (trichomoniasis) not in UK
How is campylobacter fetus var venerealis transmitted?
Natural habitat is the prepuce, glans penis and distal urethra. Service leads to mechanical transmission. Herd infection usually occurs after introduction of new infected bull.
What are the clinical signs of campylobacter fetus var venerealis?
Usually no systemic illness, females experience a mild endometritis and cervicitis with mucopurulent vaginal dischage. Cases present as repeat breeder which eventually holds, with abortion and RFM at 4-7 months or pregnancy survives to term. in herd - large number of returns, then abortions.
Do animals develop immunity to campylobacter?
Untreated bulls are usually permanently infected, cows and heifers develop immunity over 3-6 months.
How can campylobacter be diaganosed?
Isolation form post service discharges, vaginal mucus agglutination test, C foetus venerealis in products of abortion. For males - qualitative and bacteriological examination of semen, FAB on preputial washings, virgin heifer test.
How can campylobacter be controlled?
AI all stock or AI infected stock and use clean male on clean females. Two normal pregnancies by AI before resuming natural breeding advised.
What is the treatment for campylobacter?
Females not usually treated. Streptomycin will shorten course of disease. Bulls are usually culled or treated systemically plus topically (preputial irrigation and antibiotic cream). Four negative FAB or virgin heifer test advised before bull re used.
How is brucella abortus transmitted?
Infection is primarily by ingestion, with haematogenous spread at around 6 months gestation to uterus/placenta. This causes a necrotic placentitis and endometritis. In bulls, the infection localizes in the seminal vesicles and testes. It is introduced by silent carriers and excreted in fluids/faeces before and after abortion. Cattle normally only abort once but remain infected and excrete as carriers.
What are the clinical signs associated with brucella abortus?
No systemic disease. Abortion and placental retention. Some foetuses are born alive, newly infected herd, abortion seen in cows in late pregnancy, then those earlier in pregnancy. When endemic, abortions are seen in clean replacements and home bred heifers.
What does IBR cause?
Respiratory disease, milk drop and reproductive disease Non veneral infection at service or AI can lead to repeat breeding, or later in gestation to abortion. Infection in late pregnancy may lead to stillborn or non viable calves. Venereal infection at natural service can lead to infectious pustular vulvo vaginitis.
How does infectious pustular vulvo vaginitis present?
Sudden on set vulval hyperaemia, leading to vesicles and ulcers 48 hours post mating. This leads to pain, anorexia and pyrexia, preventing further service. Males develop similar preputial lesions and mating is interrupted for 2-4 weeks.
What are the definitive hosts of neospora caninum?
Dogs - they shed oocysts in their faeces. These oocysts are picked up by intermediate hosts.
What are the intermediate hosts of neospora caninum ?
Dogs, cattle, mice , horses& sheep
How does neospora cause disease in cows?
When a CONGENITALLY infected animal becomes pregnant, bradyzoite cysts multiply and spread to the placenta and foetus. the consequences may be abortion in the 3rd to 9th month of gestation, premature birth/stillbirth and a full term calf with neurological signs, a clinically normal infected calf or rarely a clinically normal uninfected calf.
What may infection with neospora during pregnancy lead to?
Infection in early pregnancy can lead to later abortion, while infection in late pregnancy can lead to a full term clinically normal congenitally infected calf.
How is diagnosis of neospora made?
Diagnosis is based on pathology and serology. There is non inflammatory necrotic foci in CNS, bradyzoites in myocardium and liver, inflammatory and necrotic placental lesions. positive maternal serology indicates exposure but may go negative, positive foetal serology indicates exposure after 17 weeks gestation.
How can neospora infection be controlled?
No vaccine in the uk or treatment. control BVD. prevent animal contamination of feed, prevent bovine/canine contact with placenta or abortion tissues, embryo transfer from valuable seropositive cows.
What is the cause of ringworm in cattle?
Trichophyton verrucosum. Spores survive for months/years. Transmitted by clinical cases and fomites.
What are the common sites for ringworm infection?
Calves - periorbital, ears, back
Adults - thorax, limbs, udder
Non pruritic, alopecic lesions, greywhite with powdery surface, often roughly circular.
What is the pathogenesis of ringworm?
Infection of keratin of hair and skin, enzymes attack keratin of actively growing hair, breaks off, mild inflammatory reaction
What is the treatment for ringworm?
Often self limiting.
Griseofulvin in feed not available in the UK.
Sodium iodide - repeat in 7 days (toxicity)
Topical enilconazol (imaverol)
Which lice species infect cattle?
Novicola bovis (biting lice)
Haematopinus eurysternus, linognathus vituli, solenopotes capillatus (sucking lice)
Describe the life cycle of lice in cattle
3-6 weeks, entirely on host, lay eggs which attach to hairs, nymphs undergo several moults to become adult, survival off host is short.
Where are lice seen in cattle?
Biting lice - neck, withers, tailhead
Sucking lice - more generalised, head neck withers brisket tail axillae groin.
What can lice be treated with?
Deltamethrin pour on, permethrin pour on, endectocides. Only eprinex can be used in dairy cows. Injectable endectocides not very effective vs biting lice.
Which mites cause mange in cattle?
Chorioptes bovis surface mite, psoroptes ovis, sarcoptes scabiei, demodex.
Describe the life cycle of chorioptes bovis?
Surface mite, life cycle is 2-3 weeks. lives off epidermal debris. Transmission via direct contact.
What type of mite is sarcoptes scabeiei?
Burrowing mite, lifecycle 10-17 days, direct contact spread or fomites, survival off animal only a few days.
What is the pathogenesis of photosensitization?
There is a photodynamic agent in the skin. Irradiation of the agent causes cell death, non pigmented areas without hair covering are most affected, causing necrosis and sloughing of skin.
Describe the difference between primary photosensitisation and secondary photosensitisation?
Primary - defective metabolism e.g porphyria, plant origin e.g st johns wort.
Secondary due to liver disease, failure to metabolise phylloerythrin (chlorophyll breakdown product) which builds up in circulation.
which type of fly are implicated in spread of summer mastitis?
What type of flies cause blowfly strike?
Lucilia sericata or phormia terranovae. Less common than in sheep, larval infestation of soiled skin especialy in warm damp conditions eg adult cattle dehorned in summer.
What are the clinical signs of warble fly infestation?
Warble larval infestation by hypoderma bovis or H lineatum- subcutaneous nodules and cysts along the back of cattle in spring should be regarded with suspicion, confirmation obtained by carefully opening swellings.
What is the cause of infectious bovine keratoconjunctivitis? (New forest eye)
Moraxella bovis + IBR, mycoplasmas, flies, dust, uv light, moraxella perhaps found on normal conjunctiva and needs enhancing factors.
What are the clinical signs of new forest eye? (infectious bovine keratoconjunctivitis)
Uni or bilateral conjunctivitis, chaemosis, discharge, purulent, blepharospasm, photophobia, cornea - central white/cloudy raised lesion, oedema, after 6 days > vascularisation, mild anterior uveitis.
What is the treatment for infectious bovine keratoconjunctivitis?
Antimicrobial therapy with either topical clxacillin, chlortetracycline, or subconjunctival injection with 1.25ml procain penicillin or 1ml oxytetracycline, or systemic oxytetracycline LA, florfenicol or ceftiofur. In an outbreak - isolate affected cattle if possible.
What is silage eye? (listerial uveitis)
An opthalmitis believed to be associated with listeria monocytogenes is recognised in cattle and sheep related to the feeding of big bale silage from ring feeders. seen more commonly in cattle. Risk of direct ocular contact with the silage. consistent isolation of L monocytogenes from conjunctival swabs from affected animals.
What are the clinical signs of silage eye?
Lacrimation, blepharospasm, photophobia, swollen, folded iris, miosis. Within 2-3 days bluish white corneal opacity spreading centrally, white focal aggregations of fibrin in anterior chamber. In advanced cases - pannus and vascularisation. Very painful.
What is the treatment for listerial uveitis?
Response to topical treatments is poor. Subconjunctival injection of a combination of oxytetracycline and dexamethasone usually halts the progression of clinical signs when given in the acute stages of the disease. The eye will usually return to normal in a few days to a week, depending on initial severity of the problem. In sheep subconjunctival treatment is effective.
What is the causative agent of ovine infectious keratoconjunctivitis?
Mycoplasma conjunctivae - present in eyes for up to 3 months after recovery. More severe in ewes than lambs.
What are the clinical signs of ovine infectious keratoconjunctivitis?
Tear staining, blepharospasm, then progresses to stage 2 and cornea becomes cloudy due to keratitis, pannus and vascularisation spreads from limbus, very irritation. stage 3 - ocular discharge becomes more mucopurulent, may be shallow ulceration. stage 4- blind, corneal ulceration, anterior uveitis, anterior chamber may rupture resulting in permanent blindness.
How does ovine infectious keratoconjunctivitis occur?
Introduced by carriers, spread by close contact, in winter during feeding/yarding housing, wind and snow. in summer weaned lambs - high stocking rates, handling of the face and head whilst drenching, dust, long grass and flies.
What is the treatment for ovine infectious keratoconjunctivitis?
Tx recommended to prevent the risk of permanent blindness. Affected animals separated, ideally housed. Single i/m injection of long acting oxytetracycline is very effective in halting the development of clinical signs or curing in 4 days. Treatment of choice in a group of affected ewes. Topical application of aureomycin powder to the surface of the eye can be used in mild cases. Topical chlortetracycline repeated in intensive lambs.
Which type of urolithiasis is common in male sheep?
magnesium ammonium phosphate hexahydrate (struvite) calculi, associated with feeding concentrates high in phosphate and magnesium.
Where do calculi usually lodge in the sheep?
Lodge within the urethra just proximal to the sigmoid flexure or within the vermiform appendix.
What are the clinical signs of urolithiasis?
Frequent tail swishing and foot stomping. wide stance, stretching, dog sitting, tenesmus, painful bleating, teeth grinding, mm congested and HR and respiratory rate are increased. nil or only drops of blood tinged urine are voided.
What are the sequelae to a urinary blockage?
back pressure doesnt usually cause bladder rupture but urine leaks acros bladder wall resulting in uroperitoneum. rupture of urethra / penis commonly occurs in cases neglected after a few days with extensive subcutaneous swelling extending from the scrotum cranially to the prepuce.
How can urolithiasis be confirmed via laboratory tests?
BUN and creatinine can be increased by many times the normal range
What is the treatment for a urinary obstruction?
Blockage is relieved normally during clinical exam when the penis is extruded and vermiform appendix excised with production of a free flow of urine. Catheterisation of the urethra after excision of the vermiform appendix and back flushinng is rarely possible. Surgical correction of urolithiasis involves a sub ischial urethrostomy under caudal block but there are potential complications. Tube cystotomy has been reported to be succesful in some breeding rams but requires GA and placement of a foley catheter.
How can urinary calculi be prevented in rams?
Urine acidifiers such as ammonium chloride are commonly added to rations. sodium chloride has been added to rations to promote water intake. provision of roughage promotes saliva production and water intake. fresh clean water must always be available and frequent checks must be made for frozen pipes.
Describe urolithiasis in cattle when compared to sheep.
Partial/complete obstruction very uncommon in cattle. rupture of urethra more common than in sheep. Surgery in standing patient under low extardural block is more successful than shepe because hydronephrosis does not develop but is a salvage procedure only in cattle near slaughter weight.
How does pyelonephritis occur in cattle?
Occurs sporadically in cattle resulting from ascending infection with cystitis and ureteritis. more common in older beef cattle following an unassisted calving.
What is the common cause pyelonephritis in cattle?
What are the clinical signs seen with pyelonephritis in cattle?
weight loss, poor appetite, fever, poor milk yield, cows calf fails to thrive. frequent attempts to urinate, flow rate is slower than normal , tail swishing with an arched back maintained for much longer than normal after urination. flecks of blood and pus are passed at end of voided urine. Grossly thickened ureters palpable on rectal examination. Dilation of renal calyces, echogenic flocculent material within the renal pelvis and renal enlargement are suggestive of pyelonephritis.
What is bacillary haemoglobinuria?
Causes sudden death in cattle and sheep caused by toxins of cl haemolyticum (cl novyi type D). focal anaerobic areas in liver caused by migrating liver flukes allow spores to germinate with release of toxin. Haemoglobinuria is rarely witnessed. If seen alive animals are isolated, arched back, febrile with rectal bleeding and bloody faeces. there is no effective treatment.
What is babesiosis in cattle?
Tick transmitted babesia bigemina and babesia bovis. Clinical signs o fever, depression, anorexia, pronounced tachycardia, tachypnoea, anaemia and haemoglobinuria manifest after 1-3 weeks. Death follows rapidly in untreated cattle. Treatment with imidocard.
What is a sandcrack?
loss of continuity of horn fibres of the palmar/plantar hoof wall extending for a variable distance from the coronet towards the bottom of the hoof wall. Sandcracks result from damage to the periople and underlying coronary band. There is often sudden onset of severe lameness when impacted material leads to pus formation and pressure on the sensitive laminae of the wall. Usually front feet are more often affected.
What is thimbling?
Horizontal fissure of the hoof wall. Poor horn production during a severe toxaemic condition such as coliform mastitis or metritis apears as a horizontal fissure in the hoof horn of all eight digits. As this defect in the wall grows down to about two thirds of its length three to four months later it weakens and may separate from the healthy horn proximally. The corium remains intact distal to the horizontal fracture holding the distal hoof horn attached at the toe. this fissure moves when weight is taken tensing the corium and causing pain and lameness. All four feet are affected.
How do white line abscesses occur?
White line abscesses arise following bacterial entry into the white line area, usually found in the lateral claw of the hind foot on the abaxial border close to the junction with the heel. the condition is more common in dairy cows that spend long periods standing / walking on poorly maintained surfaces and tracks. impaction with small stones/dirt - entry o fbacteria with multiplication forms an abscess which may extend and discharge at coronary band. Affected cattle often present with sudden severe lameness of the affected leg with only the toe touching the gorund.
What is interdigital skin hyperplasia?
Excess epidermal and hypodermal tissue occupying part of the interdigital space. Usualy appears as a protruberance of skin at the front of the interdigital space. Usually doesnt cause lameness unless it becomes so large taht excoriation leads to superficial infection.
What is slurry heel caused by?
affects almost all dairy cows during late winter months, new horn growth affects the weight bearing function of the hoof which predisposes to corium damage, sole ulcer and white line diease. Caused by prolonge exposure to slurry during the winter housing period. Dichelobacter nodosus infection has also been suggested.
How does slurry heel present?
Does not usually cause lameness alone. there is necrosis of the horn of the heel and heel sole area varying from small blackish pited areas of the horn up to black cracks penetrating deeply towards the corium of the heel sole area.
What is a sole ulcer?
A specific circumscribed lesion of the sole at the sole heel junction nearer to the axial than the abaxial wall affecting dairy cows. never seen in growing cattle and rarely in beef cows. The highest prevalence occurs during late winter after cattle have been housed for several months. Sole ulcer affects the lateral digits often involving both hind feet.
How do sole ulcers occur?
Pressure damage to the corium caused by compression at the posterior axial border of the pedal bone. build up of new horn consequent to chronic necrotic pododermatitis is an important factor.
What is the usual clinical preentation with a sole ulcer?
Sudden onset of severe lameness, may stand with the toe of the affected digit on the edge of the cubicle, may abduct the leg to weight bear on the unaffected medial claw, much new overgrown soft horn on the lateral claw containing the obvious sole haemorrhage.
How does septic pedal arthritis occur in cattle?
Following deep penetration of the distal interphalangeal joint by nails and other metal objects, or following extension from sole ulcer lesions in the lateral hind claw of dairy cows.
How does septic pedal arthritis present?
10/10 lame with marked muscle atrophy of the affected limb after 7-10 days. History of poor milk yield/body condition. marked swelling of drainage LN which may be five to ten times its normal size although the popliteal LN is difficult to palpate. The foot is hot, swollen and very painful. Marked swelling above the coronary band on the abaxial aspect extending to the bulb of the heel but discharging sinuses are uncommon except for neglected cases. The swelling above the coronary band on the abaxial aspect of the hoof wall extending around to the bulb of the heel is consistent with a diagnosis of septic pedal arthritis.
What is the treatment for a septic pedal arthritis?
Further antibiotic therapy is useless in cattle with infection of the distal interphalangeal joint. digit amputation under iv regional anaesthesia gives good results. use IV flunixin, then 25-30 mls lignocaine solution in a superficial vein after application of a tourniquet.
What is digital dermatitis in cattle?
Infectious contagious disease causing severe lameness in adult dairy cattle, the condition is uncommon in beef cows and growing cattle. Caused by a spirochaete.
How does digital dermatitis present clinically?
Lameness is variable. in severe cases the weight is borne at the toe leading to excessive growth at the heel bulbs. The early lesion is a distinct moist area of skin approx 2-5 cm in diameter above the cleft of the bulbs of the heel. there is erosion of superficial skin with a yellow green diptheritic membrane covering the lesion.
What is the treatment for digital dermatitis?
Remove all impacted faecal material overlying the lesion. thoroughly clean the lesion then apply topical oxytetracycline aerosol. repeat treatments are frequently necessary. Daily footbaths containing lincomycin or tylosin are frequently used to control herd outbreaks but ensure that cows dont drink these. formalin or copper sulphate footbaths appear to have no effect on transmission or development of this condition.
What is superfoul in cattle?
A peracute form of interdigital necrobacillosis. Very sudden onset lameness. Swelling and widening of the interdigital space with extensive tissue necrosis, can rapidly progress to involve the navicular bursa, flexor tendon sheath and distal interphalangeal joints. The foot is very swollen and cow 10/10 lame.
What is the treatment for superfoul?
Immediate action is very important. under IV regional anaesthesia, debride the interdigital lesion and pack with 2-4 500mg clindamycin tablets. apply bandage. treat with tylosin 20mls injected IM twice daily for atleast 3 days. Administer flunixin or ketoprofen.
What are antibiotic footbaths used for?
The treatment of acute raw digital dermatitis lesions. They are expensive, off license and so require a 7 day milk withold and can cause severe problems if drunk by cows. Bet to use to reduce acute active digital dermatitis infection or strategically through the winter every 4-6 weeks.
What are chemical disinfectant footbaths used for?
Used on a regular basis as a control measure to disinfect the cows feet to prevent new infections and the spread of infection within the herd. formalin must not be used on acute digital dermatitis lesions - very painful.
What is acetonaemia associated with?
It is a metabolic disease of high yielding milking cows associated with an inadequate supply of energy to sustain the high milk yields.
What is fatty liver syndrome?
This term is used to describe the mobilisation of fat that frequently occurs around calving and during the first month of lactation in high yielding dairy cows. This is thought to be a normal occurence in high yielding cattle. If greater than 20% fat is deposited in the liver it can interfere with liver function and result in exacerbation of energy problems and the development of acetonaemia.
What is carbohydrate converted into in the rumen?
VFAs such as acetate and butyrate which are ketogenic and propionate which is glycogenic.
What factors influence the occurrence of acetonaemia?
Inadequate energy content of the ration for high yielding dairy cows, inadequate intake of the diet, secondary acetonaemia due to inappetance following a primary disease eg. LDA, excessive intakes of ketogenic food eg silage with high levels of butyric acid, poor rumen function - includes sudden changes in diet or excessive levels of poor concentrate feeding.
What are the clinical signs of acetonaemia?
Usually occur sin the first month of calving but may occur at other times if the energy deficit is severe. wasting form is the most common form - cow loses body condition over a period of days or weeks, there is loss of appetite with refusal to eat concentrate feeds and a sudden drop in milk yield, the faeces are often dark and firm with a waxy appearance. A small number of cases of clinical ketosis will develop neurological signs due to a hypoglycaemic encephalopathy. Signs vary from the animal being jumpy to a frenzied delirium. There may be head pressing, circling, wandering, licking at any available object, salivation and depressed appetite.
How is a diagnosis of clinical acetonaemia made in cows?
History - usually high yielding cows, first month after calving.
Clinical biochemistry - low plasma glucose below 3mmol/l, but may be normal. mobilisation of body fat - elevated NEFA levels over 0.7mol/l indicate increased levels of fat mobilisation. Ketone bodies - Levels of B hydroxybutyrate in the serum/plasma - over 3mmoll.
How should cows with clinical acetonaemia be treated?
Use of 400ml 40% glucose intravenously. This only lasts for 2-4 hours. Oral administration of glucose precursors such as proplene glycol or glycerine twice daily by drench. Glucocorticoid hormone therapy stimulates gluconeogenesis reducing the levels of ketone bodies. vitamin b12 is essential for the metabolism of prorionate and some people drench cows with cobalt to promote vit b12 synthesis.
Which effects may NEB in early lactation have on milk?
Depression on milk protein - due to long term NEB. Increase in milk butterfat, due to increased levels of VFAs for butterfat synthesis.
What is fat cow syndrome and how does it occur?
This is the extreme manifestation of NEB and fat mobilisation in early lactation and occurs due to excessive body condition score in fat dry cows prior to calving (BCS >4 at calving) this results in a depressed DMI, and these cows thus enter a state of severe NEB in early lactation. Fat is then deposited in massive quantities in the liver leading to disruption of liver function.
How can acetonaemia be prevented in early lactation?
Correct dry cow management - should calve at condition score 2.5-3. Transitional cow management in the late dry period. Provision of a suitable ration to cows in late dry period/early lactation. Ensure that protein and energy in the diet is balanced, maximise dry matter intake in the late dry period/ early lactation, good nutritional management. ensure excellent cow comfort. regular monitoring of nutritional status. medication with sodium monensin to improve proprionate production in the rumen.
What is ovine pregnancy toxaemia? (twin lamb disease)
seen in last mont of gestation in ewes carrying two or more lambs, with a prolonged period of energy shortage - poor forage quality, inadequate concentrates, ewes in poor body condition score below 2. the rapid growth of the foetus in late pregnancy results in a marked increase in glucose requirements of the gravid uterus. Initially ewes are isolated from the flock, refuse to feed. neurological signs then progress due to development of hypoglycaemic encephalopathy. Progression to a profound depression and recumbency. High mortality rate.
How is diagnosis of ovine pregnancy toxaemia made?
frequently made on clinical signs and history. confirmation of diagnosis is by serum B-o butyrate levels over 3mmol./l. PM will reveal fatty infiltration of the liver.
What is the treatment of ovine pregnancy toxaemia?
160ml oral electrolyse and glucose solution or 50 ml propylene glycol orally 4 times daily. 100ml of 40% glucose iv as well as calcium if required, concentrate feeds and water, good bedding, shelter, induction of parturition, if the ewe is more than 136 days pregnant.
How does milk fever occur?
Due to the massive increase in requirement for calcium at the start of lactation, some degree of hypocalcaemia occurs in all cows, however only when this becomes severe and the cow fails to respond to the increased calcium demands do the clinical symptoms of milk fever develop.
Which factors affect development of milk fever?
Hypomagnesaemia - low magnesium interferes with release of PTH, ability of PTH to act on target tissues, hydroxylation of vitamin d3 in the liver. Low calcium levels stimulate PTH secretion and thus mobilisation of calcium from bone and absorption from the gut during the dry period. Metabolic alkalosis predisposes cows to milk fever.
What are the clinical signs of milk fever?
they occur around parturition and are progressive over a period of 10-24 hours. Initially there is a loss of appetite, dullness and lethargy. normal or slight depressed rectal temperature. initial hypersensitivity and hyperaesthesia, with grinding and muscle tremors, stiffnes of legs, straight hocks and paddling of feet when standing. cows will be reluctant to move, with incoordination and ataxia. They then progress to recumbency with cow initially in sternal with a lateral kink (s bend) in the neck then progressing to the head and resting on the shoulder. Increased heart rate, dilated pupils, gut stasis and severe depression. cows then become comatose in lateral recumbency, very weak with elevated heart rate. Other possible complications include uterine inertia, prolapse of the uterus and musculoskeletal damage.
How can diagnosis of milk fever be made?
history of recent or imminent calving, usually high yielding dairy cows, clinical signs, and response to treatment with calcium borogluconate, biochemistry;
blood calcium levels below 1.5mmol/l cause clinical signs, hypophosphataemia below 1.0mmol/l also frequently seen, hypomagnesaemia during the dry period may result in milk fever due to the critical need for magnesium in calcium homeostasis. this may mean that tetany and hyperaesthesia persist into the later stages.
What is the treatment approach to an individual case of milk fever?
Usually will have already been given a subcut injection of calcium by the farmer. Take a blood sample for measurement of calcium, magnesium and phosphorous levels, give a thorough clinical examination, administer 400ml of 40% calcium borogluconate solution by slow IV injection via the jugular vein using a flutter valve which will provide 12g calcium. Some veterinary surgeons also administer magnesium and phosphorous at the same time. Give 400ml calcium borogluconate subcut at the same time as iv injection to prevent relapses occuring. Remove calf/restrict milking for 24 hours to prevent calcium withdrawal, good nursing management. If the blood sample reveals hypomagnesaemia, this should be treated with 400ml of 25% magnesium sulphate administered subcut.
How can milk fever be controlled in the herd during a breakout?
magnesium supplementation, prophylactic administration of calcium (drenches or gels and boluses), vitamin d3 injections prior to calving, milk withdrawal - no pre calving milking, removal of calf at birth, withdrawal of calf colostrum by hand if required, no milking out for 3-4 days after calving.
How can milk fever be prevented all together?
Dietary restriction of calcium during the dry period - limit to less than 50g per head per day.
Manipulation of the Dietary cation anion balance. Metabolic alkalosis predisposes cows to milk fever as the raised pH prevents PTH from acting on its receptor thus blocking the mechanisms of PTH depending calcium mobilisation from bone and renal production of 1,25-dihydroxy cholecalciferol.
what is DCAB?
dietary cation anion difference
= (Na+ and K+) minus (Cl- and S-).
The aim is to reduce DCAB to between -100 to -200mEQ/kg DM by increasing Cl= and S= or reducing Na+ and K+ thus inducing a mild metabolic acidosis. Use predominantly low potassium forages such as maize silage, wholecrop wheat or straw and increase the anions using magnesium chloride. There are also a number of DCAB mineral mixes that are added empirically to the diet.
What is lambing sickness?
Ovine hypocalcaemia, commonly seen in ewes in lat pregnancy and may also occur sporadically in early lactation. it is more common in older sheep and ewes in any body condition may be affected. It is frequently associated with stressful husbandry events.
What are the clinical signs of ovine hypocalcaemia?
Clinical signs are due to muscular paralysis and are similar to those observed in milk fever in cattle. Ewes have a rapid respiratory rate with passive reflux of ruminal contents down the nose. Frequently misdiagnosed as a case of respiratory disease. Diagnosis is by clinical signs, history and response to treatment.
What is the treatment of ovine hypocalcaemia ?
for a 70kg ewe administration of 20-40mls of warm 40% calcium borogluconate by slow Iv injection and 50-10ml subcutaneously.
what is the amount and concentration of magnesium in the extracellular fluid dependant on?
1. Absorption of magnesium from the GI tract.
2. Requirement for magnesium for milk production, tissues and endogenous losses.
3. Excretion by the kidneys - excess dietary magnesium is excreted via urine.
Which factors influence the availability of magnesium to the cow?
soil levels vary considerably. pasture species (legumes, weeds and herbs contain more magnesium than grasses), daily dry matter intake regulates daily intake of magnesium. sodium is required to carry magnesium across the rumen wall. Rumen PH - magnesium solubility declines rapidly as rumen pH rises especially above pH6.5. This may be a factor in grazing of lush spring grass. High levels of ammonia inhibit magnesium absorption, either directly or indirectly by raising ruminal pH. Magnesium absorption is reduced when energy levels in rumen are reduced. Lush spring pastures are low in fibre which increases the rate of passage through the rumen, leading to insufficient time for absorption.
What is the pathophysiology of grass staggers?
Hypomagnesaemia - will occur if the intake and absorption of magnesium is less than the demands of lactation and metabolism for magnesium. the onset of clinical signs is related to the concentration of magnesium in the CSF, which only begin to fall at low blood magnesium concentrations. A vicious circle then occurs due to the stress and release of catecholamines resulting in severe clinical signs and tetany.
What are the clinical signs of hypomagnesaemia?
Sudden death - with disturbed soil around the feet of the animal indicating paddling.
Acute - Initial apprehension, nervousness, hyperaesthesia with high head carriage, twitching of the muscles and incoordination. Rapid progression with collapse into lateral recumbency, convulsions leading to coma and death. Progression into convulsions may be precipitated by stress. 30% of cows showing acute hypomagnesaemia will die although spontaneous recovery can occur.
Subclinical - cows may appear slightly nervous, reluctant to be milked, depressed DMI and loss of milk yield.
How can hypomagnesaemia be diagnosed?
History - Typically occurs in lactating cows at grass during spring and autumn and suckler cows with calves at foot with insufficient supplementation. Usually acute onset with signs of hyperaesthesia and convulsions. Plasma level of below 0.8mmol/l magnesium.
PM levels - in CSF 0.6mmol/l in freshly dead animals. In urine - no magnesium in urine. In freshly dead animals magnesium levels in the atreous humour are below 0.25mmol/l and vitreous humour (stable for 48 hours pm) are below 0.55mmol/l.
What is the treatment approach to an individual case of acute hypomagnesaemia?
Take a blood sample prior to treatment for measurement of calcium, magensium and phosphorous levels. Administer 400ml 40% calcium borogluconate, 5% magnesium hypophosphite by slow IV injection and 400ml magnesium SULPHATE by subcut injection. It may be necessary to control seizures, choices include pentobarbitone, xylazine, acp. Ensure adequate dietary intakes to prevent relapses. Also blood sample 5 other animals from herd - as likely to have hypomagnesaemia as well.
How can hypomagnesaemia be controlled/prevented?
MAgnesium supplementation of at least 5g magnesium from the diet. Most common method is inclusion in the concentrate ration. Also possible to medicate the water supply with soluble magnesium salts. Use of magnesium chloride or sulphate will help in DCAB manipulation. Mineral salts - magnesium salts are unpalatable so ad lib not satisfactory but can be incorporated into TMR. Dusting/spraying of pastures possible during high risk periods with finely ground calcined magnesite every 10-14 days. Intra ruminal boluses also possible but only release quite small amounts of magnesium.
How can ovine hypomagnesaemia be diagnosed?
Serum concentartions below 0.6mmol confirms the diagnosis. Investigation of hypomagnesaemia as a cause of sudden death can be confirmed by fresh CSF and urine magnesium concentrations below 0.6mmol/l or fresh aqueous humour magnesium concentration below 0.4mmol/l.
What is a downer cow?
Cow has been down for more than 24 hours, is not suffering from hypocalcaemia, no obvious condition e.g mastitis, toxaemia or injury. It is usually related to calving and the animal is in sternal recumbency.
What are the standard differentials for a downer cow?
Traumatic - pelvic fractures, sacroiliac luxation, rupture of the gastrocnemius tendon, dystocia, ruptured uterus, internal haemorrhage, exhaustion.
Neurological - obturator paralysis, sciatic paralysis, peripheral nerve paralysis, general neurological conditions such as BSE, botulism, tetanus.
Metabolic - hypocalcaemia, hypomagnesaemia, fat cow syndrome, rumen acidosis.
Toxaemia -a cute coliform mastitis, acute metritis, RDA, volvulus, peritonitis, traumatic reticulitis. Once the cow has been down for 6 hours then ischaemic necrosis and muscle damage results which may become irreversible after 12 hours of recumbency in the same position.
What questions should you ask when taking history regarding a downer cow?
How long has the animal been recumbent, when did the cow calve, were there any problems related to calving, was any assistance required, have any treatments been given previously, is the cow trying to get up, can she move around, where did the cow become recumbent, what degree of nursing and TLC has been provided.
What examinations should you do on a downer cow?
full clinical exam, all four quarters of udder, vaginal exam for metritis, rectal exam to check uterus and pelvic fractures, crepitus, dislocation. Neurological examination to check for sensation and deep pain of distal limb and ability to move the hind limbs. Manipulation of the hind limbs to check for crepitus, swelling, ability to move the limb, muscle damage and pain. Check if any attempts to rise - good prognosis.
What tests can you do to diagnose the problem in a downer cow?
Blood sample for calcium, magnesium, phosphate levels, energy status, liver enzymes AST GLDH and GGT if fat cow syndrome suspected. Also assessment of muscle damage - by the time a cow has been down for a couple of days there will be some degree of muscle damage. Can be used as a prognosticindicator. Myoglobin levels can be measuredin both serum and urine and gives an indication of degree of muscle damage. CK is released by damaged muscle cells and levels can be very high but has a short half life and onlyr emains elevated for 1-2 days thus indicative of ongoing damage. AST is not muscle specific and may be raised folowing liver damage. Will remain raised for 1-2 weeks following muscle damage.
What treatment can be attempted for a downer cow?
Good nursing care. Dy clean comfortable bed. Turning of cow every 3 hours to prevent pressure damage. provision of good quality food. provison of ad lib water. Treatment of underlying diseases - IV calcium borogluconate should be administered. Anti inflammatory drugs - useful to reduce pain and tissue damage as well as improving demeanour and appetite. Assistance in rising using bagshawe hoist, cow nets/harness etc.
Describe papillomatosis in cattle?
Bovine papillomavirus causes warts on the teat. There are two main types - flat or rice grain fibropapillomas seldom of clinical significance but more florid type of projecting fibropapillomas can cause problems if teats are badly affected as may interfere with milking. Most cases are seen in heifers and resolve before they enter the milking herd. May need to cut off large warts or can try autogenous vaccine from warts. Can be spread via milkers hands and utensils.
What is herpes mammillitis and how does this affect cattle
Caused by bovine herpes virus 2. this virus is unrelated to herpes virus causing infectious bovine rhinotracheitis. Disease usually seen in autumn winter months. Initially widespread vesicles form on teats and base of udder which quickly rupture to give painful ulcerative lesions. these ulcerative lesions become covered in dried serum exudate which forms thick brown scabs. Healing takes place over 2-3 weeks. Symptomatic treatment of skin lesions with antiseptic udder creams and iodine based teat dips may help. Try and limit spread.
What is pseudocowpox?
A parapoxvirus closely related to those causing orf in sheep and papular stomatitis in catle. immunity is short lived so often have endemic infection in herds. Initial erythematous and oedematous painful lesions appear on teats which soon become raised orange papules and then small dark red scabs. Vesicles are rare with this disease. The scabs will be shed after 10-12 days leaving the classical raised horshoe or ring lesion which is pathognomonic for pseudocowpox.
How does udder impetigo cause disease in cattle? What bacteria causes udder impetigo?
Severe infection of the udder skin with staphylococci can give rise to multiple small pustular lesions which can sometimes spread onto the teats. This is controlled by improving environmental hygiene and topical treatment of skin lesions with antibacterial washes.
Which cows usually are affected by udder oedema?
Mainly a problem in periparturient heifers. The exact cause is not known. In severe cases there is massive oedema of udder and teats extending along the ventral midline. Most cases resolve soon after calving when milking is initiated but in severe cases treatment may be required. milking can be started pre calving or calving can be induced with corticosteroids. Diuretics injections will aid in elimination of oedema.
What are teat chaps?
Horizontal cracks in the teat skin which can cause discomfort when being milked or suckled. they act as a good resevoir for contagious mastitis pathogens. Teat chaps can be caused by badly fitting teat cup liners and poor environmental conditions along with extreme cold temperatures.In beef cows th lesions can start with aggressive suckling by old calves prior to weaning then fly bite damage will exacerbate the lesions. In dairy cows, teat dips containing glycerine or lanolin will help prevent chaps and in beef cows, fly control and weaning calves before they get too old will help prevent problems.
What is hyperkeratosis of the teat?
Seen in cattle, commonly due to malfunctioning milking machines. Hyperkeratosis is caused by prolapse/eversion of the streak canal lining which then can become traumatised and infected. Teat end scoring can be used as a way of monitoring milking machine function and is often part of structured mastitis investigation.
Which bacterium usually secondarily infects teat end lesions?
Fusibacterium necrophorum, leading to dark scabby lesions known as blackspot.
How could a teat end laceration caused by trauma be treated in a dairy cow?
conservative - if they do not involve the teat cistern they should be cleaned thoroughly with mild antiseptic solution and any loose or devitalised skin trimmed off using a scalpel blade or sharp scissors. Healing by second intention will occur and if the cow will not tolerate being milked then a sterile teat cannula can be inserted to allow milk to be trained at milking time.
Surgical repair of teat injuries is rarely successful and most wounds break down due to secondary infection. Full thickness teat lacerations where the teat cistern has been breached will require surgical repair otherwise a leaking fistula will develop.
what are blind quarters?
occasionally newly calved heifers are presented with blind quarters. If milk can be felt filling the teat cistern then all that needs done is to open the teat orifice which is sometimes non patent. If no milk can be felt filing the teat cistern then this suggests a membranous obstruction at the base of the gland cistern.
What are teat peas?
Small fibrous lesions which can be free in teat lumen or attached by a stalk to the mucosal lining and cause obstruction to milk flow by blocking the opening to the streak canal. they can usually be removed by enlarging the teat orifice then squeezing it out.
How do contagious pathogens cause mastitis? Where is the resevoir and the trasmission method?
Reservoir - cow udder or teat skin, transmission is during milking from cow to cow. they have bacterial adhesive properties.
What are the main control measures for contagious mastitis pathogens?
milking routine, post milking teat dip, dry cow therapy.
What are the typical SCC and bactoscan with contagious mastitis pathogens?
SCC tend to be high
Bactoscan tend to be low
Name the main contagious pathogens causing mastitis in cows
Coagulase neg staphylococci
How do environmental pathogens cause mastitis?
The reservoir of infection is in the environment and they are transmitted between milking to the cow from the environment. The bacteria do not have adhesive properties.
What are the main control measures for environmental pathogens causing mastitis?
Environmental hygiene, pre milking teat dip, optimise teat end defences, maximise immune response.
What are the typical SCC and bactoscan numbers like with environmental pathogens in mastitis?
SCC - tend to be low
(except strep uberis)
Bactoscan - tend to be high
What are the natural defence mechanisms of the udder?
Teat skin, teat canal barrier lined with keratinised epithelium which secretes keratin into the canal after milking to form a solid seal and prevent bacterial entry. Cows that have large pendulous udders and cone shaped teats are more prone to mastitis. Even if bacteria have managed to penetrate the teat canal defences there are a number of other mechanisms to remove bacteria from the udder including lacto ferrin (an iron binding protein that is present in high numbers during the dry period and prevents the growth of bacteria by removing iron from the udder secretion).
Lacto peroxidase is an enzyme that is bacteriostatic on gram positive bacteria and bacteriocidal on gram negative bacteria.
How does mastitis with staph aureus occur?
The primary reservoir is the udder, although it can persist on the teat skin. it has a particularly strong adhesive properties such that a cow shedding infection in her milk can infect the next 6-8 cows by the same cluster. The majority produce B lactamase.
What are the three main types of mastitis recognised with staph aureus infection?
Peracute gangrenous mastitis - cows usually have very high temperature initially with heat pain redness and swelling of the udder. the cow is systemically ill and will become recumbent with severe depression. the udder is cold and clammy developing a blue black discolouration and the udder secretion is reddish brown, watery and sometimes with gas.
Acute mastitis - similar to other forms of acute mastitis with clots in milk.
Chronic mastitis - staph aureus is notoriously difficult to treat, leading to the formation of chronic infections with extensive fibrosis and induration of the udder. Reason for poor treatment rates include poor antibiotic penetration due to extensive udder fibrosis, production of B lactamase by the majority of staph aureus strains, persistence of bacteria within macrophages and other cell types. development of L forms, capsules and bacterial dormancy that renders the bacteria insensitive to antibiotic treatments, insufficient duration of antibiotic treatment.
What are coagulase negative staphylococci? How do they cause mastitis?
A group of bacteria including staph chromogenes, staph hyicus, staph simulans, staph epidermis, staph hominis, staph xylosus. They commonly colonise the teat end and teat canal and may only be a sample contaminant , but may invade the udder under certain circumstances leading to high SCC and clinical mastitis during early lactation.
How does strep agalactiae cause mastitis?
It is highly contagious and is readily transmitted between cows during the milking process it is usually brought into the herd via puchase of milking cows or via the relief milkers hands. it is primarily an infection of the udder although it can colonise the teat canal and teat skin. milk from infected quarters contains massive amounts of bacteria. response to antibiotic therapy is good.
Describe the types of mastitis seen with E coli?
Peracute mastitis - common in early lactation, and presents as a life threatening condition, the cow may be anorexic, pyrexic with diarrhoea, and udder will be hot, hard swollen and painful with a yellow watery secretion. the temperature becomes subnormal and the cow becomes dehydrated and endotoxaemic due to the release of endotoxins. the condition may be fatal. in contrast to peracute mastitis caused by staph aureus, gangrene rarely develops and non fatal cases will completely recover.
Subclinical mastitis can also occur when the only changes detectable are an increase in SCC and bacterial numbers in the milk
Chronic recurrent mastitis may occur in cows with a poor immune response.
What are the normal components of milk?
2.6% casein, 3.8% butterfat, 4.6% lactose and has a pH of 6.7.
What is decreased in milk during mastitis?
casein, lactose and butterfat, total proteins, calcium, phosphorous ,total milk yield, stability and keeping quality.
What is increased in milk during mastitis?
RBC, WBC, sodium, chloride, bacteria, pH, milk conductivity.
What are the clinical signs of mastitis?
SCC and bacteria are raised in subclinical mastitis and are detectable prior to clinical signs. changes in the milk may be detectable especially if foremilking is practised. mastitis can lead to changes from caseous lumps to clots in the milk to watery secretions. It is not consistently possible to determine the organism producing mastitis from clinical signs alone. Changes in the udder are detectable seen as hot painful swollen quarters. systemic illness in the cow may be seen especially in mastitis caused by staph aureus, strep uberis and coliforms.
What are the methods of detecting subclinical mastitis?
somatic cell counts and bactoscan results.
How can somatic cell count be measured?
automatic electronic methods (fossomatic method)
Californa mastitis test is a simple cowside test which crudely estimates the SCC via a gelling reaction with a detergent reagent. It can be performed during milking and the results are available immediately. it can help to identify individual quarters with high scc in order to take samples for bacteriology and decide on treatment options.
List the values which qualify as premium, standard and penalty for somatic cell counts in cows milk? How are these penalised/rewarded?
premium 400,001 -10ppl.
What factors affect the somatic cell count?
Clinical and subclinical mastitis raise SCC. Mastitis organism - contagious pathogens such as staph and strep tend to give high scc, whereas coliforms tend to be eliminated rapidly. poor agitation of the bulk tank prior to sampling can give high results. older cows tend to have higher cell counts due to prior infections. Concentration effect occurs with loer yields. Cell counts may fluctuate due to seasonal calving patterns and at afternoon milking. Cows that are milked three times daily tend to have lower SCC. Stress and management factors can lead to variations in the scc.
What is bactoscan test?
This measures the total number of bacteria present in a milk sample. it has replaced the total bacteria count which measured the number of bacterial colonies grown from milk after 72 hours and thus was a measure of total number of viable bacteria in the milk sample.
List the values which are considered premium, standard and penalty for bactoscan in cows milk?
Premium 500,001 -5.0ppl, subsequently -10.0ppl
What are the potential sources of bacteria in the milk?
Mastitis pathogens form the udder - numbers excreted from mastitis quarters can be over 100,000,000ml especially if strep uberis and strep agalactiae are involved. Poor washing of teats prior to milking will lead to bacteria entering the milk as well as predisposing to mastitis. Poor cleaning of the milking equipment after use and poor refrigeration of milk leads to bacterial multiplication.
How does the milking machine have an effect on incidence of mastitis?
Act as a fomite - the milking machine can spread infection. It can cause damage to the teat end. The keratin in the teat canal acts as a blotting paper soaking up material and this is removed by milk flow. Impact forces of the milking machine are a reverse flow of milk back up agains the teat end.
How do post milking teat dips help reduce mastitis?
Removal of contagious mastitis pathogens form the teat skin, removal of bacteria from teat sores, improving the teat skin quality. (emollients in post dips)
How do pre milking teat dips help reduce mastitis?
Disinfecting the teat and reducing superficial teat contamination, reducing the number of bacteria in the bulk milk, reduces the incidence of environmental mastitis.
What are the main aims of dry cow therapy?
Treatment and cure of existing infections eg staph aureus. Prevention of new infections. typically summer mastitis. but now research has shown also coliform mastitis and strep uberis.
Which types of dry cow therapy are available?
1. antibiotic dry cow therapy
2. External teat sealants - dries to give a physical seal around the teat. need to be re applied twice weekly.
3. Internal teat sealants - inert paste containing 65% bismuth subnitrate. Remains at the base of the teat cistern preventing introduction of new bacterial infections during the dry period.
when should culling a cow with mastitis be considered?
Cows that have had three or more outbreaks of mastitis int he same quarter over the same lactation or 5 cases of mastitis in all quarters in the same lactation and a high SCC for three months should be culled as they will probably never be cured.
What is the response of strep agalactiae like to antibiotics?
The response of strep agalactiae to antibiotic therapy is very good and it is sensitive to almost any antibiotic. As the primary reservoir for this is the udder it can be eliminated by the use of blitz therapy.
What are the reasons for failure of antibiotic therapy to resolve cases of mastitis?
Delay in the detection and treatment of cases of mastitis. Establishment of chronic infections especially staph aureus and strep uberis. Constant reinfection of the quarter due to teat end damage, teat sores etc, inappropriate antibiotic usage, duration of treatment too short or mastitis caused by organisms non responsive to antibiotics eg yeast.
What is the aetiology of summer mastitis. When does it occur, in what animals and what are the bacterial causes?
It is a disease of dry cows and heifers, occurs at grass during the summer months. Bacterial causes include arcanobacterium pyogenes, peptostreptococcus indolicus, streptococcus dysgalactiae as well as a variety of other bacteria including microaerophilic cocci. The three main bacteria are believed to act synergistically to cause summer mastitis. The major factor in the transmission of infection is thought to be the head fly (hydrotea irritans). These flies live in bushes and trees and can only fly during dry conditions and low wind speed.
What are the clinical signs seen with summer mastitis?
The affected quarter is swollen, hard, painful and hot with an enlarged teat. The udder secretion is thick and clotted with foul smelling green/yellow pus. Severely affected animals are pyrexic, stiff and lame due to the painful quarter. Oedema may extend around the udder and up inside the leg. Affected animals may abort and may die if prompt treatment is not administered.
What is the treatment of choice for summer mastitis?
Parenteral antibiotic injections, intramammary antibiotics, NSAID injections to reduce pyrexia, swelling and pain, stripping of udder manually as often as is practical, remove from other cows.
How can summer mastitis be controlled in the long term?
Reduce exposure - keep cows away form susceptible fields, fly control and sprays, sealing of teat canal for dry cows, dry cow therapy.
Describe the approach to treatment of an individual case of coliform mastitis?
Thorough clinical exam. Common clinical findings include severe depression, recumbency, subnormal rectal temperature, diarrhoea, hard quarter with yellow watery secretion and signs of endotoxaemia.
Fluid therapy - generalised endotoxaemia results in an initial vasoconstriction folowed by vasodilation, hypovolaemia, reduced cardiac output and inadequate tissue perfusion. Options include oral fluid, IV isotonic fluids (too expensive) or intravenous hypertonic fluids which are the treatment of choice - rapid intravenous infusion of 3 litres of hypertonic sodium chloride after which the cow will drink up to 40L of warm water.
NSAIDs - to reduce pyrexia, couteract endotoxaemia and reduce pain.
Antibiotics - the debate over the usefulness continues. most will administer broad spectrum antibiotics at high dose rates.
Calcium borogluconate as many cases are hypocalcaemic. Quarter stripping and oxytocin - essential to remove inflammatory products form the udder and should be performed every 2 hours initially. Cows need good nursing care - comfortable lying area etc, multivitamin injections, iv glucose.
How can environmental hygiene be improved to control environmental mastitis?
Cubicles - correct size, type of bedding, sand is good, straw yards often too wet, need to apply fresh bedding daily, calving boxes often neglected , must be clean and dry, regular scraping of rear of cubicles, passageways, needs to be adequate ventilation to prevent condensation/high humidity, high concentrate feeding will give loose dung, high rates of stocking leads to increased faecal soiling and high humidity.
What are thermoduric bacteria?
Bacteria that withstand pasteurisation temperatures over 63C and thus levels are indicative of a wash up problem.
What are psychotrophic bacteria?
They are found in dust and grow best at low temperatures. (2-10C)The value gives an indicator of poor pre milking teat disinfection.
What is the voluntary waiting period after calving?
A period of time where the cow needs to recover after calving, the uterus involutes, expels any infection and ovarian cyclicity resumes. Even if the cow does express signs of oestrus at this time, the cows will not be served as the likely success rate will be poor. This period when the farmer decides not to inseminate cows after calving is the VWP. This should last for the first 42-50 days afte calving.
What is the current average conception rate in UK dairy herds?
33% - it will take an average of three services for each successful conception.
When can pregnancy be confirmed?
Transrectal ultrasound scanning from 30 days post insemination or manual rectal palpation from 6-8 weeks post insemination.
What is the calving index?
Measures the calving interval from one calving to the subsequent calving. It is comprised of the calving to first service interval, interval between the 1st and subsequent services, conception rate and pregnany length. Aim is 365 days.
How is the predicted calving interval calculated?
Calving to conception interval plus 282 days.
Name one method of double checking the calving interval?
To look at average days in milk figure for the herd - if you double DIM and add a 60 day dry period this should approximately equal the calving interval in a herd that calves all year round.
What are the target calving intervals for 7000 litre lactation average, 8000 litre, 9000 litre, 10,000 litres?
up to 7000 litre lactation - 365 days aim
7000-8000 - 375 days
8000-9000 - 385 days
over 10,000 litre lactation average - 400 days
What is the 100 day in calf rate?
This is the percentage of cows that are pregnant by 100 days in milk and is a similar measure to the calving to conception interval.
What is the 200 day not in calf rate
This is the percentage of cows that are not pregnant by 200 days in milk. Target is less than 10%.
What is the pregnancy rate (pregnancy risk)
the percentage of cows eligible to become pregnant in a given time frame that do actually become pregnant. the timeframe usually used is 21 days.
Which groups of cows may be examined on a routine herd health fertility visit?
Post natal checks
Oestrus not observed or not seen bulling
Cows with abnormal cycles
Failure to conceive - repeat breeder cows that are not pregnant after three or more services.
How long is the average dairy cow in oestrus?
Which measures would suggest that oestrus detection is an issue on the farm? (missing cows in oestrus)
Non service events are recorded, long calving to first service interval, poor pregnancy rates of cows presented for vet PD, poor heat detection or submission rates
Which measures would suggest that oestrus identification is an issue on the farm (serving cows when not in oestrus)
High number of services occuring 0-17 days after previous oestrus, dissapointing conception rates, can be definitively diagnosed by milk progesterone analysis on the day of service (should be low)
How can a farmer maximise expression of signs of oestrus in cows?
Have an adequate loafing area for cows to display signs of oestrus. Avoid over crowding. PRovide non slippery floor surfaces, groove concrete if necessary. avoid heat stress in the summer by improving ventilation and reducing relative humidity. minimise negative energy balance/body condition loss in early lactation. reduce social stress by minimising group changes, having adequate trough space, enough cubicles etc. lame cows are less active when in oestrus.
Which methods can be used to improve oestrus detection?
3 periods of observation each day lasting 20-30 minutes.
Tail paint/chalk - on the tail head that is rubbed off when the cow is mounted.
Oestrus mount detectors - examples include kamars, bovine beacon etc. These have a change in colour when activated by pressure when cow is mounted.
Activity meters - electronic devices attached to cow via neck collar or leg. when a cow is in oestrus activity will increase by 400% which is then flagged up by the computer system.
Milk progesterone testing - low milk progesterone when in oestrus.
Natural service - bulls or vasectomised bulls.
Reproductive management systems - contracting out oestrus detection and inseminations to an external AI technician.
Oestrus synchronisation protocols.
which tests must be done for stud bulls?
TB, brucella, trichomonas fotus, IBR, campylobacter fetus, EBL, BVD are staturoy. some studs will do johnes, leptospira and Q fever additionally.
How should frozen semen be thawed?
in 35C water for 1/4ml straw 7 seconds and 1/2 ml straw for 15 seconds.
How does embryo transfer work?
It involves superovulating the donor cow, inseminating her to fertilise the multiple ova shed and non surgically recovering the resultant embryos seven days later. These can then be examined, graded and transferred fresh into synchronised recipients which are also at day 7 of their oestrous cycle or frozen and stored for future use. Superovulation utilises commercially prepared follicle stimulating hormone to encourage a group of developing follicles to overcome the dominant follicle suppression and continue developing to ovulation with concomitant maturation of the oocysts.
When is embryo collection performed?
day 7 of the oestrous cycle. embryos enter the uterine lumen from the oviduct at approx day 4 of the oestrous cycle and although embryos can be collected succesfully from the uterus between days five to nine a 7 day collection allows recovery of the most flexible stages of emrbryo for both freezing and fresh transfer.
What flushing media is used for embryo collection?
Dulbecco's phosphate buffered saline - is infused into the uterine lumen to allow slight distension before drainage by gravity flow along with the embryos and ova into a collection filter.
How are embryos frozen?
partial dehydration of the embryo in a cryoprotectant (10% glycerol and 1.5M ethylene glycol). Step wise addition or removal is required for 10% glycerol in increasing or decreasing gradients, whereas one step thawing of embryos frozen in ethylene glycol can be performed as it crosses cell membranes more rapidly.
What are the main products of rumen fermentation?
Volatile fatty acids - acetate, butyrate and propionate. Higher levels of fibre lead to a higher proportion of acetate (main precursor of milk butterfat), high levels of concentrate feeding lead to a higher proportion of propionate. Other end products are ammonia, microbial cells, gas (co2, methane and hydroen).
What effects does a high forage ration have on rumen function?
High forage ration > high levels of effective long fibre > rumination for 10 hours/day > good saliva production > rumen pH 6.5-7 > increased acetate, decreased propionate, higher milk butterfat.
What effect does high levels of concentrate have on rumen function?
Low levels of fibre >poor rumination > poor saliva prodution > rumen pH below 6 > decreased acetate, increased propionate, lactic acid > ruminal acidosis, poor production, cow health problems.
What is metabolisable protein composed of?
Microbial protein (synthesised from ERDP and NPN) and bypass protein (DUP).
How long should fibres be for inclusion in TMR?
2.5cm-10cm long. Physical form of the food is critical as stimulation of rumination requires long fibre.
What BCS should a cow be during the far off dry period?
2-1 months prior to calving hsould be viewed as a period to allow the cow to recuperate after calving and get her into the correct body condition score at calving of 2.5-3.0.
What is the transitional period?
The period from 3 weeks before calving to 3 weeks post calving. Feeding during this critical period is critical to the success of the subsequent lactation. A successful transition will lead to increased DM intakes, reduced disease problems and increased milk production during early lactation.
What BCS should a cow be in at calving?
2.5-3. Fat cows have a depressed DMI. body condition scores should only be altered during the far off dry period.
Which factors affect milk quality?
Stage of lactation - butterfat and protein tend to decrease as milk yield increases. Milk quality tends to decrease as animal gets older. Channel island breeds hav ehigher milk quality. nutrition is the major influence of milk quality. other diseases including mastitis and liver fluke can affect milk quality.
How can the level of butterfat in the milk be altered?
Increasing the amount of effective long fibre in the ration will increase butterfat levels. High levels of concentrate feeding will lead to increased proprionate production and decreased acetate production in the rumen, leading to a FALL in butterfat levels. Rumen pH may be altered by the addition of sodium bicarbonate to buffer the rumen and raise acetate production. The quantities required are high and there are problems with palatability. Inclusion of saturated hard fats will increase butterfat levels, provided their inclusion do not exceed 6%. Unsaturated soft fats will actually dcrease milk fat by depressing fibre digestion.
How can the level of protein in the milk be altered by diet?
Milk protein nearly always reflects a long term energy status. Maximise DMI during early lactation to minimise the extent of any NEB. Use a mixture of forages/TMR to stimulate intakes and energy supply. Feed higher levels of maize silage. Increase levels of concentrate feeding will supply more energy to the cow. Feeding of bypass starch will increase milk protein. the previous points to try and increase levels of energy in the diet will only work as ruminal acidosis does not develop.
how does Subacute ruminal acidosis occur?
Increased quantities of rapidly fermentable carbohydrates that result in acid production in the rumen and a consequent fall in rumen pH below the optimum range of 6-7.
What are the clinical signs of subacute ruminal acidosis?
Loose faeces, with excessive faecal soiling of hindquarters. Closer examination of the faeces may reveal fibrin casts, undigested cereal grains and long fibres. Cows swishing their tails when there are no flies, due to gut or urine irritation, reduction in milk butterfat, reduction in milk yield with cows not milking to expectation, reduction in DMI, individual animals variably go off their food with consequent reduction in milk yield, increased incidence of nutritional related diseases such as NEB/acetonaemia, LDAs, poor fertility, lameness and other periparturient diseases.
What are the risk factors for the development of SARA?
inadequate effective long fibre in the ration. Overall lack of fibre, lack of effective long fibre, or cow chooses not to eat fibre. Excessive levels of concentrate feeding, particularly starch and sugars, poor transitional diet, with sudden changes in diet especially at calving, variable DMI, slug feeding of concentrates in parlour.
How can a diagnosis of SARA be made?
Assessment of ration - quantitiy and quality of effective long fibre, visual assessment of ration in front of cows. Assessment of cows using rumen fill, faecal consistency and examination of faeces. dung from SARA cases tends ot have long fibres, undigested grains or fibrin casts. Atleast 60% of the cows should be chewing their cud whilst resting. Rume n pH measurement is required for definitive diagnosis. a pH sample of rumen fluid is taken from 12 cows and SARA is defined as a rumen pH of less than or equal to 5.5 in at least 30% of the animals sampled.
Which plants contain alkaloids?
yew, laburnum. They are usually bitter tasting
What effects do alkaloid poisonous plants have?
Poisoning is often fatal. They induce toxic effects by mimicking or blocking the action of neurotransmitters. the signs of acute alkaloid poisoning include excess salivation, dilation or constriction of the pupil, vomiting, abdominal pain, diarrhoea, in coordination, convulsions and coma.
How do pyrrolizidine alkaloids cause toxicity?
They are transformed in the liver to reactive pyrrols which exert their toxic effects in cells causing necrosis, inhibition of mitosis or vascular damage. Pyrrolizidine alkaloid poisoning usually results in chronic liver disease e.g ragwort.
How do cyanogenic glycosides cause toxicity?
e.g linseed and cherry laurel contain an enzyme system capable of converting glycosides to hydrocyanic acid. HCN inactivates the cytochrome oxidase system in the mitochondria starving cells of oxygen. clinical signs include dyspnoea, convulsions, muscle tremors and death. Diagnosis - pm indings of bright red mucosae and a smell of bitter almonds in the rumen.
How do goitrogenic glycosides cause toxicity?
present in brassica crops and white clover, can cause goitre, reduced growth, diarrhoea. sudden onset blindness in cattle and seep and digestive disturbances in growing atle grazing on rape are also thought to be associated with glucosinolate poisoning. Brassica crops contain variable amounts of both glucosinolate and thiocyanate goitrogens.
How do cardiac glycosides cause toxicity?
eg digitoxin and digitalin present in foxyglove, lily of the valley and oleander. Moderate intoxication results in bradycardia, depression, regurgitation and diarrhoea, while larger amounts of toxin cause various cardiac irregularities.
How do saponins cause toxicity?
eg present in ivy - most saponins are absorbed very slowly but large quantities can cause gastroenteritis.
what are the clinical signs of nitrite poisoning?
chocolate coloured blood and opaque. PM findings include chocolate brown discolouration of blood/tissues, pulmonary congestion and petechial haemorrhages in the heart muscle and trachea.
What are the clinical signs of oxalate poisoning?
eg rhubarb and sorrel - free circulating oxalate may damage the lung capillaries and cause pulmonary oedema. Continuous ingestion of small amounts of soluble oxalates causes nephrosis due to precipitation of calcium oxalate crystals in the lumen of the renal tubules.
What is primary photosensitisation?
Cases of photosensitisation often follow the movement of sheep from poor to lush green pasture such as silage aftermaths and are associated with failure to adapt to increased amounts of chlorophyll. Certain plants such as st johns wort and buckwheat contain photodynamic agents that are absorbed and carried systemically to the skin. Clinical signs can appear within 2-3 days of exposure to photosensitising agents. The accumulation of photosensitive metabolites under the skin and their reaction with sunlight causes necrotic damage. affected skin is oedematous and often oozes fluid.
What is hepatogenous photosensitisation
Photosensitisation can occur when the biliary excretion of phyloerythrin, a normal degradation product of chlorophyll, which is normally excreted in bile, is obstructed due to various liver diseases. High levels of phylloerythrin make the skin sensitive to sunlight. Hepatotoxic plants can cause photosensitisation. Hepatotoxic plants e.g bog asphodel and ragwort can cause photosensitisation.
how does blue green algae cause toxicosis?
Forms blooms on still water, and contains peptides that are potent hepatotoxins. the toxins are chemically stable and not inactivates by the usual treatments for drinking water.
What are the signs of tannin poisoning?
e.g oak leaves and acorns. Dark red urine and serous ocular nasal discharges, diarrhoea, dysentery. PM findings include a uraemic smelling carcase, large numbers of acorns in the rumen, subctuaneous haemorrhages and oedema.
When does chronic copper poisoning occur?
After the livers capacity for lysosomal copper storage has been exceeded, resulting in release of copper into the peripheral circulation causing intravascular haemolysis and jaundice.
What are the clinical signs of acute copper poisoning?
Acute in onset, depression, anoreixa, rapid heart and respiratory rates, subnormal rectal temperature, blue green coloured mucoid diarrhoea, collapse and death within 24 hours.
What are the clinical signs of acute lead poisoning?
blindness, muscle tremors, colic, frothing at the mouth, staggery gait. the disease progresses rapidly to recumbency with intermittent convulsions and bouts of opisthotonus, muscle tremors, facial and ear twitching, champing of the jaws and hyperaesthesia to touch and sound.
What are the clinical signs of subacute lead poisoning?
Dullness, inappetance, incoordination, blindness and gait abnormalities. Affected animals often stand immobile for very long periods of time. other clinical signs include muscle tremors, hyperaesthesia, salivation, grinding of the teeth and abdominal pain. Ruminal atony and constipation are seen followed by fetid diarrhoea o and abdominal pain.
Why does copper deficiency occur?
it can occur rarely as a primary deficiency but more commonly due to antagonism by sulphur, iron and molybdenum in the rumen. most copper eaten is passed through the gut unabsorbed.
Which factors influence the absorption of dietary copper?
Sulphur, molybdenum, iron,
What is the major transport protein for copper?
What are the clinical signs of copper deficiency in cattle?
Depigmentation (greying/brown) of the coat in black cattle, defective keratinisation - dry thin sparse hair coat, bone defects widening of the epiphyses of the distal limb bones and enlargement of the costochondral junctions, il thrift, anaemia, cardiac hypertrophy leading to sudden death, diarrhoea - classically seen immediately after turnout onto pastures with high molybdenum concentrations. Swayback is NOT seen in calves.
What are the clinical signs of copper deficiency in sheep?
Swayback (enzootic ataxia) - due to severe copper deficiency of pregnant ewes in mid to late gestation. Congenital forms - typical signs include stillbirths, births of weak lambs, neurological signs seen within a few days of birth and include ataxia, inability to stand, staggering gait and weakness of the hindlimbs.
Delayed swayback occurs in lambs 2-8 weeks of age. signs are similar to the congenital form. Depigmentation and discolouration of the fleece in dark coloured sheep, loss of wool crimp, distortion of the wool fibres and reduction in wool quality.
How can copper deficiency be diagnosed?
Signs of clinical disease.
Plasma/serum copper levels
Liver copper levels
Superoxide dismutase - expensive. Erythrocyte or liver SOD.
Response to treatment - may be attempted in cattle but not sheep due to risk of copper toxicity.
How can copper be supplemented in the diet?
Sheep are highly susceptible to copper poisoning so should only be supplemented if clinical disease has previously been diagnosed. For cattle - can attempt oral copper sulphate, copper oxide needles which lodge in the abomasum, intra ruminal boluses, injectable compounds, inclusion in compound feeds - banned for sheep, but may be included in concentrates fed to cattle. It is also possible to give free acess minerals and medication of water supply.
How can swayback be prevented in sheep?
Although swayback is progressive, it may be worth treating mildly affected lambs to stop progression of the disease using very small doses of copper. all remaining pregnant ewes should be given copper by injection or bolus. All surviviing lambs should be dosed to prevent cases of delayed swayback. House sheep during the last 6-8 weeks of pregnancy and provide supplementary feeding during late pregnancy.
What are the function of selenium and vitamin E?
Both selenium and vitamin E play complimentary independent roles as cellular antioxidants. they help protect cells against damage by lipid peroxidases and free radicals, which are produced during the normal cellular oxidative metabolism. Failure of this protection leads to membrane damage and then tissue necrosis. Tissues which have the highest rates of oxidative metabolism are thus most susceptible to damage, especially muscle (skeletal, cardiac, respiratory).
What are the clinical signs of vitamin E deficiency?
Nutritional muscular dystrophy (white muscle disease). Congenital form is seen as stillbirths or the birth of weak calves/lambs that fail to thrive and suckle and usually die within a few days. The delayed form is usually seen in calves or lambs at 1-4 months of age. signs are usually precipitated by exercise or stress. Stiffness and discomfort, inability to stand, reluctance to move or get up, myoglobinruia, respiratory distress, dyspnoea or sudden death if cardiac muscle affected.
Ill thrift - this is usually observed as poor growth rates and ill thrift in growing calves and lambs.
How can diagnosis of selenium/vit E deficiency be made?
Diagnosis of WMD by CK and AST levels or PM findings - white necrotic lesions in the myocardium and skeletal muscles.
Soil and pasture levels have good correlation with animal selenium status. Selenium levels in the blood and liver are dependent on current daily in take - so measure short term intakes.
Glutathione peroxidase levels in blood - a selenium containing enzyme and is the standard biochemical test for selenium deficiency. As erythrocyte GSHP levels depend on selenium levels during erythropoeisis and RBCs live for several months, blood levels reflect long term selenium status (2-4 months).
How may iodine deficiency occur?
primary deficiency - low iodine content in the soil occurs in the west of the UK.
secondary deficiency due to goitrogens - thiocyanate impair iodine uptake in the thyroid by competitive inhibition. thiouracil act by disrupting the iodination of thyroid hormones and prevent the conversion of inactive t4 to t3.
Selenium is also required for the conversion of t4 to t3.
What are the the clinical signs of iodine deficiency?
Goitre - due to compensatory mechanisms involved by the lack of thyroid hormone production.
Stillbirths or weak calves/lambs
Poor production - poor milk yield/wool in sheep.
How can a diagnosis of iodine deficiency be made?
soil and pasture iodine levels, goitre, thyroid histopathollogy, thyroid iodine levels, iodine levels in the blood urine and milk. Thyroid hormone levels - t4 levels reflect the thyroid and iodine status of the animal. BEWARE t4 will be high in cases of iodine deficiency secondary to thiouracil goitrogens as they prevent conversion of t4 to t2.
When should metabolic profile samples be taken?
may or june - best for baseline comparison with results in later year.
July or august - valuable to test in summer calving herds. difficult to assess whether nutritional requirements of high yielding cows are being met at this time as grass growth is often unpredictable and variable.
Autumn grazing period - allows identification of over estimation of nutritional contribution from autumn grass.
Winter feeding period - a test two or three weeks after cows have been exposed to winter feeding regime gives a good indication of balance of the total diet.
What groups of cows should be sampled when doing metabolic profile sampling of cows?
Early lactation - high yieldiers will almost inevitably be in energy deficit at this time. The greatest energy gap will usually be around 2 weeks post calving.
Mid lactation - these cows would be over 100 days calved. they will have full potential dry matter intake and should be pregnant again. This group is good control group for comparison with early lactation cows. It is important to monitor body condition at this stage.
Dry cows - dry cow management vital for optimum productivity. Cow condition and biochemical status in the 2 weeks prior to calving give valuable clues to potential problem areas.
What are the common mistakes made with metabolic profile sampling?
Cows that have been calved for more than 3 weeks should not be included in the early lactation group. Inclusion of too many cows that are not representative of the herd. Cows with long standing health or reproductive problems. Sampling immediately before or after a major nutritional or management change.
What is the optimum range of Beta hydroxybutyrate in cows?
below 1.0mmol/litre and for dry cows at the end of pregnancy is below 0.6. This is a ketone body present in the blood of all animals. the concentration increases as the animal is under increasing energy stress.
What is the optimum range for non esterified fatty acids in cows? (NEFA or free fatty acids)
below 0.7mmol/l and for dry cows at the end of pregnancy below 0.4mmol
What is the optimum range for glucose in the plasma in cows?
the optimum range in plasma is over 3.0mmol/litre. This is different from values in whole blood or serum neither of which are as accurate. Glucose is not as sensitive to changes in energy balance as BHB or NEFA because of homeostatic control.
What does it mean if a cow has high BHB/NEFA and low glucose (or normal glucose)?
This indicates a dietary energy problem but not necessarily a dietary deficiency. Uncorrected this situation constrains milk and milk protein yield and fertility. Resistance to disease may be reduced. more supplementary feed may be required. Other possible causes of this situation are single supplementary feds to large at milking or at other times, too little forage available conserved or grazing, access to forage restricted, poor quality forage, unpalatable forage poor handling of forage allowing deterioration and loss of nutrients, forage too low in fibre, an excess of digestible undegradable protein or water deprivation. May also be possible that there is no dietary energy problem i.e where milk yields are good and condition is not being lost the reason being that blood testing was carried out too close to feeding or to major diet changes.
What is the optimum range of urea nitrogen in the blood for cows?
1.7mmol/litre. Urea often analysed for interpretation is no different provided the correct range is used. Urea is 2.14 times ureaN. blood ureaN reflects very well the intake of effective rumen degradable protein ERDP and its balance with fermentable metabolisable energy. If a cow has low urea N values in their blood this shows inadequate ERDP in the rumen and erpresents a situation inhibiting productivity but it does not distinguish between a low dietary content and a low intake of a diet containing an adequate proportion of ERDP.
What are the optimum values of albumin in the blood?
optimum over 30 g/litre. Albumin is a protein which is synthesised by the liver. When levels are low this reflects liver health or a poor amino acid supply from the diet. this effect is usually long term.
What are the optimum levels of globulin in the blood?
Below 50g/l. Globulins are antibodies of the type formed in response to chronic inflammation.
What is the lower critical temperature of a calf?
at 2m/s air speed lower critical temp of 4 week old calf is 10C.
What age are calves usually infected with rotavirus? What are the typical clinical signs?
8-14 days old. Acute onset diarrhoea, yellow/green faeces, reluctance to stand and suck, mild depression and salivation.
How is rotavirus diagnosed?
PAGE test on fresh faeces. Sample four or more calves for herd problem.
What age does coronavirus cause diarrhoea in calves?
up to 20 days old.
What are the clinical signs of corona virus?
Diarrhoea, depression, faeces containing mucus and milk curds. The disease can rapidly progress to weakness, recumbency, severe dehydration and death. Coronavirus infections cause diarrhoea in calves up to 20 days old.
How does coronavirus differ from rotavirus?
Coronavirus replicates in the epithelial cells causing severe damage in the small intestine and progresses caudally into the colon.
What are the clinical signs of e coli infection?
Yellow/white diarrhoea which affects calves 1-3 days old, without mucous or blood
what is best antibiotic treatment for septicaemia?
What are the clinical signs of cryptosporidiosis?
beef calves age 10-21 days, profuse yellow green diarrhoea with much mucous present, mild dehydration but calf rapidly looses condition.
Which stain is used to identify cryptosporidiosis?
What is licensed for prevention and treatment of cryptosporidiosis?
Halofuginone lactate. For prevention calves should be dosed for seven consecutive days starting within one to two days of birth.
What are the signs of coccidiosis?
There is a sudden onset of profuse foetid diarrhoea containing mucous and flecks of fresh blood. There is considerable straining of the perineum and tail. Straining with a partial eversion of the rectum which may result in prolapse, is characteristic of severe infections.
How do you work out how much to supplement a calf with bicarbonate
base deficit x bicarbonate space x dehydrated calf weight
What is thromboembolic meningo encephalitis?
common in the USA following Histophilus somni respiratory disease. Animals are obtunded, ataxic, sternally recumbent. Hopeless prognosis.
what is the cause of pustular vulvovaginitis in cows?
Bovine herpes virus, also the same cause of IBR.
What are the clinical signs of IBr?
febrile, purulent ocular and nasal discharge, conjunctivae are oedematous, tear staining of the face, very depressed, no oral lesions but drooling of saliva, small erosions on the nasal septum leading to diptheritic plaques.
How is IBR diagnosed?
Fluorescent antibody test (FAT) from cells from the corneal sac.
What are the clinical signs of BRSV?
increased respiratory rate, frequent coughing, serous nasal discharge, no ocular involvement. secondary bacterial invasion frequently occurs. Rectal temperature varies depending on whether secondary infection present.
How is BRSV diagnosed?
BAL to obtain virus identified by FAT. Or paired serology 2-3 weeks apart.
What does rispoval 4 vaccine contain?
BRSV, IBR, Pi3 and BVD.
What is enzootic/cuffing pneumonia?
Mycoplasma dispar may act in conjunction with PI3 infection. Insidious onset disease more commonly encountered in young weaned dairy replacement heifers where young susceptible calves are mixed with or placed in pens adjacent to older recovered cattle.
What does M bovis infection in cattle cause?
Mastitis, pneumonia, polyarthritis
What is a pulmonary thrombo embolism from the caudal vena cava ?
an uncommon condition which develops following the haematogenous spread of a large number of septic emboli from a thrombus ini the caudal vena cava. Pulmonary arterial thombo embolism occurs with eventual fatal rupture of pulmonary arterial aneurysm.
What is the main bacterial isolate from cases of chronic suppurative pulmonary disease?
What is the pathophysiology of fog fever?
Ingestion of large amounts of the amino acid L tryptophan and its conversion in the rumen to 3 methyl indole and indole acetic acid results in acute pulmonary emphysema, fog fever has a sudden onset, causing severe respiratory distress in cows 1-2 weeks after moving onto lush silage.
What is farmers lung?
An extrinsic allergic bronchiolo alveolitis which develops in housed adult cattle following repeated exposure to mouldy hay containing spores derived from micrpolyspora faeni and thermoactinomyces vulgaris. Sudden onset severe dyspnoea, frequent coughing with production of thick mucous.
When is vegetative endocarditis most commonly seen?
2-4 months after parturition.
What are the clinical signs of vegetative endocarditis?
Effusion of the hock, carpal and all four fetlocks possible. Spend long periods in sternal recumbency, adopt an arched back apearance when standing and continually shift weight from one leg to another. Heart rate may be irregular and elevated over 100 bpm but there might be no murmur. There may be jugular distension and a marked jugular pulse. lesions involving tricuspid valve may result in ascites and peripheral oedema. Evidence of pain in endocarditits (elbow abduction, arched back, slow guarded movement) may lead to confusion with pleurisy, TPR.
What are the clinical signs of Dilated holstein cardiomyopathy?
Clinical signs include marked peripheral oedema, jugular distension, ascites and pleural effusion. Heart sounds often muffled due to pleural /pericardial effusion.
What is the treatment for actinobacillus lignieresii?
5 day course of streptomycin or potentiated sulphonamides, or iodides
What are the possible sequelae to barley poisoning?
Fungal rumenitis, chronic bloat, secondary liver abscessation with F necrophorum and actinomyces pyogenes, laminitis, Cerebro cortical necrosis.
What conditions can interfere with normal eructation and cause secondary bloat?
failure of oesophageal groove, acitnobacillosis or papillomatosis of oesophagus, physical obstruction/choke, physical pressure on oesophagus/vagal nerve by enlarged mediastinal/bronchial LNs common in 3-6month old stirks following chronic pneumonia, thoracic mass e.g thymic lymphosarcoma, tetanus, vagal indigestion, cereal overfeed/acidosis.
Which leptospirosis serovars most commonly affect cattle?
Borgpetersenii serovar hardjo
interrogans serovar hardjo