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Pathology and Epidemiology of Bovine Yersiniosis

Matt Ball, Senior District Veterinarian, North Coast LHPA

Posted Flock & Herd August 2010


As district veterinarians we have the potential to create and store records of great value for researchers and epidemiologists. The North Coast LHPA has decided to maintain its paper based disease folders for this reason. Good records stored on a disease basis allow comparisons between current disease levels with that occurring in the past. It also allows basic epidemiological analysis such as looking at data to form hypotheses about disease causation and for some diseases the carrying out of a basic case control study.

This paper outlines an example of how a review of disease records and the literature assisted the authors understanding of a common local disease syndrome, allowed simple epidemiological calculations and suggested areas where further epidemiological studies could be done. These suggestions are useful to provide to students wishing to undertake honours projects during their undergraduate veterinary science degree.


Yersinia is a genus of gram negative bacteria in the family Enterobacteriaceae. Both Yersinia pseudotuberculosis and Yersinia enterocolitica can be associated with enteric disease (Carter 1995). Yersinia pseudotuberculosis is considered the main agent for outbreaks of enteric Yersiniosis in domestic cattle of New South Wales (Thompson 2003).

The epidemiology of enteric yersiniosis in Australian bovidae is complex (Hum, Slattery & Love 1997). Causal factors remain unsubstantiated. Observations on disease outbreaks on the North coast of NSW suggest a complex interaction between the agent, host and environment.

Outbreaks often occur under stressful environmental circumstances (Hum, Slattery & Love 1997). Cold weather, flooding, marshy lowlands, frosts, transport and poorly nourished animals may be typical stressors.

Outbreaks are widely reported to follow winter flooding. This has given rise to the common name of 'flood mud scours'.

Callahan et al. (1988) described key features of the 'flood mud scour' syndrome during outbreaks in 1983 to 1985. During these years the syndrome was observed during winter and early spring. Typically, affected cattle 'had access to low lying poorly drained pastures which were waterlogged either by recent flooding or persistent heavy rain. In many cases, fine silt remained on the pasture after flood waters had receded' (Callinan et al. 1988).

In the observed syndrome all cattle were older than 6 months of age. If found alive animals had all or some of recumbency, lethargy, inappetance, dehydration, pyrexia and diffuse diarrhea. Faeces were found to be watery, smelly and sometimes tinged with blood. Sometimes animals were simply found dead. On biochemical analysis the majority of animals were hypoproteinaemic and at necropsy macroscopic features of enterocolitis were observed. On histopathology the tips of small intestinal villi were replaced with gram negative bacteria and neutrophils. Yersinia pseudotuberculosis was cultured as the dominant organism from 85% of intestinal samples.

When administered early in the course of the disease animals responded well to tetracycline antibiotics. During the outbreaks the average morbidity rate was estimated at 8% and the case fatality rate at 58% (Callinan et al. 1988).

Callinan et al. (1988) used culture and histopatholgical information to define a pathogenic association between the agent Yersinia pseudotuberculosis and the disease syndrome being observed. They described the colonisation of distinct macroscopic lesions with bacteria consistent with Yesinia and the culture of Yesinia pseudotuberculosis from these intestinal lesions. They concluded that Yersinia is important in the pathogenesis of the syndrome but that its role as a primary pathogen still required further confirmation.

There is limited information in later literature that further explores the causal relationship between Yersinia and the NSW 'flood mud scour syndrome'. Slee et al. (1988) discuss a similar syndrome in Gippsland between 1985-1988 where Yersinia was cultured from 222 scouring cattle. They concluded from clinical, haematology, serology, bacteriology and histopathology data that cattle are a common host for Yersinia pseudotuberculosis and that clinical and fatal disease occur occasionally from the bacterium. They comment that the factors leading to clinical disease are unknown.

Earlier Hodges and Carmen (1985) had emphasised the fact that Yersinia pseudotuberculosis can be isolated from clinically normal cattle.

Papers from a NSW veterinary conference in 2003 indicate that NSW government pathologists accepted specific 'intestinal microscopic lesions as being virtually pathognomonic' for Yersiniosis and that history, clinical signs and culture of the organism provides 'additional support for the diagnosis' (Thompson 2003).


The author analysed laboratory reports dated between January 1st 1999 and 24th August 2009 that were stored in the 'Yersinia' disease folder of the Lismore office of the North Coast Livestock Health and Pest Authority. These reports primarily related to cases of disease within the Tweed Lismore district.

During this period there were 25 records where Yersiniosis was listed as the final conclusion for enteric disease. This was on the basis of microbiology alone (19 cases) or both microbiology and histopathology (6 cases). It is important to recognise that 25 is likely to be only a very small proportion of the number of outbreaks that have occurred in the Tweed-Lismore district over the last ten years. Some outbreaks would not have had veterinary attendance.

There has also been good awareness regarding Yersiniosis and many producers and private veterinarians treat for the condition without laboratory confirmation.

Of the 25 cases, 22 were selected because in these Yersinia pseudotuberculosis was cultured as a profuse population without the need for selective enrichment media. The three cases were discarded because the culture of Yersinia seemed at odds with the history, clinical signs or other pathology. In the 22 cases the history, clinical signs and histopathology were very similar to the syndrome described by Callinan et al. (1988).

Exceptions to the typical syndrome of acute disease in adults included one case of disease in a younger calf and one case where clinical disease extended over 2 weeks. In most histories there is mention of either low condition score of the animals or poor available pasture. Key data from selected cases is summarised in Table 1.

Outbreak Date Population at risk Reported Mortalities Reported morbidity Attack rate (%) Case fatality rate (%)
1 O6/99 50 0 1 2 0
2 06/99 100 4 4 8 50
3 08/99 200 0 6 3 0
4 08/99 350 12 0 3.4 100
5 08/99 30 2 0 6.7 100
6 08/99 40 2 3 12.5 40
7 08/99 50 3 2 10 60
8 09/09 23 6 0 26 100
9 09/00 150 2 2 2.6 50
10 10/00 10 0 1 10 0
11 08/03 45 6 6 26.7 50
12 09/03 10 0 1 10 0
13 09/03 50 0 1 2 0
14 09/06 100 0 1 1 0
15 06/08 100 1 1 2 50
16 07/08 4 2 2 100 50
17 08/08 20 0 1 5 0
18 09/08 66 7 0 10.6 100
19 07/09 40 2 1 7.5 50
20 07/09 50 3 0 6 100
21 07/09 20 4 0 20 100
22 08/09 84 5 3 5.9 62.5
TOTAL 1592 61 35
AVERAGE 72.4 2.8 1.6 12.8 48.3
TABLE ONE: 22 cases of Yersiniosis Tweed-Lismore District 1999-2009

The case fatality rate of 48.3% is similar to that estimated by Callinan et al. (1988) of 58%.

Analysis of the laboratory data supports the strong seasonal nature typically described for Yersinia outbreaks. Over the ten year period cases were only reported between June and October (Chart 1). August 1999 had 5 outbreaks alone which has pushed the seasonal trend towards the right in Chart 1. If cases from 1999 are excluded from the data the peak in the seasonal trend occurs more in July than in August. The seasonal nature of the syndrome strongly suggests that environmental influences are important.

Graph of yersinia cases
Chart 1

There is an association between rainfall and the disease outbreaks (Chart2). The greatest number of cases occurred when mean monthly rainfall is low.

Graph of rainfall
Chart 2

Heavy rainfall, floods and general pasture inundation with water can occur in the Lismore region in late autumn and early winter. The ideal environmental conditions for a Yersinia outbreak may occur sometime after heavy rainfall and flooding. For example, in 2009, 4 disease outbreaks occurred in July and August when an extreme flooding event occurred in late May. A causal association between flooding and disease is suggested by the flooding preceding the disease event and by the biological plausibility of Yersinia being available at a high infective dose following its multiplication in anaerobic and moist conditions. But is this association being seen consistently?

Lismore City Council sumarises significant flood events on its webpage (Lismore City Council 2008). There is not a consistent association with these flood events and timing of disease outbreaks (Table 2). Between 1999 and 2009 six years had confirmed cases of Yersiniosis. In only three of these years was there a significant flood event. In 2005 a large flood occurred in June but there were no confirmed cases of disease that season.

Year Number of outbreaks Significant flood event Month of flood
1999 8 No
2000 2 No
2001 0 Yes Feb
2002 0 No
2003 3 No
2004 0 No
2005 0 Yes June
2006 1 Yes Jan
2007 0 No
2008 4 Yes Jan
2009 4 (up to 24 August) Yes May
Table 2: Lismore floods and disease outbreaks by year

Recognition of the local variance in weather conditions is also important. Some areas of the Tweed-Lismore region will receive much higher rainfall than average while others will receive less. Localized flooding can also occur. Collecting rainfall data and any history of localised flooding for the paddock locations of each outbreak would be useful. Particular paddocks where disease occurred may have experienced wet, swampy or recent heavy floods when the wider region did not.

For example, one outbreak in 2009 was very localized and exposure was assumed to be from an area where the 'bowl' shape of the land retained water and left a heavy layer of silt (photo1). Cattle had chosen to preferentially graze in this area. Similar data could be obtained from other outbreaks by retrospective studies.

Image of green paddock
Photo 1: Bowl shaped area near river. Soil holds water extremely well at this site. Water tends to stay over pasture for prolonged period. When water recedes a thick layer of silt remains for some time.

A number of authors have described an association between outbreaks of Yersiniosis and low temperature (Radiostits 1997). This association is supported from analysis of the lab data and mean monthly minimum temperatures in Lismore (Chart 3). Because there is moisture throughout most of the year temperature is probably the limiting climatic factor for Yersiniosis outbreaks. If the temperature is too high Yersinia cannot survive in the environment. (Chart 3)

Graph of temperature and disease
Chart 3

Nutritional status of cattle also follows a seasonal pattern on the North Coast. Nutrition is largely derived from pasture which has a seasonal decline in winter. There is an association between the seasonal decline of pasture and the seasonal peak in Yersinia cases (Chart 4). Pasture availability is at its lowest when cases are most common. Radostits (1997) discussed that good nutrition may have a role in preventing Yersiniosis. This may also explain why cases do not occur in summer.

Graph of pasture availability and disease
Chart 4

Trace element deficiencies and internal parasitism have also been suggested as being factors associated with Yersiniosis (McLennan and Kerr 2000). McLennan and Kerr specifically discuss copper and selenium deficiencies. The Tweed-Lismore district has well recognised copper and selenium deficiencies and internal parasites are the most common syndrome diagnosed. These associations may simply be confounding factors. It may be that any host stress may predispose to clinical expression of Yersiniosis.

Image of bovine intestines on post-mortem
Intestines from cow with Yersiniosis - Lismore saleyards


In 2009 there were numerous reports of Yersinia pseudotuberculosis by North Coast district and private veterinarians. In one case 5 deaths were reported from a property in Chelmsford. Two sick cattle with lethargy and scours were also identified. Deaths had all occurred over a 36 hour period. All cattle were female and in good condition. A necropsy on one cow identified yellow liquid ingesta in intestines. There was significant serosal inflammation of the ileum and jejunum. The mucosal lining of the jejunum and ileum had multifocal red-purple 1-2mm ulcerations.

Bloods from a sick animal and tissues from the necropsy were submitted for testing. Haematology and biochemistry on the sick cow revealed a PCV of 52, plasma protein of 44 and marked degenerative changes in the leucocytes. A profuse population of Yersinia pseudotuberculosis was cultured from pooled faeces and two sections of ileum. On histopathology there were clouds of coccobacilli and degenerating inflammatory cells within the mucosa (microabscesses). The villi were congested and lymphatics of the lamina propria dilated.

Following the diagnosis the source of infection was located as an area of silt covered paddock adjacent to the river. Flooding had occurred a few weeks earlier.

In another one case a cow fell down at the Lismore saleyards. This cow had appeared well when she left her Byron Bay property the day before. The cow was euthanased and at necropsy severe inflammation of the intestines was noted. A profuse growth of Yersina pseudotuberculosis was grown in the laboratory.


Yersiniosis on the North Coast of NSW is a multifactorial disease. Thrushfield (2006) describes 'necessary' and 'sufficient' causes of disease. Yersinia pseudotuberculosis is a 'necessary' cause of Yersiniosis on the North Coast of NSW. You cannot get disease if it is not present. However it will not cause disease on its own. Yersinia pseudotuberculosis combines with a number of host and environmental factors to produce 'sufficient' cause for disease.

Further research would be needed to specifically identify the components and sets of sufficient causes. It is likely that the most important sufficient cause is composed of Yersinia pseudotuberculosis, host stress and ambient temperatures beneath a certain threshold.

Animals become exposed to Yersinia by oral ingestion of any Yersinia that have survived and multiplied in water and feed. This survival and multiplication is probably assisted if the paddocks have been covered in water and if environmental temperatures are low.

Exposure would happen to a range of species and in all age groups. Unweaned calves may have a lower rate of exposure simply because they are not grazing. This may be one factor that explains why disease is more common in cattle over 6 months of age. It is possible that a low level of exposure in unweaned animals may lead to a protective immunity.

Following exposure Yersinia becomes a common inhabitant of the intestine in both domesticated and wild animals.

With 99,000 cattle and a diversity of native and pest animals there is likely to be a very large animal reservoir on the North Coast ensuring survival of the bacterium and continued environmental contamination.

Wild animal reservoirs and cattle 'carriers' excrete Yersinia organisms in their faeces onto pasture and into waterways leading to environmental contamination. Radostitis et al. (1997) report this as the 'major method of transmission'. The seasonal nature of the disease on the North Coast of NSW suggests that this passive pasture contamination will not lead to an outbreak unless it is combined with environmental factors favouring survival and multiplication of the agent in soil, pasture and/or water.

It is assumed that a massive environmental reservoir of Yersinia builds up when the survival and multiplication of the organism in favoured by wet and low oxygen conditions. Yersinia is facultatively anaerobic and has an ability to survive and multiply in water at low temperatures. The wet and anaerobic conditions in localised North Coast paddocks after flooding would favour the growth of Yersinia compared to most other bacteria. Such growth can continue unchecked if ambient temperatures are not too high.

Yersinia multiplies to a level on pasture that infection and clinical disease is more likely. Radostitis et al. (1997) describes this as 'heavy infection pressure'. Once a small number of cattle have succumbed to this heavy infection pressure they will further increase environmental contamination by excretion of bacteria in their faeces.

The history from Case 22 suggests that cattle became exposed to the organism at a point source in time. Out of the 8 affected animals 4 died within 48 hours of each other and the other 4 had clinical signs within the next few days. Transmission from one animal to another animal is probably not the major factor compared to all affected animals having ingested a large infective dose from pasture.

Following oral exposure to Yersinia cattle can have a bacteraemia and then a full spectrum of gastrointestinal syndromes:
1. septicemia and rapid death
2. acute severe hemorrhagic diarrhoea, dehydration and death
3. chronic subtle signs of ill thrift and diarrhoea and
4. infection without clinical signs but shedding organism in faeces (Hum, Slattery & Love 1997; Callinan et al. 1988).

The range in severity of clinical signs is likely to be related to a number of host factors. Not all cattle succumb to the 'heavy infection pressure' described by Radostitis et al. (1997). They suggest that this is because infection mainly occurs in those 'debilitated from other influences'. Herds will be more likely to have an outbreak if their immune status is compromised by stressors such as lactation, pregnancy, weather conditions, energy and/or protein imbalance, micronutrient deficiency, transport, change of feed or concurrent disease. Persistent pestivirus infection and uncontrolled parasites are examples of concurrent diseases on the North Coast that could predispose to both Yersinia infection and clinical disease.

Path diagram for yersiniosis causality
Path diagram of causality for Yersiniosis on north coast of NSW


Frequency calculations are important for diseases within a district as they can assist management decisions for field veterinary services. For example, is a specific program on Yersiniosis justified for the North Coast or should it simply remain a component of the passive surveillance program.

Some measures of frequency for Yersinia outbreaks have already been identified in Table 1. For each outbreak the proportion of the population at risk that became affected with disease (attack rate) was calculated. The average attack rate was found to be 12.8%. The proportion of animals affected with the disease that die (case fatality rate) was also calculated for each outbreak and on average found to be 48%.

Outbreaks of Yersiniosis are significant for individual producers.

Caution is needed in the interpretation of the frequency calculations from laboratory reports. The mortality and morbidity data on the laboratory reports is only a reflection of the situation at the time of sampling. True mortality and morbidity figures are probably significantly higher as outbreaks would continue for a period of time after sampling.

In addition mild clinical cases would not be detected on many properties where stock are not frequently or closely examined. The actual morbidity is likely to be higher compared with the mortality. Estimated case fatality rates for this disease are probably too high. The accuracy of mortality and morbidity data on the laboratory reports could be checked by retrospective interviews with affected producers.

While Yersinia outbreaks are a significant problem for affected producers how much are they a problem for the district as a whole?

The total population at risk from the laboratory data was 1592 and the total mortalities was 61. The risk of developing disease (Incidence risk) can be measured by calculating the proportion of non-diseased animals at the start of a period that became diseased during the period (Dohoo et al. 2003). There was a 4% chance of an individual cow dying from Yersiniosis during the ten-year period.

29 (47.5%) of the mortalities occurred within a single year (1999). There was a 3% chance of an individual animal dying in this year which can be extrapolated to 30% for 10 years. It is difficult to determine whether the higher number of cases in 1999 represents a true increase in the incidence risk of the disease.

The district veterinarian at that time may have had a greater professional 'interest' in Yersiniosis and responded to a greater number of mortalities compared to the following veterinarian (Robertson 2009). District veterinarians in the region changed in late 2000. Around this time there were also changes in policy relating to the charging of laboratory services by the NSW Government. This may have lowered the rate of submissions by the veterinarian.

It may be that the number of laboratory reports for 1999 is closer to the actual number of outbreaks when compared to subsequent years. A 3% chance of developing disease is relatively significant.

If the number of cases was truly lower in 2000-2009 it may be because control measures were more effective.

Effective awareness campaigns may have led to earlier detection and treatment of suspicious cattle by producers and private veterinarians. This could have reduced the number of mortalities and request for laboratory confirmation. One example of awareness during the period was a widely circulated publication on 'Beef Cattle Health on the North Coast' which outlined the need for early use of oxytetracycline in suspected cases.

Overall any of the calculated figures on incidence risk may not be particularly meaningful as many Yersinia mortalities will have occurred without attendance by a district veterinarian and laboratory confirmation. It is difficult to estimate the number of these mortalities without a widespread survey of producers and private veterinarians.

The investigation of mortality events is a large role of district veterinarians. A proportional disease measure may be useful to assess the relative importance of Yersinia. Between 1 January and 27 August 2009 the author investigated 26 mortality events. One of those events was confirmed by laboratory testing to be Yersinia. Therefore over the 8-month period 3.85% of mortalities referred to the author for investigation were Yersinia. In comparison 19% of the mortalities were diagnosed by the author as black leg. While proportional disease measures may not be useful for prelevance of disease in the district it could be useful in determining priorities. For example, if a specific objective was to reduce mortalities in the district then currently an awareness program for correct use of vaccines may be more effective than one for the early treatment of Yersiniosis.


Because Yersinia are facultative intracellular parasites and because the enteric infections they cause can be acute and fatal early and adequate treatment is important (Carter 1995).

Producers need to increase observation of their stock once an index case is identified. Any further clinical cases need to be detected early and treated immediately with oxytetracycline. Ideally clinical cases should be separated from the rest of the herd. For some herds preventative treatment of at risk cattle with antimicrobials may be appropriate.

Recognizing the likely source of infection is important and if possible cattle should be moved to a new area.


The suggested role that poor nutrition and other stress have in causing Yersiniosis indicate that prevention should be based on stress minimisation. Hum et al. (1997) comment that control of stress factors is important for prevention of Yersiniosis.

Disease from Yersiniosis on the North Coast can probably be prevented by good husbandry that minimises nutritional and other stressors. Producers should set suitable stocking rates, manage pastures appropriately and supply supplementary feed in winter. When identified selenium and copper deficiencies should be addressed. A monitoring program for gastrointestinal parasites and strategic drenching is needed.

The high-risk time for the disease on the North Coast is in winter. Producers can identify the water holding and flood prone areas of their properties and if possible graze cattle on other paddocks in winter. Some properties may be able to fence off high risk areas.

Good farm biosecurity and management to control other endemic disease such as pestivirus and internal parasites may also be preventative. Controlling pests such as rodents would be sensible.

Awareness by government and private veterinarians is an important prevention strategy. The clustering of cases within a year suggests that following an index outbreak for the year an 'early warning' could be provided to producers considered at risk.


The epidemiological features of Yersinia where it is 'carried' in non-clinical cattle and the large wildlife reservoir would make an eradication campaign on the North Coast of NSW ineffective. Reducing the impact of the disease rather than attempting eradication is a sensible approach to Yersiniosis. A suitable strategy is to continue producer awareness activities related to the likely factors involved in causing Yersiniosis and to the importance of early detection and treatment.


The Yersinia syndrome on the North Coast of NSW as described by Callinan et al. (1988) has continued over the last ten years. Although the precise causal factors of the syndrome are still not well defined a likely causal web can be created. Collection of further data by surveys of affected producers and use of GIS mapping to combine property locations and climatic data may be helpful.

The creation and analysis of disease data stored in district offices can be invaluable for epidemiological studies. Whether it is by a paper filing system or by an electronic system district veterinarians should be able to retrieve adequate disease data to review local or emerging syndromes.

LHPA staff should ensure that they utilize the resources of the NSW I & I library system to assist with undertaking literature reviews.


  1. Callinan, R.B, Cook, R.W, Boulton, J.G, Fraser, G.C and Unger D.B 1988, 'Enterocolitis in cattle associated with Yersinia pseudotuberculosis infection', Aust. Vet. J. vol 65, no.1, pps. 8-10
  2. Carter, G.R 1995, Essentials of Veterinary Microbiology, 5th edn, Williams and Wilkins, North Providence, PA
  3. Dohoo, I. R, Martin W.S and Stryhn, H 2003, 'Measures of disease frequency', p 65-84 Veterinary Epidemiologic Research AVC Inc, Canada
  4. Hodges, R.T and Carman, M.G 1985, 'Recovery of Yersinia pseudotuberculosis from the faeces of healthy cattle', New Zealand Veterinary Journal vol 33, no. 10, pps 175-6
  5. Hum, S, Slattery, S and Love, SCJ 1997, 'Enteritis associated with Yersinia pseudotuberculosis infection in a buffalo', Australian Veterinary Journal vol 75, no. 2, pp. 95-97
  6. Lismore City Council www.lismore.nsw.gov.au
  7. Lismore had extremely heavy rains (BOM 1999)
  8. McLennan, M.W and Kerr, D.R, 'Yersiniosis and trace element deficiency in a dairy herd', Australian Veterinary Journal vol 78, no.1, pps.28-29
  9. Radostits, O.M, Blood D.C, Gay, C.C 1997, Veterinary Medicine- A Textbook of the Diseases of Cattle, Sheep, Pigs, Goats and Horses, 8th edn, W.B Saunders, London
  10. Robertson, I 2009, - Principles of Epidemiology, Unit Information and Learning guide, Murdoch University, Perth
  11. Slee, K.J, Brightling, P & Seiler R. J. 1988, 'Enteritis in cattle due to Yersinia pseudotuberculosis infection'
  12. Spier, C 1990, 'Treatment of Yersinia infection with tetracyclines', Australian Veterinary Journal vol 67, no.12, p. 471
  13. Thompson, K 2003, 'Alimentary Tract', Gross Pathology of Ruminants: Proceedings 350, Post Graduate Foundation in Veterinary Science, University of Sydney, Camden, p. 14
  14. Thrushfield M 2006, 'The Cause of Disease' , Veterinary Epidemiology, Third Edition, Blackwell Science, pp34-45


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