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Ehrlichiosis

Ehrlichiosis is also refered to as canine rickettsiosis, canine hemorrhagic fever, canine typhus, tracker dog disease, and tropical canine pancytopenia. It is a tick-borne disease of dogs that is caused by the organism Ehrlichia. Dogs, cats, and in rare instances, humans are affected. German Shepherd dogs are known to be particularly affected by the disease. more...

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Erlichia

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.

Disease Overview

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 lowered peripheral blood cell counts. The second stage, called the subclinical phase, has no outward signs and can last for the remainder of the dog's life, during which the dog remains infected with the organism. In some dog breeds, such as the German Shepherd dog, the third and most serious stage of infection, the chronic phase, will commence. Very low blood cell counts (pancytopenia), bleeding, bacterial infection, lameness, neurological and ophthalmic disorders, and kidney disease, can result. Chronic ehrlichiosis can be fatal.

Treatments

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.

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 subclinical phase. Clinical signs of the chronic phase include pale gums due to anemia, bleeding due to thrombocytopenia, vasculitis, lymphadenopathy, respiratory dyspnea, coughing, polyuria, polydipsia, lameness, ophthalmic diseases such as retinal hemorrhage and anterior uveitis, and neurological disease. 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.

Diagnosis

Diagnosis is achieved most commonly by serologic testing of the blood for the presence of antibodies against the ehrlichia organism. Many veterinarians routinely test for the disease, especially in enzootic areas. It should be noted, however, that during the acute phase of infection, the test can be falsely negative because the body will not have had time to make antibodies to the infection. As such, the test should be repeated. In addition, blood tests may show abnormalities in the numbers of red cells, white cells, and platelets, if the disease is present. 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.

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Human granulocytic ehrlichiosis in Estonia - Letters - Letter to the Editor
From Emerging Infectious Diseases, 11/1/03 by Tiina Prukk

To the Editor: We report a case of a 24-year-old woman living in a rural area of Estonia who had weakness, chills, and diarrhea on May 10, 2002 On day 5 of the illness, she was admitted to the Department of Infectious Diseases, University of Tartu, with high fever (38.5 [degrees] C) and muscle pains throughout her body Examination showed mild jaundice painful and enlarged liver, and inability to move. Throat was erythematous, and enlarged lymph nodes were palpable on the neck.

Laboratory findings included the following: leukopenia 2.04x[10.sup.9]/L; erythrocytes 4.08x[10.sup.12]/L; hemoglobin 130 g/L; thrombocytopenia 36x[10.sup.9]/L; eosinophils 0%; basophils 1.0%; monocytes 7.5%; lymphocytes 38.0%; neutrophils 51.0%; reactive lymphcytes 2.0%; plasma cells 0.5%; C-reactive protein 38 mg/L (normal <5 mg/L); bilirubin 95 [micro]mol/L (normal <17 [micro]mol/L); aspartate aminotransferase 121 U/L (normal <31 U/L); alanine aminotransferase 108 UL (normal <31 U/L); and alcaline phosphatase 200 U/L (normal 35-104 U/L). Ehrlichiosis was suspected by clinical symptoms and leukopenia, thrombocytopenia, and elevated transaminases.

Human granulocytic ehrlichiosis (HGE) is an emerging tick-borne disease described for the first time in 1994 in the United States (l). The first European case of HGE was reported in Slovenia in 1996 (2). Infection with Ehrlichia phagocytophila, the agent of HGE, occurs in areas endemic for Borrelia burgdorferi (3). In Estonia, Lyme borrreliosis is frequently diagnosed in humans but the occurrence of ehrlichiosis has not been established for this region, despite our having found some seropositive results in Lyme borrreliosis patients (4).

This case of ehrlichiosis is the first diagnosed in Estonia. The initial diagnosis was based on a typical clinical spectrum of symptoms and clinical laboratory findings, which are relatively nonspecific, making the diagnosis problematic (5). Polymerase chain reaction results for Ehrlichia were negative, and we did not find morula in the blood smear. Indirect immunofluorescence assay (IFA, MRL Diagnostics, Cypress, CA) was used as a confirmatory serologic test. However, results of this assay are often negative during the initial phase of the disease (5,6). On day 7 of illness, the serologic results for immunoglobulin (Ig) M type antibodies to Ehrlichia were positive (1:20) and negative for IgG. The diagnosis of ehrlichiosis was established, and therapy with doxycycline was started. After 4 days, the patient became afebrile, and on day 6 she left for home. One month later, the titers of both types of antibodies to Ehrlichia were increased: IgM titer was 1:160 and IgG titer was 1:128; 6 months later, IgM antibodies were negative, and the IgG titer remained unchanged.

Our patient had a typical spectrum of clinical and laboratory changes to Ehrlichia, but not very specific findings of infection with E. phagocytophila. The results of IFA, i.e., IgM antibodies in the beginning of the disease and increasing titer of IgG antibodies during the course of the disease, confirmed the diagnosis. Granulocytic ehrlichiosis should be considered in patients with tick-associated fever.

References

(1.) Bakken JS, Dumler S, Chert SM, VanEtta LL, Eckman MR, Walker DH. Human granulocytic ehrlichiosis in the United States: a new species emerging? JAMA 1994;272:212-8.

(2.) Petrovec M, Lotric-Furlan S, Avsic-Zupanc T, Strle F, Brouqui P, Roux V, et al. Human disease in Europe caused by a granulocytic Ehrlichia species. J Clin Microbiol 1997;35:1556-9.

(3.) Bjoersdorff A, Wittesjo B, Berglund I, Massung RF, Eliasson I. Human granulocytic ehrlichiosis as a common cause of tick-associated fever in Southeast Sweden: report from a prospective clinical study. Scand J Infect Dis 2002;34:187-91.

(4.) Prukk T, Nilsson I, Bjoersdorff A, Wadstrom T. Seroprevalence of ehrlichiosis in south-Estonia. Budapest: First Congress of the European Society for Emerging Infections; 1998.

(5.) Lotric-Furlan S, Avsic-Zupanc T, Petrovec M, Nicholson WL, Sumner JW, Childs JE, et al. Clinical and serological follow-up of patients with human granulocytic ehrlichiosis in Slovenia. Clin Diagn Lab Immunol 2001;8:899-903.

(6.) Olano JP, Walker DH. Human ehrlichioses: diagnostic challenges and therapeutic recommendations. Infect Med 2002;19: 318-25.

Address for correspondence: T. Prukk, Department of Infectious Diseases, University of Tartu, Lina 6,51004, Tartu, Estonia; fax: 372 7 374232; email tiinap@cut.ee

Tiina Prukk, * Kylliki Ainsalu, [dagger] Ene Laja, [double dagger] and Ada Aigro [double dagger]

* University of Tartu, Tartu, Estonia; [dagger] Internal Medicine Clinic of Tartu University, Tartu, Estonia [double dagger] United Laboratories of Tartu University Clinics, Tartu, Estonia

[double dagger] United Laboratories of Tartu University Clinics, Tartu, Estonia

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