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Tick Borne Diseases of Sheep

Bruce Watt, Tablelands Livestock Health and Pest Authority, Bathurst and Michelle Dennis, Faculty of Veterinary Science, University of Sydney

Posted Flock & Herd August 2010
"Mosquitoes and tsetse flies may grab the headlines, but blood-sucking ticks are the major transmitters of disease between animals and humans in the northern hemisphere. They can carry an astonishing range of pathogens from viruses to protozoans and they feed indiscriminately on mammals and birds."


Worldwide, ticks are vectors for some of the most economically significant diseases of sheep. Tick-borne fever caused by Anaplasma phagocytophila and spread by the tick Ixodes ricinus is a serious and increasing constraint to sheep production on northern Europe. Ticks transmit other bacterial and rickettsial diseases in sheep. In Britain, Ixodes ricinus also predisposes sheep to Staphylococcus aureus causing tick pyaemia and tularaemia in northern Europe and the United States.

Ticks are regarded as a vector for caseous lymphadenitis in North America. Across the former USSR and elsewhere, ticks spread Anaplasma ovis. In Africa and the Caribbean ticks transmit Ehrlichia ruminantium, the cause of heartwater. Ticks transmit the protozoan diseases Babesia mortesi and B ovis in Europe, Russia and India and Theileria ovis and hirci in Africa, Asia and Europe. Ticks also spread the viral diseases louping-ill in England and Nairobi sheep disease in Africa.

In Australia, Haemophysalis spp ticks occasionally infested sheep without producing significant disease while Ixodes holocyclus can cause sheep to suffer tick paralysis. As ticks are widespread in Australia, exotic tick borne diseases have the potential to threaten our sheep industry if introduced.



Tick-borne fever (TBF) is now a widespread problem for the sheep industry from Scotland to Scandinavia. The causative agent has kept taxonomists gainfully employed for decades. It was first tentatively named Rickettsia phagocytophila. The protozoa then spent time as Cytoecetes phagocytophila and Ehrlichia phagocytophila. It now seems to be most commonly referred to as Anaplasma phagocytophila although as a zoonosis the agent is referred to as granulocytic Ehrlichia (GE) (Jubb and Kennedy 2007, Sumption 2007).

While other blood parasites show a predilection for the red cell fraction, A. phagocytophila attacks granulocytes. Initial clinical signs relate to a febrile response, however subsequent symptoms are a consequence of suppressed immune function. During the acute febrile stage, up to 90% of circulating granulocytes contain intracytoplasmic inclusions of A. phagocytophila (accentuated with Giemsa and polychrome methylene blue stains). Following the febrile stage, transient severe neutropaenia develops; however, at this stage, organisms are no longer found in blood smears.

Affected sheep are susceptible to a range of infections including tick pyaemia, bacterial (usually staphylococcal) septicaemia with localisation in joints and lungs, Pasteurella and presumably Mannheimia pneumonia, louping-ill and listerial infection. Pregnant ewes often abort with a high mortality rate.

Australian sheep veterinarians confronted with TBF would initially risk diagnosing the secondary problem rather than identifying the primary agent. The radiomimetic effects of ptaquilocide from bracken and rock fern intoxication might also resemble TBF. However, the toxic consequences of fern ingestion while relatively common in cattle are rarely reported in Australian sheep.


The disease tick-borne fever due to Anaplasma phagocytophila results in destruction of white cells and so a susceptibility to concurrent infections. When lambs of from 2-10 weeks of age are bitten by the tick Ixodes ricinus, staphylococci either from the skin or from the mouthparts of the tick contaminate the bite wound. Bacteraemia ensues and abscesses form in a number of tissues, especially the joints, tendon sheaths, and muscles, and less commonly the liver, lungs, kidneys, and meninges.

Affected lambs become ill, lame and lose weight (Watkins 2000).

Tick pyaemia would resemble other causes of neonatal arthritis. A diagnosis of tick pyaemia might be made if ticks were found on lambs with purulent staphylococcal arthritis, abscessation elsewhere and neutropaenia.


Ovine anaplasmosis (unlike bovine anaplasmosis) is a mild and often undiagnosed disease of sheep in the former USSR, north and South Africa, the United States, Argentina, the Mediterranean region, and the Middle East. Ovine anaplasmosis predominantly affects older sheep in the spring and summer when ticks are active. Anaplasma ovis, the causative rickettsia parasitises red cells; infected red cells are removed by splenic and other macrophages, resulting in extravascular haemolysis. Affected sheep are therefore icteric, anaemic, weak and febrile. Mortality rates rarely exceed 5% (Jensen and Swift, 1974).

Australian sheep veterinarians might mistake ovine anaplasmosis for Mycoplasma ovis infection. The clinical signs and mortality pattern seems similar. However, in our experience, M. ovis is virtually confined to young Merinos 4-6 weeks post marking and mulesing whereas ovine anaplasmosis appears to primarily affect older heep and presents as a progressive disease with emaciation.


Heartwater is a serious impediment to livestock production in sub-Saharan Africa and parts of the Caribbean. The causative agent is a rickettsia, Ehrlichia ruminantium (previously Cowdria ruminantium) that is spread by ticks of the Ambylomma genus. A wide range of domestic and wild ruminants is affected although recent introductions from naive areas are most at risk. The disease has a predilection for early mature animals, while lambs and calves less than three weeks of age are resistant (Jubb and Kennedy, 2007, Sumption, 2007). Mortality rates can reach 100% in breeds of sheep that are not native to endemic areas.

The striking pathology from which this disease derives its name is due to the predilection of Cowdria ruminantium for endothelial tissues. Organisms parasitise vascular endothelial cells and cause increased capillary permeability, leading to serous effusion in the pleural, peritoneal, pericardial cavities and in mediastinal and retroperitoneal tissues. There is widespread oedema, often involving the lungs, brain, lymph nodes, and spleen. As such, the lymph nodes of the head and neck and the spleen are often strikingly enlarged (Jubb and Kennedy, 2007).

E. ruminantium have a tropism for the capillary endothelium of the brain. Infrequently, petechial and ecchymotic haemorrhages may be distributed throughout CNS tissue. Perinuclear morulae of E. ruminantium can be demonstrated within endothelial cells through microscopic examination of a squash or smear preparation of cerebral tissue.

Parasitism of cerebral endothelial cells results in impaired CNS perfusion, which accounts for clinically evident nervous signs. Affected animals also initially have a high biphasic fever. In less acute cases, the nervous signs may be accompanied by profuse, foetid diarrhoea (Geering and Forman, 1987).

Australian veterinarians confronted by heartwater in sheep might initially suspect lead poisoning. Peracute cases would resemble anthrax. On post-mortem, the extensive serous effusions into body cavities are characteristic of heartwater and the hydropericardium not always present in cattle dying of heartwater is a more constant feature in sheep. Enterotoxaemia also causes endothelial damage and so is characterised by a pericardial effusion and generalised tissue permeability. However, an enlarged spleen while seen in anthrax is not normally a feature of enterotoxaemia. The post-mortem picture of marked pulmonary oedema, hydrothorax and a reddened gastrointestinal mucosa in stock dying subsequent to the consumption of the wild sunflower (Verbesina enceliodes) and sunflower daisy (Wedelia asperrima) might also resemble heartwater (Seawright, 1982).


Ticks spread Babesia ovis and B. motasi in southern Europe, North Africa and the Middle East (Sumption, 2007). It is an important disease in areas infested with the tick Rhipicephalus bursa. Following infection the protozoa directly invades red cells causing intravascular haemolysis. Consequently, affected animals develop anaemia, jaundice and haemoglobinuria. Pyriform parasites are easily demonstrated within red cells of blood smears from clinically affected animals. Smears of blood collected from peripheral vessels (such as from tail tip or skin scrape) may yield higher numbers of parasitized red cells.

In Australia, copper poisoning and bacilliary haemoglobinuria would resemble ovine babesiosis. Ovine babesiosis should be considered in the absence of a history and biochemistry supporting copper poisoning or liver pathology supporting bacilliary haemoglobinuria and in the presence of ticks.


Theileria in sheep mirrors the diseases in cattle. The more pathogenic form, malignant ovine theileriosis, due to Theileria hirci has a very similar distribution to bovine tropical theileriosis due to T. annulata. The disease also proliferates in the lymphatic system as do the more pathogenic bovine strains. It is endemic across tropical and sub-tropical Africa and Asia. The disease is seasonal based on tick availability and on the breed and immune status of the local sheep (and goat) population. In the acute form of the disease mortality rates can be high and affected animals are febrile. Schizonts develop within lymphocytes and macrophages and can be found in smears of blood and/or lymph nodes. Infected mononuclear cells disseminate throughout the lymphoid tissue, causing lymphoid hyperplasia and reticuloendothelial hyperplasia that is evident grossly as widespread lymphadenomegaly.

If lymphoid hyperplasia is severe enough to result in lymphatic obstruction, regional oedema and serous cavity effusions may develop. Piroplasms (merozoites) infect erythrocytes and can identified through examination of a blood smear. Erythrocyte parasitism results in extravascular haemolysis, which may be evidenced grossly by anaemia, icterus, and splenomegaly (Radostits, et al 2007). Benign ovine theileriosis, caused by either T. ovis or T. separata is an inapparent African disease. As with the 'benign' strains of bovine Theileria, it is a disease of the red cells and rarely associated with overt clinical signs (Radostits et al, 2007).

Australian veterinarians confronted with ovine theileriosis might first consider those diseases that are also on the list of differential diagnoses for M ovis infection (because the haemolysis is extravascular) or ovine babesiosis (mentioned above). The enlarged lymph nodes might suggest lymphoma. The organism should be apparent on blood smears.


Louping ill is a viral disease spread by ticks. While it is an important disease of sheep, other domestic animals can be affected as can red grouse and man. It is unpredictable, in some flocks causing no apparent disease while in others causing serious disease and mortality. As the ticks only survive off the host in a moist mat of rotting vegetation, it is a disease of the 'rough upland pastures' of Britain and Ireland (Reid, 2009).

Similar tick borne encephalitides, Russian spring-summer encephalitis (RSSE) and Central European encephalitis (CEE), occur in northern Eurasia. In each of these tick borne viral diseases, the virus cycles between ticks and small mammals and birds then 'spills over' to sheep and also cattle and goats (Geering and Forman, 1987).

Following a bite from an infected tick in susceptible sheep (especially lambs and young replacement sheep), the virus multiplies in the brain causing acute polioencephalomyelitis. Clinical signs occur in from 5 to 60% of infected sheep. These signs pertain to the nervous system and include behaviour changes, weakness, locomotory disturbances, paralysis and death. Surviving sheep develop life-long immunity. In Britain, a vaccine is available.

In Australia, the viral encephalitides would resemble neurological diseases such as listeriosis and phalaris staggers in sheep. These diseases might be suspected in the absence of an alternate diagnosis and if ticks were present. Histopathology may support the diagnosis, as there are few differentials for endemic causes of encephalitis in sheep. The inflammation characteristically confines to grey matter, which may suggest an unusual aetiology. In some cases encephalitis includes a neutrophilic infiltrate (which is unusual for viral encephalitis), and which may be difficult to differentiate from Listerial encephalitis (Jubb and Kennedy, 2007). However, predilection for histological lesions is to the cerebellar grey matter and ventral horns of the spinal cord, whereas lesions of Listeria are often most severe in the brain stem area. Therefore, it is important that these areas of CNS tissue are submitted for histopathology.


Nairobi Sheep Disease (NSD) is one of the most pathogenic diseases of sheep and goats (Edelsten 1975). It is confined to east and central Africa but Ganjam virus, a closely related variant causes a less pathogenic disease in Asian goats. NSD virus is not spread by direct contact. It is characterised by acute haemorrhagic gastroenteritis. Initially affected sheep are febrile, depressed and anorectic. Foetid diarrhoea follows. Superficial lymph nodes are enlarged and some animals have a blood stained nasal discharge. Abortion is a common sequel. Counter intuitively, mortality rates are higher in native African breeds that exotic breeds such as Corriedales and Romneys.

In Australia, Nairobi Sheep disease would resemble arsenic poisoning, coccidiosis and salmonellosis. However, a blood stained nasal discharge is not a feature of these diseases. NSD might be suspected if these diseases were ruled out and in the presence of ticks.


Borna is a tick borne disease of horses and sheep. Cattle goats and deer are occasionally infected. This viral meningo-encephalitis causes sporadic outbreaks of high mortality in central Europe (Geering and Forman, 1987).

Sheep are particularly susceptible to tularaemia, an infection caused by Francisella tularensis. Tularaemia occurs across the North America, Europe, Russia, china and Japan (OIE Centre for Food Security and Public Health). Affected sheep are septicaemic and so are febrile, with lymphadenopathy and malaise. Lambs and young ewes are particularly susceptible to fatal infection while other ewes suffer abortions and stillbirths. (Jensen and Swift, 1974)

Ticks occasionally act as vectors for a range of other diseases. Seddon commented that Haemophysalis humerosa and other ticks are a reservoir for Coxiella burnetii (1968)


The Bush Tick (Haemophysalis bispinosa) is an introduced tick whose preferred host is cattle. It is regarded as a potential vector for Theileria in cattle. However, it has been recorded on sheep as well as horses, pigs and dogs. As it is a coastal tick, it rarely causes significant infestations in sheep (Seddon, 1968). The indigenous Wallaby Tick (H. bancrofti) occurs in scrubby or timbered country and has been recorded on sheep. It is also a potential vector for bovine Theileria.

The introduced Brown Dog Tick (Rhipicephalus sanguineus) is a serious pest of dogs in tropical and sub-tropical Australia and can infest sheep in pastoral Queensland. The Ornate Kangaroo Tick (Ambylomma triguttatum) occurs widely throughout inland Australia. While its preferred host is macropods it can infest sheep, cattle, horses and dogs. These ticks can occasionally burden western NSW sheep attaching to the face and especially the ears where they cause significant worry to the stock (Seddon, 1968).

Ixodes holocyclus, the dog paralysis tick has caused considerable losses of sheep on the Atherton tablelands and has affected sheep near Pennant Hills (outer Sydney). As this tick is very susceptible to desiccation, it has a strict coastal distribution, outside the main sheep areas of Australia. Affected sheep were noted to become weak before collapsing into sternal recumbency. Keratitis is apparently a common feature of the disease and may precede paralysis (Seddon, 1968).

No discussion on tick borne diseases of Australian sheep would be complete without reference to Trypanosoma melophagium. This benign blood parasite was transmitted by the sheep 'tick' Melophagus ovinus (Turner and Murnane, 1930). The sheep 'tick' or ked however appears to have gone the way of catarrh, dispatching T. melophagium with it.


Human tick borne diseases, most notably tick-borne encephalitis and Lyme disease, have increased dramatically especially in the former states of the USSR post communism. While there is some speculation about the reason for this one suggestion is that increased poverty and wealth have induced people into the tick infested forest areas. The tick borne viral encephalitides (LIV, RSSE and CEE) not only affect people working or relaxing in forests. As the viruses are excreted in milk, outbreaks have also occurred in people consuming the milk of infected sheep and goats (Geering and Forman, 1987).

Granulocytic Erhlichosis agents following tick bites initially produce 'flu-like' symptoms. However, these agents are also immunosuppressive causing life threatening complications in people (Sumption, 2007).

Crimean-Congo haemorrhagic fever (CCHF) is a serious tick borne viral zoonosis. Sheep and a range of other vertebrates host the disease without effect. However, people are at risk both from infected ticks and from infected animal tissues (Sumption, 2007). NSD virus has been reported to cause fever and joint pain in people in Uganda (Geering and Forman, 1987).

Tularaemia, an infection from the bacterium Francisella tularensis is spread by a range of arthropod vectors but also by ingestion, inhalation and direct contact. More than one hundred species of temperate northern hemisphere mammals host the bacterium and sheep are particularly susceptible. In people case fatality rates from the wide range of unpleasant syndromes associated with F. tularensis is up to 35% if untreated (OIE Centre for Food Security and Public Health).


  1. Centre for Food Security and Public health. Tularemia http://www.cfsph.iastate.edu
  2. Edelsten RM (1975) The distribution and prevalence of Nairobi sheep disease and other tick-borne infections of sheep and goats in Northern Somalia. Trop Anim Hlth Prod 7, 29-34
  3. Geering WA and Forman AJ (1987) Animal Health in Australia, Volume 9 Exotic Diseases, p 149-151
  4. Jensen R and Swift BL. (1974) Diseases of Sheep, pp 297-299
  5. Jubb KVF and Kennedy PC and Palmer N. (2007). Pathology of Domestic Animals, 5th Edition, vol I, p 420; vol III, p 239, 244.
  6. Seawright, AA. (1982) Animal Health in Australia, Vol 2. Chemical and poison plants. pp109-110
  7. Seddon, HR. (1968) Diseases of Domestic Animals in Australia Part3 Arthropod Infestations, p 66
  8. Sumption K. (2007) Tick-borne disease of sheep, in Martin WB and Aitken ID Diseases of Sheep. Third edition, p 312
  9. Ticks and politics. The rise of tick-borne diseases in Eastern Europe www.wellcome.ac.uk
  10. Turner AW and Murnane D (1930) Trypanosomes in the blood of Victorian sheep. II. On the presence of Trypanosoma melophagium in the blood of Victorian sheep and its transmission by the sheep 'tick' Melophagus ovinus. Journal of the Council for Scientific and Industrial Research, Australia, 3, 121-122, cited by LL Callow Animal Health in Australia Vol 5 Protozoal and Rickettsial Diseases (Australian Government Printing Service, Canberra, 1984)
  11. Watkins GH. (2000) Arthritis, in Martin WB and Aitken ID Diseases of Sheep. Third edition, pp 251-2


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