Bovine Flashcards
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?
> 2 months
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?
Cytopathic 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?
280-285 days.
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?
day 16
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?
Genetics
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?
- Parity
- Retained placenta
- Uterine infection
- Twins
- Hypocalcaemia.
- Selenium deficiency
- Suckling frequency
- Dystocia
- Climate - heat stress
- hydrops
What is post partum vaginal discharge called?
LOCHIA
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?
Dystocia/assisted calving RFM 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?
GnRH
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.
