Cattle Diseases Guide:

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mikey:
Blackleg
Clostridia are group of anaerobic, spore-forming organisms found in the soil/environment, which produce rapidly fatal disease by secretion of potent toxins. Conditions such as botulism, blackleg, bacillary haemoglobinuria, malignant oedema and tetanus are all caused by clostridia.

Botulism

Botulism is a lethal food poisoning in cattle caused by eating material that contains Clostridium botulinum toxins. The incubation period before clinical signs appear varies from a few hours to two weeks, making it difficult to identify the causative material eaten by affected animals. The most common manifestation of the disease in cattle is a subacute disease with restlessness, incoordination and difficulty to swallow developing into recumbency, paralysis and death within 1-7 days.

The bacteria and the disease occurrence are world-wide. In the UK, cases are likely to occur either due to ingestion of contaminated silage or contact with animal carcasses or skeletons of dead animals containing the toxin. The use of poultry litter as fertiliser on cattle pastures has been identified as a risk factor, due to the poultry mixed with the litter.

Bacillary haemoglobulinuria

Bacillary haemoglobulinuria is a rapidly fatal disease caused by C. oedematiens type D. The disease is associated with liver damage primarily caused by liver fluke. The condition is fairly rare in the UK. Young stock or dry cows inspected less regularly are often found dead. In lactating cows, a sudded drop in milk yield associated with high fever is seen. Other clinical signs include ruminal stasis with or without apparent abdominal pain, rapid breathing, dark red urine, jaundice and death within a short time of the onset of clinical signs.

Spores of C. oedematiens type D can be found both in the soil and in the livers of normal cattle on farms where the disease occurs.

Blackleg

Blackleg infection is caused by Clostridium chauvoei and is almost allways associated with wound infection in cattle. Most cases occur in young stock between 10 months and two years of age. Feet or legs and the tongue are often the predilection site. Within 48 hours there is a high fever and if limb muscles are involved the animal becomes stiff and unwilling to move. Skin discolouration, subcutaneous oedema and gas production may be present and perineal oedema is sometimes seen. Infections of the head may produce marked oedema and even bleeding from the nose. Death usually follows a period of anorexia, profound depression and prostration.

The spores of C. chauvoei survive well in the soil.

Malignant oedema

Malignant oedema is caused by the infection of wounds with bacilli of the genus Clostridium (C. oedematiens type A; C. chauvoei; C. perfringens; C. sordellii; C. septicum). The condition is fairly rare and sporadic, but outbreaks involving several animals may occur after an event that has caused bruising or wounds (e.g. penning for a short period). Clinical signs appear rapidly after infection and at the site of infection a swelling will develop which will 'pit' on pressure. Gas may be detected, as the skin becomes darkened and tenser. A high fever is present and toxaemia develops. The animal dies within 1 - 2 days.

Tetanus

Tetanus is caused by the toxin tetanospasmin released from the spore-forming bacillus Clostridium tetani. The disease in cattle occurs most often after surgical intervention or difficult calving after spores gain entry to a wound. Germination of spores occurs only if the microenvironment is anaerobic. After germination of the spores within the wound the C. tetani bacilli proliferate and produce toxin.

The incubation period can be very variable from 3 days to several months but most cases occur usually after about 10 days. At first the animal appears slightly stiff, becomes unwilling to move and develops a fine muscle tremor. The temperature rise is variable (39 - 42°C). The general stiffness of the limbs, head, neck and tail increases after 12 - 24 hours. The animal shows hyperaestesia and repeated spasms. Mastication becomes difficult due to tetany of the masseter muscle (lockjaw), food is chewed with difficulty, the animal drools saliva and bloat often occurs. There is retention of the urine and constipation. The animal becomes recumbent, with the legs rigidly extended, opistotonos and the jaws become rigid. The animal usually dies due to respiratory failure 3 - 4 days after the onset of clinical signs. Milder cases, which develop more slowly, can recover over a period of weeks or even months.


mikey:
Blackleg (Clostridial myositis)
Cases of blackleg often increase when animals are turned out or moved to new pastures, so farmers need to be aware of the signs so that action can be taken to prevent further disease

What is Blackleg?
Blackleg is a highly fatal disease of muscle caused by the bacterium Clostridium chauvoei. Infection begins when bacterial spores are eaten (usually as result of eating soil, but occasionally from contaminated feed). These spores enter the bloodstream and travel to organs and tissues throughout the body (particularly muscles). They remain dormant until a trigger (usually an injury) stimulates them. The trigger reduces blood flow and thus the supply of oxygen to the tissues. In the absence of oxygen the bacteria multiply and produce a local infection. As they grow, the bacteria produce poisons that destroy the surrounding tissues. This damage shows as the characteristic black muscle with gas. The poisons do not stay in the muscle but enter the bloodstream, resulting in animal that very rapidly goes downhill and dies. The disease is most commonly seen in calves between six months and two years of age, but occasional cases are seen in adults and it can occur in younger animals (particularly if they have not had sufficient colostrum). Disease is definitely more common in animals that are growing well
Clinical Signs
Lameness may be seen before death if you’re lucky
In a few cases the first sign seen is tongue and throat swelling with the tongue protruding
However, the most common sign is sudden death in an otherwise apparently normal animal
The carcass often looks like a much less fresh carcass, with bloating and gas under the skin
Bloody discharge from the nose, mouth and other body openings are also seen
Diagnosis
A post mortem is essential to diagnose blackleg. Many other diseases cause sudden death and need to be ruled out. The most important of these is anthrax, which must be ruled out before a PM is done
The changes in the muscle are characteristic, but the extent of the damage can vary considerably. Some cases have black oozing muscle throughout the hindquarters, others have much smaller areas of damage which may not involve the limbs at all.
It is worth getting further lab tests done to confirm it is Cl. chauvoei as other clostridial bacteria can cause similar muscle damage Don’t do a PM on farm. Opening the carcass can liberate bacteria which will form spores to contaminate the ground and subsequently infect other cattle.
Treatment
In very early cases very high doses of penicillin may prevent death, but the extent of muscle damage means that in most cases this will not be economic
Prevention
As the bacteria are present in the soil, preventing access to soil by not grazing freshly sown pastures with youngstock can reduce the risk, but vaccination is really the only effective means of controlling blackleg. The main choice is between vaccination against Cl. chauvoei alone or with vaccines that are effective against other clostridial disease. Ask your vet for advice

With clostridial vaccines, like all vaccines, care should be taken to follow the manufacturers' instructions. The best protection is a two-dose course followed by annual revaccination. Other regimes can be effective but check with your vet before using these. Vaccination takes 10-14 days to become effective, so it’s best to vaccinate before a problem occurs or a risk period is encountered.



mikey:
Bloat In Cattle
There was an increase in the number of reports of bloat from NADIS vets this spring. Bloat is most commonly seen in spring and autumn, when grass growth is at its peak. It is one of the most common causes of death in adult cattle at grassp>

What is bloat?
Bloat is simply the build up of gas in the rumen. This gas is produced as part of the normal process of digestion, and is normally lost by belching (eructation). Bloat occurs when this loss of gas is prevented. There are two sorts of bloat. The least common type is gassy bloat, which occurs when the gullet is obstructed (often by foreign objects such as potatoes) or when the animal can’t burp (such as with milk fever or tetanus). The second type of bloat is frothy bloat, which happens as the result of a stable foam developing on top of the rumen liquid, which blocks the release of the gas. This is by far the most common form of bloat, and unlike gassy bloat, it is highly seasonal with peaks in the spring and autumn. This is because the foam is formed by breakdown products from rapidly growing forages (particularly legumes such as clover and alfalfa). These increase the viscosity (stickiness) of the rumen fluid and prevent the small bubbles of gas formed by rumen fermentation from coming together to form free gas that can be belched off

Clinical Signs
Distended left abdomen is the most obvious sign
Usually associated with pain, discomfort, and bellowing.
Death can occur within 15 minutes after the development of bloat
Gaseous bloat is usually seen in one or two animals. Frothy bloat can affect up to 25% of cases
In some cases sudden death may be the first sign seen by the stockman, although in such cases it is likely that there will be other cattle with bloat that are still alive
Diagnosis
On the clinical signs described above
History of access to lush pasture
Passing a stomach tube will distinguish between gassy and frothy bloat. If it’s gassy bloat a stomach tube passed into the rumen will allow the gas build-up to escape through the tube. No such gas is seen in frothy bloat.
Treatment
Passing a stomach tube is the best treatment for gassy bloat. Once the gas has been released, the cause of the obstruction should be looked for.
In a few cases a trochar and cannula punched through the side into the rumen will relieve gassy bloat when a stomach tube has not worked. But such cases are rare, and as the trochar provides a tremendous opportunity for introduction of infection, it should only be used as a last resort.
For frothy bloat, antifoaming agents that disperse the foam should be given by stomach tube. Old-fashioned remedies such as linseed oil and turpentine are effective but newer treatments such as dimethicone or polaxolene are easier to give as the effective dose is much smaller.
If an outbreak of frothy bloat occurs all cattle on that pasture should be removed immediately and put onto a high fibre diet (hay or straw), and any cows showing bloating signs treated with an anti-foaming agent. The pasture should not be grazed for at least ten days.
Prevention
It is much more effective to prevent bloat than treat affected animals. Management and planning can significantly reduce the number of cases. To prevent frothy bloat: 1)
If possible avoid using high-risk pastures at high-risk times. Pastures with a history of bloat problems or with a high clover content should not be used for cows soon after turnout.
Stagger turnout with buffer feeding as this will allow the rumen to adapt to the new diet. In particular try and keep up fibre intakes at risk periods.
If you have to use high-risk pastures, introduce the cattle to them slowly. In some cases restricting access to as little as ten minutes per day at the start may be necessary to prevent bloat.
Avoid starting to graze high-risk pastures when they are wet.
Administer anti-foaming agents daily if bloat is a severe problem. If this is the case and you can strip graze then spraying antifoaming oils (emulsified with water) onto the grass can significantly reduce labour costs.
Remove high-risk animals. Some animals have recurrent bloat despite prevention and treatment.

mikey:
Bluetongue (BTV)
Bluetongue is an insect-borne, viral disease primarily of sheep, occasionally goats and deer and, very rarely, cattle. The disease is non-contagious and is only transmitted by insect vectors. The disease is caused by a virus belonging to the family Reoviridae.
Species affected
Primarily a disease of sheep but other species such as goats, cattle, buffaloes, camels, antelopes and deer can be infected. Humans are not affected.
Distribution
The virus is present in most countries of Africa, the Middle East, India, China, the United States, and Mexico. Bluetongue virus infection, without associated clinical disease, is present in Southeast Asia, Papua New Guinea, northern South America and northern Australia. A strain of bluetongue virus was first identified in Australia in 1975 from trapped insects but despite its long-term presence, it has not caused any clinical disease.
Key signs
The disease is characterised by fever, widespread haemorrhages of the oral and nasal tissue, excessive salivation, and nasal discharge. In acute cases the lips and tongue become swollen and this swelling may extend below the lower jaw. Lameness, due to swelling of the cuticle above the hoofs and emaciation, due to reduced feed consumption because of painful inflamed mouths, may also be symptoms of this disease. The blue tongue that gives the disease its name occurs only in small number of cases. Convalescence of surviving sheep is slow. The high fever in sheep results in wool breaks, which adds to production losses.
Spread
The virus cannot be transmitted between susceptible animals without the presence of the insect carriers. The incidence and geographical distribution of bluetongue depends on seasonal conditions, the presence of insect vectors, and the availability of the susceptible species of animals. The insect carriers, biting midges, prefer warm, moist conditions and are in their greatest numbers and most active after rains.
Persistence of the virus
Bluetongue virus does not survive outside the insect vectors or susceptible hosts. Animal carcases and products such as meat and wool are not a method of spread. Survival of the virus within a location is dependent on whether the vector can overwinter in that area.
Control strategy
The strategy is to contain the outbreak and minimise trade impact by:
using a combination of quarantine and movement controls to prevent spread
treatments and husbandry procedures to control vectors, reduce transmission and protect susceptible animals
tracing and surveillance to determine the extent of virus and vector distribution
zoning to define infected and disease-free areas.
There is no justification for stamping out but some animals may need to be destroyed for welfare reasons. It is not possible to eradicate the bluetongue vectors.

Note: The Exotic Animal Disease Response Agreement only apply to bluetongue disease in its classical virulent form.

© The State of Queensland (Department of Primary Industries and Fisheries) 1995 - 2007.
Post-Mortem Blue Tongue Pictures
Bluetongue is an insect-borne viral disease to which all species of ruminants are susceptible. The virus is transmitted by a small biting midge of the Culicoides genus rather than from animal to animal. The virus does not affect humans. Bluetongue is a notifiable disease and, where suspected, should be reported to Animal Health.

VLA is involved in the surveillance for the disease and was responsible for the detailed post mortem examinations of the first cases in the UK. The images below illustrate the pathology associated with this disease as shown by the first 3 cattle cases in East Anglia.

 
Cow 1 bluetongue case – clinically affected Highland cow. Extensive superficial erosion of the muzzle with a mucopurulent nasal discharge
 
 
Cow 1 bluetongue case – clinically affected Highland cow. Diffuse reddening of the dental pad with multifocal haemorrhages on the upper lip and dental pad
 


 
Cow 1 bluetongue case – clinically affected Highland cow. Ocular discharge visible at the medial canthus (wrinkling of the cornea reflects post mortem change)


 
 
Cow 1 bluetongue case – clinically affected Highland cow. 'Coronitis’: skin reddening around and above the coronary band intensifying distally with serous crusting at the coronary band
 


 
Cow 1 bluetongue case – clinically affected Highland cow. Multifocal haemorrhages with oedema visible on the cut surface of the submandibular lymph node
 
 
Cow 1 bluetongue case – clinically affected Highland cow. Extensive ecchymotic subepicardial haemorrhages


 


 
Cow 1 bluetongue case – clinically affected Highland cow. Extensive subendocardial haemorrhages in the left ventricle






 
 
Cow 2 bluetongue case – Gloucester cow. Identified as PCR positive. Multiple pinpoint haemorrhages in the skin around the bases of the teats. There were also scattered petechial haemorrhages on the skin of the ventral abdomen. No other lesions distinctive of bluetongue were seen in this cow
 


 
Cow 3 bluetongue case – clinically affected Friesian/Holstein cow. Focally extensive necrosis at the mucocutaneous junction of the nares.





 
 
Cow 3 bluetongue case – clinically affected Friesian/Holstein cow. Focally extensive area of haemorrhage (with associated ulceration not clearly visible in this image) on the ventral surface of the tongue. There are multifocal pinpoint haemorrhages covering most of the ventral surface of the tongue
 


 
Cow 3 bluetongue case – clinically affected Friesian/Holstein cow. Focally extensive haemorrhage involving the bulbar conjunctiva with associated subconjunctival petechiation
 
 
Cow 3 bluetongue case – clinically affected Friesian/Holstein cow. Generalised lymph node enlargement with oedema



 

mikey:
Bovine Diarrhoea Virus (BVDV)
(BVDV)
BVDV is one of the commonest causes of infectious abortion. It is also associated with a wide range of diseases from infertility to pneumonia, diarrhoea and poor growth. BVDV is normally the most important viral cause of disease in cattle in the UK (at least outside of an FMD outbreak!)

What is BVDV?
BVDV is a member of the family of pestiviruses. Other diseases associated with other pestiviruses include classical swine fever and border disease in sheep. Pestiviruses infect cloven-hoofed stock only, BVDV has been found in pigs and sheep (indeed many cases of border disease are caused by BVDV not border disease virus)

Clinical Signs
Calf diarrhoea
o Mild diarrhoea of a few days duration.
o This was the initial disease associated with BVDV but is rare as a syndrome in the UK.
o In the US a new type of BVDV has been identified associated with outbreaks of severe diarrhoea with very high death rates.


Mucosal disease
o Sudden onset weight loss and inappetance in cattle between 6 and 24 months of age (usually 12 to 18)
o Drooling and salivating
o Profuse foul smelling diarrhoea
o Usually only one or two animals infected at any one time
o Erosions and reddening on gums, cheek, tongue and muzzle
o Over 90% die within 7 days
o Only occurs in calves persistently infected while in the uterus with BVDV


Unthrifty calves
o Small at birth or fail to grow properly
o May be blindness, incoordination
o Hair loss or abnormal hair
o Other defects such as bulldog face can be present


Calf pneumonia
o BVDV infection suppresses the immune system, so calves with BVDV have a significantly higher risk of developing viral pneumonia
o Pneumonia generally more severe than that caused by infection with other viruses alone


Infertility
o Infection <16 days after service – apparently normal return to oestrus but reduced herd pregnancy rate
o Infection >16 days after service, but in early pregnancy – embryo loss and delayed return to oestrus
o Infection mid to late pregnancy – abortion or stillbirth
o Not all pregnant cattle infected by BVDV will show infertility, some will fight off infection and have normal calves
o Other cattle, particularly if infected before 120 days, will have apparently normal calves but these calves will be
persistently infected spreading the virus and being at high risk of developing mucosal disease. These animals are often referred to as PIs
Diagnosis
BVDV causes such a wide range of disease it is rare to be able to diagnose cause on clinical signs alone (except for IBR infections which can have a characteristic conjunctivitis)
Testing the blood for antibodies and/or virus is the best method of diagnosis.
A paired blood sample for antibodies is useful for pneumonia, diarrhoea and infertility. If the first sample is taken when the animal is ill and the second two to three weeks later, a rise in antibodies suggests that there was active infection
For most cattle with mucosal disease there will be no rise in antibodies. However, because they are persistently infected with BVDV, their blood will be virus positive
Some unthrifty calves will show a rise in antibodies, others will have virus in the blood, but some will have neither. In the latter case a diagnosis of BVDV is made on the presence of other animals excreting virus or having raised antibodies.
Prevention and control
There are two routes for control.

The first and best is to eliminate BVDV from the herd by testing and slaughtering. In most herds BVDV is spread by PIs. Getting rid of these PIs and closing the herd can be significantly economically beneficial. Discuss with your vet the testing options, which can include testing the milk for virus and antibodies as well as the more routine blood testing. The problem with this route is that it may take two or more attempts to eliminate BVDV from the herd and becoming closed is vital because as BVDV is extremely common

The second route is vaccination. This can be used in combination with blood testing. There are two vaccines available in the UK for adult cattle, both of which claim to prevent the effects of BVDV on fertility. Ask your vet for advice as to which vaccine to use and when to use them


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