CASE NOTES


REVIEW OF TICK FEVER OUTBREAKS IN NSW 2011-2012

Paul Freeman, NSW DPI, Wollongbar

Posted Flock & Herd April 2013

INTRODUCTION

The cattle tick (Boophilus microplus) transmits the blood parasites causing babesiosis (B. bovis, B. bigemina) and anaplasmosis (A. marginale) (commonly called "tick fevers") during feeding on their hosts. NSW has been using regulation to restrict the entry of cattle tick into NSW for over 100 years as a means of controlling outbreaks of tick fever. Outbreaks of tick fever occur periodically in NSW and can cause major mortalities in affected herds. This review will focus on the key epidemiological features of tick fever outbreaks in NSW over the past 2 years involving 10 properties and 117 cases with 59 mortalities in total.

Table I. Summary information in the ten outbreaks

BIOLOGY OF PARASITE AND HOSTS

The cattle tick is a one host tick with all three developmental stages: larvae; nymph and; adult, occurring on the one host. Each stage lasts around 7 days and after their final blood feed, adult female ticks drop off the host to lay eggs which then hatch into larvae. The environmental period of the cattle tick life cycle can last up to 9 months.

Babesia spp. organisms are spread exclusively by cattle ticks during feeding on hosts. Transovarial transmission occurs with Babesia spp. resulting in a proportion of infected larvae from hatchings. There is no carrier state in cattle.

Anaplasmosis, like babesiosis, is spread by cattle ticks, however, unlike Babesia spp. infection there is no transovarial transmission, so spread from cow to cow requires close contact, usually involving male ticks (which can live for up to 2 months) moving from infected to susceptible hosts. Anaplasma can also be spread mechanically and by intrauterine transmission. Infection is almost always introduced into a herd via an introduced long-term infected carrier animal.

Cattle, buffalo and deer are primary hosts for cattle tick in Australia. However, tick fever has only ever been reported in cattle in Australia.

While only one infected tick is necessary to cause tick fever, on a population basis most ticks do not carry Babesia infection. Only around 1/500 to 1/5000 are Babesia infected, so large numbers of ticks are needed to induce multiple tick fever cases

The tick fever organisms exclusively parasitise erythrocytes and the clinical signs relate to erythrocyte destruction and the associated immune response to their presence.

SPATIAL SPREAD OF OUTBREAKS

Eight properties with tick fever diagnosis were located on the far north coast of NSW, one other was near Quirindi in the central west of NSW, with another at Deepwater in the New England region (Figure 1).

Figure 1. Map showing locations of tick fever outbreaks

TEMPORAL SPREAD

The majority of new cattle tick infestations are detected in the autumn, and most of the tick fever outbreaks have also occurred around this time (Table II).

Table II: Dates of first and last cases of tick fever in both years and for all properties

The duration of outbreaks in the ten properties is graphically depicted in Figure 2. In one case the outbreak extended for over 80 days.

Figure 2: Time in days from first to last case on each of 10 properties

Ongoing transmission within herds requires high environmental cattle tick populations. In NSW, where cattle tick infestations are eradicated by regular repeated treatments, tick fever outbreaks are generally short-lived. In cases 3 and 4 the property owner was not using the whole of the property for grazing. Some paddocks were free of stock for several months before being restocked. This allowed cattle tick populations to build up even in the presence of regular acaricidal treatment. Once this practice was discontinued, new cases of tick fever ceased. By grazing the whole property, cattle act as vacuum cleaners for infective tick larvae. If this is combined with 21 day treatments of all susceptible stock, very few adult females survive to lay eggs.

SOURCE OF INFECTION

In seven of the outbreaks there was direct or indirect contact with animals which originated from the tick infested area of Qld. For example, direct contact was responsible at Deepwater (Property No. 5) where two bulls were introduced legally from Qld about 2 months before the first case of tick fever occurred.

Indirect contact was responsible for six outbreaks. Properties 2, 3 and 4 all had common ownership, and the owner of Property 1 was a close relative of this owner. Animal movements between all four properties had occurred. A bull introduced in 2008 as a calf at foot from tick infected Qld on to Property No. 4, was moved to Property No. 1 in July 2010. This bull had evidence of chronic cattle tick infestation when examined in March 2011. He was almost certainly carrying some Babesia-infected ticks which dropped off at Property 1 and laid eggs. The hatching of these eggs would have included some Babesia-infected larvae which would have attached to other animals in herd 1 resulting in cases of tick fever. The bull never showed any signs of tick fever while at Property 1.

The owner of Properties 2, 3 and 4 had introduced many animals from tick-infested Qld over the years, with some of these being vaccinated against tick fever. Some may have been naturally infected. It is also known that this same property owner had been treating his cattle for "ticks" for some time before cattle tick was confirmed in his herd. This treatment was suppressive (not at 21 day intervals). This was adopted as a control strategy only as the owner thought he simply had a grass or paralysis tick problem. The combination of high cattle tick numbers and the presence of one or more cattle which would have had tick fever organisms in their blood would have allowed a build up of Babesia-infected ticks. The movements of animals between the four properties would have spread these infected ticks, resulting in tick fever cases on all holdings.

The origin of the cattle ticks on property 4 is unknown. They may have been introduced from Qld with stock purchases. However, they had been treated prior to entry into NSW and were not acaricide resistant. It is more likely, however, that they were acquired locally and were able to build up because of the initial inadequate treatment program and the regular inter-property movements. The cases on Properties 2 and 3 would also probably have originated from Property 4.

The onset of tick fever on Property 7 was preceded by the regular straying of a neighbour's Lowline bull. This bull and one other animal in the neighbouring herd had been introduced from Queensland's cattle tick zone and had not been treated prior to introduction. Cattle ticks were detected on both properties although no cases of tick fever occurred in the neighbouring Lowline herd.

On Property 9 near Quirindi, tick fever cases occurred around 2 weeks after a mob of Hereford cows were introduced to a paddock previously grazed by Qld origin cattle. These Qld origin cattle were purchased out of Moree saleyards and had moved from a property near Paterson, Qld. in the infected zone, to a common ownership property in the Moree area around 12 months previously. Normally animals moving to higher status tick zones need to be treated on the tick line in Qld. However, records to verify that this occurred could not be located. It is likely that these Qld origin cattle were tick infested when purchased at the Moree saleyards and at least one generation of hatchings occurred on the Quirindi property allowing a build up of infective larvae on pasture. Cattle tick sampled at the Quirindi property were of the Ultimo strain (high synthetic pyrethroid resistance and low amitraz resistance, consistent with Qld origin). The Qld origin cattle were confined to only a small area of the Moree property and had no contact with other cattle resident on the property and when sent to the saleyards the paddock was left empty. No cattle ticks were detected when the resident cattle on this Moree property were inspected during tracing investigations.

Cases 6, 8 and 10 had undetermined sources of tick fever infestation. Property 6 is located on the NSW/Qld border and had only a single case of B bigemina infection detected in a bull at slaughter. There was no history of any clinical illness on the property. Inspection of the 1200 head held did not detect any cattle tick. Properties 8 and 10 are also located close to the Qld border and have had previous cattle tick infestations associated with poor biosecurity.

ETIOLOGIC AGENTS

B bigemina was diagnosed in the bull from Property 6 but in all other 9 cases B bovis was diagnosed.

On Properties 3, 4 and 5 (all under common management) anaplasmosis was also diagnosed concurrently with B. bovis infection. However, the Anaplasma infection was only associated with ill effects on Property 5, where it caused abortions. At the time of the babesiosis diagnosis, the herd was undertaking a cattle tick eradication program and Imidocarb was administered to all stud animals prohylactically. The cattle tick eradication program was based on 21 day moxidectin pour-on treatment as there was no plunge dip available. The manager was instructed to allow all cattle access all paddocks within a 21 day period to act as vacuum cleaners for larvae on pasture. However, cattle ticks were still present on some stock at the fourth inspection and treatment. This suggested that larval exposure was still occurring and some areas were probably grazed infrequently.

The owner of Property 5 had made multiple introductions of animals from the Tick infected area of Qld over the years, and this was the probable source of Anaplasma infection for this herd. As most of the 13 aborting cows were not sampled, it was uncertain what proportion of these were due to Anaplasma infection rather than babesiosis. Unlike B. bovis infection, pyrexia is not a strong feature in Anaplasma infection and abortion is regarded as a consequence of anaemic anoxia. The illness is more prolonged and jaundice is common. Also unlike B bovis infection "redwater" or haemoglobinuria does not occur with anaplasmosis. Table III provides a snapshot of the clinical signs and pathology seen in the cases that were examined.

Table III. Signalment and pathology seen during the outbreaks

ACKNOWLEDGEMENTS

Geoff Payne, Larry Falls, Bob McKinnon, Keith Newby, David Thomson and Matt Ball all provided information or reports used during the compilation of this summary.

REFERENCES

  1. Burns, B.M., Fordyce, R.G., Holroyd, R.G. "A review of factors that impact on the capacity of beef cattle females to conceive, maintain a pregnancy and wean a calf - Implications for reproductive efficiency in northern Australia" Animal Reproduction Science 2010; 122: 1-22
  2. Bowman A., Nuttall P. (editors) Ticks: Biology, disease and control. Cambridge University press 2008

 


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