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The first I heard of this disease was when I took a Babe into my vet for a health check just a couple days after I got her.  I had been waiting for her for a long time and she had been ill prior to my getting her.  Even though I was told she had been tested heart worm negative I had my vet recheck her just for my piece of mind.  She had come from an area in the country with very little heart worms and had not even been tested for it until I asked about it.  This time my paranoia paid off because in addition to testing for heart worms my vet also tested for C.E. And she was absolutely, no doubt about it, positive!

We had spent quite a while talking and working with Babe before this test was done.  There had been so many things which had not been thought out well before I got her and she had been treated incorrectly for months with a variety of drugs.  Treating the symptoms of the problem instead of considering that they were symptoms of a bigger problem.  I understand that this is the single most common problem with healing with C.E.  There is a tendency to not put the problems together in one package, all caused by one disease.

This disease is carried by the brown dog tick and is more common in areas with a larger tick population/infestation.  Keeping and maintaining tick free kennels will help but doesn't assure an animal will not be infected, but it helps.  There are 2 phases of the disease, acute and chronic.  The acute variety usually shows within the first 3 weeks or so of being bitten.  Some symptoms are fever, runny eyes/nose, swollen lymph nodes among others.  This variety responds well to treatment  in a short amount of time...usually going into remission and a return to health.

Chronic C.E. however usually can wait several months before signs start to show. Prolonged high temp, dehydration, no appetite, inability to keep food down, weight loss and lots of others as well. This phase of the disease, with proper medication, may have a good life.  Both varieties require antibiotics in the form of tetracycline. Up until recently this has been the only drug available in the US for treatment but just recently another one which has been used abroad has come here...I am unclear at this point if it is simply for research or wither we can actually get it for our babies. I will keep you all posted as L learn more about that aspect. Unfortunately the chronic form of the disease can kill.

Since this disease affects the immune system you really need to be careful about booster vaccinations.  I have had to make the decision to not give her a 6 month Parvo booster at this time until she is stronger and we can learn more about what the consequences might be. Right now my little Babette has good days and bad days.  She gets her medication 3 times a day and is also taking antibiotics in an olive oil based eye drops in both eyes for ulcers she has on both corneas...  We have 2 weeks to go on that and then will go in for testing.

This disease is out there.  It has been reported in every state and worldwide as well.  You cannot get it from an infected dog but you can from an infected tick. If you have a dog with the problem,  would like to share your story or have more links I would be delighted to have the info to add here!


An Overview of Canine Ehrlichiosis

Lauren Bockino, B.S.; Paula M. Krimer, DVM, DVSc; Kenneth S. Latimer, DVM, PhD; and Perry J. Bain, DVM, PhD

Class of 2003, Ross University, School of Veterinary Medicine, St. Kitts, West Indies (Bockino) and Department of Pathology (Krimer, Latimer, Bain), College of Veterinary Medicine, University of Georgia, Athens, GA 30602-7388

Barbara's Dogs by Tom Martin


The Ehrlichiae are a group of small, gram-negative, pleiomorphic, obligate intracellular cocci that infect different blood cells in various animal species and in humans. There has recently been a reclassification of the family Anaplasmataceae to which the Ehrlichiae belong.8 According to this new classification there are two leukotrophic diseases in dogs that are caused by bacteria in the genus Ehrlichia, namely, Canine Monocytic Ehrlichiosis (caused mainly by Ehrlichia canis) and Canine Granulocytic Ehrlichiosis (caused by Ehrlichia ewingii). It should be noted that cross-reactivity and co-infection is common among the ehrlichiae.7 Classically, canine ehrlichiosis presents as a rather non-specific multisystemic disorder with the primary complaints being depression, lethargy, mild weight loss, vomiting, diarrhea, and anorexia, with or without hemorrhagic tendencies. Furthermore, patients may present with uveitis and/or retinal petechiae, polymyositis, polyarthritis, and central nervous system signs.2 Hematologic abnormalities most commonly associated with canine ehrlichiosis include nonregenerative anemia and thrombocytopenia. Serum chemistry commonly reveals hyperglobulinemia (monoclonal or polyclonal gammopathy), hypoalbuminemia, and low albumin-globulin ratio.5

Canine Monocytic Ehrlichiosis (Ehrlichia canis)

Canine Monocytic Ehrlichiosis (CME), caused by E. canis, is an acute to chronic disease of monocytes, and is the ehrlichial disease most extensively studied. This organism is primarily transmitted by Rhipicephalus sanguineus, the brown dog tick. It is seen mostly in the southeastern and southwestern United States, although it is recognized in all states and worldwide. Amblyomma and Dermacentor ticks have also been implicated in transmission of this disease.3 Dogs may present with variable clinical signs, but thrombocytopenia with bleeding tendencies is the most consistent presenting complaint in dogs in both the acute and chronic stages of the disease.1 During the acute stage, splenomegaly and lymphadenomegaly are common. In the chronic stage, widespread hemorrhage and increased mononuclear cell infiltration of organs may also be evident. Hematologic changes include nonregenerative anemia, thrombocytopenia, and leukopenia. Pancytopenia may occur as a result of hypoplasia of all bone marrow precursor cells, more commonly in the severe chronic phase.4 Some dogs may develop a secondary immune-mediated hemolytic anemia (IMHA) and have an acute hemolytic crisis, and, thus, a positive direct antiglobulin (Coombs') test.1

Canine Granulocytic Ehrlichiosis (Ehrlichia ewingii)

Canine Granulocytic Ehrlichiosis (CGE) caused by Ehrlichia ewingii, is a disease of neutrophils and, rarely, eosinophils. CGE classically presents with mild signs including fever, lethargy, anorexia, weight loss, vomiting, diarrhea, severe but transient thrombocytopenia, and transient mild nonregenerative anemia with ineffective erythropoeisis. Commonly, the major presenting clinical signs associated with E. ewingii include lameness and joint swelling due to polyarthritis. This form of ehrlichiosis is generally seen in the southern and mideastern United States.1,4 Ticks including Ixodes pacificus, Dermacentor variabilis, Rhipicephalus sanguineus, Amblyomma americanum (especially in North Carolina), and Ixodes scapularis (damminni) have been implicated as vectors.3,6

Pathogenesis of Ehrlichiosis

The pathogenesis of infection with E. canis is the most extensively studied; therefore this discussion will focus on this particular species.

Infection occurs through salivary secretions of the tick at the attachment site during ingestion of a blood meal or through blood transfusions. If the adult Rhipicephalus sanguineus engorges on the dog during the acute stage, it can transmit the disease to other dogs for at least 155 days following detachment.1 Transmission by Rhipicephalus sanguineus is transstadial: the tick acquires the bacteria by feeding on an infected dog in either the larvae or nymph form and the tick transmits the disease to another dog as either the nymph or adult form. The life cycle of Ehrlichia is not yet completely understood but it is thought that it occurs in three intracellular forms. The initial bodies are small spherical structures (1-2 micrometers in diameter) which are believed to develop into larger multiple membrane-bound units known as morulae. The morulae are inclusions within the cytoplasm of the leukocyte as seen in Figure 1. This morula is thought to then dissociate into small granules called elementary bodies.

Figure 1. Ehrlichia canis seen in a membrane-bound inclusions (morulae) within the cytoplasm of a monocyte (buffy coat smear, Wright stain).

After an incubation period of 8-20 days, the acute phase of infection occurs which lasts 2-4 weeks. At this time, the organism multiplies within circulating mononuclear cells and the mononuclear phagocytes within the liver, spleen, and lymph nodes. The infected cells are then transported in circulation to the rest of the body, with a predilection for the lungs, kidneys and meninges. Cells infected with ehrlichia adhere to the vascular endothelium and induce a vasculitis and subendothelial tissue infection. This subsequently leads to platelet consumption, sequestration, and destruction that results in the thrombocytopenia seen during this acute phase. Variable leukocyte counts and anemia may also develop progressively during this stage.1 After 6-9 weeks, dogs will either eliminate the parasite (if immunocompetent) or develop a parasitemia in which clinical signs absent to mild to severe. This stage is also characterized by variable persistence of thrombocytopenia, leukopenia, and anemia. Dogs that cannot mount an effective immune response will become chronically infected.1


Definitive diagnosis of CME requires visualization of morula within monocytes on cytology, detection of E. canis serum antibodies with the indirect immunofluorescence antibody test (IFA), polymerase chain reaction (PCR) amplification, and/or gel blotting (Western immunoblotting).

On cytology, ehrlichiae stain dark blue to purple with Romanowsky stain. The morulae are well-defined, round to oval, eosinophilic to basophilic bodies found in host membrane-lined vacuoles within the cytoplasm of the mononuclear cells.1

In dogs experimentally infected with E. canis, the IFA test has detected serum antibodies as early as 7 days after initial infection, although some dogs do not become seropositive until 28 days post-infection. If ehrlichiosis is highly suspected clinically in a seronegative dog, serology should be repeated in 2-3 weeks. In the past, titers of IgG antibodies of >1:80 have been considered diagnostic,1 but the most recent research has indicated that titers <1:80 should be deemed suspect and serology should be repeated in 2-3 weeks or a PCR or Western immunoblotting should be considered. A diagnosis should be made and treatment instituted when clinical signs and clinicopathological abnormalities consistent with canine ehrlichiosis are found.2

There are a few potential downfalls of using the IFA test for the diagnosis of E. canis infection. One major concern exists in endemic areas with dogs that are chronically infected and have a positive titer, but are otherwise healthy or show non-specific clinical signs. In these dogs, a positive antibody titer does indicate past exposure to E. canis, does not prove that ehrlichiosis is necessarily an active infection or the cause of the presenting clinical signs. In dogs with non-specific clinical signs, a repeat IFA test after 1 or 2 weeks may be beneficial to differentiate between primary E. canis infection and another secondary disease. Antibody titers to E. canis should increase with active infection. Furthermore, one must consider co-infection with multiple tick-borne diseases caused by agents such as other Ehrlichiae, Rickettsia species, Bartonella species, and Babesia canis. Disease caused by any of these agents may be clinically, hematologically, and serologically indistinguishable from each other. In addition, the immunodominant proteins of E. canis have been shown to serologically cross-react with those of E. chaffeensis (the agent that causes Human Monocytic Ehrlichiosis). Studies have shown that serologic testing by IFA could not consistently distinguish between infections of these two species. Interpretation of E. canis serology should include the consideration of the disease process, cross-reactivities with other ehrlichial species, the possibility of multiple tick-borne infections, and persistent IFA antibody titers post-treatment. Antibody titers be used to gauge the success or failure of treatment of CME. Treatment success should be based on remission of clinical signs, a decline in E. canis antibody titers and a concurrent decrease in gammaglobulin concentrations.7

PCR amplification is also a sensitive method for the detection of acute E. canis although there are currently several potential limitations. It is recommended that this method be used in addition to serology for the initial diagnosis of ehrlichiosis, not instead of it.2

The diagnosis of CGE differs from that of CME as E. ewingii has not yet been cultivated in an in vitro system, therefore antigens have not been available for comparative serological testing. Diagnosis of CGE requires visualization of morula within neutrophils in peripheral blood (Figure 2), joint effusions, and PCR or Western immunoblot.3 In a study using Western immunoblots, sera from dogs that were experimentally infected with E. ewingii were tested on E. canis antigens. Although there were no reactions with the dominant E. canis antigens, the sera produced binding patterns similar to those of anti-E. canis sera with high molecular proteins. This also may help with the diagnosis of CGE.7

Figure 2. A segmented neutrophil from a dog that contains morula of a granulocytic species of Ehrlichia, most commonly Ehrlichia ewingii (blood smear, Wright stain).


Treatment and Prevention

The mainstay of prevention of canine ehrlichiosis is tick control. The drug of choice for treatment for all forms of ehrlichiosis is doxycycline for at least one month. There should be dramatic clinical improvement within 24-48 hours following initiation of treatment in dogs with acute-phase or mild chronic-phase disease. During this time, platelet counts begin to increase and should be normal within 14 days after initiation of treatment.1,2 Polyarthritis associated with E. ewingii may be self-limiting.3 Previous infection does not confer lifelong immunity, and dogs can become reinfected with the same or other ehrlichial species after re-exposure to infective ticks.



1. Ettinger SJ, Feldman EC: Textbook of Veterinary Internal Medicine: Diseases of the Dog and Cat, vol. 1, 5th ed. W.B. Saunders Co., Philadelphia, 2000, pp. 402-406.

2. Neer TM, Breitschwerdt EB, Greene RT, Lappin, MR: Consensus statement on ehrlichial disease of small animals from the Infectious Disease Study Group of the ACVIM. J Vet Intern Med 16:309-315, 2002.

3. Goldman EE, Breitschwerdt EB, Grindem CB, Hegarty BC, Walls JJ, Dumler JS: Granulocytic ehrlichiosis in dogs from North Carolina and Virginia. J Vet Intern Med 12:61-70, 1998.

4. Neer TM: Canine monocytic and granulocytic ehrlichiosis. In: Greene CE (ed): Infectious Diseases of the Dog and Cat, 2nd ed. W.B. Saunders Co., Philadelphia, 1998, pp.139-147.

5. Varela F, Font X, Valladares JE, Alberola J: Thrombocytopenia and light-chain proteinuria in a dog naturally infected with Ehrlichia canis. J Vet Intern Med 11:309-311, 1997.

6. Wolf L, McPherson T, Harrison B, Engber B, Anderson A, Whitt P: Prevalence of Ehrlichia ewingii in Amblyomma americanum in North Carolina. J Clin Microbiol 38:2795, 2000.

7. Waner T, Harrus S, Jongejan F, Bark H, Keysary A, Cornelissen A: Significance of serological testing for ehrlichial diseases in dogs with special emphasis on the diagnosis of canine monocytic ehrlichiosis caused by Ehrlichia canis. Vet Parasitol 95:1-15, 2001.

8. Ehrlichia Research Laboratory, College of Veterinary Medicine, The Ohio State University, Columbus, OH

The watercolor "Barbara's Dogs" by Tom Martin, New Moon Illuminations, is used with permission of the artist.



This page is a special feature of Working Dogs Cyberzine

Canine Ehrlichiosis

Clinical Name: Ehrlichiosis, Ehrlichia

Dogs get ehrlichiosis from the brown dog tick, which passes an Ehrlichia organism into the bloodstream when it bites. There are three stages of ehrlichiosis, each varying in severity. The acute stage, occurring several weeks after infection and lasting for up to a month, can lead to fever and disorders of the blood. The second stage, called the sub clinical phase, has no outward signs and can last for up to five years. If the infected dog’s immune system is unable to eliminate the Ehrlichia organism, the third and most serious stage of infection, the chronic phase, will commence. Lameness, neurological and ophthalmic disorders, kidney disease, and anemia and other blood disorders can result. Chronic ehrlichiosis can be fatal.

Antibiotics, administered for an extended period of time, are effective at eliminating the infection. Dogs with severe cases of chronic ehrlichiosis cannot be cured, but supportive care and treatment of diseases secondary to the infection, such as anemia, can help stabilize the dog.

Clinical Signs and Symptoms

The acute stage of the disease, occurring most often in the spring and summer, begins one to three weeks after infection and lasts for two to four weeks. Clinical signs include a fever, petechiae, bleeding disorders, and vasculitis. There are no outward signs of the sub clinical phase, which can last for up to five years. Clinical signs of the chronic phase include pale gums due to anemia, thrombocytopenia, vasculitis, lymphadenopathy, respiratory dyspnea, coughing, polyuria, polydipsia, lameness, ophthalmic diseases such as retinal hemorrhage and anterior uveitis, and neurological disease.


Diagnosis is achieved most commonly by serologic testing of the blood for the presence of antibodies against the Ehrlichia organism. During the acute phase of infection, however, the test can be falsely negative because the body will not have had time to make antibodies to the infection. Thus, the test will need to be repeated if the first result is negative. In addition, blood tests will show abnormalities in the numbers of red cells, white cells, and platelets. Uncommonly, a diagnosis can be made by looking under a microscope at a blood smear for the presence of the Ehrlichia organism, which sometimes can be seen within a white blood cell.


Ehrlichiosis is a tick-borne disease of dogs that is caused by an organism called Ehrlichia. There are several species of Ehrlichia, but the one that most commonly affects dogs and causes the most severe clinical signs is Ehrlichia canis. The brown dog tick, or Rhipicephalus sanguineous, that passes the Ehrlichia to the dog is prevalent throughout most of the United States, but most cases tend to occur in the Southwest and Gulf Coast regions where there is a high concentration of the tick.

There are three stages of the Ehrlichia canis infection: acute, sub clinical, and chronic. Approximately one to three weeks following the infection, clinical signs of the acute phase begin and typically last for two to four weeks. The sub clinical phase, which does not produce outward clinical signs, lasts for up to five years. If the dog’s immune system is unable to eliminate the organism during this stage, the chronic phase will occur and may last for years, depending on the severity of the infection. Dogs that are severely affected can die from this disease.

Although people can get ehrlichiosis, dogs do not transmit the bacteria to humans; rather, ticks pass on the Ehrlichia organism. Clinical signs of human ehrlichiosis include fever, headache, eye pain, and gastrointestinal upset.

Transmission or Cause

The Ehrlichia organism is passed to the dog through the saliva of a tick called Rhipicephalus sanguineous. These ticks are prevalent throughout most of the United States, but most cases of infection tend to occur in the Southwest and Gulf Coast regions.


Supportive care must be provided to animals that have clinical signs. Subcutaneous or intravenous fluids are given to dehydrated animals, and severely anemic dogs may require a blood transfusion. Treatment for ehrlichiosis involves the use of antibiotics such as doxycycline for a period of at least six to eight weeks; response to the drugs may take one month. In addition, steroids may be indicated in severe cases in which the level of platelets is so low that the condition is life threatening.


The prognosis is good for dogs with acute ehrlichiosis. For dogs that have reached the chronic stage of the disease, the prognosis is guarded. When bone marrow suppression occurs and there are low levels of blood cells, the animal may not respond to treatment.


Prevent tick infestation by avoiding tick-infested areas. In addition, there are many methods for controlling fleas, including medicated shampoos, dips, sprays, the Preventic® collar, or Frontline®. If tick control is not feasible, tetracycline at a lower dose can be given daily for 200 days during the tick season in endemic regions.

Article republished here with permission from
Copyright(c) 2000 by



by Holly Frisby, DVM

Drs. Foster & Smith, Inc.
Veterinary Services Department

Canine ehrlichiosis is a disease of dogs and wild canids (e.g., wolves) and is found worldwide. Canine ehrlichiosis is also known by other names such as "tracker dog disease", "tropical canine pancytopenia", "canine hemorrhagic fever", and "canine typhus". It affected a large number of military dogs in the war in Vietnam.

What causes ehrlichiosis?

Ehrlichiosis can be caused by several organisms including Ehrlichia canis, E. equip, E. platys, E. ewingii, and possibly others. The Ehrlichia organisms are what we call rickettsia which on the evolutionary scale are between bacteria and viruses.

How is Ehrlichia transmitted?

Ehrlichia is transmitted by the brown dog tick, Rhipicephalus sanguineus. The immature form of the tick feeds on an animal infected with Ehrlichia. When these immature forms or a mature form of the tick feeds on another animal, the Ehrlichia is passed on to that animal. The Ehrlichia can remain alive in the developing tick for up to 5 months. This means a tick could become infected in the fall, and infect a dog the following spring.

Because the disease is transmitted by the brown dog tick, it can occur wherever brown dog ticks are found. Almost every state in the United States has reported a case of ehrlichiosis.

What are the symptoms of ehrlichiosis?

Ehrlichiosis can have three phases. Signs of the acute phase of the disease usually develop 1-3 weeks after the bite of the infected tick. The acute phase of the disease generally lasts 2-4 weeks. The Ehrlichia enter certain cells of the body and reproduce inside of them. These cells are found in the lymph nodes, spleen, liver, blood, and bone marrow. As a result of the infection the lymph nodes, liver and spleen are often enlarged. Anemia, fever, depression, lethargy, loss of appetite, shortness of breath, joint pain and stiffness, and bruises are often seen.

In the sub clinical phase the animal may show only slight anemia. During this phase the dog either eliminates the Ehrlichia from the body or the infection may progress to the chronic phase.

The chronic phase generally develops 1-4 months after the tick bite and can be either mild or severe. Weight loss, anemia, neurological signs, bleeding, inflammation of the eye, edema (fluid accumulation) in the hind legs and fever may be seen. Blood tests show that one or all of the different blood cell types are decreased. One cell type, the lymphocyte may increase and be abnormal in appearance. This can sometimes be confused with certain types of leukemia. If a dog becomes chronically infected, the disease can keep coming back, especially during periods of stress.

A decrease in the number of platelets (platelets help the blood clot) in the blood is the most common laboratory finding in all phases of the disease. Changes in the protein levels in the blood are common. The most common protein, albumin, is decreased and other types of protein called "globulins" are increased.

Since one tick could be infected with and transmit more than one disease (e.g., haemobartonellosis or asbestosis), it is not all that uncommon to see a dog infected with more than one of these diseases at a time which generally causes more severe symptoms.

How is ehrlichiosis diagnosed?

A highly accurate blood test which tests for the dog's antibodies (proteins produced to fight off the infection) to Ehrlichia is available. It is called the indirect immunofluorescent antibody (IFA) test. The antibodies may not be detected in the early phase of the disease since it takes some time for the body to make them. As the disease progresses, the antibody level will rise significantly. Often two tests will be done 2 weeks apart and the results compared. Dogs with an active infection will show a significant rise in the amount of antibody present.

A newer test called the ELISA test is becoming more available and the test can be run in your veterinarian's laboratory. This test also determines the amount of antibodies present.

The antibodies can last for one or more years after the infection, but they do not make the dog immune to ehrlichiosis - the dog could get reinfected.

Sometimes the organism can be seen inside cells on a blood smear. To find them, a small drop of blood is spread over a microscope slide, stained and examined under the microscope. The organism can only be found in the blood stream for about 3 days during the acute phase of the disease. So this method of diagnosis could miss some cases of the disease.

How is ehrlichiosis treated?

The antibiotics tetracycline or doxycycline are used. Treatment is for 2-3 weeks. Some dogs will need blood transfusions or intravenous fluids depending on the severity of the disease. Generally the prognosis during the acute phase is good if the animal is properly treated. Dogs who go on to the chronic phase have a poorer prognosis. German shepherds and Doberman pinschers tend to have a more severe chronic form of the disease.

The drug imidocarb dipropionate is sometimes used in conjunction with the antibiotics. It is given as an injection, but may not be available in all areas.

Some of the damage caused by Ehrlichia may be due to the dog's own immune response to the organism. For this reason, high doses of corticosteroids (e.g., prednisolone) are often given during the early phase of the disease.

How can I prevent ehrlichiosis in my pet?

Tick control is the main way to prevent ehrlichiosis. Products which repel and kill ticks such as Biospot for Dogs are excellent choices. Tick collars containing the active ingredient amitraz (Preventic collars) are also used, sometimes in conjunction with Biospot in those areas with high tick infestations. If a large number of cases of ehrlichiosis are diagnosed in an area, some veterinarians recommend placing dogs on low doses of tetracycline or doxycycline during the tick season.

There is no vaccine for ehrlichiosis.

Can people get ehrlichiosis?

Yes. The common symptoms in people include fever, chills, headache, and muscle aches. Other less common symptoms include nausea, loss of appetite, weight loss, abdominal pain, cough, diarrhea and change in mental status.

People do NOT get infected directly from a dog, but through a tick bite. Human ehrlichiosis may be spread by a different tick than the brown dog tick. Research suggests the Lone Star tick may be involved. Also, the Ehrlichia species most often implicated in human infections is E. chaffeensis.


Couto, DG. Rickettsial Diseases. In Birchard, SJ; Sherding, RG (eds): Saunders Manual of Small Animal Practice. WB Saunders Co., Philadelphia PA; 1994;124-5..

Harrus, S; Bark, H; Waner, T. Canine monocytic ehrlichiosis: An update. Compendium of Continuing Education for the Veterinary Practitioner 1997;19 (4) :431-444.

Olson, JG. Ehrlichiosis. In: Zoonoses updates from the Journal of the American Veterinary Medical Association. American Veterinary Medical Association, Schaumburg IL; 1995:74-75.


Dr. Ibulaimu Kakoma DVM PhD

First I want to thank Jan and Bob for giving me the opportunity to make some remarks and to congratulate them for undertaking such heavy and well executed responsibility to address this important issue. Their basic premise was to reach the owner/breeder and also to establish dialogue with the veterinary clinicians and scientists outside the vet's office. I think they have achieved both. The owners and breeders will gather tremendous information from this article in a language they will understand since there is a minimum of technical jargon to cloud their reading enthusiasm. The veterinarian and scientist will get the challenging message that the 21st century clients have modern tools to watch everything we do and publish and they are looking for a practical product for their pet.... at times regardless of how much it will cost. The clients are also prepared to work with us to the extent possible and when they question our training they are not vet bashing but trying to develop a dialogue.

The authors are right in indicating that diseases have no borders. Today the definition of a tropical disease could not have been more nebulous and blurred! That is why we have task forces in USA and Europe to deal with "Emerging diseases" which show up suddenly and unexpectedly. In some ways ehrlichiosis meets that definition.

This raises the issue of training in tropical medicine. The authors' point is well taken that veterinary curricula are facing the challenge to accommodate the problems of newly emerging diseases, such as ehrlichiosis.

Extra attention needs to be paid to this segment if future veterinarians are going to be prepared for diseases that just emerge here or encountered in missions overseas. It is gratifying to know that there is a Society of Tropical Veterinary Medicine and "Intervet" which expose our veterinary community to so- called foreign diseases. The USDA at Plum Island along with the CDC are examples of establishments that have enormous resources to educate all of us on these issues.

Bob and Jan bring up the issue of the complexity of ehrlichiosis. In fact the disease is more of a syndrome. Readers will appreciate this from articles such as that written by David Huxsoll who has so neatly categorized the stages of the disease. The spectrum of syndromes and disease entities imitated by ehrlichiosis are incredible, emphasizing the need to carefully rule out ehrlichiosis for common infectious diseases.

The warning signs may certainly be subtle. Can one rule out ehrlichiosis by the IFA test and should we treat all animals which are IFA positive? First, a positive IFA test simply means "current or previous exposure" ........treatment or recovery does not guarantee a negative IFA.

Any patient positive in the IFA and presenting with signs consistent with ehrlichiosis should definitely be treated. Indeed empirical treatment is reasonable if in the clinician's assessment waiting for the IFA results could endanger the patient. IFA could certainly be negative during the very early phase of the disease even when severe signs are evident.

Therefore, in the writer's opinion a clinical assessment may supercede the IFA status. A positive IFA test excludes a dog from being a blood donor and membership of a breeding stock for the fear of transmitting the disease and every effort should be made to research into methods of terminating the carrier state.

Provided the treatment is prescribed and monitored by a veterinarian, it seems less risky to treat IFA positive animals resident in a non-endemic area than to risk a severe disease. In an endemic area, however, treatment on the basis of the IFA test per se cannot be justified since the patient will again be exposed and the synergistic advantage between antibodies and the cellular immune system may be of value in fighting the new infection. In other words, in areas where the diseases are common practically every dog has been exposed and treatment can only be justified on the basis of the clinical disease.

The relatively low endemicity in many parts of North America means that supervised treatment of early diagnosed( by IFA or PCR) cases is worthwhile to prevent costly potential worsening of the patient's condition or even death, as mentioned by Bob and Jan. They have shared with us their private experiences in which intervention helped some cases and when the problem was recognized too late the patient could not be saved. It must be emphasized, however that empirical treatment with antibiotics must be carefully evaluated and monitored to avoid abuse of these important compounds.

The other issue raised is "early diagnosis". The PCR test is showing promise and perhaps in future it will be available routinely. Because the test is DNA-based, it offers the most specific and sensitive detection method which confirms that the patient is definitely infected and treatment would be indicated without any doubt. Finally, we must join the authors in a crusade to find alternative drugs to doxcyline and tetracyline in case we encounter resistance to these drugs or we are treating mixed infections ( e.g. ehrlichiosis and babesiosis). A case in point is Imizol® a well tested drug used in may parts of the world but not legally available for dog treatment in USA. (Since the article was written in 1996 , unfortunately, little has changed. However, one important change is the fact that Imizol is now available and your vet should be able to easily obtain it. This drug is given by injection in a series, normally, of two shots two weeks apart. - Bob Wilson 1/14/2000). Compassionate users of Imizol® have reported impressive results in cats and dogs suffering from ehrlichiosis and we should continue research to facilitate approval by the FDA. The ultimate goal should however be the development of a vaccine for this disease complex and for that we need to work with the breeder, the owner, industry and academia. This mission is noble according to the wishes of friends such as Pajti, Jake, Bear, Saucy and many others born in the Hendricks and Mair families.

For those searching for additional reading please search under the following scientists: Ewing, S; Huxsoll, D; Breschwerdt, E; Dawson, J; Lewis, G E; Holland, C J; Ristic, M R; Dutta; Rikihisa, Y; Madigan, J; Dumler; Bakken; Nyindo; Roult; Long, M; Goetz; Palmer, G; Walker, D; and many other scientists.

Ibulaimu Kakoma,DVM PHD
Urbana IL.
January, 1996


The purpose of this document is to help dog owners as well as their veterinarians become aware and learn more about a dreaded and deadly killer that is claiming the lives of dogs in all 50 states.

We also encourage you to reproduce the document should you wish to pass it on to others. We only ask that it be the complete document so that nothing is taken out of context and to give credit to those who labored so diligently in its preparation.

While a lot of detail is contained in this document, it is thought and hoped that it will be shared with the dog owners' veterinarian. Many vets are not familiar with ehrlichiosis, do not appreciate the magnitude of the problem or have treated it as something else failing to treat the underlying cause. This is in no way meant to condemn the veterinary community. As you will see, they are reacting to what they perceive as signs of diseases they are more familiar with, which is a very logical approach but not one that will work with ehrlichiosis. The nature of this disease is such that it mimics a great many other diseases, and this tends to confuse and complicate treatment.

There are many forms of the disease attributed to the organisms in the genus ehrlichia that are genetically related, including one of the species recently found in humans which causes the disease HGE (Human Granulocytic Ehrlichiosis). Another is E. equip species which causes illness in horses. This is a different species than E. risticii which causes Potomac Horse Fever and is also found in dogs. Other identified species are E. sennetsu, human pathogen, E. ewingii and E. platys, both canine pathogens. The species E. ewingii has been reported in dogs in Minnesota, and likely occurs in other states as well.

The two keys to success are early recognition and treatment.

Treatment with proper antibiotics can be quite dramatic in these cases, whereas treating an ehrlichiosis patient with steroids or drugs other than the tetracycline family will almost certainly lead to tragedy.


This section is for the clinician. Please form a picture in your mind of the following: A client comes into your clinic with her dog. She is a good client, her dog gets his vaccinations regularly, is on heartworm preventive, and is obviously well cared for.

But today it is apparent she is very worried about her pet. You glance at the dog - a middle-aged pleasant animal who looks a bit tired. "Doctor", the owner begins, "He just isn't himself lately - he doesn't want to play anymore, and he always enjoyed retrieving his ball. His coat isn't as nice as usual - he seems to be turning gray early - he's only 5 years old! We've noticed his breath is really bad, and sometimes he doesn't want to eat. Then he will eat fine for a few days, but he will throw up yellow stuff. His eyes are really red too - and sometimes they have a glassy reflective look like they do at night in a headlight. He used to love to sleep with us, but now he seems to have trouble getting up on the bed. And he's always drinking water - I don't remember him ever drinking so much water. And I've never known him to have so many accidents; he always used to be so clean - now sometimes he doesn't even ask to go out - he just goes on the floor like he doesn't care. What could be wrong with him Doctor? I'm really worried...."

O.K. Doctor, what do you think? Impossible for one dog to have so many problems? Neurotic owner? Better take a look.....with the dog up on the table, you take his temp - normal. Eyes are pretty red - allergies? Coat does look a bit dull, but you've seen worse. You ask about the food he is eating - how much exercise he is getting - has his routine changed lately?

Chances are good that this dog may be sent home with different food, vitamins or a coat additive, advice to cut back on the evening water so there won't be so many accidents. Maybe he is just bored and needs more attention. Still, it wouldn't be a bad idea to do a CBC. What about his difficulty in getting up on the bed - could he be developing arthritis? Seems kind of young - but maybe he's just getting old before his time. Then the CBC comes back within normal limits - white count is a little depressed, but not that bad. He seemed to have a slight cough - could be a mild case of kennel cough that he just can't shake. Amoxicillin for a couple of weeks should take care of that.

Sound familiar? This is beginning to happen in veterinary clinics all over America every day. Because the signs are run-of-the-mill, it is not the sort of case that even the most detailed veterinarian is going to get too excited about. We would like to change that, because there is a very good chance that the dog just described is suffering from a type of infection often considered as rare - ehrlichiosis. The fact is, ehrlichiosis is not rare at all, and through this paper, we hope to dispel that myth - because that myth is resulting in countless deaths of pet dogs and even cats - and each and every one of these pets was someone's special friend. It doesn't have to be that way.

Perhaps the most critical thing for the clinician to remember is to look at the big picture. Does a client's pet really have several ailments affecting different systems, or could it be suffering from ehrlichiosis which in essence, affects all systems?

What about the purebred show dog with autoimmune disease? It is easy to assume this is a genetic problem inherent in the breed but why not give the dog the benefit of the doubt and consider ehrlichiosis as a possible cause. Response to treatment with proper antibiotics can be quite dramatic in these cases, whereas treating an ehrlichiosis patient with steroids is almost certainly signing its death warrant.

Today's veterinarian will also acknowledge that today's pets travel far and wide with their owners. As a result, the diseases and vectors are no longer limited to specific regions. Ticks thrive in cold as well as warm climates and where the tick goes, so goes the ehrlichiosis.


Surprisingly, Ehrlichia has been around for a lot longer than most people realize. It was first described in 1935 in Algerian dogs. However, in 1962 , a number of military dogs (German Shepherds) that had been stationed in Vietnam died from complications of Hemorrhagic Fever. It was later determined to have been caused by the ehrlichia species E. canis.

Even more surprising is that the rapid spread and reports of the disease have only occurred in the last few years. Today it has been and continues to be reported in all 50 states, Canada, Europe, Asia, South America and Africa.

Ehrlichiosis is related to Rocky Mountain Spotted Fever and shares similar signs, though rarely does a victim of ehrlichiosis display the rash that is associated with RMSF. Lyme disease also shares some of the same signs, but technically is in a separate category. Lyme disease is caused by a spirochete (a spiral shaped bacteria) and although it is transmitted by ticks, as are most of the rocketries, Lyme disease is sensitive to a wider range of antibiotics, and Lyme disease has never been linked to fatalities as are many of the rickettsias. The rickettsial group is unique in that it's members share some traits of a virus, and some traits of a bacteria, but they are classified with bacteria.

While doxycycline is frequently used to treat Lyme disease other drugs have been used. Amoxicillin is a recent trend in the treatment of Lyme disease but has no effect whatsoever on ehrlichiosis. As both Lyme disease and ehrlichiosis share some signs a misdiagnosis of ehrlichia as Lyme disease could prove fatal to both dogs and humans if not treated with the proper drug.

Rickettsias actually parasitize the white blood cells, which is why they are so devastating to their victims. Essentially, they cripple the immune system by inhibiting the basic function of the bone marrow - that of making new cells to replace old and dying cells.

Once a human or animal is stricken with ehrlichiosis, white cells die off faster than the bone marrow can replace them. These dead cells migrate primarily to the spleen which enlarges as a result. Frantically, the bone marrow works to form new, healthy cells. In its haste, it sends out immature cells which do not work efficiently. Quite often these immature cells are almost indistinguishable from those seen in leukemic patients. Advanced Ehrlichiosis is, in fact, often misdiagnosed as leukemia or lymphosarcoma.

To complicate things further, ongoing research suggests that chronic ehrlichiosis may lead to various cancers, especially leukemia and lymphosarcoma. There is speculation that it may predispose animals to other forms of cancer as well. Because of its effect on the nervous system, ehrlichiosis is also sometimes misdiagnosed as brain cancer. It does, in fact, affect many dogs neurologically and can cause seizures, problems with coordination, changes in temperament, or obsessive-compulsive behavior (such as repeated licking or other repetitive behaviors.)

Causes of death by ehrlichia are usually due to internal hemorrhage including hemorrhage into the brain, severe autoimmune disease, multiple secondary infections due to a compromised immune system or complete failure of one or more internal organs such as heart, liver, spleen, etc.


With the exception of E. risticii, most rickettsias are believed to be spread through contact with ticks. E. risticii is particularly difficult as no vector (the insect agent of transmission) has been clearly identified. Ongoing research indicates that a tick could be implicated but a variety of possible vectors exist. Flies, mosquitoes, chiggers, and fleas, are all being considered as possible insect vectors.

Carriers (reservoirs) of the disease may include mice, rats and other mammals who have constant exposure to various insects (but are themselves unaffected by the disease). It was once thought that cats and even dogs could act as reservoirs for E. risticiiand not develop signs of disease. In the last few years this has not proven to be consistent as more and more domestic dogs and cats have developed serious illness after natural infection with E. risticii.

Newly infected domestic animals (who may ultimately succumb to the disease) may serve as carriers for insect vectors, who then pass the infection to another animal. At least one of the species, E. risticii, can be passed through the placenta to puppies. It can also be passed from infected donor animals used in veterinary clinics. None of the species are thought to be passed through breeding, but we have been unable to locate any current research in this area.

The two species that have, to date, been most commonly reported in dogs are E. canis and E. risticii. It is possible to be infected with both species which presents a particularly nasty challenge. It is fortunate that both respond to the same method of treatment.

There is no breed that has shown either a greater or lesser immunity to the disease and there are a great variety of breeds, including mixed breeds, that have contracted ehrlichiosis.

While it was initially found primarily in the Southwestern States, today it is found throughout the US. The human form has had the highest number of reported cases in Wisconsin and Minnesota but it too is found in many other locations in the US.

It should also be noted that it has been fatal in humans whereas Lyme disease has yet to claim its first victim.


The disease typically courses through three stages. The first is the early or acute stage (which usually mimics a mild viral infection.) The signs in this stage may be very subtle and could go unnoticed. Without proper treatment the animal will go on to a sub clinical (second) stage or may advance to the chronic (final) stage. During the acute stage most, if not all, damage is reversible and a full recovery is possible. It is during this stage that treatment is most effective, which emphasizes the need for early detection.

Once the chronic stage is reached, the rickettsial organism has taken up residence within the bone marrow. At this point the damage done is often irreversible. It is not unusual for dogs in this final stage to suffer massive internal hemorrhage, or succumb to sudden stroke, heart attack, renal failure, splenic rupture or liver failure, resulting in death. A peculiarity about the disease is - these dogs often do not look or act as though they are in a terminal stage of disease until their final hour.


If there is any one element of this disease that makes it especially deadly, it is the ability it possesses to mimic other diseases. Perhaps the best description of ehrlichiosis is "the AIDS of the canine world". The detection of the disease has, so far, only been successfully accomplished through IFA (indirect fluorescent antibody test) which detects the presence of antibodies. This test is, however, not infallible; dogs sometimes test negative in the acute phase due to their immune system's delay in forming antibodies. They may also test negative, or with a low titer, when in the chronic stage (the immune system at this point may be giving up the battle.)

Regardless of the what the titer is, any positive should be considered indicative of infection and treated quickly and aggressively. A dog with a negative titer who has signs should still be treated, then re-tested at a later date.

Although E. canis and E. risticii appear to be the most common species to infect dogs, other species are out there which won't be detected if the laboratory is testing strictly for E. canis or E. risticii. (Another reason to treat the signs even if the titer test is negative.) CBC panels have been used but they are too non specific to be reliable. There are many cases where a dog's CBC has been "within normal limits" yet the dog died of ehrlichiosis!

CBC Panel abnormalities are often so borderline, they may be overlooked by the vet as inconsequential. An example could be a dog who appears to have sufficient platelets, yet is showing signs of internal hemorrhage (blood in urine, bruising on mucosal surfaces, coughing, bloodshot eyes etc.) This can happen because the platelets have lost their ability to function normally - they can actually lose their adhesiveness which hinders their ability to form a normal blood clot.

When abnormalities are seen in a CBC Panel, they may include a reduction in platelets, mild anemia, high WBC (usually in new infections), low WBC (usually in chronic cases), high sedimentation rate (due to dead cells outnumbering healthy cells), high alkaline/phosphatase ratio, and other slight abnormalities. Kidney function tests may show high BUN and creatinine. In these cases, the diet should be altered to lessen the strain on the kidneys.

The following laboratories are experienced in running the IFA test for various species of ehrlichia, including E. risticii. In some laboratories discounts may be available, either when testing for several species of ehrlichial infection in the same dog (a "rickettsial panel") or if multiple dogs (such as in a breeding kennel) are tested at the same time ("bulk testing"). Be sure to inquire about any discounts before blood is sent.

Blood must be spun down to separate the serum component which is then shipped via overnight mail in a cold pack. Direct any questions about this procedure to the laboratory where you are sending the sample.


Colorado State University's Veterinary Diagnostic Laboratory
University of Illinois
Laboratory of Veterinary Diagnostic Medicine
ATTN: Dr. Kakoma
P.O. Box "U", 2001 S. Lincoln
Urbana, IL 61801
PH: 217/333-1620 or 217/333-1859
FAX: 217-222-4628

Protatek Reference Laboratories
ATTN: Dr. Cynthia Holland
574 E. Alamo Street
Chandler, AZ 85225
PH: 602/545-8499

Dr. T. McElwain
Washington State University
Vet Diagnostic Lab
Pullman, WA 99164

Dr. E.B. Brietschwerdt
Dr. M.G. Levy
North Carolina State University
College of Vet Medicine
4700 Hillsborough Rd.
Raleigh, NC 27606

Dr. D. Huxsoll
Louisiana State University
School of Vet Medicine
Baton Rouge, LA 70803


Perhaps the greatest challenge in battling ehrlichiosis is in detecting and accurately assessing the signs. This has been one of the major reasons for the disease being under-reported and misdiagnosed. In most cases the early signs are very subtle. In all cases the signs mimic those caused by other diseases.

In the acute phase of infection, ehrlichiosis appears much the same as any viral infection. The animal often runs a fever, may lose his appetite and/or act depressed, the eyes may have a glassy appearance, etc. These signs may even disappear of their own accord in a few days time. Animals who are especially stoic may pass through this phase without anyone even noticing. This stage of the disease almost always clears up without treatment. It is, however, during this stage that treatment can be most effective in eliminating the disease.

Virtually any unusual sign is worthy of note as there are generally more than one. The animal may act depressed or tired with a diminished interest in playing. Acute infections of E. risticiiwill sometimes involve diarrhea and/or vomiting (often this is vomiting of bile only). The animal usually refuses food for a few days, may lose weight, and will probably want to be left alone. E. risticii is often misdiagnosed as parvo or corona infection, and occasionally the signs of E. risticiiare very similar to those of kennel cough.

It is when ehrlichiosis is not treated in this first stage with the proper antibiotics that it goes on to wreak havoc in the system of its canine victim. The following list of signs should be carefully reviewed as recognition of the signs will more than likely be the first indication of the disease. Remember that while few dogs display all of the signs, most will show several. Again, stoic dogs are the most difficult to diagnose; trust your instincts and remember that you are the best judge of what is normal in your own dog and what isn't. In one case of a Border Terrier who had both E. canis and E. risticii, the only sign noticed by the owner was the dog lost interest in play - something he had always enjoyed to the utmost. As we have indicated, any change in behavior is enough to warrant precautionary measures.

Breeders may observe unique signs due to their experience with pregnant and nursing bitches as well as puppies. A female dog with signs previously too subtle to be noticed, may develop serious illness during pregnancy, or she may deliver dead or ailing puppies. In these cases, breeder and veterinarian must work in cooperation with one another in order to make the correct diagnosis.

We would like to thank and are eternally grateful to Susan Netboy for the excellent job she has done in compiling the following list. Susan is very active in greyhound rescue and was one of the first to realize the scope of ehrlichiosis as well as babesiosis in rescued greyhounds. It should be of concern to all that greyhounds make up a very large percentage of the blood donor dogs, both at university veterinary school hospitals, and at many veterinary clinics. Rickettsias are readily spread through blood transfusion.


Information gathered by Susan Netboy:

EHRLICHIOSIS is an infectious blood disease. A reduction in cellular blood elements is the primary characteristic of the disease. Although the organism lives and reproduces in the white blood cells (leukocytes); it has a particularly devastating effect on the lymphatic system and will ultimately affect multiple organs, systems, and cells: respiratory, circulatory, central nervous system, kidney, brain, liver, spleen, endothelium.

Additionally, the severe depression of the immune system created by the disease opens the door to secondary bacterial infections and other complications. Because the onset of visible signs is likely to be gradual in the chronic phase and subtle in appearance, alertness to the following conditions is imperative in order to catch the disease while it is still treatable:

  1. weakness
  2. cough
  3. labored breathing
  4. fatigue
  5. pneumonia
  6. intermittent fever
  7. arthritis
  8. muscle wasting
  9. discharge from nose or eye
  10. depression
  11. weight loss
  12. anorexia
  13. increased thirst and urination
  14. incontinence
  15. sensitivity of the skin
  16. head tremors
  17. disorientation
  18. seizures
  19. neck or back pain
  20. bleeding tendencies
  21. pallor due to anemia
  22. retinal hemorrhages
  23. bleeding into the skin
  24. rash
  25. nose bleeds
  26. spontaneous bleeding
  27. abdominal tenderness
  28. swelling of the legs
  29. swollen lymph nodes

Certain features of ehrlichiosis may mimic the following diseases:

  1. systemic lupus erythematosus
  2. brucellosis
  3. blastomycosis
  4. endocarditis
  5. immune mediated diseases
  6. thrombocytopenia
  7. pancytopenia
  8. myelophthisis
  9. cancer of the spleen or liver
  10. Valley Fever
  11. plasma cell myeloma
  12. leukemia

It is recommended that ehrlichiosis be ruled out before accepting these diagnoses as a definitive cause of the illness or condition. Ehrlichiosis is known to be prevalent in racing greyhounds; there is no question amongst veterinarians who have dealt with the disease that it must be taken seriously and aggressively treated. Testing is simple and definitive; a positive titer at any level needs to be treated. Very good results can be obtained with readily available, inexpensive treatment of a 7 to 8 week course of tetracycline or doxycycline at the correct dosage. (For further information contact: Susan Netboy at (800) 446-8637) Contents Copyright (c) 1995, Greyhound Friends For Life. Last Modified: August 15, 1995.


Due to the rapid spread and inadequate publicity the single biggest failure has been the failure to recognize and test for the disease. Perhaps the strongest recommendation that can be made is to eliminate ehrlichiosis first as a possible cause by treating with appropriate antibiotics to see if the animal responds. If an animal has any of the above signs an excellent path would be to take blood for a Indirect Fluorescent Antibody (IFA) test and start the animal on doxycycline immediately.

If the titers return as negative, but the animal is responding to treatment, he should be kept on the antibiotic and re-tested in a couple of weeks. The IFA test looks for the presence of antibodies produced by the dog's immune system and it may take as long as 30 - 45 days for the immune system to respond with the production of enough antibodies to detect. As doxycycline does not affect the production of antibodies it will not interfere with the test results.

We strongly advise against waiting for a positive result before treating with doxycycline. Vets should also be cautioned about the use of steroids in a dog who may have ehrlichiosis. If Lyme disease is the suspect then treat with doxycycline. Although some chronically-infected dogs may need steroid treatment, this should always be done in conjunction with doxycycline treatment and only as a last resort measure. In cases where the vet feels more than one disease may be involved, ehrlichiosis should be given the first priority.

In acute cases there is usually a dramatic response to treatment. A case in point involved a Border Terrier owned by one of the authors. He presented with signs consistent with renal failure, and renal failure is not usually treated with doxycycline. However, the owner was aware that the dog had been exposed, and the signs had come on quite suddenly. There was also apparent (though slight) enlargement of the spleen and liver. The vet then reluctantly agreed to treat with doxycycline along with other supportive therapy.

When the test results came back 48 hours later, the vet was alarmed at the apparent indication of chronic renal failure. However, re-examination and testing of the patient showed dramatic improvement - 2 days on doxycycline had brought kidney function back within the normal range, the heart rate had returned to normal, and dehydration was no longer evident. Subsequent IFA titer tests showed the dog was indeed positive for both E. canisand E. risticii. Due to the decision to treat immediately, this dog is still alive, enjoys excellent health, and has normal kidney function at age 7 1/2 years. This also makes the drug a diagnostic tool as well as treatment. If the signs disappear with treatment it is almost a virtual certainty that the dog has been infected and blood tests should be run to make the confirmation.

Most cases have shown a good response to treatment with the tetracycline family of antibiotics. Doxycycline is the preferred drug as it has less potential side effects and better penetration of certain bacteria (Merck). Inoculations as well as injectable antibiotics should not be administered to a dog suspect for ehrlichial infection, as reactions have been reported, some of which proved fatal to the patient (the immune system is already taxed due to the action of the disease.)

Another drug, Imizol®, has also proven very effective, but unfortunately it is not readily available in the US and is still considered experimental. (Since the article was written in 1996 , unfortunately, little has changed. However, one important change is the fact that Imizol is now available and your vet should be able to easily obtain it. This drug is given by injection in a series, normally, of two shots two weeks apart. - Bob Wilson 1/14/2000).

The suggested treatment with doxycycline has been 5 to 10mg per day per Kg. (according to the Merck Manual.) Some dogs have been treated at a rate of 20 mg per kg body weight per day (or 200 mg for the typical 22 pound dog, divided into two daily doses given 12 hours apart) with excellent results. Most cases have shown that the higher dosage is more effective, but its use will be dictated by the animals tolerance. It should be administered for at least a 6 week period. Due to the high dosage Merck also suggests vitamin supplementation with vitamins B and K due to the reduction in the animals ability to synthesize those vitamins in the large intestine. In some cases wrapping the tablet in a piece of bread or adding to rice will facilitate administering the drug as well as helping to prevent nausea which may occur in some animals on the high dosage.


We hope that this will be a help in spotting the signs and treating ehrlichiosis early and effectively. More importantly, we hope that it will create an awareness in owners, breeders and veterinarians to watch for the subtle signs of this disease. If caught early it is curable.

For those who read this and can influence pharmaceutical companies to develop a vaccine as has been done for Lyme disease, we will consider our mission complete.


WE THANK the many veterinarians, veterinary technicians, breeders and owners who have shown genuine concern for the animals suffering from ehrlichiosis, and share our determination to push for more widespread testing, treatment, and hopefully a vaccine. We would also like to make a special mention and thanks to Michelle Tjaden who, in addition to providing a great deal of reseach information, had the first dog (Border Terrier) from which the first culture of E. risticii was grown by Dr. Kakoma. We would also like to thank Barbara Mair who has researched this disease with a vengeance and was instrumental in getting DNA testing underway; and to Dr. Jutta Hammermuller, who, working closely with Mrs. Mair and Dr. Kakoma, gave generously of her time and expertise to figure out how to conduct PCR/DNA tests on dogs.

A very special thanks has to go to Dr. Ibulaimu Kakoma who is an Associate Professor of Microbiology/Immunology at the College of Veterinary Medicine at the University of Illinois Champaign. Dr. Kakoma is a Doctor of Veterinary Medicne as well as a microbiologist and is an expert on the subject of tick borne diseases. He has written many articles on the subject of ehrlichiosis and continues his research today. He took many hours out of his busy schedule to discuss various issues and agreed to write the Foreword at the beginning of this article. Dr. Kakoma is fully dedicated to the eradication of ehrlichiosis and has been instrumental in providing technical assistance, not only for this document, but to our mutual attempts to attract and convince drug manufacturers to develop a vaccine.

WE DEDICATE this paper to our memories of Saucy, Jake, Bonnie, Clancey, Duke, Keeley, Pajti, Emma, Penny and the many many other beloved pets who lost their battle with ehrlichiosis, and left an empty spot in the hearts of their owners that can never be filled. All of these dogs succumbed to an insidious killer we now know as ehrlichiosis because, at the time, there was not enough widespread knowledge to prevent it. We created this paper to provide that knowledge to help prevent others from the same fate and dedicate this paper to those stoic little animals so they will not have died in vain.


Bob Wilson - Border Terrier Owner

In the process of putting this document together I was asked by several people around me as to why I seemed so focused on the subject. Many who have experienced this type of tragedy would prefer to move on and try to forget the incident. My answer was that I guess that I preferred to learn from history rather than be doomed to repeat it.

There is no question that it is a valid answer but the real reason was that you had to know Jake. She came into my life at a time when turmoil was the norm and I was finding myself emotionally drained. While Jake's arrival five and a half years ago didn't solve the problem it made my life bearable and gave it a purpose. I found myself changing my lifestyle to adapt to hers. We were constant companions and virtually inseparable. Jake went to the office with me, spent countless hours in the car with me and slept with me. It was almost a joke amongst many of my friends as they knew that if they invited me somewhere where there was any possibility of bringing Jake that she had to have an invitation or I might not show. She gave me more love than I knew existed and in return I gave her more love than I knew I had. She read me like a book and knew when I needed a friend and when I needed to go play ball with her. She was my best buddy.

On October 30, 1995 that relationship came to an abrupt and sad end with her death from what we now know as ehrlichiosis. It was only 30 days prior to her death that I learned about this insidious killer and by then it was too late. If life was 36" in diameter I had just had a 34" hole blown in mine. There has never been the death of any living thing that has so profoundly affected me. It is a loss that still haunts me to the depth of my soul.

Because there seemed to be no clear-cut reason for the disease I went on a quest to learn all I could about it. Unquestionably Jan Hendricks, a co-author of this document, was my major source of both information and consolation. Jan is a Border Terrier breeder and was where Jake came from. Her dedication to the breed and maintaining its' high standards is nothing short of awesome. It was through our discussions that we decided to try to put all of the known information in one place. This document very simply would not be if it were not for her dedication.

There are many others who provided information to this document that space does not allow us to mention. Several, however, simply have to be recognized. Susan Netboy who is involved with Greyhound Friends for Life which is a rescue organization has done a great deal of work in "spreading the word". A significant part of her work on ehrlichiosis is contained in this article. A very special thanks to Lynda Adame who runs the "Tick Net" on the Internet. That group now has over 55 members who regularly share information on ehrlichiosis and babeiosis and it's treatment.

We hope that this document will help you avoid the pain , sorrow and problems that we have all experienced with this silent and insidious killer.

January 1996


Canine Ehrlichiosis

What it is

Ehrlichiosis, often called tick fever or tropical canine pancytopenia, is a tick-transmitted disease affecting dogs. The brown dog tick carries the organism causing Ehrlichiosis and transmits the disease while feeding on the dog’s blood.


The disease has two phases, acute and chronic. The acute phase occurs 1-3 weeks following tick exposure. Clinical signs of illness are rather nonspecific and may include listlessness, swollen lymph nodes, anorexia, fever, and discharge from the nose and eyes. The signs of the chronic phase may include those mentioned for the acute phase plus nosebleeds or other abnormal bleeding and weight loss. The chronic phase may occur several months following the acute phase.

In both phases, the damage done to the body relates to destruction and decreased production of all blood cells (red blood cells, white blood cells, and platelets). This leads to anemia, decreased resistance to disease, infection and abnormal bleeding. German Shepherds seem especially susceptible to the disease.


Although clinical signs and a history of prior tick infestation are helpful, accurate diagnosis depends upon blood testing.


The acute phase of the disease usually responds to treatment within a short period of time. The chronic phase is difficult to treat and may require several months of therapy. Treatment for both phases usually involves specific antibiotics, but may include other supportive care.

Unfortunately, the chronic form of the disease can be fatal.


The best prevention of the disease is to keep your dog free of ticks. This should include checking the skin daily for ticks, treating the dog with tick products (tick dips, powders/sprays, or baths), and having your home and yard sprayed for ticks.

About The Brown Dog Tick….

  1. It is the most widely distributed of all ticks in the United States.
  2. The preferred host is the dog and it seldom attacks man or other animals.
  3. It feeds on the blood of dogs.
  4. It infests dog kennels, runs, backyards, and will readily infest the home. Usual hiding places in the home include baseboards, window casing, furniture, curtains, and carpet.
  5. The tick life cycle has three stages, with each stage requiring a blood meal before maturing to the next stage. The complete life cycle may be as short as two months, or as long as two years.
  6. Controlling the brown dog tick requires treatment of infested premises by the homeowner or a pest control operator, as well as treatment of the dog. Your veterinarian can advise you as to proper treatment methods for your dog.

This information is supplied by the Arizona Veterinary Medical Association in cooperation with your Veterinarian.





Tetracycline Antibiotics (Monodex, Vibramycin, Terramycin)
Jennifer Prince, DVM
Veterinary Services Department, Drs. Foster & Smith, Inc.


Tetracyclines are antibiotics which is available in multiple forms. Does not kill bacteria, but slows their growth. Not for use in pregnant or nursing dogs or puppies.

Generic Names
Doxycycline, Oxytetracycline, Tetracycline

Brand Names
Monodex, Vibramycin, Terramycin, Achromycin (for eyes), Panmycin Aquadrops

Combination Drugs
Albaplex contains tetracycline and novobiocin
Delta Albaplex contains tetracycline, novobiocin and prednisolone

Type of Drug

Form and Storage
Tablet, capsule, oral suspension, powder for injection, and as an eye drop and ointment
Unless otherwise stated by the manufacturer, the products should be stored in tight, light-resistant containers at room temperature. Once the powder is reconstituted (mixed with sterile water) it should be stored at room temperature and used within 12 hours for intravenous (IV) injection or 24 hours for intramuscularly (IM) injection.

Indications for Use
Treatment of spirochetes (like the Lyme disease organism), Chlamydia, Rickettsia (like Ehrlichiosis and Rocky Mountain Spotted Fever), and gram positive and gram negative bacteria. Some bacteria are developing resistance to tetracyclines. Tetracyline has been used with variable results to decrease facial staining from tears, although it is not approved for this use.

General Information
Tetracycline is FDA approved for use in dogs and cats. Oxytetracycline is approved for use in large animals. Doxycycline is not approved for use in veterinary medicine, however, it is a common and accepted practice to use oxytetracycline and doxycycline in dogs and cats. Available by prescription. Tetracycline antibiotics are bacteriostatic which means they work by interfering with the growth cycle of the bacteria allowing the body time to fight the infection.

Usual Dose and Administration
Dogs: Oxytetracycline 9 mg/pound by mouth (capsules) every 8-12 hours. Tetracycline 10 mg/pound by mouth (liquid, tablets, oral suspension) every 8 hours by mouth. For facial tearing in dogs use 2-4 mg/pound daily or 50 mg/dog per day. Results vary. Doxycycline 2-5 mg/pound every 12-24 hours by mouth (tablets, capsules, oral liquid).
Cats: Oxytetracycline and tetracycline 9 mg/pound every 8-12 hours by mouth. Doxycyline 2 mg/pound every 12 hours by mouth (tablets, capsules, oral suspension). Type used and the duration of treatment depends on the disease being treated and the response to treatment.

Side Effects
May see vomiting, diarrhea, or lack of appetite. Cats have more difficulty tolerating tetracycline and may also show signs of stomach pain, fever, hair loss, and depression. Rarely seen are photosensitivity, liver damage, and blood disorders.

Not for use in animals hypersensitive (allergic) to them.

Not for use in pregnant, nursing animals, or growing animals as it may slow bone growth and discolor teeth (turn teeth yellow, brown, or gray) in young animals.

Use with caution in animals with liver or kidney disease and if using other medications that affect the liver or kidney.

Delta Albaplex has the maximum benefit if used in the first 48 hours of treatment then Albaplex should be used for the rest of the treatment.

Drug or Food Interactions
Products given by mouth such as antacids, vitamins, minerals, Pepto-Bismol, or Kaopectate may decrease the absorption of the tetracycline antibiotic. It is recommended to give these products at least 3 hours before or 2 hours after the tetracyclines.

In humans, tetracycline has caused an increase in serum (blood) levels of digoxin (a heart medication) that may last several months after discontinuing the tetracycline.

Oxytetracycline and tetracycline are better absorbed on an empty stomach. Doxycycline is absorbed even with food in the stomach.

Side effects may be reduced if given with food.

Unlikely after oral (by mouth) overdoses. May see vomiting, lack of appetite, or diarrhea.



Haemobartonella canis
Holly Frisby, DVM
Veterinary Services Department, Drs. Foster & Smith, Inc

Haemobartonellosis is a tick transmitted (and sometimes flea transmitted) disease that affects both cats and dogs. Haemobartonellosis targets the red blood cells which are responsible for carrying oxygen. In cats, it is called feline infectious anemia.

What causes haemobartonellosis

Haemobartonellosis is caused by Haemobartonella canis and H. felis. H. canis and H. felis are not typical bacteria. They belong to a group of microorganisms called mycoplasma, which are the smallest free-living type of 'germs'.

How are H. canis and H. felis transmitted?

Fleas and ticks become infected with Haemobartonella by feeding on an infected animal. When the flea or tick then feeds on another animal, the Haemobartonella are passed on. Because Haemobartonella live in the blood cells, they could be spread via a blood transfusion from an infected animal to a noninfected one. In the cat, Haemobartonella can also be spread from the queen (mother cat) to her kittens. There is evidence bitches can also pass Haemobartonella to their puppies, but is has not been proven.

What are the symptoms of haemobartonellosis in dogs?

In the dog, the disease is generally not apparent unless the dog has previously had its spleen removed (splenectomy), has a suppressed immune system (e.g., from taking cancer chemotherapy), or is infected with other organisms such as Ehrlichia. The spleen is responsible for filtering the blood and its job is to remove and destroy damaged red blood cells, like those seen in haemobartonellosis. That is why a dog without a spleen is more susceptible - there is nothing to remove the infected cells (and the Haemobartonella) from the blood stream.

Since one tick could be infected with and transmit more than one disease (e.g., haemobartonellosis, ehrlichiosis, babesiosis), it is not all that uncommon to see a dog infected with more than one of these diseases at a time.

How is haemobartonellosis diagnosed?

Sometimes the organism can be seen inside cells on a blood smear. To find them, a small drop of blood is spread over a microscope slide, stained and examined under the microscope. The number of organisms in the blood stream can fluctuate dramatically. There can be many observed in one sample, and a sample taken two hours later may reveal none. .

How is haemobartonellosis treated?

Antibiotics such as tetracycline, oxytetracycline or doxycycline are given for three weeks. In some animals it is necessary to give one or multiple transfusions.

How is haemobartonellosis prevented?

As with other diseases transmitted by fleas or ticks, flea control and tick control are the foundations of prevention. Products which repel and kill ticks and fleas such as Bio Spot for Dogs are good choices. For dogs, tick collars containing the active ingredient amitraz are also used, sometimes in conjunction with Bio Spot in those areas with high tick infestation.

Can people get haemobartonellosis?

There have been no reported cases of haemobartonellosis in people.



Hepatozoon canis
Holly Frisby, DVM
Veterinary Services Department, Drs. Foster & Smith, Inc.
Hepatozoon canis is a one-celled parasite that is transmitted by ticks, usually the Brown Dog Tick, Rhipicephalus sanguineus. Because of the long time interval between becoming infected and developing illness, this disease is not just seen during the tick season, but all year round. It is not a very common disease in the United States, but when it does occur it’s usually in Texas and the surrounding states. This parasite infects dogs, coyotes, and fox.

What are the signs of disease caused by H. canis?

Most infections with H. canis do not cause illness. It can cause serious disease, however, in animals with concurrent disease such as ehrlichiosis and babesiosis, or in animals with suppressed immune systems. Signs of disease include fever, loss of weight, loss of appetite, nasal discharge and weakness of the rear limbs. A mild anemia and bloody diarrhea may also be seen. As the disease progresses, lameness, severe muscle pain, and an inability to rise are often observed. These signs may occur on and off for years. To better understand how H. canis causes these signs, let’s look at the life cycle.

What is the life cycle of this tick-borne parasite?

When an infected tick is eaten by a dog, H. canis is freed and migrates through the dog’s intestine to the liver, spleen, lymph nodes, heart and muscles. Inside the cells of these organs, the parasite reproduces by dividing and eventually ruptures the cell. The parasite then moves into different cells to continue the process of maturing and rupturing cells. The damage caused by the rupturing of these cells causes the severe muscle pain. Eventually the more mature forms enter particular white blood cells.

When a tick bites the dog, the tick takes in the white blood cells. H. canis reproduces in the tick, and when eaten, the tick will infect another dog. H. canis does not move to the salivary glands of the tick, so it is NOT transmitted by a tick bite – only by eating the tick.

How is infection with H. canis diagnosed?

A diagnosis of H. canis infection is made by microscopically examining the blood and finding the parasite in particular white blood cells called neutrophils. A great increase in the number of this certain type of white blood cell is a characteristic sign of this disease. Finding the parasite in a muscle biopsy is a very reliable method of diagnosing this disease.

In some severely affected dogs, the point at which the muscles attach to the bones may become inflamed. These bony changes may be seen on radiographs (x-rays).

How can infection with H. canis be treated and prevented?

There is no effective treatment or vaccine for this disease. Certain drugs such as imidocarb in combination with other drugs have sometimes been successful in lowering the number of organisms in an animal. Using supportive care, such as aspirin, some cases will respond but they will not be cured.

Tick control will be helpful in preventing the spread of this parasite. Using a tick preventative such as Bio Spot on your dog would be helpful since the ticks most commonly eaten by a dog are the ones it finds while grooming.

Georgi, JR; Georgi, ME. Canine Clinical Parasitology. Lea & Febiger. Philadelphia, PA; 1992;90-94.

Sherding, RG. Toxoplasmosis, Neosporosis, and Other Multisystemic Protozoal Infections. In Birchard, SJ; Sherding, RG (eds): Saunders Manual of Small Animal Practice. WB Saunders Co. Philadelphia, PA; 1994;142-143.

Sousby, EJL. Helminths, arthropods and protozoa of domesticated animals. Lea & Febiger. Philadelphia, PA; 1982;689-690.





J. S. Mathew, BVSc, MS & S. A. Ewing, DVM, Ph D
Department of Infectious Diseases and Physiology, College of Veterinary Medicine, Oklahoma State University, Stillwater, OK 74078-2006

Ehrlichiosis is a disease that affects a variety of animals including human beings; caused by obligatorily intracellular bacteria belonging to the genus Ehrlichia . There are several species assigned to this genus and those for which the vectors are known are transmitted by ixodid ticks. Ehrlichial organisms infect predominantly white blood cells of their vertebrate hosts; one exception isEhrlichia platys which infects dog platelets. The organisms appear in clusters known as morulae in the cytoplasm of infected cells. Ehrlichial organisms are classified as agranulocytic or granulocytic  based on the cells they infect and one that infect platelets. The species currently assigned to the genus Ehrlichia are as follows:

Ehrlichia canis (Donatien and Lestoquard 1935), Moshkovski 1945

Ehrlichia canis was the first ehrlichial organism to be discovered and is the type species of the genus E. canis has worldwide distribution and is the cause of canine agranulocytic ehrlichiosis. This organism is known to be transmitted transstadially by the brown dog tick, Rhipicephalus sanguineus under natural conditions. Dogs are likely to be long term carriers but can be cleared if treated properly with tetracyclines. E. canis can be cultured in vitro in mammalian-derived cell line (DH82) and in an invertebrate cell line (IDE8).

Clinical signs of E. canis infection

Acute infection:
Pyrexia (103-1060F), lethargy, anorexia, weight loss, bronchial sounds, dyspnea, cyanosis and often death if not treated. Hematological findings include severe thrombocytopenia (<25000/ul), mild anemia, and leukopenia.

Chronic infection:
Depression, abdominal tenderness, scrotal and limb edema, petechial hemorrhages of mucus membranes, epistaxis, melena, retinitis leading to blindness, uveitis, corneal edema, and miosis; neurological abnormalities include hyperesthesia, anisocoria, and seizures. Hematological findings include hyperproteinemia, hyperglobulinemia, and hypoalbuminemia.

Ehrlichia ewingii, Anderson, Greene, Jones, and Dawson 1992

E. ewingii is the causative agent of canine granulocytic ehrlichiosis first identified in 1969 at Oklahoma State University, Oklahoma, USA and recognized as a distinct species in 1992. This organism infects neutrophils and eosinophils and produces a milder disease than that produced by E. canis infections. Experimental transmission studies suggest that this agent can be transstadially transmitted by lone star tick, Amblyomma americanum . This agent has not been cultured in vitro.

Clinical signs

Acute infection:
Most often asymptomatic and there may be mild fever (102-1030F), anorexia and lethargy. Hematological findings include mild thrombocytopenia, leukopenia and mild normocytic normochromic anemia.

Chronic infection:
Chronic cases are thought to be characterized by arthritis but the relationship has not been proved experimentally and synovial fluid often contains granulocytes infected with ehrlichial organisms.

Ehrlichia platys, French and Harvey 1982

Ehrlichia platys which infects dog platelets is the only Ehrlichia spp that infect cells other than leukocytes. It causes infectious cyclic thrombocytopenia (ICT). The disease is characterized by severe thrombocytopenia(<15000/ul) occurring at regular intervals. The disease is often asymptomatic but thrombocytopenic animals may hemorrhage after accidents or during surgery. The vector for this agent is not known, though R. sanguineus is suspected.

Ehrlichia risticii, Holland, Ristic, Cole, Johnson, Baker, and Guetz 1985

Ehrlichia risticii is the causative agent of Potomac horse fever or equine monocytic ehrlichiosis. Natural infections were also reported in dogs with symptoms resembling E. canis infection. This organism is very closely related to Ehrlichia sennetsu (see below). Potomac horse fever is prevalent in midwestern and northeastern United States and also reported from Europe and India. The mode of transmission of this agent is unknown, but recent reports suggest oral transmission. Trans-placental transmission of this agent also has been reported. Infections are more prevalent during summer months and have about 5-30% mortality rate.

Clinical signs

Pyrexia, anorexia, enteritis, watery diarrhea, colic and laminitis. Hematological findings include thrombocytopenia and leukopenia.

Ehrlichia equi, Lewis, Huxsoll, Ristic and Johnson 1975

Ehrlichia equi causes equine granulocytic ehrlichiosis originally reported from the Sacramento Valley in California, USA. This organism is closely related to or possibly identical with Ehrlichia phagocytophila and the human granulocytic ehrlichial (HGE) agent (see below).The mode of transmission of this agent is unknown, but Ixodes spp. are suspected as vectors. E. equi infections normally occur during fall, winter and spring. The laminitis commonly observed with E. risticii infection is absent in equine granulocytic ehrlichiosis.

Clinical signs

Fever, anorexia, petechial hemorrhages and edema of legs

Ehrlichia bovis (Donatien and Lestoquard 1936), Moshkovski 1945

Ehrlichia bovis is the cause of bovine mononuclear or agranulocytic ehrlichiosis in cattle. The disease is reported from Africa, Middle East, India and Srilanka, but not reported from USA. This agent was originally isolated from circulating monocytes of Moroccan cattle to which Hyalomma spp. ticks were transferred from cattle imported from Iran. The disease is known as "Nopi" or "Nofel" in West Africa.

Clinical signs

Clinical signs include fever, anorexia, incoordination and enlarged lymph nodes

Ehrlichia phagocytophila (Foggie 1952), Philip 1962

Ehrlichia phagocytophila is the bovine/ovine granulocytic ehrlichial agent reported from Great Britain. This agent is now thought to be similar or nearly identical to E. equi or HGE. Cross-immunity between the bovine and ovine strains is incomplete. About 6-50% of granulocytes show the parasite during the acute phase of infection. The organism is transmitted by the sheep tick, Ixodes ricinus.

Clinical signs

Signs include fever, reduced milk production, weight loss, and perhaps abortion. Hematologic findings include leukopenia and thrombocytopenia

Ehrlichia sennetsu, Missao and Kobayashi 1956

The disease caused by this agranulocytic ehrlichial agent has been known to exist in southwest Japan since the 19th century. The disease has been variously known as Hyuganetsu disease, sennetsu ehrlichiosis, glandular fever, and infectious mononucleosis. Mice are highly susceptible to this agent and are routinely used for laboratory cultivation of the parasite. This agent is serologically related to E. risticii. The vector is unknown, though eating of a particular fish has been suspected to be a source of infection.

Clinical signs

Acute febrile illness, lethargy, weakness, diarrhea and generalized lymphadenopathy. Hematological findings include lymphocytosis as the most consistent finding.

Ehrlichia chaffeensis, Anderson, Dawson, and Wilson 1991

Ehrlichia chaffeensis is the causative agent of human (predominantly agranulocytic) ehrlichiosis. The first case was reported from Michigan, USA, in 1986. This agent infects predominantly agranulocytes but is thought to infect granulocytic series of cells occasionally. Disease can be fatal in immuno-compromised patients. Dogs can be experimentally infected with this agent. White-tailed deer are likely reservoir hosts and experimental transmission of this agent between white-tailed deer by the lone star tick, Amblyomma americanum, has been demonstrated. E. chaffeensis is serologically closely related to E. canis and E. ewingii. This agent has been successfully cultured in vitro in DH82 cells.

Clinical signs

Fever, headache, malaise, myalgia, inappetence, nausea, vomition, renal failure, and encephalopathy. Hematological findings include thrombocytopenia and leukopenia; serum chemistry shows elevated hepatic aminotransferase levels.

Human Granulocytic Ehrlichia (HGE)

Human granulocytic ehrlichial agent specifically infects human granulocytes and was first reported from Upper Midwest, USA in 1990. The agent is found by 16S rDNA analysis to be very closely related to E. equi and E. phagocytophila. HGE can be experimentally transmitted by the black-legged tick, Ixodes scapularis (Fig. 6). The disease caused by HGE can be fatal if not diagnosed and treated promptly.

Clinical signs

Fever, anorexia, headache, confusion and neurological abnormalities in advanced stages.


Clinical signs with hematological findings are very useful in the diagnosis of ehrlichiosis. Confirmed diagnosis is by demonstration of morulae in a peripheral blood smear, which is often difficult. Serology using IFA or FIAX can be used for the diagnosis of agents for which antigens are available; they include all the agranulocytic ehrlichial agents (except E. bovis), E. platys, E. ewingii and E. equi. Modern techniques like polymerase chain reaction (PCR) are very useful for the accurate diagnosis of ehrlichial infections of all types.


Tetracycline antibiotics are the drug of choice for treating infections caused by all species of Ehrlichia. They are very effective and can completely eliminate the organisms if treated properly and to date no drug resistance has been reported. Other antibiotics, like chloramphenicol and rifampin, are also effective against ehrlichial agents.


Effective vaccines are presently unavailable.


Since ticks are the major vectors in most cases, tick control is essential in the prevention of ehrlichiosis. Prompt treatment of vertebrate hosts with correct dosage of antibiotics will eliminate infection and prevent carrier status.


Ticks: What Makes Them Tick?
Race Foster, DVM
Marty Smith, DVM
Drs. Foster & Smith, Inc.
The word tick means different things to different people. Many individuals actually have an 'acarophobia' or fear of ticks. To us at Drs. Foster and Smith, Inc. who live among the great woods of Northern Wisconsin, ticks have other meanings. The first emergence of ticks is a sure sign of spring. They are the one indication that we can always count on. The World Championship Tick Races are held in the nearby town of Park Falls, Wisconsin. Literally, hundreds of participants enter this annual event. Their prized ticks are placed at the center of the arena and the first tick to exit the ring is declared the winner!

What are ticks?

Ticks are not insects like fleas, flies and lice, but are arachnids like mites and spiders. There are approximately 850 species of ticks worldwide. Scientists have classified ticks into two families based upon their structure. The family Argasidae contains the argasid ticks, which are soft-shelled. Their body lacks a hard shell (scutum) which is the protective outer covering found on some ticks. Argasids also have a ventral (on the underside) head and when viewed from above, their head cannot be seen.

The other tick family is named Ixodidae and these ticks possess the hard outer covering and therefore are termed hard-shelled ticks.

The following is a listing of the common hard-shelled (Ixodid) ticks and their habitats:

Amblyomma americanum is the Lone Star Tick and is found throughout the South, east of the Rocky Mountains.

Amblyomma maculatum is the Gulf Coast Tick, and that is where it resides.

Dermacentor albipictus is also called the 'Winter tick' , 'Moose Tick' or 'Elk Tick' and is found in the northern and western United States as well as Canada.

Dermacentor andersoni is the Rocky Mountain Spotted Fever Tick and transmits the deadly disease for which it is named.

Dermacentor variabilis is one of the most famous of all. Its name is also the American dog tick and lives in the entire eastern 2/3 of the United States.

Rhipicephalus sanguineus is the king of ticks. It is called the Brown Dog Tick and is a serious threat to kennels anywhere in the United States.

Ixodes scapularis is a tiny little tick with a huge threat. It is also known as the deer or black-legged tick. It has one claim to fame and that is it transmits Lyme disease.

All of the above are 'hard-shelled' ticks. There are more, but these are the most frequently encountered.

The soft-shelled ticks or Argasids are fewer in number. The one most known is Otobius megnini also known as the spinose ear tick. It is most common in the southwest and as one might guess, loves to attach itself and feed on ears.

Tick Anatomy

All ticks have three pairs of legs during the immature stage and four pairs as an adult. They crawl but cannot fly. Wings are absent. In addition, ticks possess a sensory apparatus called Haller’s organ. This structure senses odor, heat, humidity, and you. This is how the ticks locate their food source. They climb upon tall grass and when they sense an animal is close by, they crawl on.

What do ticks eat?

A tick's diet consists of blood and only blood. Your blood, dogs’ blood, cats’ blood, and most blood. The tick imbeds its mouthparts into the animal's (or human's) skin and sucks the blood. Except for the eggs, ticks require a blood meal to progress to each successive stage in their life cycle.

What is the life cycle of ticks?

Comparative sizes of the life stages of the deer tick

Most ticks are what we call three host ticks, that is, during their development which takes two years, they feed on three different hosts. All ticks have four stages to their life cycle: egg, larvae (seed tick), nymph, and adult. Let's look at the life cycle of the deer tick, as an example.

Adult female deer ticks lay eggs on the ground in spring. Later in the summer (depending on moisture and temperature), the eggs hatch into larvae. The larvae, which are smaller than the period at the end of this sentence, find an animal (the first host, which is usually a bird or rodent), live off its blood for several days, then detach and fall back onto the ground. For deer ticks, this most commonly occurs in the month of August. In the ground, the well-fed larvae now molt into the next stage and are called nymphs.

Each female tick lays approximately 3,000 eggs.

The nymphs remain inactive during the winter months and in spring become active. The nymph now finds an animal (the second host - a rodent, pet or human) and feeds again. Once well fed, the nymph detaches and falls back to the ground. Here it molts and changes into an adult. Throughout the fall, both adult male and female ticks now find another animal (the third host - a rodent, deer, pet or human) and feed on blood and mate. Once well fed, both males and females fall back to the ground. The male now dies and the female lives through the winter and lays eggs in the spring, completing the cycle. If the adults cannot find a host animal to feed on in the fall, they will survive in the leaf litter until the next spring when they will feed, mate and produce eggs.

Other species of ticks may be at peak activity for each life stage at different times of the year than the deer tick we described. Your local university or health department may have information on peak tick activity in your area.

What diseases do ticks transmit?

Ticks can transmit:

  • Babesiosis (Piroplasmosis)
  • Cytauxzoonosis
  • Ehrlichiosis
  • Haemobartonellosis
  • Hepatozoonosis
  • Lyme Disease
  • Rocky Mountain Spotted Fever
  • Tularemia



07 August 2001

Alex Morrow MVB BA PhD MRCVS of the Royal (Dick) School of Veterinary Studies, Edinburgh, addresses a topical issue with information from Vetstream’s CANIS and FELIS

The Pet Travel Scheme has not only opened up international borders to pets, some diseases never before seen by most UK vets have made the journey back to our shores. Among the most important exotic diseases likely to be seen in animals that have returned from abroad are those transmitted by ticks. Tick activity tends to be greater in summer months, the time when most dogs are likely to be taken to endemic areas. Several cases of Babesiosis have been seen in dogs that were taken abroad by their owners – unfortunately some of them were fatal. Canine ehrlichiosis is another important tick-borne disease that can also have fatal consequences. The challenge facing the UK veterinary profession is how to recognize and treat these novel diseases or to advise owners on their prevention.


This is a serious tick-transmitted protozoal disease caused by Babesia spp. Dogs imported into areas where the disease is endemic are particularly at risk and can die within a day of the clinical signs appearing. Concurrent infection with the tick transmitted rickettsial parasite Ehrlichia canis is likely.

The geographic distribution of the disease is almost worldwide in tropical, subtropical and warm temperate climates: Africa, Asia, Southern Europe, Russia, Central Asia, Central and South America and parts of the USA. In endemic areas, the prevalence of infection in dogs can be high but the clinical disease tends to occur primarily in puppies and young adults. Usually these dogs gradually develop a level of immunity to the disease, but remain carriers thus providing a reservoir of infection.

Two species of Babesia are involved: Babesia canis and B. gibsoni. There are three strains/subtypes of B. canis with the most predominant in Europe being B. canis canis, which is transmitted by the tick Dermacentor reticulatus. B. canis vogeli, transmitted by Rhipicephalus sanguineus is found in northern Africa and North America and B. canis rossi, transmitted by Haemaphysalis leachi occurs in Southern Africa. B. gibsoni is transmitted by R. sanguineus and H. bispinosa and causes a more chronic form of the disease. It occurs in North America, North and East Africa and Asia including India, Japan and parts of China.

The ticks acquire the piroplasms of Babesia spp when they ingest blood from an infected dog. Sporozoites, the infective stage, form in the salivary glands of the tick and are transmitted to the dog when the tick feeds. The parasites invade the dog’s erythrocytes, which then either rupture or are removed by phagocytosis. Intravascular and extravascular haemolysis and erythrocyte phagocytosis leads to haemoglobinuria, bilirubinuria and jaundice, while the inflammatory response contributes to endothelial damage. The incubation period is 10-20 days. The haemolytic crisis seen in acute infections results in anaemia, hypoxia and metabolic acidosis. The pathology is that of anaemia varying from a marked rapidly developing type in highly susceptible dogs to a more chronic manifestation, with jaundice, in dogs reared in endemic areas. The inflammatory response probably accounts for the associated complications. In complicated cases single organ failure tends to predominate, although multiple organs are often affected. Neurological signs can occur from the sludging of parasitised erythrocytes in small blood vessels, or from metabolic changes. Other complications include renal failure and acute respiratory distress syndrome.

The disease may occur in a hyper-acute, acute or chronic form. The hyper-acute form is characterised by sudden onset, shock and rapid death. In the chronic form there is intermittent fever and decreased appetite with or without jaundice.

Diagnosis of this condition in the UK is obtained from the history, clinical signs and also haematology.



  • Dog has visited endemic area and been exposed to tick vectors.
  • May be history of lethargy, exercise intolerance and/or lameness/stiffness.
  • Anorexia and weight loss.v
  • Anuria/oliguria.
  • Dyspnoea.
  • Neurological signs.

Clinical signs

  • Pyrexia.
  • Signs of haemolytic anaemia, eg depression, ‘water-hammer’ pulse, pale mucous membranes, haemoglobinuria.
  • Splenomegaly.
  • Lymphadenopathy.
  • Jaundice.
  • Complications may also be seen including stomatitis, gastritis and enteritis, respiratory distress, congested mucous membranes, neurological signs including incoordination, collapse, nystagmus and seizures, keratitis and iritis, and (rarely) rhabdomyolysis. Haematological abnormalities include a regenerative anaemia, thrombocytopaenia and leukocytosis. The definitive diagnosis of babesiosis is obtained from Giemsa (or Wrights) stained blood smears that demonstrate the parasite in the erythrocytes. As few organisms are present in the blood, it is preferable for the sample to be taken from peripheral capillaries such as in the ear tip or nail bed. Centrifugation on Percol density gradients enhances the chance of detection. B. canis is pear-shaped (4-5 um long) and usually occurs in pairs, with up to eight or more present, whereas B. gibsoni appears singly as smaller (3 um) round or oval bodies (1 x 3.2 um) but occasionally larger elongate forms half the width of the cell are present. Serology may be useful in chronic cases.

Therapy is targeted at eliminating or reducing the parasite load and reversing the anaemia, if severe. In uncomplicated cases diminazene aceturate (3.5 mg/kg IM) is the drug of choice, but this should not be used in severe cases. It is effective against B. canis, but less so against B. gibsoni. It has a low therapeutic index and overdosage results in nervous signs. Imidocarb dipropionate (5 mg/kg IM) is also effective against B. canis but not against B. gibsoni (NB a sterile abscess may form at the inoculation site). Phenamidine isethionate (1.5 mg/kg SC on two consecutive days) is also used in the treatment of B. canis and B. gibsoni infections.

It should be noted that high doses of diminazene and phenamide can sometimes induce fatal toxicity in dogs.

Trypan blue (10 mg/kg as a 1% solution given IV) suppresses parasitaemias and alleviates the clinical signs but it does not eliminate infection and recurrence of clinical signs can occur.

Blood transfusion is indicated in the severely anaemic patient (haematocrit value of <0.1 l/l). Fluid therapy may also be required in severely affected patients to counteract haemoconcentration, acidosis and shock. It is important to monitor the respiratory rate and pulmonary sounds of patients receiving fluid therapy – especially if they were already showing signs of respiratory distress.

Recovery in mild-moderate cases can be apparent within 24 hours of treatment. In dogs with icterus, recovery may be prolonged, but the prognosis is generally good when treatment has been initiated early and there are no complications. Dogs may become carriers and recurrence of clinical signs can occur due to stress. Recurrent infection is possible if the animal has not been exposed to the parasite for a prolonged period.

Prevention of infection can be achieved by the use of acaricides and the daily removal of ticks. Prophylactic treatment should be considered when dogs are taken to endemic areas. Imidocarb dipropionate, 6 mg/kg can prevent the occurrence of clinical disease for 4-6 weeks while allowing a degree of immunity to develop in exposed dogs. Doxycycline, 5–20 mg/kg daily has been claimed to prevent symptoms developing, especially when used at the higher dose rate. Vaccines are available in some countries but strain variation can limit their protective activity.


Ehrlichiosis is a tick-transmitted rickettsial disease in which, depending on the Ehrlichia spp involved, mononuclear cells, granulocytes or platelets are parasitised. In dogs raised in endemic areas infection is common but this rarely develops into clinical disease. However, disease is very common in dogs imported into endemic areas.

The distribution of Ehrlichia spp is determined by the distribution of the vector ticks and this includes most of the tropics, subtropics, warm temperate climates and Finland. E. canis, transmitted by Rhipicephalus sanguineus, is endemic in Africa, the Middle East, Asia, the Caribbean, USA, Central America, parts of South America and Southern Europe. E. ewingii is present in the USA and Northern Europe and E. platys is present in the USA, Israel, Taiwan and Southern Europe. Although the vector tick species of E. ewingii and E. platys are not known for certain in the former case it probably includes Amblyomma and Dermacentor species. R. sanguineus, often referred to as the kennel tick, can survive over 500 days as unfed adults, remaining infective for at least 150 days, allowing them to over-winter and pass on the infection the following spring. The preferred feeding sites of the adult tick on the dog are the ears, along the back of the neck and between the toes but in heavy infestations they may be found almost anywhere.

Canine monocytic ehrlichiosis caused by E. canis, is the most important form of canine ehrlichiosis. It can present in an acute or chronic form, the latter when severe being referred to as tropical canine pancytopaenia. The clinical manifestations of canine granulocytic ehrlichiosis, caused by E. ewingii, are similar to but much milder than the acute form of canine monocytic ehrlichiosis while canine cyclical thrombocytopaenia, caused by E. platys, is not usually accompanied by clinical signs.

Infection occurs via salivary secretions when an infested tick ingests a blood meal. The incubation period of E. canis infection varies between eight and 20 days followed by acute, subclinical and in some cases chronic phases. It is an obligatory intracellular parasite multiplying inside cytoplasmic vacuoles in mononuclear phagocytic cells. Spread haematogenously, the parasite causes splenomegaly, hepatomegaly and lymphadenopathy. Vasculitis can develop affecting various organs including the lungs, kidneys and possibly the meninges. Immune mechanisms play a major role in the pathogenesis of the disease. Thrombocytopenia, anaemia and leukopenia are often seen during the acute phase due to bone marrow suppression and may persist during the subsequent subclinical phase. The disruption of platelets can result in haemorrhages, especially epistaxis. Severely affected animals are susceptible to secondary infections.

A lymphoproliferative syndrome can be seen with persistent latent infection, resulting in the accumulation of large numbers of plasma cells in various organs including lymphopoietic tissues, the kidneys and meninges. This chronic form can develop several weeks or even years after the primary clinical episode and is known as tropical canine pancytopenia. Not all dogs develop the chronic form of the disease but German Shepherd dogs appear to be more susceptible.

E. platys causes a cyclical riskettsiaemia of approximately ten day intervals with thrombocytopenia of diminishing severity as immunity develops.

Diagnosis of ehrlichiosis from the clinical signs is difficult as there are a number of presentations of the disease and clinical signs during the acute phase tend to be non-specific. History and haematology provide essential guidance.



  • Dog has visited endemic area and been exposed to tick vectors.
  • Depression, lethargy, stiffness/lameness.
  • Anorexia, weight loss, vomiting (haematemesis).
  • Increased bleeding tendency.
  • Ocular disease or blindness.
  • Seizures and other neurological signs.

Clinical signs of Canine monocytic ehrlichiosis Acute phase:

  • Sudden onset.
  • Depression.
  • Fluctuating temperature.
  • Splenomegaly and lymphadenopathy.
  • Limb and scrotal oedema.
  • Respiratory signs.
  • Petechiae and ecchymoses of the skin and mucous membranes. Many dogs appear to recover from the acute phase without treatment and pass into the subclinical phase.

Chronic form:

  • Dyspnoea.
  • Ventral oedema.
  • Petechial and ecchymotic haemorrhages on hairless skin or mucous membranes and prolonged bleeding time on venipuncture.
  • Epistaxis.
  • Haematuria.
  • Hypotension and shock secondary to blood loss.
  • Neurological signs, eg signs of meningoencephalitis (arched back, severe neck and back pain), paraparesis or tetraparesis, ataxia, hyperaesthesia and convulsions can occur during the acute or chronic phases.
  • Ocular changes, eg conjunctivitis, corneal oedema, anterior uveitis, hypaema, subretinal haemorrhage, retinal detachment and blindness
  • Skin lesions, eg alopecia and crusting.

Haematological changes in canine monocytic ehrlichiosis include thrombocytopaenia (consistently seen in all stages), non-regenerative anaemia and leukopenia with severe pancytopaenia developing in the chronic form. A hypergammaglobulinaemia is seen in all phases although it is somewhat lower during the pancytopaenia phase. Definitive diagnosis of E. canis infection is obtained by demonstration of the organism in mononuclear cells in Giemsa-stained peripheral blood smears or smears from the buffy-coat layer of untreated animals in the acute phase. The organisms can be seen in small groups or tightly packed clusters, known as morulae, up to 4 um in diameter in the vacuoles in the cytoplasm of these cells. The overnight incubation of buffy-coat and plasma in culture vessels containing flying coverslips greatly enhances the detection rate of infected mononuclear cells. However, demonstration of the organism in stained smears is often not possible, even in the acute phase. Cell culture reisolation of the parasite is the most sensitive and definitive for early diagnosis – but, due to the length of time required to obtain a result, it is really only suitable for research purposes. Serological tests are useful as demonstration of the organism in blood smears is difficult. Needle aspirates of spleen, lymph nodes and bone marrow should be checked for the presence of a plasmacytosis in tropical canine pancytopenia.

E. ewingii is seen as morulae in neutrophils and eosinophils, with E. platys detected as basophilic inclusions in platelets. v The treatment of choice for canine monocytic ehrlichiosis is doxycycline (10-20 mg/kg/day for a minimum of 3 weeks), on its own or preferably along with Imidocarb diproprionate (5 mg/kg IM or SC in a single dose repeated after 14 days). The combination is believed to be more effective in preventing the development of chronic infection and is particularly useful where mixed infections with Babesia canis are suspected.

Tetracyclines (22-25 mg/kg TID for at least 3 weeks) could be given as an alternative to doxycycline, except in uraemic cases when doxycycline is preferred. Chloramphenicol (50 mg/kg PO or IV TID for 14 days) can be used instead of tetracyclines when discolouration of tooth enamel is a concern.

Supportive therapy including fluid therapy, blood transfusion and vitamin supplementation may also be required. Glucocorticoids (prednisolone 1-2 mg/kg BID) should be considered until immune-mediated thrombocytopenia and anaemia resolve. However, the use of immunosuppressive drugs in dogs with rickettsial disease should be undertaken with caution, especially as these animals could also be infected with other tick-borne infections.

The prognosis is good for animals that undergo appropriate treatment during the acute phase. Chronic infections occur in those that don’t receive proper treatment, eg treated for too short a time period, and this can lead to the development of tropical canine pancytopenia, which is refractory to treatment. Recovered animals are usually immune to further infection but they become carriers and may experience relapses when stressed.

Control can be achieved by the use of acaricides, including acaricide impregnated collars Prophylactic treatment, using low doses of tetracyclines, 6.6 mg/kg orally, should be considered for dogs on relatively short visits to endemic areas or during periods of maximum tick activity.

Further sources: 1. Lobetti R G (1998) Canine babesiosis. Comp Cont Educ Pract Vet 20, 418-431.
2. Harrus S & Hylton B (1997) Canine monocytic ehrlichiosis – an update. Comp Cont Educ Pract Vet 19, 431-444.
3. Waner T, Keysary A, Bark H, Sharabani E & Harrus S (2000) Canine Monocytic Ehrlichiosis – an overview. Israeli J Vet Med 54, 103–107.




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Updated 01-07-04