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This is an almost invariably fatal disease of
cattle of worldwide distribution.
INCIDENCE
The disease is not that common and usually arises
as a single-animal incident.
AETIOLOGY
MCF is caused by a herpesvirus, which is excreted
by healthy sheep. The viruses are not transmitted naturally between
cattle hence cattle are dead-end hosts.
CLINICAL SIGNS
Affected cattle show the following signs:- inappetance,
marked loss of condition, extreme depression and high fever, occasionally
with nervous signs such as excitement and muscle tremors. There
is marked enlargement of superficial glands and sooner or later,
a copious discharge appears which accumulates around the eyes
and nose. Excessive salivation occurs and breathing difficulties
and snoring due to the accumulation of the discharge. Inflammation
and congestion around the eyes can result in blindness.
Usually mouth lesions are present when the temperature
first rises. In addition to congestion, distinct ulcers develop
inside the cheeks. Erosions also occur on the palate. Halitosis
becomes very marked as the disease progresses.
The character of the faeces varies considerably
from case to case. Constipation may be present but usually at
least during some part of the course of the condition, diarrhoea
occurs, varying in quality from scanty soft faeces to profuse
diarrhoea.
Further prominent signs include widespread,
moist skin lesions and urine infections.
Cattle which develop malignant catarrh usually
die within 5-10 days and the fever usually persists almost until
death.
EPIDEMIOLOGY
In most countries in the world, sheep are believed
to be the reservoir for infection of cattle and to harbour the
virus without developing clinical signs. In Britain, confirmed
cases are usually known to have had contact with lambing ewes
and most cases are seen during the period between February and
June.
The disease in cattle seems to be non-contagious
to other cattle.
DIAGNOSIS
A confident diagnosis can almost always be made
on consideration of the wide spectrum of clinical signs. In addition,
the histopathological lesions (and their wide distribution) are
sufficiently characteristic to be looked upon as confirmatory.
TREATMENT
None. (MCF should be looked upon as an invariably
fatal disease; if claims are made regarding successful treatment,
then there should be doubts about the original diagnosis).
CONTROL
No vaccine exists.
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A chronic mild to moderately severe dermatitis
depending on the mite involved. Chorioptic mange is generally
mild while sarcoptic mange can be very severe. Psoroptic mange
is also severe but is not common in U.K.
AETIOLOGY
Chorioptes bovis, Sarcoptes scabiei and Psoroptes
ovis var bovis.
PREVALENCE
Mange in cattle is common in Britain but is
often ignored or goes unrecognised. It is more common in beef
cattle which are housed together in the winter. More than one
animal is usually affected at a time and the whole herd may well
be affected.
CLINICAL SIGNS
Chorioptic mange causes excess scaling and flaking
of the skin with mild pruritis. A marked itch is usually seen
with sarcoptic mange which is often called ‘neck and tail
mange* indicating common sites. Lesions are often widespread,
and if the condition affects adult cows, the back of the udder
may well be affected. In bulls the lesions often commence on the
underside of the body. Lesions in many cases are mild with minimal
loss of hair. Severe cases are less common and in these there
may be quite marked loss of hair with thickening of the skin and
excess scaling. Areas where the hair is reduced or lost do not
have well defined borders. Generally mange is a dry crusty condition
in cattle but in severe cases, the hair may have a wet, damp appearance.
There may be fissures on the thickened skin.
PATHOGENESIS
The pruritis associated with mange results in
secondary abrasions caused by licking and rubbing and the activity
of the burrowing Sarcoptes can cause marked skin thickening.
EPIDEMIOLOGY
The disease is spread mainly by direct contact
since mites cannot survive for more than a few days off the host.
Cattlemen may acquire a temporary infection with Sarcoptes.
DIAGNOSIS
This is based on clinical signs usually in groups
of cattle during winter or spring. Confirmation is by microscopical
examination of a skin scraping. Chorioptic mites are very numerous
and are readily found because they are on the surface of the skin.
Sarcoptic mites may be more difficult to find.
TREATMENT
Ivermectin and doramectin are effective in the
treatment of sarcoptic and psoroptic mange and are an aid in the
control of Chorioptes bovis. Both drugs have long meat withdrawal
periods (21-42 days) and cannot be used in milking cows. Other
suitable drugs are amitraz and the organophosphorus compound phosmet;
these can be used in dairy cows as the milk withdrawal periods
are less than 2 days.
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DEFINITION
Inflammation of the mammary gland which may
manifest as clinical mastitis when the milk is grossly abnormal
or subclinical mastitis when the milk appears normal.
ECONOMIC IMPORTANCE AND INCIDENCE
Mastitis, along with lameness and infertility,
ranks as one of the major sources of economic loss to the U.K.
dairy industry, both in the effects of the disease itself and
the number of cows culled because of repeated incidents of mastitis.
The incidence of mastitis is affected by various
factors including
(I) Age of the animal
The incidence of mastitis increases with age.
This is particularly the case with regard to the incidence of
Streptococcal infection.
(ii) Stage of lactation
The incidence of clinical mastitis is highest
in early lactation with a marked peak during the first few days
post-partum. On the other hand, the incidence of subclinical mastitis
increases steadily as lactation proceeds and is particularly obvious
with Streptococcus agalactiae infections.
(iii) Management of husbandry
Many different management and husbandry practices
can affect the incidence of mastitis, but by far the most important
is hygiene particularly with reference to the milking regime.
AETIOLOGY
Mastitis can be caused by a number of micro-organisms
especially bacteria such as Streptococcus agalactiae, Streptococcus
dysgalactiae, Streptococcus uberis, Staphylococcus aureus and
Actinomyces pyogenes. Other bacteria occasionally involved include
Proteus vulgaris, Pseudomonas aeruginosa, Klebsiella spp, M.bouzgenitalium
and M.bovimastidis. Tuberculous mastitis caused by Mycobacterium
bovis is extremely rare. Leptospiral and fungal mastitis may occur.
CLINICAL MASTITIS
Four degrees of clinical mastitis are recognised.
1. Very Severe (Peracute) Clinical Mastitis
Usually occurs very shortly after calving. Sudden
onset with the cow changing from being apparently normal to severely
ill within a period of 12 hours. Both local and systemic reactions
are evident. The local reaction is very severe with one or more
quarters (more frequently hind quarters) becoming hard, hot, swollen
and painful. The secretion is small in amount, thin, serous, may
be bloodstained, and is often foul-smelling.
The systemic reaction is characterised by marked
fever and may proceed to a fatal toxaemia. Other clinical features
include marked depression, anorexia and a markedly abnormal gait
due to the pain associated with the local reaction. Foetal membranes
are often retained. Recumbency is common.
If the animal survives affected quarter(s) may
become gangrenous (particularly associated with Staphylococcal
infections). The quarter becomes cold to the touch, discoloured
blue-black and, if death does not occur, sloughs off within 1-2
weeks. Very severe (peracute) clinical mastitis is often associated
with Staphylococci or E.coli.
Clinically severe E.coli mastitis presents as
follows:
Initially anorexia, pyrexia and in some cases
diarrhoea are seen. The udder and milk may appear normal. However
within twelve hours the udder becomes hot, swollen and painful
and the secretion is abnormal being yellow in colour and containing
small clots. The fever is usually transient and by the time clinical
signs develop in the udder and milk the temperature may be normal.
Gangrene rarely develops.
2. Severe (Acute) Clinical Mastitis
More common than the very severe form and may
occur at any stage of lactation. However it also most frequently
occurs shortly after calving.
There is a marked local reaction. The onset
is rapid with one or more quarters becoming hot, swollen and painful.
The secretion is thin and serous, but contains large yellow clots
which often clog the teat orifice. Pus may also be present.
The systemic reaction is characterised by moderate
fever. This frequently subsides within one or two days, but persists
if the lesion spreads or septicaemia develops.
A wide variety of micro-organisms may be responsible
for this form of mastitis. Amongst the most common are staphylococci,
streptococci and coliforms.
3. Mild Clinical Mastitis
Can occur at any stage of lactation. Usually
there is only a local reaction. Any systemic reaction is mild
and transient. The local reaction is mainly evident as changes
in the milk. The secretion is thinner than normal, containing
small clots and in many cases pus. Repeated episodes of mild clinical
mastitis in the same lactation are common and this is referred
to as "chronic" mastitis.
Again a wide variety of bacteria may be responsible,
although staphylococci and streptococci are most frequently isolated.
4. Chronic Mastitis
This term is applied to a wide range of chronic
lesions within the udder; from a localised area of abscessation
to a completely fibrosed quarter. When localised abscesses are
present the milk may be normal, but they commonly break down and
give rise to episodes of clinical mastitis. Abscesses may also
break through the skin of the udder. Affected animals remain a
constant source of infection for the rest of the herd.
Terminal fibrosis and atrophy are the end-point
of most forms of mastitis (proliferative lesions are the exception,
the most notable of which is tuberculous mastitis). Once the acute
inflammatory signs of an episode of mastitis disappear, they are
followed by acinar involution, fibrosis and atrophy. If small,
the lesions will be confined to the areas around the base of the
teat, but if larger they may involve the greater part or even
the whole of the quarter. The teat wall may also be affected.
Fibrosis causes induration which can be recognised
on palpation. Atrophy results from contraction of the fibrous
tissue. The secretion from a quarter undergoing fibrosis and atrophy
is usually normal in appearance, although reduced in amount.
OTHER SPECIFIC FORMS OF CLINICAL MASTITIS
1. Summer Mastitis
Although severe clinical mastitis is generally
confined to lactating cows, summer mastitis is a severe clinical
mastitis which affects dry cows, in-calf heifers and, on occasion,
bulling heifers. The cause is Actinomyces pyogenes, probably spread
by flies. As the name implies it occurs during the summer months,
particularly when warm and wet. Initially the affected quarter
becomes swollen, hard and painful. There is either no secretion
or just a little watery fluid. This local reaction is usually
accompanied by a severe systemic reaction with marked fever. Affected
animals may die. Later there is a secretion of thick yellow pus
which has a foul smell. The udder then becomes indurated with
the formation of multiple abscesses. These frequently burst through
the wall of the udder, most commonly at the base of the teat.
Gangrene does not develop but the quarter may
slough.
2. Mycoplasmal Mastitis
The species of Mycoplasma most commonly involved
in Britain is M.bovis. There is a sudden onset with all four quarters
being involved and milk yield falls to almost zero. The udder
is usually swollen, particularly in early lactation. The quarters
are smooth and hard but virtually painless. The secretion initially
appears normal but on allowing to stand a fine sandy material
settles out leaving a turbid whey-like supernatant. Later the
secretion resembles colostrum and may contain a little blood.
Eventually it becomes purulent but large clots are not seen.
Mycoplasmal mastitis may be a persistent problem
where the problem is not correctly diagnosed and treatment is
inadequate.
3. Leptospiral Mastitis
Leptospirae of a number of serotypes (especially
L.hardjo) can cause mastitis in cattle. Clinical signs include
fever, jaundice and abortion but there is a sudden fall in milk
yield for 3-5 days. All quarters can be affected and the milk
produced may be stained with blood or be brownish or yellowish
in colour. The udder is flabby in this condition
SUBCLINICAL MASTITIS
By definition, the udder and milk secretion
are clinically normal (although, of course, fibrosis and atrophy
may be present from a previous clinical attack).
However, due to the small, active lesions which
exist there is a high cell count in the milk. A high bacterial
count may be present. In addition, the milk yield is reduced,
butter fat and solids not fat are depressed and the milk has poor
keeping qualities. Since the lesions are progressive, subclinical
mastitis is often a precursor to clinical mastitis and after an
episode of clinical mastitis, the infection may persist at the
subclinical level. Even without clinical incidents some degree
of fibrosis and atrophy will eventually become clinically apparent.
On most farms with a high incidence of clinical mastitis the vast
majority of the cows will have subclinical mastitis.
The milk from a normal quarter will have a cell
count of 100,000 cells/ml, but counts up to 250,000 cells/ml are
acceptable. Naturally high counts occur during the first week
after calving and at drying off.
The usefulness of cell counts is not in the
individual animal but as a means of monitoring the herd as a whole.
Account should be taken of the trend in cell counts (bulk sample
performed once a month) over a six month period, rather than the
individual monthly count (for reasons such as a high proportion
of the herd being dried of!).
As a general guide, continuing counts of <500,000
cells/ml, suggest that a severe mastitis problem is unlikely,
whereas counts of 1,000,000 suggest the opposite. Total bacterial
counts are carried out by the milk boards on bulk milk samples
as a means of assessing hygienic quality on a monthly basis.
Micro-organisms which cause mastitis can infect
the mammary gland by invasion of the teat canal, e.g. streptococci,
staphylococci, coliforms (E.coli, Klebsiella sp., Proteus sp.
and Pseudomonas sp.) yeasts, salmonellae, mycoplasmas and Actinomyces
pyogenes. The last three organisms may also invade the udder by
the haematogenous route, as do Leptospira spp. and Mycobacterium
bovis.
EPIDEMIOLOGY
A few bacteria which cause mastitis are obligate
udder pathogens e.g. Streptococcus agalactiae, but the majority
can also grow on skin (A.pyogenes, S.dysgalactiae, S.aureus) or
are contaminants from the environment e.g. E.coli, Pseudomonas
and Klebsiella spp. (in sawdust). In all cases, incorrectly-adjusted
milking machines and poor hygiene can contribute to the spread
of established mastitis and predispose to infections from the
environment. In many cases there is evidence to link the reflux
of infected milk into teat canals or even the skin of the teats
with subsequent cases of mastitis. This is particularly obvious
with Mycoplasma mastitis. Streptococci such as S.agalactiae can
persist for up to 3 weeks on cloths and S.dysgalactiae and staphylococci
can survive for long periods on milkers hands. Outbreaks of Pseudomonas
mastitis are often connected with the contamination of water tanks
or teat dips with the organism and those of coliform mastitis
with sawdust bedding in loose-housed animals. Klebsiella spp.
are particularly associated with sawdust. Flies are common vectors
of infections especially of A.pyogenes in summer mastitis occurring
in any cows or heifers at pasture.
Carriers are an important source of disease
and sub clinically or chronically affected animals can act as
sources of infection for healthy animals in the herd. Carriers
of streptococci, staphylococci, coliforms, mycoplasmas and A.pyogenes
may all initiate outbreaks of mastitis, particularly if brought
into a non-immune herd. The use of intramammary antibiotics and
teat siphons may also predispose to certain types of mastitis,
particularly to those associated with fungi (especially Candida
and other yeasts), Nocardia, atypical mycobacteria and mycoplasmas,
all of which may be resistant to the intramammary antibiotic preparations
currently available.
DIAGNOSIS
Based on:
Assuming a careful clinical examination diagnosis
of "mastitis" is not difficult. However clinical differentiation
of the various bacteriological types is at best difficult and
usually impossible. Summer mastitis, mycoplasma mastitis, tuberculous
mastitis and leptospiral mastitis can be diagnosed clinically.
It is also possible to differentiate between very severe ‘peracute*
staphylococcal mastitis and very severe ‘peracute* E.coli
mastitis in most circumstances which will allow rational therapy.
Cell counts and bacteriology are essential in assessing the nature
and severity of the problem.
Accurate bacteriological results are necessary
for the identification and rational treatment and control of mastitis.
Samples should be taken after the teat has been washed with disinfectant
and water, dried and swabbed with alcohol. Foremilk should be
discarded and milk should be taken into a sterile container held
at an angle to preclude contamination of the sample with hair
etc.
TREATMENT
LACTATING COW TREATMENT
Mild clinical mastitis is usually diagnosed
and treated by the farmer using intramammary tubes. On the basis
of probably efficacy penicillin/aminoglycoside combinations have
as successful a "cure" rate as any other antibiotic;
they have short withdrawal times and are cheap.
Acute and per-acute cases are best treated by
systemic injection. Intramammary treatment with the same antibiotic
is appropriate but this would probably be only in the uninfected
quarters since frequent stripping out and inflammation makes intramammary
treatment of the infected quarter worthless.
The immediate main aim of the antibiotic is
to halt the septicaemia and hopefully also to kill the bacteria
in the udder. Since the problem is so acute, since isolation of
the causative organism is too slow, and since differentiation
of the two main bacteria responsible is not always possible on
clinical grounds, the aim is to use an antibiotic reasonably effective
against these two organisms. Antibiotic therapy in acute mastitic
cases is probably secondary to fluid therapy in terms of altering
the prognosis. Large volumes of fluid given intravenously can
be life-saving.
DRY COW TREATMENT
All quarters in all cows be treated with a "dry-cow"
intramammary tube at drying-off.
Treatment in the ‘dry* period is
To prevent new infections (60% of all new infections
arrive in the dry period, and 90% of these via the teat canal
in the first 3 weeks of the dry period).
To remove "chronic" subclinical infection i.e. those
leading to persistent high cell counts.
They prevent "summer mastitis" - but this is rarely
a reason for their use.
A second infusion after 4 weeks of the dry-period may be valuable
if there is a high incidence of infection.
TEST DIPS
In reducing high cell counts, teat dips and
hygiene are extremely important.
The teat dips should be iodophors, or glutaraldehyde,
or hypochlorites in high concentration. Others such as chlorhexidine
and quaternary ammonium compounds give poorer efficacy.
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(milk fever)
DEFINITION
This metabolic disorder occurs around parturition
in mature dairy cows and is characterised by general muscle weakness
and circulatory collapse.
AETIOLOGY
In every cow and heifer the concentration of
calcium in the blood falls at or just after calving. When this
fall is excessive, milk fever develops. Only about 50 per cent
of the calcium in the blood is immediately available. During gestation
the gradual increased demand for calcium by the calf is met by
an increased absorption from the gut. At calving there is a sudden
increase in the demand for available calcium as colostrum/milk
is produced. The calcium in the blood suddenly drops as a result
of a temporary inability by the newly calved cow to replace this
calcium. It is when this drop is excessive that clinical signs
of milk fever become apparent.
During the first day of lactation, the demand
for calcium is about three times the total available. However,
it takes about two days for the calcium homeostatic mechanisms
to adjust to this sudden demand associated with the onset of lactation.
Around calving, there is stasis of the intestinal
tract for a short period and the animal*s appetite is decreased.
While the food intake of heifers drops only slightly, that of
a mature cow may decrease to only 20 per cent of her normal intake.
This period of reduced calcium intake, which can persist from
8 to 20 hours, is crucial in determining the degree of hypocalcaemia
because absorption from the gut constitutes the dominant or only
source of calcium.
Furthermore, as a cow gets older the amount
of calcium which can be mobilised quickly from the bones decreases
progressively. This means that there is an increased dependence
on diet as a major source of calcium and this makes the individual
increasingly susceptible to hypocalcaemia when her food intake
is suddenly decreased. Cattle fed a diet high in calcium during
the last few weeks before calving are particularly susceptible
to the development of milk fever because they become entirely
dependent on absorption from the gut with resorption from the
bones almost nil. Conversely, when cows are fed very little calcium
before calving, active bone resorption is stimulated and susceptibility
to clinical milk fever is reduced presumably because such individuals
are not solely dependent upon dietary sources.
EPIDEMIOLOGY
Milk fever is a modern disease and almost invariably
affects high yielding dairy cows. There is no doubt that within
breeds, the condition occurs regularly in certain families. This
disorder is rare in heifers, uncommon in second calvers with the
highest incidence being in 5 to 6 year old cows. Although cases
arise throughout the year, the incidence is highest in Britain
in the late summer and autumn. About 10 per cent of the cases
occur during the two days before calving while 80% occur in the
3 days following calving.
CLINICAL SIGNS
A cow with milk fever can progress to death
through three clinically recognisable stages:
Prodromal stage. The cow is apprehensive tending
to paddle especially with her hind legs. There are widespread
muscle tremors and slight hyperaesthesia. There is smooth muscle
paralysis which results in an inability to swallow, consequently
inappetance and low thirst, ruminal stasis with the passing of
small amounts of dry faeces or none or all, and the suspension
of urination. These signs can regress spontaneously or they can
become more severe. In the latter instance, the cow falls down
and, after trying to get to her feet several times, she will lie
in sternal recumbency with her hind legs stuck out awkwardly.
Sternal recumbency. Once an individual has become
recumbent, spontaneous recovery is very unlikely. The cow becomes
increasingly hypoaesthetic and tends to lie with her head tucked
into her flank. Her temperature is subnormal, her muzzle dry and,
because of ruminal stasis, ruminal tympany becomes obvious. The
degree of hypoaesthesia becomes worse and eventually the cow goes
into lateral recumbency.
Lateral recumbency. The respiratory rate decreases
(10/minute) and groaning respirations may be heard. The heart
rate increases but the heart sounds become increasingly more difficult
to hear. The papillary reflex is absent and the pupils become
more and more dilated. There is a worsening of the above signs
and the affected individual eventually dies.
In the few cases which occur before calving,
there is the added complication of uterine inertia. Therefore,
in those cases which develop immediately after calving, it is
advisable to check that there is not another calf in the uterus.
Other complications include uterine prolapse and retained placenta.
TREATMENT
Any individual suspected of being hypocalcaemic
should be treated promptly and, if possible, before she becomes
recumbent. Before milk fever is diagnosed and drug therapy instituted,
other causes of recumbency such as physical injury and infectious
diseases should be considered and ruled out as far as is possible.
Therapy is based upon the parenteral administration of a warmed
solution of calcium salts with calcium borogluconate being the
most frequently used. Optimal responses have been obtained alter
the administration of the equivalent of about 8g calcium. Since
one bottle (400m1) of a 20 per cent solution of calcium borogluconate
supplies the equivalent of 6.8g calcium, it is better to use the
40 per cent solution in which there is the equivalent of 13.5g
calcium in 400m1. It is common practice to give half the volume
intravenously and half subcutaneously but this has not been shown
in Britain to improve the recovery rate. Calcium salts should
be given slowly (400ml over 10-15 minutes) because of the effect
of overdosage on the heart.
Following treatment, many cows will then eructate,
defaecate and get to their feet within 15 minutes. Those in lateral
recumbency will first rise into sternal recumbency and then stand
up after about two hours. Cows with milk fever should be allowed
to get to their feet in their own time because if forced to by
to get up, they can easily injure themselves particularly on slippy
concrete floors.
The recovery rate in uncomplicated cases is
about 75 per cent with about 15 per cent of the total having to
be culled or dying because of complications. About 20 per cent
of apparently successfully treated cases will relapse and require
a second course of therapy. If a cow does not get to her feet
within three days the prognosis is poor because of the development
of muscle necrosis.
A small proportion of cases remain recumbent
(downer cows) following calcium therapy. It has been shown that
the longer therapy is delayed after the onset of clinical signs
the lower is the recovery rate.
PREVENTION
Nutritional management. A high calcium diet
before calving increases the incidence of milk fever by increasing
the individual*s dependence on diet as a source of calcium and
reduces skeletal mobilisation. Conversely, a low calcium diet
reduces the incidence of milk fever. However, in Britain where
a large proportion of a normal dairy cow*s diet is grass-based,
it is difficult to devise a diet which will supply less than 50g
calcium per day. Cereals are relatively low in calcium and therefore
the feeding of barley for 3-4 weeks before parturition is to be
recommended. Feeding cereals also reduces the pH of the rumen
content and it has also been shown that an acid diet also reduces
the incidence of milk fever by increasing the calcium absorption.
In the U.S.A. the feeding of a high phosphorus/low
calcium ration to cows during the last month of pregnancy reduced
the incidence of milk fever. However, such diets tend to be unpalatable
and expensive although the addition of 5 per cent monosodium phosphate
in the concentrate ration may be useful. Cows should not be overfed
especially with energy to prevent the development of the fatty
liver syndrome.
Administration of Vitamin D and metabolites
or analogues.
A single injection of 10 million units of Vitamin
D from 2~to 8 days before calving will significantly reduce the
incidence of milk fever in susceptible cows. If the cow then does
not calve this regime can be repeated every eighth day until calving
does occur.
Vitamin D3 preparations are very effective at
increasing serum calcium concentrations. Dosing is recommended
at 24 to 48 hours before calving in order to produce protection
from milk fever. A second injection can also be given 72-96 later
but it is recommended that this is followed by corticosteroid
treatment to ensure that the cow calves within 48 hours. Its disadvantages
are twofold: firstly the date of parturition may be uncertain
and secondly it depresses serum magnesium concentrations and it
is advised that it is important to ensure that the magnesium intake
of cows in late pregnancy is adequate.
On farms where previous experience has shown
that the incidence of milk fever is likely to be high, every cow
may be given 400ml of calcium borogluconate subcutaneously after
calving.
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DEFINITION
Bovine virus diarrhoea (BVD) and mucosal disease
(MD) are two conditions caused by the same virus, BVD virus. BVD
is an acute transient, often asymptomatic condition which occurs
following infection of susceptible calves or adult cattle. There
may be transient diarrhoea but mortality is negligible. Mucosal
disease is, in contrast, a sporadic condition of low morbidity
but high fatality. Clinically apparent illness may be of short
duration but can be prolonged. Diarrhoea is a major feature, mouth
lesions are almost invariably present and interdigital ulceration,
lameness and skin lesions are common. Mucosal disease occurs in
animals persistently infected with BVD virus as a result of infection
prior to birth; these persistently infected animals produce no
antibody against the virus. Infection with BVD virus can also
result in embryonic deaths, abortions and congenital abnormalities.
INCIDENCE
Infection with BVD virus is common in British
cattle. Over 60% of adult cattle are seropositive. Acute outbreaks
of diarrhoea in adult animals (BVD) are rare. Cases of mucosal
disease occur sporadically, usually in animals 6-18 months of
age although cases do occur outside this age range. The introduction
of infection into a previously unexposed group of pregnant cattle
can result in significant losses in calves both pre and post-natally.
The virus can cause an inapparent infection
of animals and may persist in a variety of tissues following infection
of the foetus.
PATHOGENESIS
Of critical importance to the outcome of infection
with BVD virus is the gestational status of the animal infected
and, in pregnant animals, the age of the foetus, as well as the
strain of virus involved.
Infection of previously unexposed, non-pregnant
animals results in transient illness of 1-2 weeks duration. Most
cases are subclinical but occasionally there is a transient diarrhoea.
Infected animals develop neutralising antibody and virus is eliminated
from the body.
Infection of previously unexposed pregnant animals
with virus results in similar effects to those above in the cow
but transplacental spread of virus to the calf also occurs with
consequences which vary most importantly according to the stage
of gestation.
At any stage of gestation, virus infection may
result in foetal death. This will be apparent variously as early
embryonic death with return to service and apparent infertility,
as obvious abortion or as stillbirths; there may also be production
of weak or undersized calves. Animals infected between 100 and
150 days of gestation, may have abnormal brain and nervous system
development.
Infection occurring in the foetus before the
development of immune competence at about 120 days may not result
in foetal death or gross or even microscopic abnormalities. However,
the calves produced are persistently infected with BVD virus.
Virus is present in many organs and tissues and remains so for
life. No antibody is produced against the virus and it appears
that the presence of virus early in foetal life results in a failure
to recognise it as ‘non-self* and therefore there is development
of a specific immunotolerance with persistent infection and no
antibody production.
The production of persistently infected calves
is important for two reasons. Firstly, these animals continually
excrete large amounts of virus in a variety of secretions throughout
life and are an important source of infection for other animals,
especially as they may be clinically normal. Transmission can
occur by ingestion, inhalation, transplacentally or, with persistently
infected bulls, venereally. Secondly, only persistently infected
animals may, subsequently, succumb to mucosal disease.
Not all animals persistently infected with BVD
virus will develop mucosal disease. A number survive to adulthood
and may become pregnant and any calves produced will also be persistently
infected. Persistently infected calves may also be stunted and
are more likely to succumb to other common diseases such as calf
diarrhoea or pneumonia.
MUCOSAL DISEASE
Course
Short lived acute cases of mucosal disease lasting
only 1-2 weeks before death do occur. Chronic cases may last for
1 to 2 months or longer with successive crops of lesions developing
and fading. Virtually all animals with recognisable mucosal disease
will eventually die.
CLINICAL SIGNS
Depression is common. Inappetance is common
and sometimes there is complete anorexia. The animal is usually
wet around the lips and muzzle, and saliva tends to be held in
the mouth, possibly because swallowing causes discomfort. Diarrhoea
is commonly present, often continuous but sometimes intermittent.
Oral lesions are usually diffuse and any part of the oropharynx
may be affected. Vesicles are seen. Gums are often reddened and
numerous small irregular shaped shallow ulcers appear. These superficial
erosions and ulcers often become confluent and covered with a
thin light-coloured diphtheritic membrane. Handling of the tongue
can cause some pain.
Mucosal disease virus has not been clearly associated
with respiratory tract signs .Erosions and ulcerations on the
nose may develop a diphtheritic membrane. The nostrils usually
have a profuse discharge. There is often crusting at the nose-skin
junction. Eyes may be congested with moderate discharge.
Ulceration of the skin of the interdigital cleft
is common and the ulcer is usually quite large and irregular in
outline. Sometimes there is under-running of the horn and lameness
associated with laminitis. In longstanding or recovered cases
there may sometimes be thickening of the coronary band and parallel
marks on the hoof associated with previous laminitis. There is
marked loss of condition.
If pregnant animals are affected they may abort.
DIAGNOSIS
Diagnosis of cases of mucosal disease should
be relatively easy on the basis of clinical and/or pathological
findings. In such clinical cases, if confirmation is required,
examination of blood samples should reveal a persistent viraemia
and an absence of neutralising antibody. Virus may also be detected
in nasal or ocular discharges. At post mortem, virus may also
be detected in lymph nodes, alimentary tract lesions and other
tissues.
Fully susceptible animals, both virus and antibody
negative, will usually seroconvert within 3 weeks of infection.
It should be apparent that within a herd both virus detection
and antibody analysis would be required to differentiate between
immune, susceptible and persistently infected animals which might
succumb to mucosal disease in the future and are a source of risk
to other stock.
CONTROL
Control of BVD-MD within a herd may not be justifiable
on the grounds of cost and can only be done effectively on the
basis of knowledge of virus and antibody status of animals in
the herd.
In fattening stock, detection of persistently
infected animals would allow elimination of those likely to die
from mucosal disease. In an infected breeding herd, the main object
of control should be to ensure that all animals are immune before
they are bred: this should prevent foetal losses, and production
of weak calves or calves likely to die from mucosal disease. Vaccination
can be effective in controlling the problem.
In known BVD-MD free herds it is important that
infection should not be introduced into groups of susceptible
breeding animals. This means that bought-in stock should preferably
be both virus and antibody free or, at the least, virus negative
and antibody positive. It should be noted that both tests are
essential in assessing status - antibody analysis alone is unsatisfactory.
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Diarrhoea in calves during the neonatal period
(i.e. the first four weeks of life) is very common. Various microbiological
agents have been associated with the syndrome and the fate of
affected calves is dependent on the severity of the biochemical
changes. Diarrhoea caused by Salmonella is described under Salmonellosis.
AETIOLOGY
E.coli has been associated with neonatal calf
diarrhoea since before the beginning of this century. Particular
strains of E.coli are more effective than others at inducing disease.
There are also numerous viruses and other microbiological agents
that have been identified in diarrhoeic calf faeces; rotavirus,
coronavirus, parvovirus, enterovirus, astrovirus, calicivirus,
small cubic virus and a villous epithelial cell syncytia inducing
virus. The two most important, and certainly most studied, viruses
are rotavirus and coronavirus. Both these viruses will produce
diarrhoea in colostrum-deprived calves, although strain differences
do exist.
Among the other agents which have been associated
with diarrhoea in neonatal calves, the small protozoan parasite
of the genus Cryptosporidium is the most important.
The relative importance of E.coli, viruses and
Cryptosporidium in the aetiology of neonatal calf diarrhoea has
not been fully ascertained. E.coli are not often isolated from
calves more than 10 days old, whereas rotavirus and coronavirus
are mainly detected in the faeces of calves between 5 and 15 days
old. These two viruses can be demonstrated in up to 60% of calves
with diarrhoea.
INCIDENCE
Surveys of neonatal mortality are variable but
figures of between 2% and 8% are not uncommon. It is suggested
that approximately 50% of neonatal calf mortality is due to gastrointestinal
associated conditions. This may represent 100,000 calves per annum
being lost in the United Kingdom.
CLINICAL SIGNS
Only the clinical syndrome associated with E.coli
is sufficiently distinct to enable an clinical diagnosis to be
made with reasonable accuracy. Even then, confirmation by laboratory
techniques would be required.
The syndrome produced by E.coli occurs in very
young calves, usually less than 5 days of age and frequently as
young as 24 hours old. The onset of the syndrome is very sudden,
and the diarrhoea is very profuse, with a brownish-yellow colour.
Affected calves can lose up to 15% of their bodyweight within
24 hours of the onset of diarrhoea. They quickly become dull,
lethargic and dehydrated. Mortality rates can be very high among
affected calves.
Generally, however, neonatal calf diarrhoea
occurs mainly during the second and third weeks of life, but death
occurs only in a proportion of affected calves. When death occurs
it usually does so after three or four days of profuse diarrhoea,
during which time there is marked loss of weight and increasing
dullness. The faeces, which become progressively more fluid, rarely
contain blood, and tend to impart a yellowish stain on the hindquarters
and tail. If the diarrhoea continues calves become recumbent,
or have great difficulty in rising and are very weak. Some calves
become reluctant to feed early in the course of the condition,
whereas others continue to take milk readily even after they become
recumbent. Eventually, severely affected calves go into lateral
recumbency and become comatose.
Cases which ultimately recover rarely reach
the stage of recumbency although weakness, dullness and loss of
weight are common. Although many such calves are diarrhoeic for
several days, the faeces are usually less fluid than those of
calves which ultimately die. In calves which recover, it is common
to find that the hair is lost in those regions where faecal staining
has occurred. Many calves which apparently recover from neonatal
calf diarrhoea fail to grow as well as animals which have not
been affected, and also appear to be more susceptible to pneumonia.
Calves which have died as a result of severe
diarrhoea are severely dehydrated. If the illness has lasted for
several days they are also very thin and have little perirenal
fat. Many have a grossly distended urinary bladder, presumably
due to the fact that calves do not urinate while recumbent.
PATHOGENESIS
The cause of death in severe neonatal calf diarrhoea
is the severe depletion of fluid and electrolytes resulting from
the diarrhoea. Briefly, in calves which are fed milk until death,
diarrhoea results in a fall in plasma sodium and bicarbonate concentrations
and in blood pH, whereas a rise is found in plasma urea and chloride
concentrations. Plasma potassium concentrations are variable,
but frequently are raised and myocardial potassium concentrations
are consistently low. There is a fall in the plasma volume.
It is postulated that the diarrhoea results
in metabolic acidosis which results in rapid respiration. As a
result of acidosis, potassium is withdrawn from the heart muscle
which results in terminal cardiac failure.
EPIDEMIOLOGY
Several major facts have emerged from epidemiological
studies of calf mortality both in this country and North America,
the most important of which is that although the feeding of colostrum
to newborn calves does not guarantee survival, colostrum deprivation
invariably results in death. Dairy calves first obtaining colostrum
from a bucket have a higher mortality rate than similar calves
which first ingest colostrum by suckling their dams. Calves born
in byres have a much higher mortality rate than calves born in
either yards, boxes or in the field. The mortality rate is highest
in the first week of life and thereafter it decreases exponentially.
The mortality rate in calves in a particular calf-house is directly
proportional to the length of time that the building has been
occupied by young calves. The mortality rate in dairy calves is
at its highest between January and April each year. Ayrshire and
Channel Island calves appear to be less resistant to neonatal
disease than are Friesians. As the size of the adult cow herd
increases, the mortality rate among the calves also increases.
The mortality is higher, and the seasonal mortality pattern is
much more marked, in Scotland than elsewhere in Great Britain.
Little is known about the situation in bought-in
calves although it is known that currently at least one million
calves are sold for rearing each year. Many such calves have to
be freighted long distances to reach the rearing (i.e. northern
and eastern) parts of the country and this entails frequent mixing
of individuals during transit and at markets and holding centres.
It has been shown that the mortality rate in these calves reaches
a peak one week after arriving at their destination and that the
mortality rate increases as calves travel northwards. However,
it must be stressed again that no detailed investigation has studied
the disease situation in these calves. The fact that many of them
are two or three weeks of age when sold probably would tend to
reduce the incidence of neonatal calf diarrhoea and other conditions
such as salmonellosis and respiratory
disease must obviously also be considered as possible causes of
death.
IMMUNOLOGY
Precolostral calf serum is devoid of immunoglobulins
and calves are dependent upon acquiring these immunoglobulins
from colostrum which is usually a particularly rich source. After
a feed of colostrum, immunoglobulins together with other whey
proteins are absorbed through the intestinal epithelial cells
of a calf*s intestine. Macromolecular absorption in newborn calves
is remarkable for the speed and extent at which it proceeds, but
the efficiency of absorption rapidly decreases after birth. The
factors responsible for the cessation of macromolecular absorption
in calves are not fully understood.
It has been found that wide variations exist
in the serum immunoglobulin concentrations of colostrum-fed calves.
Moreover, a direct correlation exists between a calf*s serum immunoglobulin
concentration and that calf*s chances of survival. Many calves
with little or no serum immunoglobulins die during the neonatal
period, many of them from colisepticaemia,
the rest from the effects of diarrhoea. With slightly higher concentrations
colisepticaemia does not occur although deaths are still common
as a result of diarrhoea. With higher serum immunoglobulin concentrations
diarrhoea can occur but calves rarely die.
A very profound seasonal variation in the serum
immunoglobulin concentrations of dairy bull and heifer calves
has been found to occur in the west of Scotland with low mean
values occurring between November and April of each year and high
mean values between May and October. This seasonal variation is
due to the different management techniques that summer and winter-born
dairy calves are subjected to in this area. In the winter, most
dairy calves are born in the byre and first obtain colostrum from
a bucket whereas in the summer, most calves are born in the fields
and first obtain colostrum by suckling their dams. Dairy calves
which first obtain colostrum by suckling their dams usually absorb
greater amounts of colostral immunoglobulins than do bucket-fed
calves, hence the latter*s higher mortality rates.
The amount of immunoglobulin absorbed by a calf
has been shown to be a function of first, the age when fed and
second, the mass of immunoglobulin presented. The cessation of
immunoglobulin absorption is now known to occur progressively
from birth not suddenly at 24-30 hours after birth. This makes
the timing of the first feed critical and the value of subsequent
feeds of colostrum apparently of only marginal importance in relation
to serum immunoglobulin levels.
DIAGNOSIS
In all outbreaks of neonatal diarrhoea, steps
must be taken to eliminate the possibility of salmonellosis. Confirmation
of one or other of the possible microbiological agents can be
readily carried out by diagnostic laboratories
TREATMENT
Almost every available chemotherapeutic agent/antibiotic
has been used in the treatment of neonatal calf diarrhoea at some
time or other and most with very limited success. Most of the
trials which have been carried out have been uncontrolled and
few have considered the immune status of the call. The most frequently
used treatment regimes consist of antibiotic therapy, combined
with some form of food withdrawal and/or fluid replacement.
Fluid therapy has often been used in conjunction
with antibiotics. It is clear that the electrolyte and fluid imbalance
associated with neonatal calf diarrhoea is a complex disaster
resulting in acidosis which, in turn, is probably responsible
for death in that it initiates cardiac failure by depleting myocardial
potassium. Any attempt at fluid therapy should be based upon a
knowledge of the fluid and electrolyte status of a calf and should
be administered under conditions of intensive care. Particular
care is required in the correction of acidosis in the scouring
calf.
The withdrawal of milk is frequently advocated
as an adjunct to the treatment of diarrhoea. Certain proprietary
preparations for oral replacement therapy contain appropriate
ions and substances such as glycine, glucose and citrate to assist
absorption of the electrolytes and are claimed to be of value.
CONTROL
The use of prophylactic antibiotics to control
diarrhoea in home-bred calves can be expensive and frequently
is not successful. It is the only course open to people purchasing
calves for rearing although much of the trouble in these units
can be prevented by delaying the purchase of calves until they
are about one month old.
The control and subsequent prevention of disease
in homebred dairy calves in a closed unit which is experiencing
trouble should be based on those factors mentioned previously
- reducing pathogen challenge and increasing the resistance of
the calf.
Attempts should be made to increase the amounts
of colostral immunoglobulin absorbed by each calf. In view of
the fact that wide individual and possibly breed variations exist
in colostral concentrations of antibody it is essential to feed
as large a volume of colostrum as possible, which has no lasting
ill effects on newborn calves. It is necessary to ensure that
indoor calvings during winter occur in loose boxes or yards.In
any case, the stockman must convince himself that a newborn calf
has suckled to satiation (this may take 20 minutes) as early as
possible.
Occasionally, despite precautions it is found
that a calf with low serum imnmunoglobulin concentration has been
produced. This is not due to an inability to absorb colostrum
but is a result of either delayed feeding or ingestion of only
a small quantity of colostrum. Some dams produce low volumes or
concentrations of globulin and "pre-milking" or dripping
markedly reduces the concentration of globulin from these quarters.
The odd calf with a low serum immunoglobulin level is unlikely
to experience diarrhoea if it is mixed with calves with much higher
serum levels.
If, for some reason, box calving is not possible,
then very large amounts of colostrum should be fed to calves as
soon as possible after birth. It is usually possible to feed calves
at one hour of age with up to five pints of colostrum. It is suggested
that the stockman should be urged to feed up to six pints of colostrum
as soon as possible after birth, but at least within the first
4 hours of life. This will not harm the calves although a transient
diarrhoea and dullness will occur a few hours after ingesting
such amounts. Even in such calves, the absorption of colostral
immunoglobulin is very significantly increased if the calves are
mothered.
Infection build-up cannot be ignored. Therefore,
periodic disinfection should be practiced and calves should be
kept in fairly small self-contained groups wherever possible.
Obviously, bought-in calves constitute a major hazard to homebred
animals and this practice is never consistent with the continued
good health of homebred animals.
Other management factors should also be considered
here. Newborn dairy calves probably thrive best at an ambient
temperature in excess of 13C (550F). Single penning is desirable,
not because it limits disease spread, but because the stockman
tending the calves gets to know individual animals much more quickly.
Successful calf rearing is a time consuming job demanding considerable
expertise.
In order to increase the concentrations of specific
antibodies to the microbiological agents associated with calf
diarrhoea vaccination of the dams in the last few weeks of gestation
has been investigated. Rotavec K99 is a vaccine currently available
in the U.K. It raises antibody levels in colostrum against both
E.coli and bovine rotavirus. Although still dependent on colostral
transfer this vaccine gives good results if used appropriately.
However, it is the failure or partial failure
in the transfer of colostral immunoglobulins from the cow to the
calf that is a major contributory factor to the severity of neonatal
calf diarrhoea. Thus increasing the level of specific antibodies
in the colostrum is of limited value to a calf which fails to
receive sufficient colostrum, at a time when its ability to absorb
that colostrum is at a maximum.
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Infection with a number of serotypes of Salmonella
spp. may give rise to a syndrome in which fever, diarrhoea (frequently
with dysentery) and deaths occur in both calves and adults but,
on occasions, in pregnant cows abortion may be the only overt
clinical sign. The disease in cattle is a source of infection
for man.
AETIOLOGY
S.dublin and S.typhimurium are the most common
causes of bovine salmonellosis in Britain. Many other serotypes
can cause disease. It should be remembered that all salmonellae
may become pathogenic under the right conditions.
INCIDENCE
Salmonellosis is an important disease of cattle
in Britain and throughout the world. The cost to the agricultural
industry is not known but it has been claimed to be of major importance
to calf rearers and is currently the second most commonly diagnosed
cause of bovine abortion.
CLINICAL SIGNS
Salmonellosis can affect cattle of all ages
but it is most frequently seen in adult cows and calves. The clinical
signs for all serotypes are similar.
Adult cattle: Initially, in acute salmonellosis,
there is rapid onset dullness and marked fever (40-41.50C) with
inappetance and a dramatic drop in the milk yield of affected
(dairy) cows. A severe diarrhoea ensues with foetid watery faeces
which may contain blood, mucus and shreds or casts of necrotic
bowel epithelium. Presumably as a result of this latter feature,
abdominal pain is often noticed. Some
Calves: Calves of any age can be affected but
it most frequently occurs between 2-8 weeks of age. The median
age for S.dublin outbreaks is 4 weeks and for S.typhimurium it
is 3 weeks.
Clinically the affected calves are very dull
with marked lethargy. Unlike calves affected by colibacillosis
which may continue to consume milk even when recumbent, calves
with salmonellosis are usually completely inappetent. There is
a marked fever, often as high as 41.50C with a profuse, evil-smelling
diarrhoea. There may or may not be dysentery. Affected calves
rapidly lose condition, become very weak, unable to stand and
emaciated. Death occurs within 2-3 days of the development of
clinical signs and the mortality can be as high as 30% and occasionally
higher. In non-treated survivors the diarrhoea may persist for
up to 2 weeks.
Following infection with S.dublin the development
of gangrene-like lesions and osteitis of the extremities has been
described with sloughing of the ear-edges, the tip of the tail
and even the distal extremities of the limbs.
PATHOGENESIS
Infection usually occurs by the oral route.
The source of organism is usually the faeces of an infected animal,
whether clinically affected or a faecal carrier, although infected
milk, uterine discharges and products of abortion may be important
where infection occurs in adult cattle. Following ingestion, the
organism may multiply within the gut. The organisms multiply within
the gut wall and from there disseminate to the systemic circulation.
Multiplication in the liver and blood stream gives rise to a septicaemia.
The ability of Salmonella spp. to produce diarrhoea is largely
associated with the invasion of the gut wall and the inflammatory
reaction. In recovery the organism may become localised in joints,
the foetus to give abortion, in the gall bladder or in other organs.
Adult animals which have recovered from S.dublin infection may
continue to excrete the organism in the faeces for several months
(perhaps for life). Those which have recovered from S. typhinurium
infection cease excreting organism after 6-14 weeks. Calves which
have recovered normally cease to excrete the organism after a
few weeks.
It is suggested that intercurrent disease such
as fascioliasis (liver fluke)
may predispose to infection.
EPIDEMIOLOGY
Host range. S.dublin infection does occur in
species other than cattle but is primarily an infection of cattle.
S.typhimurium can infect a wide variety of species and infections
may originate from any of these including wild life.
SOURCES OF INFECTION
Although there are many possible ways by which
susceptible cattle may acquire salmonella infection, the overwhelming
evidence suggests that infection is most often acquired from other
cattle which are excreting the organisms. For clinical disease
to be established in cattle it would seem that challenge has to
be relatively high.
1) Infection from other cattle. As stated above
this is the most important source of infection with S.dublin and
S.typhimurium. Infection may be introduced into a population of
cattle either by the purchase of an adult carrier or by mixing,
in market or in transit, with clinical or pre-clinical cases.
Infection may pass from adults in a herd down to the calves or
vice versa. Congenital infection of calves born at full-term does
not appear to occur, but those calves born to cows which are faecal
excretors almost invariably become infected either at parturition
or soon after birth. Intensive husbandry systems, especially loose
housing, have facilitated the spread of salmonella infection.
2) Infection from contaminated foodstuffs and
water. Although the infection rate of cattle food constituents
(e.g. bone, meat and blood meals and milk powders) can be high,
surveys of the end-products (cattle and calf cakes or pellets)
have shown a low incidence of infection and low counts of organisms.
The change to loose-housing has been associated
with an increase in the volume of slurry for disposal. S.dublin
may survive for up to 30 weeks in winter slurry, but the survival
time on grass after being spread is much shorter. Survival in
soil cores may be as long as 24 weeks. The recommendation to reduce
the risk of spread of infection via slurry is: (1) storage of
slurry for a minimum of 4 weeks; (2) pasture should not be grazed
until 4 weeks after slurry spreading. There is at least one recorded
outbreak of salmonellosis due to S.typhimurium occurring after
slurry was spread on fields at a much higher rate than normal.
Outbreaks of salmonellosis have been attributed
to cattle drinking contaminated water, effluent from knackeries,
contamination of fields due to sewage overflow, or sewage sludge.
3) Infection from other domestic animals (and
man). Few instances are recorded and often the primary source
of infection is unknown. However, it is recorded that on a few
occasions, Salmonella typhimurium infection has passed to cattle
from chickens, ducks, geese, pigs and humans.
4) Infection from wild animals. Rats may allow
a farm infection of S.typhimurium to persist. Only low infection
rates in British farm rats have been recorded although in one
case infected rat droppings in old hay were found to be the source
of infection for beef cattle. Sparrows, starlings and seabirds
have also been found to S.typhimurium rarely remain infected for
any length of time and excretion of the organism usually only
occurs for a few weeks.
Some animals which have recovered from S.dublin
infection may become intermittent excretors. Animals which merely
ingest the organism and excrete it in the faeces without becoming
infected are referred to as passive carriers.
DIAGNOSIS
In calves, time of onset (3-4 weeks of age),
the clinical signs of the disease - fever, depression, diarrhoea,
sometimes with the presence of blood, the post-mortem findings
and a history of recent purchase through markets may suggest a
diagnosis of salmonellosis. In adults the clinical signs are also
suggestive. Diagnosis must, however, be confirmed by the isolation
of the organism.
TREATMENT
Affected animals should be treated by both the
parenteral and oral routes with an antimicrobial drug. This is
possible in calves but in adult ruminants many such drugs may
disturb rumen flora if given orally. The same drug or class of
drug e.g. an aminoglycoside should be given parenterally and by
mouth as far as possible. Ampicillin, trimethoprim/ sulphonamide
combination, neomycin, spectinomycin, enrofloxacin and sulphonamides
are all available in injectable and oral forms. With drugs which
can be absorbed from the gut, injections need only be given initially.
Compounds available for oral dosing also include furazolidone
and may be given as boluses, from oral dosers, or as soluble products
for administration in drinking water or milk.
The drug of choice may be ampicillin, amoxycillin,
enrofloxacin, trimethoprim/ sulphonamide (destroyed in functioning
rumens) neomycin or furazolidone in that order. Antibiotic sensitivities
of the salmonellae involved should be taken into account if treatment
is unsuccessful or in continued outbreaks.
Calves do not usually become carriers following
treatment but adults may, and disposal of adult cases to a secure
rendering plant should be considered.
Careful nursing and management of individual
calves is of great importance and the animals should be kept under
lamps, turned regularly and fed several times daily until they
improve. It is important to impress upon the person in charge
of infected animals, adults or calves, the possibility of spread
occurring to himself and his family and strict hygiene measures
must be observed.
Prophylactic (oral) use of antibiotics should
be discouraged as in most cases low levels of antibiotics have
no effect on the excretion pattern of salmonellae. Indeed it has
been shown in man that with non-invasive salmonellosis, antibiotics
significantly increase the excretion period of the organism in
the faeces.
CONTROL
Vaccines
Currently only multicomponent dead vaccines
are available in the U.K. e.g. Bovivac (Hoechst). High serum concentrations
of absorbed colostral immunoglobulins aid survival and reduce
the severity of alimentary disturbance in calves with salmonellosis
but, unless specific antibody to Salmonella is present cannot
prevent infection.
Control measures which should be instituted
during an outbreak of salmonellosis
Isolation of clinical cases to reduce
the weight of contamination.
Recovered animals should be retained in isolation for at least
2 weeks after the cessation of diarrhoea.
Carcasses of fatal cases should be sent to knackeries capable
of producing salmonella-free products.
Ideally, adult clinical cases of S.dublin infection should be
slaughtered as recovered animals invariably remain persistent
excretors.
Clinical cases should never be sent for emergency slaughter intended
for human consumption.
Treatment of effluent in such a way as to minimise contamination
of environment.
Following an outbreak the premises should be thoroughly cleaned
and disinfected.
Restrict movement of animals either on to or off farm until final
disinfection has been carried out.
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This is a condition of colostrum deficient calves
less than one week old. It has a sudden onset and affected calves
almost invariably die.
AETIOLOGY
Particular serotypes of E.coli are associated
with colisepticaemia.
INCIDENCE
The exact incidence of this condition is unknown,
but the majority of calves which die during the neonatal period
(i.e. during the first four weeks of life) die during the first
two weeks of life, either as a result of colisepticaemia, or diarrhoea.
CLINICAL SIGNS
Many cases of colisepticaemia are said to be
‘sudden deaths", as when last observed the calf was
seen to be well. However, careful stockmen will generally have
noticed that the calf was dull, stiff and reluctant to rise and
feed. Rapid deterioration and collapse then follow. Fever (1050F-40.50C)
is frequently present but rapidly drops to sub-normal values as
the animal collapses. Diarrhoea if present at all is scanty and
a terminal event. In some cases, enlarged, puffy joint capsules
may be seen and the occasional calf displays signs of central
nervous system disturbance due to meningitis. Death ensues within
12 hours of the onset of clinical signs.
A small proportion of cases do not die but many
of these subsequently suffer from arthritic lesions (joint-ill)
and/or abscesses in the body tissues and organs, umbilicus, and,
on occasions, the central nervous system.
EPIDEMIOLOGY
This is the classic condition of the calf which
has been deprived of colostrum or has not absorbed colostral immunoglobulins
(see neonatal calf diarrhoea).
DIAGNOSIS
Relatively sudden death in calves less than
one week old which have a suitable epidemiological background,
i.e. colostrum deficient and poor hygienic conditions may indicate
a diagnosis of colisepticaemia.
TREATMENT
Because of the rapid onset and death of affected
animals treatment is usually ineffective, even with massive doses
of antibiotic.
CONTROL
This condition is easily controlled by increasing
the concentrations of passively acquired colostral immunoglobulins
in the serum of newborn calves. See Control of neonatal
calf diarrhoea.
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Ostertagia ostertagi is the most common cause
of parasitic gastritis in cattle. The disease, ostertagiosis,
is characterised by weight loss and diarrhoea and typically affects
young cattle during their first grazing season, although herd
outbreaks and sporadic individual cases have also been reported
in adult cattle.
LIFE CYCLE
O.ostertagi has a direct life cycle. The eggs
are passed in the faeces and develop within the faecal pat to
the infective third stage. When moist conditions prevail the larvae
migrate from the faeces onto the herbage.
After ingestion the larvae develop in the lumen
of an abomasal gland before they emerge from the gland to become
mature on the mucosal surface.
The entire parasitic life cycle usually takes
three weeks but under certain circumstances many of the ingested
larvae become inhibited in development for periods of up to six
months.
The presence of O.ostertagi in the abomasum
in sufficient numbers gives rise to extensive pathological and
biochemical changes and severe clinical signs. These changes are
maximal about 18 days after infection but it may be delayed for
several months when arrested larval development occurs.
In heavy infections of 40,000 or more adult
worms the principal effects of these changes are first, a reduction
in the acidity of the abomasal fluid, the pH increasing from 2.0
up to 7.0. This results in a failure to activate pepsinogen to
pepsin and to denature proteins. There is also a loss of bacteriostatic
effect in the abomasum. Secondly, there is an enhanced permeability
of the abomasal epithelium to macromolecules such as pepsinogen
and plasma proteins. The results of these changes are a leakage
of pepsinogen into the circulation leading to elevated plasma
pepsinogen levels and the loss of plasma proteins into the gut
lumen eventually leading to low blood protein levels. Clinically
these consequences are reflected as inappetance, weight loss and
diarrhoea and precise cause of the latter being unknown.
In lighter infections the main effects are sub-optimal
weight gains.
CLINICAL SIGNS
Bovine ostertagiosis is known to occur in two
clinical forms. In temperate climates with cold winters the seasonal
occurrence of these is as follows.
The Type I disease is usually seen in calves
grazed intensively during their first grazing season as the result
of large numbers of larvae ingested 3-4 weeks previously; this
normally occurs from mid-July onwards.
The Type II disease occurs in yearlings, usually
in late winter or spring following their first grazing season
and results from the maturation of larvae ingested during the
previous autumn and subsequently inhibited in their development.
The main clinical sign in both Type I and Type
II disease is a profuse diarrhoea and in Type I, where calves
are at grass, this is usually persistent, watery and has a characteristic
bright green colour. In contrast, in the majority of animals with
Type II the diarrhoea is often intermittent and anorexia and thirst
are usually present. The coats of affected animals in both syndromes
are dull and the hind quarters heavily soiled with faeces.
In both forms of the disease the loss of body
weight is considerable during the clinical phase and may reach
20% in 7-10 days. Carcass quality may also be affected since there
is a reduction in total body solids relative to total body water.
In Type I disease, the morbidity is usually
high, often exceeding 75%, but mortality is rare provided treatment
is instituted within 2-3 days. In Type II disease only a proportion
of animals in the group are affected but mortality in such animals
is very high unless early treatment with an anthelmintic effective
against both inhibited and developing larval stages is instituted.
EPIDEMIOLOGY
Dairy Herds
From epidemiological studies the following important
facts have emerged:
1. A considerable number of larvae can survive
the winter on pasture and in soil. Sometimes the numbers are sufficient
to precipitate Type I disease in calves 3-4 weeks after they are
turned out to graze in the spring. However, this is unusual, and
the role of the surviving larvae is rather to infect calves at
a level which produces patent sub-clinical infection which ensures
contamination of the pasture for the rest of the grazing season.
2. A high mortality of overwintered larvae on
the pasture occurs in spring and only negligible numbers can usually
be detected by June. This mortality combined with the dilution
effect of the rapidly growing herbage renders most pastures, not
grazed in the spring, safe for grazing after mid-summer.
However, despite the mortality of larvae on
the pasture it now appears that some can survive in the soil for
at least another year and on occasion appear to migrate on to
the herbage. Whether this is a common occurrence and whether the
larvae migrate or are transported by terrestrial populations of
earthworms or beetles is not definitely known but the occurrence
of this apparent reservoir of larvae in soil may be important
in relation to certain systems of control based on grazing management.
3. The eggs deposited in the spring develop
slowly to larvae; this rate of development becomes more rapid
towards mid-summer as temperatures increase, and as a result,
the majority of eggs deposited during April, May and June all
reach the infective stage from mid-July onwards. If sufficient
numbers of these larvae are ingested the Type I disease occurs
any time from July until October. Development from egg to larvae
slows during the autumn and it is doubtful if many of the eggs
deposited after September ever develop to larvae.
4. As autumn progresses and temperatures fall
an increasing proportion (up to 80%) of the larvae ingested do
not mature but become inhibited. In late autumn, calves can therefore
harbour many thousands of larvae but few developing forms or adults.
These infections are generally asymptomatic until maturation takes
place during winter and early spring and if large numbers of these
larvae develop synchronously, Type II disease occurs. Where maturation
is not synchronous clinical signs may not occur but the adult
worm burdens which develop can contribute to pasture contamination
in the spring.
Two factors, one management and one climatic,
appear to increase the prevalence of Type II ostertagiosis.
First, the practice of grazing calves from May
until July on permanent pasture, then moving these to hay or silage
aftermath before returning them to the original grazing in late
autumn. In this system the accumulation of larvae on the original
pasture will occur from mid-July i.e. after the calves have moved
to aftermath. These larvae are still present on the pastures when
the calves return in the late autumn and, when ingested, the majority
will become inhibited and thus increase the potential for Type
II disease.
Secondly, in dry summers the larvae are retained
within the crusted faecal pat and cannot migrate on to the pasture
until sufficient rainfall occurs to moisten the pat. If rainfall
is delayed until late autumn many larvae liberated on to pasture
will become inhibited following ingestion and so increase the
chance of Type II disease. Indeed, epidemics of Type II ostertagiosis
are typically preceded by dry summers.
Although primarily a disease of young dairy
cattle, ostertagiosis can affect groups of older cattle, particularly
if these have had no previous exposure to the parasite since there
is no significant age immunity to infection. Also, acquired immunity
in ostertagiosis is slow to develop and calves do not acquire
a significant level of immunity until the end of their first grazing
season. If they are then housed for thewinter and acquired immunity
has waned by the following spring and yearlings turned out at
that time are partially susceptible to reinfection and can contaminate
the pasture with small numbers of eggs. However, immunity is rapidly
reestablished and any clinical signs which occur are usually of
a transient nature. During the second and third year of grazing
a strong acquired immunity develops and adult stock in endemic
areas are generally highly immune to reinfection. An exception
to this rule occurs around the periparturient period when immunity
wanes, particularly in heifers, and there are reports of clinical
disease following calving. The reason is unknown but may be due
to the development of larvae which were arrested in their development
as a result of host immunity.
Beef Herds:
Although the basic epidemiology in beef herds
is similar to dairy herds the influence of immune adult animals
grazing alongside susceptible calves has to be considered. Thus
in beef herds where calving takes place in the spring, ostertagiosis
is uncommon since egg production by immune adults is low, and
the spring mortality of the overwintered larvae occurs prior to
the suckling calves ingesting significant quantities of grass.
Consequently only low numbers of larvae become available on the
pasture later in the year.
However, where calving takes place in the autumn
or winter, ostertagiosis can be a problem in calves during the
following grazing season after they are weaned. The epidemiology
is then similar to that seen in dairy calves. Whether Type I or
Type II disease subsequently occurs depends on the grazing management
of the calves following weaning.
DIAGNOSIS
In older animals the clinical signs and history
are similar but laboratory diagnosis is more difficult. A useful
technique to employ in such situations is to carry out a pasture
larval count on the field on which the animals had been grazing.
Where the level of infection is more than 1,000 larvae per kg
of dried herbage the daily larval intake of grazing cows is in
excess of 10,000 larvae. This level is probably sufficient to
cause clinical disease in susceptible adult animals or to upset
the normal functioning of the gastric mucosa in immune cows.
TREATMENT
Type I disease responds well to treatment at
the standard dosage rates with any of the modem benzimidazoles
(albendazole, fenbendazole or oxfendazole), the probenzimidazoles,
levamisole, or ivermectin. All of these drugs are effective against
developing larvae and adult stages. Following treatment calves
should be moved to pasture which has not been grazed by cattle
in the same year. The field where the outbreak has originated
may be grazed by sheep or rested until the following June.
For the successful treatment of Type II disease
it is necessary to use drugs which are effective against inhibited
larvae as well as developing larvae and adult stages. Only the
modem benzimidazoles listed above or ivermectin are useful in
the treatment of Type II disease when used at standard dosage
levels although the probenzimidazoles are also effective at higher
dose rates.
In young animals this decision is based on:
The clinical signs of inappetance, weight loss
and diarrhoea
The season. For example, Type I occurs from
July until September and Type II from March to May
The grazing history. In Type I disease, the
calves have usually been set-stocked in one area for several months,
in contrast, Type II disease often has a typical history of calves
being grazed on a field from spring to mid-summer, before being
moved and then brought back to the original field in the autumn.
Affected farms usually also have a history of ostertagiosis in
previous years.
Faecal egg counts. In Type I disease these can
be more than 1,000 eggs per gram and are a useful aid to diagnosis;
in Type II counts are highly variable, may even be negative and
are of limited value.
Plasma pepsinogen levels. In clinically affected
animals up to two years old these are usually raised.
Post-mortem examination
CONTROL
Traditionally, ostertagiosis has been prevented
by routinely treating young cattle with anthelmintics over the
period when pasture larval levels are increasing. For example,
this involves one or two treatments usually in July and September
and on many farms this prevented disease and produced acceptable
growth rates. However, it has the disadvantage that since the
calves are under continuous larval challenge their performance
may be impaired. With this system effective anthelmintic treatment
at housing is also necessary using a drug effective against inhibited
larvae in order to prevent Type II disease. Today, it is accepted
that the prevention of ostertagiosis by limiting exposure to infection
is a more efficient method of control.
This may be done by grazing calves on new grass
leys although it is doubtful if this should be recommended for
replacement dairy heifers, as it would result in a pool of susceptible
adult animals. A better policy is to permit young cattle sufficient
exposure to larval infection to stimulate immunity but not sufficient
to cause a loss in production. The provision of this ‘safe
pasture* may be achieved in two ways:
First, by using anthelmintics to limit pasture
contamination with eggs during periods when the climate is optimal
for development of the free-living larval stages i.e. spring and
summer.
Alternatively by resting pasture or grazing
it with another host, such as sheep, which are not susceptible
to O.ostertagi, until most of the existing larvae on the pasture
have died out.
Sometimes a combination of these methods is
employed.
Prophylactic Anthelmintic Medication
Since the crucial period of pasture contamination
with O.ostertagi eggs is the period up to mid-July, one of the
efficient modern anthelmintics may be given on two or three occasions
between turnout in the spring and July to minimise the numbers
of eggs deposited on the pasture. For calves going to pasture
in early May two treatments, three and seven weeks later are used,
whereas calves turned out in April require three treatments. With
some anthelmintics which have a persistent effect and prevent
infection for several weeks after administration, various regimens
are recommended. For example ivermectin at 3, 8 and 13 weeks post
turnout or doramectin at turnout and 8 weeks later.
Several rumen boluses have been developed which
release in a sustained fashion or as programmed single ‘pulse*
doses. When these boluses are administered to calves just prior
to turn-out they prevent the development of infections acquired
from overwintered larvae and so prevents the deposition of eggs
during the spring. This in turn prevents the development of high
levels of pasture contamination with larvae which are responsible
for disease.
Anthelmintic prophylaxis has the advantage that
animals can be grazed throughout the year on the same pasture
and is particularly advantageous for the small heavily stocked
farm where grazing is limited.
Anthelmintic treatment and move to safe pasture
in mid-July
This is usually referred to as the ‘dose
and move" system and is based on the knowledge that the annual
increase of larvae occurs after mid-July. Therefore if calves
grazed from early spring are given an anthelmintic treatment in
early July and moved immediately to a second pasture such as silage
or hay aftermath, the level of infection which develops on the
second pasture will be low.
The one reservation with this technique is that
in certain years the numbers of larvae which overwinter are sufficient
to cause heavy infections in the spring and clinical ostertagiosis
can occur in calves in April and May. However, once the ‘dose
and move' system has operated for a few years this problem is
unlikely to arise.
Alternate grazing of cattle and sheep
This system ideally utilises a three year rotation
of cattle, sheep and crops. Since the effective life-span of most
O.ostertagi larvae is under one year and cross infection between
cattle and sheep in temperate areas is largely limited to Trichostrongylus
axei, good control of bovine ostertagiosis should, in theory,
be achieved. It is particularly applicable to farms with a high
proportion of land suitable for cropping or grassland conservation
and less so for marginal or upland areas, but in these areas good
control has been reported using an annual rotation of beef cattle
and sheep.
The drawback of alternate grazing systems is
that they impose a rigorous and inflexible regimen on the use
of land which the farmer may find impractical. Furthermore, in
warmer climates where Haemonchus is prevalent this system can
prove dangerous since this very pathogenic worm establishes in
both sheep and cattle, but is not a problem in Scotland.
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(Husk, Hoose)
Parasitic bronchitis can occur under differing
management systems and, although the disease is basically the
same, the various syndromes will be described individually. Firstly,
the disease will be described in detail as it occurs in dairy
and dairy-cross calves in which it is most common and most important.
Secondly, it will be described in single suckled calves, thirdly
in adult cattle and finally, the reinfection syndrome will be
discussed.
HUSK IN DAIRY CALVES
This disease, which is caused by the lungworm,
Dictyocaulus viviparus, is characterised by bronchitis and pneumonia.
Typically, dairy and dairy cross calves are affected during their
first grazing season particularly if they have had access to old
pastures. Parasitic bronchitis is particularly prevalent in temperate
areas where there is a high rainfall.
AETIOLOGY
The adult lungworms, which are slender, thread-like
and up to 8cm long, are found in the lung passages. The female
worms lay eggs which hatch quickly to produce larvae which are
coughed up, swallowed and appear in the faeces. Under optimal
conditions these can develop to the infective stage in 5 days.
When ingested by a susceptible host the larvae penetrate the intestinal
wall, moult, and travel to the lungs. A few days later the young
adult worms move up into the lung passages. In a primary infection,
larvae first appear in the faeces after about 25 days.
The pathogenesis of D. viviparus infection may
be divided into 4 phases:
Penetration Phase: Days 1-7
Prepatent Phase: Days 8-25
Patent Phase: Days 26-60
Post-patent Phase: Days 61-90
CLINICAL SIGNS
The clinical signs are the result of a gradually
developing bronchitis and pneumonia. In infected calves, the sequential
development of the clinical signs are as follows:
Days l-7 -No clinical signs
Days 8-14 -Increased rapidity and depth of breathing
with coughing which initially is occasional but then becomes more
frequent.
Days 22 onwards- Frequent bouts of coughing;
increased rapidity and depth of breathing. The respirations are
harsh and correlate with the increased respiration rate; in severely
affected cases, squeaks and crackles are heard over the posterior
lung lobes. Occasionally, subcutaneous emphysema is detected.
If death occurs, it is usually between 20 and 25 days post-infection.
The severity and duration of the clinical signs
in any outbreak are dependent mainly on the number of larvae ingested
and the rate of their ingestion. Other factors include age of
the animal affected, the plane of nutrition and weather. In an
affected group, differing degrees of clinical severity are apparent
because of differing levels of infection, e.g. a few animals mildly
affected, most moderately affected, a few severely affected.
Mild group infection - occasional/frequent coughing
when calves are made to stand up or when chased.
Moderate group infection - frequent bouts of
coughing at rest, increased rate and depth of breathing.
Severe group infection - rapid respiration rate,
difficulty breathing brought on or exacerbated by exercise, frequent
bouts of harsh coughing. Although many cases may have a slightly
elevated temperature this is usually due to the damage produced
by the lungworms and not to a secondary bacterial infection.
It is usually the smallest calves within a group
which are most severely affected. A massive infection in this
type of calf can present as a sudden onset breathing difficulties
and death, due to acute heart failure, can occur during the subsequent
24-48 hours. Such cases are often in the pre-patent phase but
in general, most calves are suffering from the patent disease
when clinical signs are first noticed.
After drug therapy, the frequency of coughing
decreases, the breathing rate eventually returns to normal and
the depth of breathing becomes much less noticeable. However,
full return to normality can take weeks and even months in severe
cases.
About six weeks after clinical signs are initially
noticed, a proportion (20-25%) of convalescent individuals, which
had been severely affected, may develop sudden onset respiratory
distress with mouth-breathing. Squeaks and crackles can be heard
over the posterior lobes and the temperature is normal. These
calves usually die from acute heart failure within 24-96 hours
of their first being seen to be ill.
The name given to this form of the disease is
Post-Patent Husk.
EPIDEMIOLOGY
Generally only calves during their first grazing
season are clinically affected, since on any farm where disease
is endemic, older animals have a strong acquired immunity.
In the vast majority of husk incidents, it is
dairy calves or dairy-cross calves being reared for beef, which
are affected. However, under certain circumstances, single suckled
calves and adult cattle can develop clinical disease.
Husk is predominantly a problem in areas with
a mild climate and average to high rainfall. The majority of outbreaks
occur from late July to September, although outbreaks can occur
from June to November. Disease usually develops after susceptible
calves have been at grass for 2-5 months.
There are two main ways by which D.viviparus
infection can persist on endemic farms.
Overwintered larvae: in the British Isles, larvae
can survive on pasture from autumn until late spring in sufficient
numbers to initiate infection. A similar effect may result when
infected manure is spread onto grass in the spring.
Carrier animals: small numbers of adult worms
can survive in the bronchi of infected animals for several months.
Another factor which is involved in the dissemination
of larvae is the fungus Pilobolus. This occurs in bovine faecal
pats and when the spores are ripe, the sporangia which can carry
up to 50 larvae, are discharged into the air and onto the surrounding
herbage.
DIAGNOSIS
This is based on the clinical signs, the time
of year and a history of grazing on permanent or semi-permanent
pasture.
Dictyocaulus larvae can be detected in the faeces
of cases with patent infections.
When calves are found dead and parasitic bronchitis
is suspected, post mortem examination of the lungs should show
characterisitic signs of lungworm infestation.
TREATMENT
The anthelmintics available for the treatment
of parasitic bronchitis and pneumonia are levamisole, ivermectin,
or any of the modem benzimidazoles used orally i.e. oxfendazole,
fenbendazole or albendazole. These drugs have all been shown to
eliminate both mature and developing lungworms with a consequent
amelioration of clinical signs and a reduction in faecal larval
counts.
For maximum efficiency these drugs should be
used as early as possible in the treatment of the disease since
clinical signs associated with pulmonary pathology are not rapidly
resolved by the removal of adult lungworms.
When the disease is severe and well-established
in a number of calves the farmer should be aware that anthelmintic
treatment, while being the only course available, may exacerbate
the clinical signs in one or more animals with a possible fatal
termination. The reasons underlying this are still under study
but are apparently associated with the death, dissolution and
aspiration of adult worm material into the respiratory bronchioles
and alveoli.
In more serious cases the prognosis must be
guarded and the farmer informed that a proportion of these animals
may not recover whilst some of those that do so may remain stunted.
As well as being treated with an anthelmintic, severely affected
animals may require antibiotics if they are fevered and may be
in need of hydration if they are not drinking. The use of finadyne
(flunixin) in severely affected animals will aid recovery.
CONTROL
The only proven and reliable method of preventing
the development of parasitic bronchitis is to immunise all young
calves with the commercially available lungworm vaccines (Huskvac)
prior to their going out to grass for the first time. Both are
irradiated, live, larval vaccines which are given orally to calves
aged two months or more. Two doses of vaccine (1,000 larvae in
each) are given with an interval of four weeks between doses.
In order to allow a sufficiently high level of immunity to develop,
vaccinated calves should be protected from challenge until two
weeks after their second dose. The vaccine should not be given
to calves obviously affected with infectious calf pneumonia.
Although vaccination is effective in preventing
clinical disease, it is not 100 per cent effective against challenge
and small numbers of lungworms may be found in the bronchi of
vaccinated calves. Consequently the pastures remain contaminated
and it is important that all calves should be vaccinated before
going to grass and that a vaccination programme, once undertaken,
must be continued annually. Although these pasture larvae will
effectively boost the immunity of vaccinated calves, they can
produce clinical disease in susceptible animals.
Because of the unpredictable epidemiology of
husk control grazing management alone is not practical.
The use of anthelmintics during the grazing
season as a means of ‘immunisation* i.e. hopefully allowing
calves to become exposed to only small numbers of lungworm larvae
is also hazardous and cannot be recommended. For example, the
dose and move method used for ostertagiosis has been clearly shown
not to prevent calves developing clinical parasitic bronchitis.
Also, the various other control measures for ostertagiosis, which
rely on strategic treatments such as ivermectin at 3, 8 and 13
weeks post turnout and doramectin at turnout and 8 weeks later,
or on the use of sustained or pulse release boluses at turnout,
are not necessarily completely reliable in preventing parasitic
bronchitis.
Using some of these techniques, calves are extremely
unlikely to develop parasitic bronchitis although occasionally
disease may occur at the end of a long grazing season. Also provided
they have been exposed to sufficient lungworm infection they will
acquire a degree of immunity which will protect them during subsequent
years.
HUSK IN SINGLE-SUCKLED CALVES
The importance of husk in this type of animal
appears to be on the increase as an increasing number of beef
cows calve down in the autumn.
Calves born in August and September are usually
weaned during May and June and from weaning until they are housed
or sold in October/November, they are likely to be exposed to
infection with D.viviparus larvae. Clinical disease may become
evident around September/October around the time the calves are
sold at the autumn calf sales and parasitic bronchitis can be
an important complicating factor in cases of Transit Fever. Spring-born
single suckled calves which are grazed with their dams until they
are housed or sold do not commonly develop severe clinical parasitic
bronchitis. However, coughing as a result of a mild D.viviparus
infection is common.
Treatment is similar to that described for dairy
calves. If husk is a problem, both spring and autumn born single
suckled calves can be vaccinated successfully at grass provided
the vaccine is given prior to their encountering a significant
larval challenge in spring or early summer.
HUSK IN ADULT CATTLE
This is relatively uncommon although there appears
to be an increasing incidence in recent years, especially in dairy
animals.
The patent form of the disease is by far the
most commonly encountered although the prepatent and postpatent
forms have also been recognised. The most common presenting sign
in lactating females is a reduction in milk yield together with
the onset of breathing problems.
For adult cattle to develop husk, they must
have been shielded from a significant natural challenge for several
grazing seasons. Clinical disease results when such animals are
exposed to a significant larval challenge e.g. when cows or heifers
are put onto a field where calves suffering from clinical husk
have grazed previously.
Individual cows can also develop husk by encountering
a massive challenge e.g. while being kept in the calf paddock
or run with calves, because they are due to calve or they require
daily attention or treatment.
The drugs available for treatment are similar
to those discussed for calves but in selecting a drug for adult
dairy cows one must consider the withdrawal period for milk intended
for human consumption.
THE RE-INFECTION SYNDROME IN HUSK
This form of the disease is relatively common
as a mild syndrome, but much less frequent as a severe syndrome.
When a partially immune animal is suddenly exposed
to a massive larval challenge, significant numbers of larvae may
reach the lungs and migrate to the bronchioles where they are
simultaneously killed by the animals own immune response.
The mild syndrome is characterised by frequent
coughing and slightly increased respiratory rate.
In the severe syndrome, lactating dairy cattle
have a marked reduction in milk yield and increased rate and depth
of respiration.
This form of the disease can also occur in younger
cattle such as vaccinated calves or second year stirks and adults
which have acquired immunity either through vaccination or/and
natural infection, when they are exposed to a massive larval challenge.
The source of this larval challenge is often a heavily contaminated
field on which calves suffering from clinical parasitic bronchitis
have grazed during the previous year. The following year the vaccinated
calves, second year stirks or adults when exposed to these large
numbers of larvae may develop clinical signs of the reinfection
syndrome.
Treatment is as described for husk in adult
cattle.
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This condition develops when the skin becomes
sensitised to certain wavelengths of sunlight by the presence
of specific photodynamic agents within the tissue. Photodynamic
substances absorb energy from light, and the cells in the exposed
tissues are severely damaged as a result. There are two major
types of photosensitisation; primary, in which the photodynamic
substance is absorbed intact from the alimentary tract; secondary,
in which the photosensitisation is secondary to a disease of the
liver. A third form of photosensitisation can result from contact
of the skin with certain types of plant sap.
Some plants, such as St. John*s wort (Hypericum
perforatum), buckwheat (Polygonum fagopyrum) and wild carrot (Cynopterus
spp), contain photodynamic substances, which cause primary photosensitisation.
Some chemical compounds are also photoactive. Secondary photosensitisation
follows the effects of the mycotoxin produced by the fungus Pithomyces
chartarum or ragwort poisoning.
CLINICAL SIGNS
It is the non-pigmented thin-skinned areas of
the body with poor hair cover which are affected. Lesions are
often seen on the head and ears, along the neck and back, and
if the animal is lying down the udder and teats may be affected.
Affected animals are quite distressed and inappetent.
Initially, there is severe swelling and oedema of the white parts
of the head and ears, the latter being very pendulous due to their
increase in weight. The eyelids, face and lips also become swollen.
There appears to be severe irritation and affected animals frequently
rub themselves on objects in an attempt to alleviate the irritation
with further self-inflicted trauma. Serous exudation through the
skin occurs and this dries to form yellow crusts or scabs. This
acute inflammation is followed by death and sloughing of the affected
skin, often leaving the ears dried, twisted and withered. Regeneration
of the skin may take several weeks.
Removal of the animal to shaded, cool, and well
ventilated housing will prevent further damage to the skin, treatment
to prevent fly strike and antibiotics to control secondary infection
may be needed. If the animal has a genetic predisposition to the
disease, or suffering from liver failure then the prognosis is
poor.
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This disease is a pneumonia caused by Pasteurella
species. Weaned suckled calves are usually affected soon after
they have been housed.
AETIOLOGY
Pasteurella haemolytica biotype A serotype 1
(Al) represents about 75 per cent of the organisms isolated from
cases in Britain although P.haemolytica A2 (10%) and P.multocida
(10%) have also been found in the respiratory tracts of pneumonic
animals.
EPIDEMIOLOGY
The incidence is highest in newly purchased,
weaned, suckled calves from September to December when the majority
of the calf sales occur. Consequently, the disease is seen predominantly
in the northern and eastern areas of Britain on fattening beef
farms. However, severe outbreaks with fatalities have also been
confirmed in homebred, suckling beef calves housed with their
dams as well as in milk fed and weaned dairy cross calves. Respiratory
signs almost invariably develop within 4 weeks of suckled calves
being housed (75% within 14 days) and, once the initial incident
has passed, further group pneumonic episodes are uncommon.
CLINICAL SIGNS
Many outbreaks are called ‘transit fever*
because they develop in cattle which have only been on the farm
for a short time. Individuals are first seen to be standing alone
and not eating. In severe incidents, the food intake of the whole
group can suddenly decrease markedly. Occasional coughing may
be heard, but frequent coughing is rare. Breathing difficulty
and a nasal discharge may be common in the group, conjunctivitis
and ocular discharge have only been seen when IBR is also involved.
The morbidity and mortality rates vary greatly
from group to group and from year to year. In a study involving
2026 weaned suckled calves the morbidity rate was found to be
11 per cent and the mortality rate less than 1 per cent.
DIAGNOSIS
The epidemiological findings and the clinical
signs are usually sufficient although post mortem findings, when
available, will confirm the diagnosis. In early stages of the
disease, Pasteurellae species can frequently be isolated in pure
culture from nasopharyngeal swabs.
TREATMENT
P.haemolytica is susceptible to the penicillins,
oxytetracycline and trimethoprimsulphonamide and other broad-spectrum
antibiotics. P.multocida has a similar susceptibility pattern.
Long acting antibiotic preparations are very useful since they
obviate the need for daily handling.
The prognosis is good provided treatment is
given during the early stages of the disease.
CONTROL
It is not possible to prevent the development
of pneumonic pasteurellosis but physical stress factors should
be minimised in newly purchased, weaned, suckled calves. If such
animals are kept outside for as long as possible (at least 2 weeks)
before being housed, then the prevalence and severity of the disease
should be less. On some units, an injection of long-acting penicillin
is given when the calves are housed and it has been claimed that
this reduces the severity of the disease. Vaccination can be considered.
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Post-parturient haemoglobinuria is a disease
of high yielding dairy cows which occurs within a few weeks of
calving, and is characterised clinically by red urine and marked
reduction in milk yield.
PREVALENCE
Post-parturient haemoglobinuria affects only
dairy cows particularly those which are high yielding. It is rare
in young animals and is usually seen in cows which have had at
least three calves. The majority of cases occur around three weeks
post-calving (range 10-40 days post-calving).
In most countries the peak incidence of the
disease is during the later winter (i.e. January to March) but
in the U.K. it has also been observed in the early summer (May
and June) when pasture conditions have been poor. Although outbreaks
can occur, with each successive calving cow of the correct age
being affected, the usual situation is that only one or two animals
show clinical signs.
CLINICAL SIGNS
Red blood stained urine is usually the first
clinical sign, but this is rapidly followed by inappetance and
a marked drop in milk yield which may be the first signs recognised.
Initially the animal becomes pale but jaundice soon becomes evident.
The jaundice is frequently severe. There is marked effects on
the cardiovascular system. Constipation is usual and any faeces
which are passed tend to be dark in colour and covered in mucus.
Fever is not a feature. Affected animals are dull and extreme
weakness with a staggering gait is common. Recumbency often ensues.
If death occurs then it usually does so within
the first 36 hours of the appearance of clinical signs. The mortality
rate is variable, but as many as 60% of affected animals can die.
Those which do not die start to show obvious signs of recovery
within 5-7 days. Recovery is usually complete within 3 weeks but
full milk yield is seldom attained.
DIAGNOSIS
Diagnosis is based on history, clinical signs
and where necessary laboratory findings from blood tests..
TREATMENT
Where possible transfusion of blood should be
performed. However, it should be remembered that other cows on
the farm may be anaemic although not showing obvious clinical
signs and thus the donor animal(s) should be carefully selected.
The possibility of transmitting other diseases by blood transfusion
should be considered.
Phosphorus salts can be administered as a solution
subcutaneously, intramuscularly or intravenously. Compound preparations
containing calcium, magnesium and phosphorus contain phosphate
salts at a much lower concentration than Foston.
Supplementation of diet with bone meal.
PREVENTION
If animals are fed an adequate concentrate supplement
then the condition will be virtually eliminated. Supplementation
of the diet with phosphorus, e.g. by use of bone meal.
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This is a relatively common condition which
develops following the spread of a large number of septic emboli
(blood clots) from a thrombus in the caudal vena cava and it can
present as either a sudden onset or an insidious onset breathing
disorder.
This occurs as a clinical condition mainly following
thrombosis of the caudal vena cava. Thrombosis of the caudal vena
cava usually occurs in the part of the vein adjacent to the liver.
In most cases, this results from a liver abscess. In addition
to seeding the lungs with emboli, the hepatic veins can become
obstructed to produce chronic venous congestion of the liver with
a palpably enlarged liver.
EPIDEMIOLOGY
This syndrome is mainly seen in immature and
young adult cattle (1-3 years old). It occurs in beef and dairy
animals all the year round and all over the country.
CLINICAL SIGNS
The disease is detected initially in three forms.
(i) Animals found dead in a pool of blood having
bled through its respiratory tract. Previous signs of disease
having almost invariably not been observed.
(ii) In the vast majority of cases there is
a history of respiratory disturbance which in half the animals
will have been present for only a few days while in the other
half it will have been present for several weeks or months with
weight loss and coughing and also perhaps with acute pneumonic
incidents. Those in which the clinical syndrome has apparently
developed suddenly tend to deteriorate rapidly. The main clinical
signs are similar to those of a chronic suppurative bronchopulmonary
disease but there is usually a disproportionate degree of chest
pain which is most obvious when the animal is made to walk. Some
cases have marked thoracic pain even at rest. A variable degree
of dullness, reduced appetite and fever are also present. Palpable
enlargement of the liver can usually be detected at this stage.
Bleeding from the nose develops sooner or later and may be seen
as blood splashing around the affected animal or as clots of bright
red arterial blood hanging from the animal*s nostrils and mouth.
This sign is characteristic of pulmonary thromboembolism as a
result of thrombosis of the caudal vena cava. Following this,
the animal*s condition usually deteriorates rapidly; the amount
of thoracic pain increases. Most cases die from a massive bleeding
within two weeks of their first being seen to cough blood.
A few animals can develop signs of heart failure.
DIAGNOSIS
The development of a sudden or insidious onset
chronic respiratory condition with widespread squeaks and chest
pain should indicate possible pulmonary thrombo-embolism especially
if the animal is anaemic even although bleeding has not been observed.
Once the animal has been seen to cough up blood.
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The precise definition of pyelonephritis is
inflammation of the kidney. Normally secondary to infection.
AETIOLOGY AND PREVALENCE
In cattle, pyelonephritis is a common condition,
although sporadic in occurrence, which is almost entirely confined
to mature cattle, particularly cows, and is caused by Corynebacterium
renale. Occasionally the initial, acute, episode is severe enough
to lead to renal failure but more commonly it is a chronic, relapsing
condition and the acute phase may pass unnoticed. The economic
importance of the disease at present is unknown.
It is generally agreed that pyelonephritis is
basically an infectious and contagious disease but that there
are subsidiary aetiological factors since intact and healthy urinary
tract relatively resistant to infection. These subsidiary factors
may include trauma (e.g. service, calving) or a degree of urinary
obstruction.
CLINICAL SIGNS
There are two forms of the disease, i.e. acute
and chronic:
Acute pyelonephritis
Abdominal pain is one of the major features
of acute pyelonephritis. The animal is dull, anorexic, stands
with its back arched, frequently shifts its stance, and may periodically
kick at its abdomen. There is straining and frequent passing of
small quantities of urine which is discoloured, containing blood,
pus and tissue debris. Fever is common.
Chronic pyelonephritis
If the animal does not die in the acute phase
then it may progress to the chronic form of pyelonephritis. Chronic
pyelonephritis can, however, develop without any apparent acute
phase.
In chronic pyelonephritis there is loss of condition
and a fall in milk yield over a period of weeks, during which
there are bouts of fever and inappetance. The frequency of urination
is increased and may be accompanied by straining. The urine is
turbid, containing pus, tissue debris and frequently small clots
of blood.
DIAGNOSIS
Confirmation of diagnosis in early cases is
based on examination of the turbid, blood-stained urine from which
the organisms may be isolated. In later cases, the enlarged kidneys,
distended ureters and thickened bladder may be recognised per
rectum. The post mortem findings are characteristic.
TREATMENT
The use of large doses of penicillin for a week
or more have been said to produce complete cures in some cases.
Usually, however, there is irreparable kidney damage when the
condition is diagnosed and, although treatment can produce a temporary
improvement, relapse is the rule. Also, it should be remembered
that remission does occur in untreated animals.
CONTROL
Surveys of dairy herds have indicated that a
percentage of apparently healthy cattle harbour C.renale in the
vagina. This may be as high as 23% in herds where cases of pyelonephritis
have been recognised. There is evidence to suggest there is dissemination
of the organism to close neighbours in tethered cattle. C.renale
has also been isolated from the urine of healthy cattle and the
penile sheath of bulls.
Control measures would include general hygiene
and removal of clinical cases.
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Rape and Kale poisoning occurs when excessive
amounts of these fodder crops are ingested by cattle and is characterised
clinically by red blood stained urine.
PREVALENCE
The incidence is generally low but several cases
may occur within an individual herd. Lactating cows, particularly
those which are recently calved and lactating heavily, are usually
affected but the condition has also been described in bullocks.
EPIDEMIOLOGY
Rape and kale are used as fodder crops during
the autumn and early winter and thus the disease is seen at this
time. Outbreaks of poisoning have been associated with frosting
of the plants but this is probably related to an increase in the
toxic factor (see below) in the plant as it ages. Wet, cold weather
has also been suggested as a factor influencing occurrence of
the disease.
AETIOLOGY AND PATHOGENESIS
Rape and kale contain a toxic compound, 5-methylcysteine
sulphoxide (SMCO), which is metabolised by the rumen, absorbed
and directly or indirectly causes breakdown of the blood cells.
As the amount of SMCO in the plant increases with ageing, the
plants are most toxic once flowering and secondary growth occurs.
It should also be noted that different varieties of rape and kale
contain varying amounts of SMCO.
CLINICAL SIGNS
These are very similar to the signs seen in
post-parturient haemoglobinuria. There is red blood stained urine,
inappetance and a marked drop in milk yield. Pallor and moderately
severe jaundice develop. Other clinical signs of anaemia are evident.
Diarrhoea is a common feature. Fever is rare. Deaths may occur.
Diagnosis is based on clinical signs and history.
Blood tests may be of use.
TREATMENT
Cease feeding of rape or kale. Where considered
necessary blood transfusion may be performed on individual animals.
However the donor should be selected carefully as apparently normal
animals may be in the early stages of the disease. Reintroduction
to the rape or kale should be gradual and intake should be restricted.
PREVENTION
Use rape and kale as fodder before flowering
and secondary growth occurs when the plants are most toxic. Strip
grazing of rape or kale is usual practice but should be carefully
controlled as the toxic effect of these plants is directly related
to the amount consumed. It has been suggested that adult cows
should be limited to 15-20 kg kale per day.
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(Ringworm)
DEFINITION
A superficial skin disease usually lasting no
more than 6 months.
AETIOLOGY
Usually Trichophyton verrucosum or Microsporum
canis.
PREVALENCE
Ringworm is very common. Some self-contained
herds are free. It occurs mainly in calves but is occasionally
seen in adults. There is greater opportunity for spread when animals
are housed in winter, but it occurs all the year round.
TRANSMISSION
Direct or indirect contact. Infected premises.
Buying in calves. Rarely from man to cattle.
CLINICAL SIGNS
Lesions are most common around the eyes and
at the base of the ears. Neck, back and perineum are often affected
but lesions are uncommon on the lower limbs.
The first sign of cattle ringworm is a palpable
thickening of the affected skin. Next, the overlying hair pattern
is disturbed. As infection progresses and inflammation develops
the bases of hairs become matted with a light coloured exudate
and eventually asbestos-like crusts, grey or fawn in colour, develop.
The lesions may be present singly or coalesced into groups. They
are usually rounded and discrete, less often diffuse and confluent.
They are somewhat itchy. Hairs generally break off at the surface
of the lesion. Mechanical removal of the crust of an active lesion
reveals moist red skin and the crust later reforms.
The fungus invades the keratin of the hair follicle
and the hair shaft just above the bulb. Secondary bacterial infection
may follow. The immunity produced is not solid.
EPIDEMIOLOGY
While other species (including man) can be infected,
cattle are important as the reservoir for T. verrucosum. The fungus
can survive for years off the animal.
DIAGNOSIS
The classical mature lesion of cattle ringworm
is clinically diagnostic. Rarely, however, atypical lesions occur,
e.g. scaliness and hair loss only.
Certain stains can be diagnosed by there ability
to fluoresce under an ultraviolet light. Microscopical examination
or fungal culture can confirm the diagnosis.
TREATMENT AND CONTROL
Griseofulvin is no longer available in a form
for farm use as a feed additive. The license has been withdrawn.
The small dosage and short course recommended by the manufacturer
were not very effective in severe cases. More effective was 20mg
active principle per kg body weight daily for 14 days. Although
this involves using griseofulvin outwith the data-sheet recommendations
and appropriate withdrawal periods would be required.
Topical antifungal applications include natamycin
and eniconazole. These preparations may be more useful for individuals
or small groups of animals due to time taken to apply fluids topically
but the nil milk (and meat) withdrawal periods may be advantageous.
Evaluation of any treatment in clinical trials
is made very difficult by the spontaneous regression of the lesions
which occurs without treatment, especially alter animals are turned
out to grass in the spring. A vaccine against ringworm caused
by T.verrucosum has been marketed. The attenuated vaccine is given
from 2 weeks of age and is repeated 10-14 days later, alter which
no subsequent booster doses are required.
Sterilisation of premises is near impossible.
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Bovine renal amyloidosis is a condition of adult
cattle in which deposition of amyloid protein in the kidney results
in a disease characterised clinically by profuse diarrhoea, subcutaneous
oedema and renal enlargement.
PREVALENCE
Amyloidosis is a sporadic disease of middle-aged
to old cows i.e. more than 5 years old. From the relatively small
number of cases examined, the disease occurs most frequently in
dairy cows, often becoming clinically evident shortly after parturition.
CLINICAL SIGNS
The first feature noted by the owner is the
sudden onset of profuse diarrhoea which is followed by the appearance
of subcutaneous oedema. Occasionally, the owner may have noted
that the cow has been drinking excessively.
On initial presentation, most of the cases seen
are thin but the majority are bright without fever, and with a
relatively good appetite. The most significant clinical findings
are:
a persistent homogeneous, profuse diarrhoea
sometimes containing considerable quantities of mucus
subcutaneous oedema which occurs in the submandibular, presternal
and ventral abdominal wail areas
renal enlargement which is readily detected by palpation of the
left kidney per rectum.
Amyloid is also deposited in the gastrointestinal tract in some
cases and this can make the rectal mucosa extremely friable. In
such animals, rectal examination may cause quite severe bleeding.
Other clinical findings are marked depression
of milk yield and progressive loss of weight. Increased water
consumption often occurs, daily intake ranging from 30 to more
than 50 litres (normal, adult, non-lactating cattle of dairy breeds
may drink up to 25 litres/day). In a proportion of cases, a septic
focus e.g. chronic mastitis or chronic suppurative pneumonia,
will be evident on general physical examination.
Once the clinical signs become evident, the
disease is of relatively short duration, (usually 1-2 weeks, exceptionally
up to 1 month). Terminally, the animals become dull, inappetent,
thin, very weak and recumbent. A few cows remain bright and continue
to eat even when recumbent.
Amyloidosis can occur apparently as a complication
of certain longstanding disease processes e.g.
Chronic infections
Chronic inflammatory disease (arthritis)
Tumours
Primary amyloidosis in which systemic amyloid deposition occurs
in the absence of any predisposing factor or disease.
In cattle, many cases of amyloidosis do have
coexisting chronic septic or inflammatory foci and in the past
many cases were associated with tuberculosis. However, in a significant
proportion of animals, no predisposing disease can be found.
DIAGNOSIS
The clinical signs axe sufficiently characteristic
to give an accurate diagnosis, but a post mortem examination will
confirm.
TREATMENT
There is no effective treatment. Affected animals
should be slaughtered.
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Infection with a number of serotypes of Salmonella
spp. may give rise to a syndrome in which fever, diarrhoea (frequently
with dysentery) and deaths occur in both calves and adults but,
on occasions, in pregnant cows abortion may be the only overt
clinical sign. The disease in cattle is a source of infection
for man.
AETIOLOGY
S.dublin and S.typhimurium are the most common
causes of bovine salmonellosis in Britain. Many other serotypes
can cause disease. It should be remembered that all salmonellae
may become pathogenic under the right conditions.
INCIDENCE
Salmonellosis is an important disease of cattle
in Britain and throughout the world. The cost to the agricultural
industry is not known but it has been claimed to be of major importance
to calf rearers and is currently the second most commonly diagnosed
cause of bovine abortion.
CLINICAL SIGNS
Salmonellosis can affect cattle of all ages
but it is most frequently seen in adult cows and calves. The clinical
signs for all serotypes are similar.
Adult cattle: Initially, in acute salmonellosis,
there is rapid onset dullness and marked fever (40-41.50C) with
inappetance and a dramatic drop in the milk yield of affected
(dairy) cows. A severe diarrhoea ensues with foetid watery faeces
which may contain blood, mucus and shreds or casts of necrotic
bowel epithelium. Presumably as a result of this latter feature,
abdominal pain is often noticed. Some
Calves: Calves of any age can be affected but
it most frequently occurs between 2-8 weeks of age. The median
age for S.dublin outbreaks is 4 weeks and for S.typhimurium it
is 3 weeks.
Clinically the affected calves are very dull
with marked lethargy. Unlike calves affected by colibacillosis
which may continue to consume milk even when recumbent, calves
with salmonellosis are usually completely inappetent. There is
a marked fever, often as high as 41.50C with a profuse, evil-smelling
diarrhoea. There may or may not be dysentery. Affected calves
rapidly lose condition, become very weak, unable to stand and
emaciated. Death occurs within 2-3 days of the development of
clinical signs and the mortality can be as high as 30% and occasionally
higher. In non-treated survivors the diarrhoea may persist for
up to 2 weeks.
Following infection with S.dublin the development
of gangrene-like lesions and osteitis of the extremities has been
described with sloughing of the ear-edges, the tip of the tail
and even the distal extremities of the limbs.
PATHOGENESIS
Infection usually occurs by the oral route.
The source of organism is usually the faeces of an infected animal,
whether clinically affected or a faecal carrier, although infected
milk, uterine discharges and products of abortion may be important
where infection occurs in adult cattle. Following ingestion, the
organism may multiply within the gut. The organisms multiply within
the gut wall and from there disseminate to the systemic circulation.
Multiplication in the liver and blood stream gives rise to a septicaemia.
The ability of Salmonella spp. to produce diarrhoea is largely
associated with the invasion of the gut wall and the inflammatory
reaction. In recovery the organism may become localised in joints,
the foetus to give abortion, in the gall bladder or in other organs.
Adult animals which have recovered from S.dublin infection may
continue to excrete the organism in the faeces for several months
(perhaps for life). Those which have recovered from S. typhinurium
infection cease excreting organism after 6-14 weeks. Calves which
have recovered normally cease to excrete the organism after a
few weeks.
It is suggested that intercurrent disease such
as fascioliasis (liver fluke)
may predispose to infection.
EPIDEMIOLOGY
Host range. S.dublin infection does occur in
species other than cattle but is primarily an infection of cattle.
S.typhimurium can infect a wide variety of species and infections
may originate from any of these including wild life.
SOURCES OF INFECTION
Although there are many possible ways by which
susceptible cattle may acquire salmonella infection, the overwhelming
evidence suggests that infection is most often acquired from other
cattle which are excreting the organisms. For clinical disease
to be established in cattle it would seem that challenge has to
be relatively high.
1) Infection from other cattle. As stated above
this is the most important source of infection with S.dublin and
S.typhimurium. Infection may be introduced into a population of
cattle either by the purchase of an adult carrier or by mixing,
in market or in transit, with clinical or pre-clinical cases.
Infection may pass from adults in a herd down to the calves or
vice versa. Congenital infection of calves born at full-term does
not appear to occur, but those calves born to cows which are faecal
excretors almost invariably become infected either at parturition
or soon after birth. Intensive husbandry systems, especially loose
housing, have facilitated the spread of salmonella infection.
2) Infection from contaminated foodstuffs and
water. Although the infection rate of cattle food constituents
(e.g. bone, meat and blood meals and milk powders) can be high,
surveys of the end-products (cattle and calf cakes or pellets)
have shown a low incidence of infection and low counts of organisms.
The change to loose-housing has been associated
with an increase in the volume of slurry for disposal. S.dublin
may survive for up to 30 weeks in winter slurry, but the survival
time on grass after being spread is much shorter. Survival in
soil cores may be as long as 24 weeks. The recommendation to reduce
the risk of spread of infection via slurry is: (1) storage of
slurry for a minimum of 4 weeks; (2) pasture should not be grazed
until 4 weeks after slurry spreading. There is at least one recorded
outbreak of salmonellosis due to S.typhimurium occurring after
slurry was spread on fields at a much higher rate than normal.
Outbreaks of salmonellosis have been attributed
to cattle drinking contaminated water, effluent from knackeries,
contamination of fields due to sewage overflow, or sewage sludge.
3) Infection from other domestic animals (and
man). Few instances are recorded and often the primary source
of infection is unknown. However, it is recorded that on a few
occasions, Salmonella typhimurium infection has passed to cattle
from chickens, ducks, geese, pigs and humans.
4) Infection from wild animals. Rats may allow
a farm infection of S.typhimurium to persist. Only low infection
rates in British farm rats have been recorded although in one
case infected rat droppings in old hay were found to be the source
of infection for beef cattle. Sparrows, starlings and seabirds
have also been found to S.typhimurium rarely remain infected for
any length of time and excretion of the organism usually only
occurs for a few weeks.
Some animals which have recovered from S.dublin
infection may become intermittent excretors. Animals which merely
ingest the organism and excrete it in the faeces without becoming
infected are referred to as passive carriers.
DIAGNOSIS
In calves, time of onset (3-4 weeks of age),
the clinical signs of the disease - fever, depression, diarrhoea,
sometimes with the presence of blood, the post-mortem findings
and a history of recent purchase through markets may suggest a
diagnosis of salmonellosis. In adults the clinical signs are also
suggestive. Diagnosis must, however, be confirmed by the isolation
of the organism.
TREATMENT
Affected animals should be treated by both the
parenteral and oral routes with an antimicrobial drug. This is
possible in calves but in adult ruminants many such drugs may
disturb rumen flora if given orally. The same drug or class of
drug e.g. an aminoglycoside should be given parenterally and by
mouth as far as possible. Ampicillin, trimethoprim/ sulphonamide
combination, neomycin, spectinomycin, enrofloxacin and sulphonamides
are all available in injectable and oral forms. With drugs which
can be absorbed from the gut, injections need only be given initially.
Compounds available for oral dosing also include furazolidone
and may be given as boluses, from oral dosers, or as soluble products
for administration in drinking water or milk.
The drug of choice may be ampicillin, amoxycillin,
enrofloxacin, trimethoprim/ sulphonamide (destroyed in functioning
rumens) neomycin or furazolidone in that order. Antibiotic sensitivities
of the salmonellae involved should be taken into account if treatment
is unsuccessful or in continued outbreaks.
Calves do not usually become carriers following
treatment but adults may, and disposal of adult cases to a secure
rendering plant should be considered.
Careful nursing and management of individual
calves is of great importance and the animals should be kept under
lamps, turned regularly and fed several times daily until they
improve. It is important to impress upon the person in charge
of infected animals, adults or calves, the possibility of spread
occurring to himself and his family and strict hygiene measures
must be observed.
Prophylactic (oral) use of antibiotics should
be discouraged as in most cases low levels of antibiotics have
no effect on the excretion pattern of salmonellae. Indeed it has
been shown in man that with non-invasive salmonellosis, antibiotics
significantly increase the excretion period of the organism in
the faeces.
CONTROL
Vaccines
Currently only multicomponent dead vaccines
are available in the U.K. e.g. Bovivac (Hoechst). High serum concentrations
of absorbed colostral immunoglobulins aid survival and reduce
the severity of alimentary disturbance in calves with salmonellosis
but, unless specific antibody to Salmonella is present cannot
prevent infection.
Control measures which should be instituted
during an outbreak of salmonellosis
Isolation of clinical cases to reduce
the weight of contamination.
Recovered animals should be retained in isolation for at least
2 weeks after the cessation of diarrhoea.
Carcasses of fatal cases should be sent to knackeries capable
of producing salmonella-free products.
Ideally, adult clinical cases of S.dublin infection should be
slaughtered as recovered animals invariably remain persistent
excretors.
Clinical cases should never be sent for emergency slaughter intended
for human consumption.
Treatment of effluent in such a way as to minimise contamination
of environment.
Following an outbreak the premises should be thoroughly cleaned
and disinfected.
Restrict movement of animals either on to or off farm until final
disinfection has been carried out.
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(wire)
DEFINITION
Traumatic reticulitis is characterised by the
sudden appearance of some or all of the following signs: dullness,
anorexia, milk drop, fever, abdominal pain and intestinal stasis.
INCIDENCE
The condition is almost exclusively a disease
of adult cattle and is relatively common. It is usually a sporadic
problem of individual cattle although occasionally farmers may
experience several cases within a short period, presumably as
the result of heavily contaminated fodder. There are reasons for
believing that traumatic reticulitis occurs far more commonly
than is generally recognised. Chronic reticular adhesions are
a very frequent finding in old cows at slaughter.
AETIOLOGY
Clinical signs arise as the result of penetration
of the reticular wall by a foreign body; usually the foreign body
is metallic (a nail or a wire) but sometimes nonmetallic objects
such as stiff broom-bristles or sharp pieces of plastic may be
involved. Usually, a foreign body which penetrates the reticular
wall measures about 7-8 cm long.
PATHOGENESIS
Foreign bodies are most commonly ingested with
hay or silage and many produce no obvious signs or at most, a
transient discomfort. However, when more serious problems do arise,
the foreign body most frequently penetrates the stomach wall,
presumably after it has been trapped by the honeycomb-like folds
of the lining. Subsequent events appear to depend on the extent
to which infection spreads following penetration. In certain cases,
infection may be limited to the reticular wall (reticular abscesses)
while in others there maybe infected tracts with overlying reticular
adhesions; in very severe cases, penetration and infection may
give rise to widespread peritonitis and/or lesions in the spleen,
liver or heart.
CLINICAL SIGNS
This is usually of a sudden onset illness associated
with often complete anorexia and a marked drop in milk yield in
the case of lactating cows. Observant owners may also notice an
abnormal stance or gait, no faeces, a degree of ruminal tympany
and an expiratory grunt.
In the early stages of traumatic reticulitis
(i.e. within the first two days or so) the cow will be rather
dull, showing little interest in food and not cudding. If passed,
faeces will be very much reduced in quantity, dark-coloured and
hard. At this stage, animals usually prefer to stand, and moreover,
to stand with their hindfeet at a lower level than their forefeet
(in tethered cattle this results in an obvious preference for
them to stand with their feet in the grip or gutter). An occasional
animal will be down and if this does occur, other signs of abdominal
pain which may only have been mild while standing (and, in particular,
an expiratory grunt) will often become much more obvious. In addition,
they stand with elbows outwards, an arched back and an empty,
tucked-up abdomen. Such cases are usually reluctant to move and
when forced to do so, often assume a rather characteristic stiff
("wooden") gait.
DIAGNOSIS
With a good history and a prompt consultation
about an animal which has hitherto been untreated, a confident
diagnosis, based upon the results of a first examination, is usually
possible. Problems arise with poor histories, delays in consultation
and in cattle which have already received some form of medication,
particularly antibiotic therapy.
TREATMENT
So often the approach to a case depends on economic
considerations. Briefly, in early cases, where the diagnosis is
in little doubt and the subject is a reasonably valuable animal,
prompt surgery should be carried out and in such circumstances
the prognosis is good.
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Urolithiasis is the development of stones and
crystals within the urinary tract.
This is a disease of males, usually castrates.
Obstruction, usually caused by a single calculus (stone) is most
common in castrated males. It is especially common in cattle on
high concentrate rations in Britain.
CLINICAL SIGNS
In the early stages the animal shows abdominal
pain, kicks at its abdomen and shifts its weight between feet.
Frequent attempts to urinate are made, often accompanied by teeth
grinding, but little if any urine is passed and may be blood stained.
Examination of the tuft of hairs on the end of the prepuce will
show the presence of sand, a tiny crystalline deposit from the
urine passed before the blockage became total.
If the condition is not noticed the bladder
will rupture and/or the urethra will perforate at the site of
obstruction. This produces relief from the abdominal pain but
following bladder rupture, the abdomen will distend and the animal
become gradually uraemic. Rupture of the penile urethra will cause
accumulation of urine in the subcutaneous tissues of the ventral
body wall.
TREATMENT
The long term prognosis, in spite of treatment,
is poor so if the condition is noticed early and the animal is
fit for slaughter then that is the best option. Affected cases
are often too small or otherwise unsuitable for immediate slaughter
and in these animals surgery can be carried out to clear the obstruction
which has a good short-term prognosis and enables the animal to
be fattened for slaughter. Post operative infection is however
a significant risk.
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Winter Diarrhoea is a highly contagious disease
characterised by a brief attack of severe diarrhoea and sometimes
dysentery which occurs during the colder months of the year.
AETIOLOGY
Current evidence suggests that a coronavirus
is responsible.
PREVALENCE
This disease is quite widespread and has been
reported in North America, Britain, Sweden and Australia. The
disease can be the cause of serious economic loss in dairy herds,
for although the mortality is very low the disruption of milk
production and loss of body condition are important factors
CLINICAL FINDINGS
The disease is most serious in adult milking
cows, particularly those which have recently calved. Young stock
usually only show mild signs but diarrhoea can be present in calves
as well as adults.
The diarrhoea is very profuse, watery, homogeneous
and dark green to black in colour. There is no mucus or epithelial
shreds in the faeces but up to 10% of affected cows may have severe
dysentery. A marked fall in milk yield occurs and this may last
for up to one week. The consistency of the faeces returns to normal
within 2-3 days. Very occasionally an odd cow may develop a very
severe persistent diarrhoea which results in death.
EPIDEMIOLOGY
The disease occurs in housed dairy cattle in
the late autumn, winter, and occasionally spring. In Britain it
most frequently occurs in November, 2-3 weeks after housing. Young,
newly-calved heifers or heifers in late pregnancy are most severely
affected. Older ones are less severely affected and young stock
are unlikely to be affected at all. The disease has a very high
morbidity and it spreads rapidly throughout the adult herd, with
the majority of animals becoming ill within 7-10 days of the first
case. However the disease has normally subsided completely within
2-3 weeks of its initial appearance. The disease is thought to
be introduced to a farm by recently acquired infected cattle or
visitors. The infection of individual animals occurs orally by
the ingestion of either contaminated water or feeding stuffs.
The incubation period is 3-7 days.
DIAGNOSIS is therefore
based on:
- An epidemic occurring during the colder months
when cows are housed.
- A rapid spread of the disease from animal
to animal.
- No consistent rise in body temperature during
the diarrhoeic phase.
- Recovery of the majority of affected animals
within one week.
- No fatalities.
- Confirmation of the presence of coronavirus
in the faeces.
TREATMENT
Most affected animals recover without intervention
although tylosin and nitrofurazone could be used. Occasionally
in severe dehydration, fluid replacement may be contemplated.
CONTROL
Because of the explosive nature of the disease,
effective control measures cannot be recommended. An immunity
which persists for about 6 months is said to occur after a natural
attack but outbreaks seldom recur in the same herd within 2-3
years.
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