Diarrhoea Cattle

In Practice ● JA N UA RY 20 07 9

MAJOR INFECTIOUS CAUSES

RINDERPESTRinderpest is a highly infectious disease of ruminants and is notifiable. It has not been seen in the UK since 1877 and a worldwide eradication campaign has resulted in it being restricted to relatively small areas of Central Africa, the Middle East, and South-western and Central Asia. However, recent unexpected outbreaks of disease, such as bluetongue in northern Europe and the migration of avian flu, show that disease can spread around the

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DIARRHOEA is a relatively common clinical sign in cattle and the most frequent reason for the submission of diagnostic samples from adult cows to veterinary laboratories. There are several infectious and parasitic diseases that manifest primarily as diarrhoea and others in which diarrhoea is one of the features. These must be distinguished from non-infectious, toxic and nutritional causes. A range of laboratory tests is available to the diagnostician, which vary in sensitivity and specificity, factors that should be considered when negative results are obtained. Furthermore, confirmation of the cause of diarrhoea is not always possible in live animals and, in some cases, postmortem examination may be warranted, especially if there are concerns about the health status of the remainder of the herd. This article reviews the causes of diarrhoea in adult cattle, with particular emphasis on the clinical aspects and laboratory tests that will help to establish a definitive diagnosis.

Differential diagnosis of diarrhoea

in adult cattle ARTHUR OTTER AND MICK CRANWELL

In Practice (2007) 29, 9-19

world with the traffic in animals and animal products, and veterinary surgeons should bear this in mind.

Clinical signsRinderpest varies from peracute to subacute, and atypi-cal cases can occur. Generally, there is pyrexia, depres-sion, anorexia, hyperpnoea and tachycardia, reddening of mucous membranes, intense muco purulent lacrima-tion and excessive salivation, necrosis/ulceration and erosion of oral mucosa. Pro fuse haemorrhagic diarrhoea, with necrotic debris and mucus, and severe tenesmus is seen two to three days later. Mortality is high, with

death resulting in eight to 12 days.

Laboratory testsTests are undertaken in dedicated laboratories. Virus detection by antigen cap-ture ELISA, RT-PCR or cell culture techniques is employed. Sero logical meth-ods (competition ELISA and virus neutralisation) are available.

SALMONELLOSISInfection by salmonellae is regularly encountered

Arthur Otter graduated from Cambridge in 1985 and holds a PhD for studies on ovine listerial encephalitis. He has worked for the Veterinary Laboratories Agency (VLA) since 1991, first in the Cambridge and Carmarthen Regional Laboratories before moving to Shrewsbury in 2001. He is a member of the VLA Cattle Group.

Determining the cause of an outbreak of diarrhoea in adult cows requires thorough evaluation of management and feeding practices, as well as the collection of suitable samples from several animals for laboratory investigation

Mick Cranwell qualified from Cambridge in 1972 and subsequently spent eight years in general practice and a year as a large animal intern at the University of Guelph, Canada. He joined the VLA Carmarthen in 1981 and moved to Starcross in 1982 where he has been ever since. He has been a member of the VLA Cattle Group since its inception in 1996.

Key considerations

When investigating cases of diarrhoea, a number of key factors must be considered to help point to a likely differential diagnosis: ■ How many animals are affected?■ Is the condition acute or subacute/chronic in onset?■ Are animals housed or at pasture? ■ Is the condition affecting only adult animals or all age groups?■ Are there any additional clinical signs?■ Are feeding and other management factors involved?■ Is a zoonotic disease suspected?

Diarrhoea is a common presenting clinical sign in adult cattle and can be a diagnostic challenge

In Practice ● JA N UA RY 20 0710

in diagnostic laboratories in the UK, where two serovars – Salmonella Dublin and Salmonella Typhimurium – predominate in cattle. In the 1990s, there was an upsurge in the number of outbreaks of S Typhimurium infection in farmed livestock, chiefly cattle, caused by phage-type DT104, which showed multiple antibiotic resistance. More recently, S Dublin has re-established itself as the predominant isolate.

S Typhimurium outbreaks are not uncommonly asso-

ciated with the purchase of animals. The importation of stock can also be a source of infection with S Dublin; however, in many herds, infection becomes established in chronically infected animals and can remain latent for years without manifesting clinically, before emerging to cause disease again.

Occasional outbreaks with other salmonellae, such as Salmonella Newport, Salmonella Agama and Salmonella Enteritidis, have also been identified.

Surveillance for existing and novel causes of diarrhoea

The possible introduction of a notifiable disease, emer-gence of a novel disease or a significant change in the pat-tern of existing diseases in UK cattle are a major concern and underline the importance of sustained and thorough disease surveillance efforts. Much of the diagnostic and investigative laboratory work on cattle in this country is undertaken at Veterinary Laboratories Agency (VLA) and Scottish Agricultural College Veterinary Services (SAC VS) laboratories. Analysis of data from submissions is an essen-tial part of the ongoing ‘scanning surveillance’, and there are two main databases involved in this process:■ The Veterinary Investigation Diagnosis Analysis (VIDA) database records disease trends in England, Wales and Scotland, and began in 1975. It has regularly been modi-fied with the recognition of further diseases. Its limita-tion, however, is the lack of denominator data.■ Since 1999, the VLA has been using a database, known as ‘Farmfile’, which utilises the increased data provided with laboratory submissions from farms in England and Wales. Disease trends can be compared more accurately by analysis of the diseases as a percentage of diagnosable submissions. In addition to the monitoring of recognised diseases, the Farmfile database enables analysis of those submis-sions received in the VLA diagnostic laboratories where a diagno-sis was not established, for which a ‘diagnosis not reached’ or DNR code is recorded. These are subdivided according to the principal presenting sign (eg, diarrhoea, respiratory disease, nervous disease).

MOST COMMONLY DIAGNOSED INFECTIOUS AND PARASITIC CAUSES OF DIARRHOEA IN ADULT CATTLE IN THE UK

History Clinical signs Diagnostic tests

Salmonellosis Often associated with purchased stock, especially from markets or dealers. Infection with S Dublin can arise in herds after periods of no disease, due to chronic carrier animals

Diarrhoea and/or abortion. Occasionally results in systemic disease, with signs including pyrexia, milk drop, tachypnoea, depression

Bacterial culture using selective media. Serology is not diagnostic, but can confirm exposure

Bovine virus diarrhoea

Usual source of herd infection is the introduction of persistently infected animals, including the purchase of pregnant cows carrying persistently infected calves. Other sources include acutely infected cattle, contaminated equipment and, possibly, sheep

Acute infection is often subclinical, with occasionally severe, rarely haemorrhagic, diarrhoea. In cases of mucosal disease, illthrift, oral and/or coronary band ulceration, and watery, sometimes bloody, diarrhoea may be seen

Virus detection in heparin blood by ELISA or RT-PCR. Virus isolation from blood in cell culture. Serology shows rising titres in acutely infected cattle, while persistently infected animals remain seronegative

Johne’s disease (paratuberculosis)

Initial cases in herds in purchased cows. Subsequent cases in homebred stock

Intractable watery diarrhoea, loss of condition and decreased milk yield

Microscopy on faeces (Ziehl–Neelsen). Faecal culture using selective media. RT-PCR on faeces. Serology

Winter dysentery Usually occurs in housed dairy herds in winter. Up to 100 per cent of the herd, including young stock, may be affected over a short period

Rapidly spreading herd outbreak of diarrhoea – bloody in some herds, watery in others – with associated milk drop. Spontaneous recovery within a few days

Coronavirus ELISA on faeces is rarely positive. Serology shows rising titres in paired samples

Fasciolosis Peak incidence is seen in autumn and winter, but clinical cases can occur throughout the year. Most prevalent in the west of the UK

Diarrhoea, occasionally dysentery. Loss of condition and reduced milk yield. Oedema and anaemia in chronic cases. Can precipitate black disease

Fluke ova detection in faeces by sedimentation or flotation methods. Serology indicative of exposure although may be historical

Gastrointestinal nematode parasitism

Typically seen in first season grazing cattle. Possible in animals reared indoors (eg, bulls) or those previously given ‘blanket’ anthelmintic treatments

Diarrhoea, weight loss, depression, reduced performance

Worm egg count using the McMaster or modified improved McMaster flotation method

Coccidiosis Rare cases seen in dairy cows and heifers, often soon after turnout

Diarrhoea, sometimes profuse, tenesmus and blood staining

Coccidial oocyst count using the McMaster or modified improved McMaster method

Diagnosis not reached

Johne’s disease (positive serology)

Dietary problem

Salmonellosis: Salmonella Dublin

Bovine virus diarrhoea

Salmonellosis: Salmonella Typhimurium

Parasitic gastroenteritis

CoccidiosisMucosal disease

Winter dysentery

Other

Johne’s disease (acid-fast bacteria)

Salmonellosis: other Salmonella species

Fasciolosis

Detailed analysis and monitoring of various age groups of ani-mals is conducted on an annual basis and by season. The pie chart above shows the diagnoses, and submissions where no diagnosis was reached, for VLA submissions in 2005 for adult cattle present-ing with diarrhoea as the main clinical sign, and where reasonable testing was undertaken.


Clinical signsDiarrhoea is the most common presenting sign in cases of salmonellosis, and disease often occurs in freshly calved animals. Several animals can be affected in an outbreak. Infection with S Dublin can result in abor-tions in the same herd, but this is less common in S Typhimurium outbreaks. For both organisms, disease may be seen in calves and other species on the same premises. Zoonotic disease can also occur, not uncom-monly with S Typhimurium but rarely with S Dublin. S Typhimurium chiefly causes gastrointestinal signs in cows and calves, but S Dublin can potentially cause pneumonia, polyarthritis, meningitis, osteomyelitis, tail and ear tip necrosis, or any combination of these signs, in affected calves. Septicaemic disease is rarely encoun-tered in adult cattle. The number of affected animals varies from single cows to widespread cases in some outbreaks, particularly if animals are crowded. Mortality rates in adults are low, compared with calves, although occasional outbreaks can be associated with the deaths of several cows.

Laboratory testsThe diagnosis of salmonellosis is relatively straightfor-ward and there are a number of selective media that are employed to culture the bacteria. Brilliant green agar and selenite broth are routinely used in the Veterinary Laboratories Agency (VLA). Slide agglutination testing groups the isolates, which are then serotyped at a VLA reference laboratory. Additionally, sensitivity to a panel of 16 antimicrobials is determined for all isolates for the purpose of epidemiological surveillance.

Under the Zoonoses Order 1989, all isolates from food-producing animals in England and Wales must be reported to the local nominated officer, who is usually a senior veterinary investigation officer in the VLA, and to the local divisional veterinary manager (DVM) for isolates in Scotland. The relevant health authorities are also informed.

Problems with laboratory diagnosis by bacterial cul-ture arise occasionally if animals have received anti biotics prior to sampling or in those with chronic infections.

Serology is also available for S Typhimurium and S Dublin, but is of no value diagnostically other than for the detection of S Dublin in chronically infected herds.

BOVINE VIRUS DIARRHOEA AND MUCOSAL DISEASEBovine virus diarrhoea virus (BVDV) infection of naive animals (ie, ‘acute’ BVD) is usually asymptomatic or

associated with mild, often unnoticed, diarrhoea. A more severe, and sometimes fatal, enteritis occasion-ally occurs. The most damaging economic effects of infection are seen in pregnant cows, which may abort or produce persistently infected (PI) animals. PI animals are the chief source of infection, excreting BVDV con-stantly throughout life. They usually develop mucosal disease, a fatal form of illness, which occurs most often between the ages of six and 24 months, but can be seen in younger calves and in older animals. Disease is usually encountered in herds following contact with BVDV-infected stock, and often after the purchase of PI animals, although some infections are presumed to have been introduced by acutely infected animals, or pregnant cows carrying a PI fetus.

Clinical signsMost infections in naive cattle cause no or only mild diarrhoea, with few other recognisable clinical signs of illness. A transient reduction in milk production and appetite may occur. Cows in the first trimester of preg-nancy undergo embryonic loss or abortion, while there are more variable outcomes in mid-gestation; infection is usually asymptomatic in late pregnancy. Infection in the first trimester may also result in persistent infection of the fetus. Acute BVDV infection occasionally causes a more severe disease characterised by profuse diarrhoea, which is occasionally blood-tinged and dysenteric termi-nally, pyrexia, agalactia and weight loss. Erosions may be detectable on the oral mucous membranes, but these are usually small and easily missed. Mortality can reach 10 per cent.

Mucosal disease occurs in PI animals when, it is believed, there is a mutation of non-cytopathic BVDV to a cytopathic variant. PI animals fail to respond immu-nologically and affected animals suffer an overwhelm-ing BVD viraemia and invariably die or are euthanased. Illthrift may be recognised in some PI animals, but oth-ers are indistinguishable from their cohorts. Disease is characterised by usually profuse, watery and intractable diarrhoea, weight loss and depression. Oral/nasal ero-sions and ulceration are more common and more severe than with acute BVDV infection, although not present in all cases. Ulceration of the coronary bands and interdig-ital tissue, usually affecting all feet, may also be seen, and can be the predominant lesion in some animals. Several animals will usually be affected in a cohort over a period of a few months. Clinical disease begins suddenly and animals may be affected for two to three weeks before death occurs.

Postmortem appearance of the intestine of a cow with haemorrhagic enteritis caused by acute BVDV infection. Picture, VLA Bury St Edmunds

Diphtheresis and haemorrhagic inflammation of the intestines of a calf with Salmonella Typhimurium DT104 infection


Laboratory testsUnderstanding the epidemiology of BVD and mucosal disease, and the characteristics of the various tests avail-able, is important in the selection and interpretation of laboratory tests. It is difficult to detect BVDV in acutely infected animals as the virus titre in such animals is low and virus detection tests (eg, ELISA or immunoperoxi-dase staining [IPX]) are unlikely to be successful unless sampling coincides with the height of the viraemia. The TaqMan RT-PCR (Applied Biosystems) is more like-ly to detect virus in blood samples from such animals although, again, this will depend on when sampling is undertaken.

Using an ELISA for antibodies to BVDV on blood samples collected at least two or, preferably, more than three weeks apart, seroconversion is readily apparent in acutely exposed animals. Postmortem, virus isolation or RT-PCR undertaken on tissues may be attempted and histopathology with immunocytochemistry on freshly fixed samples should be diagnostic.

For animals with mucosal disease, and for the detec-tion of clinically unaffected PI animals, the titre of BVDV in peripheral blood is much higher and the BVDV antigen ELISA, IPX and RT-PCR all demon-strate high sensitivity. There is the potential for virus to be masked in younger animals that have a high titre of passively acquired BVDV antibody through colostral intake and, in such cases, testing at six months of age, or older, has been advocated. Virus isolation has the bene-fit that subtypes can be compared by genetic analysis. In older animals, there are few problems with the detection of virus in peripheral blood samples using any of the available tests. RT-PCR results can be obtained within a few hours and the test differentiates type 1 and type 2 isolates and cases of border disease virus infection. This has important implications for disease surveillance because, to date, all isolates in the UK have been type 1, with the exception of seven incidents where type 2 was identified. Serology in cases of mucosal disease and PI animals by ELISA should confirm persistent seronega-tive status, although occasional animals may show very low antibody titres in some tests. In the USA, immuno-cytochemical testing of ear punch samples, collected when ear tags are fitted to cattle, is used to screen for PI animals.

Postmortem examination of cases of mucosal dis-ease is diagnostic. Erosive or ulcerative mucosal lesions may occur at any level of the gastrointestinal tract, but

are most readily identifiable in the mouth, oesophagus, reticulum, rumen, abomasum and ileum. In some ani-mals, lesions may also be seen on the coronary bands, teats and vaginal mucosa. Typical histopathological fea-tures and immunohistochemistry for BVDV antigen in various tissues, including the brain, confirm diagnosis.

JOHNE’S DISEASEJohne’s disease (paratuberculosis) has increasingly been diagnosed in dairy and beef herds in England, Wales and Scotland over the past five years. The reason for this is uncertain, but it may be associated with increased stock movement, increasing herd size and intensification in the industry over this period, as well as increasing disease awareness. There is also currently much more concern and interest because of the possibility that the causa-tive bacterium Mycobacterium avium paratuberculosis (commonly referred to as Map) may be associated with Crohn’s disease in humans.

Clinical signsTypically, Johne’s disease affects cattle over three years of age, but in heavily infected herds it may be seen in growing animals as young as 12 months. There is per-sistent and profuse diarrhoea with associated gradual weight loss, and reduced milk yield in lactating cows. Signs sometimes lessen or resolve in pregnancy only to recur after calving.

Laboratory testsDiagnosis of Johne’s disease should be possible on clini-cal grounds alone in herds where several previous cases have been confirmed. It is essential to make a definitive

Mucosal disease. (left) Ulceration of the oral mucosa at the junction with the hard pad and below the incisor teeth. (above) Diffuse multifocal superficial ulceration of the abomasal mucosa

Poor condition associated with chronic diarrhoea in an adult cow with Johne’s disease. Picture, VLA Penrith


diagnosis in herds where disease has not been confirmed or suspected before and it should be borne in mind that disease is highly unlikely in closed herds where it has never occurred. However, recent evidence that Map can be found in wild rabbits associated with clinical disease indicates the possibility of spread from wildlife. Sheep can also develop Johne’s disease, and although transmis-sion of infection between cattle and sheep is thought to be rare, work in the field is ongoing to determine wheth-er the ‘S’ (sheep-associated) and ‘B’ (bovine-associated) strains of Map are absolute.

FAECES

Microscopical examination of Ziehl–Neelsen stained faecal preparations for the acid-fast Map is tradition-ally the most commonly performed test. This relies on the identification of typical small acid-fast organisms appearing in characteristic ‘clumps’. The test has a rela-tively high specificity when undertaken by experienced examiners and a result is achievable within an hour but, because the organism is passed in low numbers and intermittent shedding is common, the sensitivity of this method is poor (around 25 to 35 per cent). Hence, only one in four or, at best, one in three clinically affected animals will be diagnosed by this method. The sensitiv-ity of the test is even poorer for subclinically infected animals, so the technique is of no value for screening.

Faecal culture of Map is generally regarded to be the ‘gold standard’. It is 100 per cent specific, but has the disadvantage that intermittent or low shedders may not be detected and takes between six and 16 weeks to com-plete. Detection of infection by faecal culture depends on the particular procedure used, the stage of infection

of the animal tested and whether it is infected but not shedding, infected and a low shedder or infected and a high shedder. If the animal is a florid clinical case and a high shedder, the sensitivity may approach 80 per cent or higher.

An RT-PCR test system for bovine faeces has recent-ly been developed for Map. This has the great advantage of providing results within a week of samples being received, compared with the three months that may be needed for culture. The sensitivity of this method is comparable to bacteriological cultural techniques on solid media, while the specificity of both methods is very high.

SEROLOGY

A complement fixation test has historically been used and is still required by some importing countries. For supporting clinical diagnosis and control programmes, antibody ELISAs have been employed. These are good for confirming infection in animals with clinical dis-ease, when the sensitivity is quoted to be around 90 per cent. The sensitivity of the absorbed ELISA is high-est for animals that are both high shedders and exhib-iting clinical signs of disease. When used in control programmes for screening clinically normal livestock, the sensitivity is reported to be much lower, at around 15 to 25 per cent. The specificities of the tests are report-edly high and figures of 99 per cent have been quoted.

POSTMORTEM EXAMINATION

Gross lesions in affected cattle are strongly suggestive of Johne’s disease, with histopathology confirming the diagnosis. Lesions can be widespread in the intestine, but are usually most obvious in the ileum, caecum and

Faecal smear from a cow with Johne’s disease. Note the typical appearance of Mycobacterium avium paratuberculosis, an intracytoplasmic organism that is found in small clumps and often only in small numbers. Ziehl–Neelsen stain

VIDA-recorded incidence of Johne’s disease (based on detection of Map and serology) in adult cattle (aged ≥ two years) as a percentage of diagnosable submissions from 1999 to 2005; the vertical bars indicate 95 per cent confidence limits

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1999 2000 2001 2002 2003 2004 2005

(above) Thickened ridged appearance of the ileal mucosa from an animal with Johne’s disease. (below) Note the associated heavy infiltration of epithelioid macrophages and multinucleate giant cells in a sample of thickened ileal mucosa


proximal colon. Thickening of the wall of the intestine and a ridged appearance of the mucosa are character-istic; lymphatics are usually prominent. Local lymph nodes, particularly the ileocaecocolic node, are usually enlarged. On histopathological examination, infiltrates of epithelioid macrophages and sometimes multinucleate giant cells are found in the lamina propria and submuco-sa of the intestine and the lymph node. Intracytoplasmic acid-fast bacilli are visible in Ziehl–Neelsen stained sections, although the organisms are sparse and can be difficult to find in some cases.

WINTER DYSENTERYWinter dysentery is a highly contagious disease that is thought to be associated with bovine coronavirus infec-tion. As the name suggests, it is most commonly seen in housed animals and although all ages of livestock can be affected, it usually affects adult cattle.

Clinical signsWinter dysentery is characterised by a sudden onset of severe diarrhoea (sometimes, but not always, containing blood) or dysentery in housed cattle. Affected animals are rarely pyrexic although they may be depressed and lose condition. The disease may spread rapidly to sus-ceptible animals and clinical signs usually resolve spon-taneously in two to three days. A marked reduction in

milk yield is reported in affected milking herds. Mild respiratory disease may also accompany the outbreak of diarrhoea. Disease is sporadic and up to 100 per cent of the herd can be affected. Mortality is not reported.

Laboratory testsCoronavirus is shed in faeces. However, due to the dilu-tion factor in adult cows and probably because virus shedding largely precedes clinical signs, antigen ELISAs to detect the causative virus in faeces are often nega-tive. Antibodies to coronavirus are commonly detected in cattle, so single sample serology is unhelpful. Paired serology by ELISA for rising antibody titres on blood samples collected two to four weeks apart is more likely to be diagnostic. BVDV serology is also worth undertak-ing as BVD is the most likely differential diagnosis, and seroconversion to both coronavirus and BVDV has been reported in some herds.

PARASITIC CAUSES

FASCIOLOSISFasciolosis in the UK has traditionally been most pre-valent in western parts of Wales, south-west Eng land and south-west Scot land. However, recently and increasingly, it has been diagnosed across the UK into East Anglia. Changes in climate, with wetter warmer winters, may well be responsible by affecting the habitat of the intermedi-ate snail host Galba (Lymnaea) truncatula. Although the life cycle favours infection in late summer through autumn until housing, disease is usually chronic and so may manifest in cattle at any time of the year.

Clinical signsChronic illthrift and anaemia are often reported in cat-tle with fasciolosis, but diarrhoea has tended to be the most common main presenting sign recorded for sub-missions to VLA diagnostic laboratories where fasciolo-sis is confirmed. This is usually accompanied by weight loss, reduced milk yield and a variably reduced appetite. Anaemia and subcutaneous oedema may also occur in chronic cases. The disease is rarely fatal in cattle on a

Marked fibrosis and calcified thickening of bile ducts in the liver of a cow chronically infected with Fasciola hepatica. Picture, VLA Thirsk

Adult Fasciola hepatica liver flukes collected from an infected carcase. Picture, VLA Carmarthen

Galba (Lymnaea) truncatula, the intermediate snail host of Fasciola hepatica

Submandibular fluid accumulation (‘bottle jaw’) in a Limousin cow. This is a clinical manifestation of hypoproteinaemia and can occur in cases of Johne’s disease, fasciolosis and chronic nematode parasitism. Picture, VLA Bury St Edmunds


reasonable plane of nutrition, but can be more serious in outwintered animals receiving little supplementary feed. Many infected cattle show no overt clinical signs, but may not be performing as well as expected for the diet available. Black disease, caused by Clostridium novyi infection, may occur, as the necrotic tracts in the liver caused by parasite migration favour bacterial growth and toxin production.

Laboratory testsFAECES

Flotation and sedimentation can be used to examine fae-ces for liver fluke ova. Flotation is a more rapid method and useful for screening faeces of large numbers of ani-mals, but sedimentation has been found to be much more sensitive and can be used to examine pooled faeces as part of a herd health screening programme. For individ-

Diagnostic samples and laboratory tests

The submission of clinical samples to a diagnostic laboratory is essential for con-firmation of most of the common causes of diarrhoea, or as part of a comprehensive investigation when non-infectious causes are suspected. It is important to obtain the most appropriate samples from affected animals and factors that should be consid-ered include:■ THE NUMBER OF ANIMALS TO BE SAMPLED. For herd problems, a minimum of three to six animals is recommended;■ SAMPLE SELECTION. Submitting faeces and a blood sample from diarrhoeic cows increas-es the chance of a definitive diagnosis;■ THE TIME IN THE DISEASE COURSE. – For chronic diarrhoea, the initiating cause

may be difficult to detect. For example, in the case of fasciolosis, egg numbers can be low and excretion intermittent;– For peracute disease (eg, coccidiosis, type II ostertagiasis), diarrhoea may occur before the causative agent can be demon-strated in faeces;■ PRIOR TREATMENT. Prior use of anti biotics (eg, in cases of salmonellosis) or recent para siticidal dosing (eg, with a flukicide when testing for fasciolosis) will influence the laboratory test and negative results should be interpreted with caution;■ POTENTIAL LIMITATIONS OF LABORATORY TESTING.– For example, coronavirus detection in faeces of cows with winter dysentery is rarely successful;

– The chance of detecting liver fluke eggs is improved if the optimum amount of fae-ces is submitted for examination (eg, up to 40 g for the sedimentation method);■ THE SENSITIVITY AND SPECIFICITY OF THE LABORATORY TESTS (see table below).– The best tests are those with the high-est sensitivity and specificity characteristics (ie, they optimise the chance of detecting an organism and minimise the chance of cross reacting with others);– A high chance of false negative results should be considered for tests with poor sensitivity (eg, examination of faecal smears for acid-fast Map organisms in Ziehl–Neelsen stained preparations to identify Johne’s disease).

SENSITIVITY AND SPECIFICITY CHARACTERISTICS OF THE TESTS AVAILABLE FOR THE MOST COMMON CAUSES OF DIARRHOEA IN ADULT CATTLE

Cause of diarrhoea Sample Laboratory test Sensitivity Specificity

Salmonellosis Faeces Bacterial culture Unknown. Will depend on the stage of disease, prior treatment, and so on

100%

BVD/mucosal disease Heparin blood Antigen ELISA 95-99% 98-100%

BVD/mucosal disease Heparin blood RT-PCR (TaqMan) 95-99% 98-100% (and differentiates BVDV type 1 and type 2 and Border disease virus)

BVD/mucosal disease Clotted blood/serum IPX 95-99% 98-100%

BVD/mucosal disease Clotted blood/serum or heparin blood

ELISA (serology) ~95-100% ~95-100%

Johne’s disease Faeces Microscopical examination

25-35% High for experienced observers

Johne’s disease Faeces Bacterial culture Around 80% for florid clinical cases; approximately 45 per cent overall for infected animals

100%

Johne’s disease Faeces RT-PCR Very similar to bacterial culture on solid media 100%

Johne’s disease Clotted blood/serum ELISA (serology) 90% for clinically affected animals, but 15-25% for subclinically affected animals

99%

Winter dysentery Faeces ELISA Poor No data

Winter dysentery Clotted blood/serum ELISA (serology) No data No data

Fasciolosis Faeces Egg sedimentation High (greater sensitivity than flotation method). Egg excretion by Fasciola hepatica is variable; negative result in prepatent stage of disease

High for experienced observers

Fasciolosis Clotted blood/serum ELISA (serology) 98% 96%


Faeces Modified improved McMaster worm egg count

High. The result is a measure of adult egg-laying population (ie, acquired at least three weeks earlier). Does not detect immature parasites

High for the differentiation of trichostongyle-type eggs from other species (eg, Nematodirus species), but not possible to differentiate individual trichostrongyle species (eg, Ostertagia species, Trichostrongylus species) from eggs (larval development required)


Abomasal and intestinal content (collected at postmortem examination)

Total worm count Moderate. The worm count is a screening method to indicate the total worm burdens in abomasum and intestine. Many immature parasites can only be detected by pepsin digestion of the mucosa


Coccidiosis Faeces Oocyst count (modified improved McMaster)

High. Absolute counts are not diagnostic and do not differentiate pathogenic and non-pathogenic oocyst species – this can be done microscopically on the basis of oocyst morphology



ual animals, examination of 40 g of faeces optimises the sensitivity of the test; for composite samples, 5 g aliq-uots of faeces collected from 10 animals are required.

SEROLOGY

ELISAs that have a high specificity for antibodies to Fasciola hepatica in cattle sera or bulk tank milk have been developed. The detection of antibodies to liver fluke is evidence of infection within the last nine months, but does not necessarily indicate current infection.

BIOCHEMISTRY AND HAEMATOLOGY

F hepatica infection results in variable hepatocyte dam-age, biliary inflammation and resultant protein loss. Eosinophilia may be identified and used as a screen-ing test for prepatent infection, but is less useful once the parasites invade the biliary tree, and is also non-specific. Chronically, there may also be anaemia, which is usually non-regenerative and normocytic. The activ-ity of liver enzymes (notably glutamate dehydrogenase [GLDH], which is released by damaged hepatocytes, and L-gamma glutamyl transferase [GGT], which is an indi-cator of biliary stasis/inflammation) may be increased in the prepatent stage of disease, but there is often no increased enzyme activities or eosinophilia during the patent/chronic stage of infection.

PARASITIC GASTROENTERITISParasitic disease largely occurs in first season graz-ing animals and is therefore rarely seen in adult cattle. However, the recent re-emergence of husk as a signifi-cant cause of respiratory disease in adult dairy cows indicates the potential for changes in the pattern of dis-eases. Significant gastrointestinal parasite numbers can occasionally be found in animals that are compromised due to concurrent disease, are receiving inadequate nutrition or are in poor condition. Disease may also be identified in ‘show’ animals or bulls bred for sale that have been reared indoors and not exposed to parasites.

Clinical signsAbomasal and intestinal parasitism essentially caus-es similar disease, with diarrhoea, often profuse and watery, being the chief presenting sign. Reduced appe-tite and poor production can also result.

Laboratory testsDetermination of faecal worm egg counts using the McMaster or modified improved McMaster flotation method is reliable in experienced hands and provides a useful guide. Counts would be expected to be high with heavy parasite burdens, but this will depend on the spe-cies of parasite, the chronicity of disease and the consist-ency of the faeces (see box, above right).

Total worm counts can be performed on fresh car-case samples of abomasal and small intestinal contents. However, pepsin digestion is required to detect many of the immature parasites and should be carried out for sus-pected type II ostertagiasis. Type II ostertagiasis is more likely in housed animals after a first grazing season if they have not received effective larvicidal anthelmintic treatment at housing. Estimation of serum pepsinogen concentration is a useful biochemical indicator of abo-masal glandular inflammation. However, definitive diag-nosis relies on histopathological examination of freshly fixed tissue.

COCCIDIOSISCoccidiosis is typically diagnosed in young calves, and is the most common enteric diagnosis in animals aged three to 12 weeks old. Rare outbreaks of diarrhoea occur in older animals and are associated with acute-onset dis-ease, which usually resolves spontaneously in a few days.

Clinical signsThe principal clinical sign is diarrhoea, with or without tenesmus and blood. Variable depression and appetite reduction may also be seen. Reduced production can occur in dairy cows.

Laboratory testsCoccidial oocyst counts are determined by the McMaster or modified improved McMaster technique. Occasionally, very high counts in excess of 1,000,000 oocysts per gram are detected although low numbers of oocysts may also be significant. As disease is atypical in adult cattle, the species of oocysts should be determined to establish whether they are pathogenic (Eimeria bovis, Eimeria zuerni or Eimeria alabamensis). Histopathology is useful although mortality is unlikely in adult animals unless there are secondary complications. It is under-taken on freshly fixed ileum, caecum and proximal colon samples, which show a significant inflammatory response with destruction of crypts.

Worm egg counts

Worm egg counts are performed on faeces, or samples of lower intestinal contents from ani-mals following postmortem examination, using McMaster or modified improved McMaster flota-tion techniques. Detection of helminth eggs indi-cates that adult parasites are present in the gas-trointestinal tract of the animal. Determination of the species requires additional culture to third-stage (L3) larvae. Trichostrongyle-type eggs may include Ostertagia, Trichostrongylus, Cooperia, Bunostomum and Haemonchus species.

Egg counts can be influenced by a number of factors, particularly the age and nutritional status of the animal, and the species of parasites present. Faecal consistency should be considered when attempting to interpret egg counts: high egg num-bers in liquid samples are of greatest significance. The timing of sampling must also be borne in mind, especially after recent anthelmintic adminis-tration. It is important to consider all of these fac-tors when interpreting the significance of worm egg counts (see table below).

Note that, with all worm egg counts, only mature egg-laying female parasites are detected. The count gives no indication of the immature parasite burden.

SIGNIFICANCE OF WORM EGG COUNTS IN CATTLE

Eggs per gram Interpretation and treatment

0 to 200 Light infection

300 to 700 Moderate level of parasite infection. Anthelmintic treatment may be beneficial

700+ Heavy parasite infection. Anthelmintic treatment is recommended


TOXIC CAUSES

A range of chemicals, plants and mycotoxins can cause enteritis and diar-rhoea in adult cows. The key features of these con-ditions are summarised in the table below. All of these conditions are rare and diagnosis of most intoxications depends on knowledge of possible exposure with detection of toxic concentrations or causative agents on post-mortem examination.

WHITLOCK, R. H., WELLS, S. J., SWEENEY, R. W. & VAN TIEM, J. (2000) ELISA and faecal culture for paratuberculosis (Johne’s disease): sensitivity and specificity of each method. Veterinary Microbiology 77, 387-398

(left) Ragwort (Senecio jacobaea), one of several plants that can cause intoxication in cattle. Clinical signs include diarrhoea or constipation, abdominal pain, tenesmus, weight loss, inappetence and, occasionally, nervous signs. (above) Collapsed diarrhoeic Limousin cow with salt poisoning. Picture, VLA Bury St Edmunds

TOXIC CAUSES OF DIARRHOEA

Characteristics of disease and laboratory tests

Molybdenosis/copper deficiency

More commonly diagnosed in the past and seen in specific areas such as the ‘teart’ pastures of Somerset. Copper binds to antagonists in the soil, particularly sulphur and molybdenum, which renders much of the ingested copper unavailable for absorption. A variety of clinical signs is possible in cattle of all ages, with diarrhoea a more common feature in calves. Low liver and blood copper (measured in heparin samples preferably) and improved health status after copper supplementation support the diagnosis

Salt poisoning Seen on the marshes of Norfolk and in other coastal areas where grazing cattle drink from drainage ditches contaminated by sea water and have no alternative water source. In acute disease, there is diarrhoea, thirst, dehydration, prostration and death. In more chronic cases, there may be staggering, muscle tremors, reduced appetite and failure to thrive. Laboratory tests to support the diagnosis include sodium, chloride (lithium heparin blood samples) and packed cell volume (heparin or EDTA blood samples) estimations. Testing water salinity using a conductivity meter is also helpful

Lead poisoning Diarrhoea is a feature of chronic lead toxicity, in addition to depression, loss of condition and performance, and infertility. Lead analysis of heparin blood samples, or kidney samples in animals that die, is diagnostic

Copper poisoning Diarrhoea is an occasional sign. Haemolytic crisis occurs causing haematuria and jaundice most consistently. Liver and, preferably, kidney copper analysis is required to confirm diagnosis. Whole blood (heparin) copper concentrations in excess of 50 µmol/litre are highly suggestive of toxicity

Nitrite poisoning Typically occurs after eating brassicas or after access to fertiliser. Acute toxicity manifests as diarrhoea, abdominal pain, muscle tremors and weakness, dyspnoea, rapid weak pulse, brownish coloured mucous membranes and convulsions. Detection of methaemoglobin in fresh blood (clotted or heparin) samples provides supportive evidence

Arsenic poisoning Arsenicals are now rare, but are sometimes used in horticulture. Old mine waste used in farm walls can also be a source. Poisoning results in profuse diarrhoea (which is often haemorrhagic), weakness, salivation, incoordination, vomiting and abdominal pain. Extremely reddened abomasal mucosa is seen on postmortem examination. Analysis of heparin or EDTA blood samples, urine, faeces and milk is possible to indicate recent exposure, and of hair samples for chronic intoxication. Arsenic detection in the rumen content or liver of animals that die should be carried out

Mercury poisoning Organomercury compounds have been used as seed dressings and intoxication is possible if stock access stores. Clinical signs include diarrhoea, inappetence, incoordination and blindness. Raised mercury concentrations may be detected in heparin blood samples, urine and faeces. Analysis of mercury concentrations in samples of liver and kidney collected at postmortem examination is also possible

Oak/acorn poisoning Constipation is seen early on in the disease process, with diarrhoea, often dark/tarry or bloody, developing later. Diagnosis based on detecting acorns in rumen contents collected at postmortem examination can be difficult as disease can occur some time after ingestion. Elevated blood urea and creatinine concentrations are indicative of compromised renal function and can be used prognostically

Other plant poisons DOG’S MERCURY (MERCURIALIS PERENNIS). Principal signs include watery diarrhoea, sometimes preceded by constipation, salivation and loss of appetite. Later, weakness, jaundice and the production of pinkish or blood-stained urine is seenRAGWORT (SENECIO JACOBAEA). Principal signs include diarrhoea or constipation, abdominal pain, tenesmus, weight loss, inappetence and, occasionally, nervous signsHEMLOCK WATER DROPWORT (OENANTHE CROCATA). Principal signs include diarrhoea, abdominal pain, excess salivation or foaming at the mouth, hyperpnoea, dilated nostrils, bellowing, pupillary dilation, rapid pulse, staggering gait, circling, muscle tremors and convulsionsRHODODENDRON (ERICACEAE SPECIES). Principal signs include diarrhoea, depression, anorexia, salivation, abdominal pain, bloat, vomiting (sometimes projectile) and dyspnoeaBRACKEN (PTERIDIUM AQUILINUM). Principal signs include haemorrhagic diarrhoea, depression, anorexia, haematuria, and bleeding from other mucous membranes, such as eyes, nose and/or vagina

Potato poisoning Waste potatoes that are green or decayed and sprouting/seed potatoes can cause poisoning in cattle. Typically there are nervous signs, including restlessness, incoordination, appetite loss, excess salivation, vomiting and diarrhoea or constipation

Mycotoxicosis A range of toxic metabolites, most produced by Fusarium species, which are the most common contaminants of cereals, have the potential to cause disease in cattle, which may include diarrhoea as a clinical sign


(above left) Many, but not all, cases of malignant catarrhal fever develop the typical ‘head and eye’ form of the disease with opacity of the cornea. (above right) Variable, often severe, oral ulceration can confuse the diagnosis of malignant catarrhal fever with mucosal disease, acute BVDV infection and foot-and-mouth disease

OCCASIONAL INFECTIOUS AND MISCELLANEOUS CAUSES OF DIARRHOEA

History Clinical signs Diagnostic tests

Clostridium tertium Originally isolated from fattening cattle showing rapid-onset ataxia, and death within 12 hours. Experimental infection of calves has induced diarrhoea

Haemorrhagic enteritis. Diarrhoea, usually bloody

Anaerobic bacterial culture of faeces or intestine samples collected at postmortem examination

Yersinia pseudotuberculosis Outbreaks reported in cattle on water-logged pastures in Australia in winter and early spring

Profuse, foul-smelling, watery, brown to green-coloured diarrhoea, sometimes blood-tinged

Bacterial culture and histopathology demonstrating necrotising enterocolitis

Escherichia fergusonii Sporadic cases of diarrhoea, mastitis and abortion, clinically suggestive of salmonellosis

Diarrhoea, abortion or mastitis Pure isolates of E fergusonii in the absence of other recognised infectious or parasitic causes

Rotavirus Rapidly spreading watery diarrhoea, which resolves spontaneously in affected cattle, reported in Japanese dairy cows

Rapidly progressive outbreak of watery diarrhoea in adult cattle, recovery in three to five days, reduced milk yield

Detection of group C rotavirus in faeces by PAGE or electron microscopy

Malignant catarrhal fever Usually sporadic although occasional outbreaks have been seen. Adults or young stock may be affected. In most cases, there is a history of contact with sheep in the previous three months. Note some cases are difficult to differentiate clinically from mucosal disease. Recent cases of bluetongue in Europe have been considered similar to malignant catarrhal fever

Most disease is acute and rapidly fatal. Lesions are typically seen on the eyes, nose and mouth, and, occasionally, skin and feet. Variably extensive ulceration of tongue, hard pad and gums, unilateral or bilateral corneal opacity, and diarrhoea (occasionally haemorrhagic) may be seen

Seroconversion demonstrable using an immunofluorescent antibody test (IFAT) by the time animals are presented for examination. Occasional peracute cases will not have seroconverted. RT-PCR for ovine herpesvirus 2 on heparin blood or lymphoid tissues. Histopathology on viscera and brain collected at postmortem examination

Endotoxaemia Coliform mastitis, endometritis or other coincidental illnesses

Acute diarrhoea or dysentery Clinical history and failure to identify other causes of diarrhoea

‘Haemorrhagic bowel syndrome’

Acute collapse and death of dairy cows, usually in early lactation

Acute-onset depression, reduced milk production, tachycardia, ruminal stasis, abdominal distension and tar-like or bloody faeces, rather than overt diarrhoea

Postmortem examination confirms jejunal haemorrhage, isolation of Clostridium perfringens in anaerobic culture and exclusion of alternative diagnoses

Renal amyloidosis Rare. Usually occurs in older cows, with an insidious history that may include previous suppurative illness

Diarrhoea, reduced yield and appetite, weight loss, palpably enlarged kidneys

Hypoproteinaemia and increasing azotaemia. Histopathology required to confirm and differentiate from nephritis or nephrosis

Acidosis Excess intake of grain or concentrates (eg, after access to food stores)

Diarrhoea, depression, ataxia/drunkenness, laminitis

Rumen liquor pH <4·5 (stomach tube or postmortem sampling). Blood biochemistry can be helpful, demonstrating an increased anion gap ([Na+ + K+] – [Cl– + HCO3

–], reference range in cattle = 10 to 20 mmol/litre; values >30 mmol/litre in cases of acidosis)

Excess dietary protein High protein/low energy diets Diarrhoea, reduced production Biochemistry (blood urea) may yield supportive evidence. No definitive diagnostic tests other than to rule out other causes

Lush pasture More likely in spring and in herds that are not buffer-fed

Diarrhoea No diagnostic tests other than to rule out other causes

Poor quality roughage Poor quality feed availability Diarrhoea and loss of condition, poor production in dairy cows

No diagnostic tests other than to rule out other causes

‘Cold cow syndrome’ Sporadic reports in dairy herds in spring after turnout. May be associated with particular pastures on some farms

Ataxia or drunkenness, anorexia, depression, hyperpnoea, agalactia. In some cows, perineal oedema, muscular stiffness, cold to touch. Diarrhoea, which is occasionally profuse, generally occurs

No diagnostic tests other than to rule out other causes. Typical signs and history of recent turnout. Recovery occurs within a few days of being moved off affected pasture

PAGE Polyacrylamide gel electrophoresis

Endometritis can cause systemic endotoxaemia, which may be associated with diarrhoea

OCCASIONAL INFECTIOUS AND MISCELLANEOUS CAUSES

There are many other potential causes of diar-rhoea in cattle. Several infectious agents have been identified in the fae-ces of diarrhoeic cattle, but their significance has not been clearly established. Diarrhoea can be a feature of dietary changes and a sign of systemic disease. The features of various of these conditions are sum-marised in the table below.

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in dairy cattle: 22 cases (1997-2000). Journal of the American Veterinary Medical Association 221, 686-689GUNNING, R. F. & WESSELS, M. E. (1996) Clinical coccidiosis in a herd of dairy cows. Veterinary Record 139, 497-498MAWATARI, T., TANNEICHI, A., KAWAGOE, T., HOSOKAWA, M., TOGASHI, K. & TSUNEMITSU, H. (2004) Detection of a bovine group C rotavirus from adult cows with diarrhea and reduced milk production. Journal of Veterinary Medical Science 66, 887-890SILVERA, M., FINN, B., REYNOLDS, K. M. & TAYLOR, D. J. (2003) Clostridium tertium as a cause of enteritis in cattle. Veterinary Record 153, 60

SUMMARY OF THE CAUSES OF DIARRHOEA

Acute diseases Chronic diseasesIndividual animals Herd outbreaks Individual animals Herd outbreaks

RinderpestFasciolosis Fasciolosis Fasciolosis FasciolosisSalmonellosis Salmonellosis Salmonellosis

Johne’s diseaseBVD: mucosal disease BVD: acute infection BVD: mucosal disease

Winter dysenteryMolybdenosis/copper deficiency

CoccidiosisParasitic gastroenteritis


Malignant catarrhal fever

Ragwort poisoning Ragwort poisoningAcorn poisoningAcidosis

EndotoxaemiaRenal amyloidosis

Dietary problems (eg, lush pasture, feed change)

Dietary problems (eg, excess protein, poor quality roughage)

Salt poisoningArsenic poisoningMercury poisoningPlant poisoning‘Cold cow syndrome’

SUMMARY

Diarrhoea in adult cattle presents a considerable diag-nostic challenge. Arguably, very few cases can be confi-dently diagnosed on clinical grounds alone. Laboratory tests are essential for confirming or ruling out several of the infectious and parasitic causes of diarrhoea when considering differential diagnoses. It is, however, impor-tant to bear in mind that few tests are 100 per cent sen-sitive and that, in some cases (eg, faecal screening for Johne’s disease), a negative result does not rule out the diagnosis, rather it remains unconfirmed. Repeated test-ing of individuals and, with herd outbreaks, testing of a representative number of affected animals, are often necessary to make a definitive diagnosis.

AcknowledgementsThe authors would like to thank colleagues who have provided photographs and commented on aspects of this article.

Further readingAL-MASHAT, R. R. & TAYLOR, D. J. (1984) Sporolactobacillus spp. In enteritis of cattle. Proceedings of the 4th International Symposium on Neonatal Diarrhoea. Veterinary Infectious Disease Organisation Conference, University of Saskatoon, Saskatoon, Canada, October 3 to 5, 1983. pp 654-665BAIN, M. S. & GREEN, C. C. (1999) Isolation of Escherichia fergusonii in cases clinically suggestive of salmonellosis. Veterinary Record 143, 511CALLINAN, R. B., COOK, R. W., BOULTON, J. G., FRASER, G. C. & UNGER, D. B. (1988) Enterocolitis in cattle associated with Yersinia pseudotuberculosis infection. Australian Veterinary Journal 65, 8-11DANIELS, M. J., HENDERSON, D., GREIG, A., STEVENSON, K., SHARP, J. M. & HUTCHINGS, M. R. (2003) The potential role of wild rabbits Oryctolagus cuniculus in the epidemiology of paratuberculosis in domestic ruminants. Epidemiology and Infection 130, 553-559DENNISON, A. C., VANMETRE, D. C., CALLAN, R. J., DINSMORE, P., MASON, G. L. & ELLIS, R. P. (2002) Hemorrhagic bowel syndrome

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