section name header

Basics ⬇

Outline

BASICS

Definition!!navigator!!

Seasonal, tick-borne disease caused by a granulocytotropic rickettsial organism, Anaplasma phagocytophilum (previously Ehrlichia equi).

Pathophysiology!!navigator!!

  • Caused by a Gram-negative bacteria, present inside granulocytes
  • Ixodes scapularis (the black-legged tick or deer tick) is the likely primary vector for the disease in the eastern and midwestern USA and Ixodes pacificus (the western black-legged tick) in the west
  • Existence of a maintenance or sylvatic host likely represents a wild reservoir, such as rodents; horses are considered dead-end hosts and are not directly contagious
  • Disease transmission occurs when infected ticks feed on the horse for 2–36 h
  • Incubation period is 8–25 days after experimental infection using ticks as vectors
  • The agent affects granulocytes (both neutrophils and eosinophils) and causes a vasculitis and interstitial inflammation, leading to edema, petechial hemorrhages, ataxia, and hemolytic anemia
  • Infection can result in pancytopenia, especially thrombocytopenia
  • Severe myopathies have occurred concurrent with the infection

Systems Affected!!navigator!!

  • Behavioral—mentation alteration (i.e. lethargy) of varying degrees
  • Hemic/lymphatic/immune—vasculitis, leading to edema and mucosal hemorrhages; hemolytic anemia
  • Musculoskeletal—reluctance to move, limb edema
  • Nervous—vasculitis in the CNS, leading to ataxia and recumbency
  • Cardiac—arrhythmias have been associated with myocarditis secondary to vasculitis within the myocardium
  • Myopathy—rare

Incidence/Prevalence!!navigator!!

  • High prevalence in the Sierra Nevada foothills and northern coastal range of California and many areas of eastern and midwestern USA. Anywhere the tick vector is present is at risk for the disease
  • Seroprevalence studies in northern California show a prevalence of 3.1–10.3%, depending on geographic location, and >50% seropositivity among horses on premises known to be enzootic for the disease
  • The disease is seasonal, having its highest occurrence during the late fall, winter, and spring

Geographic Distribution!!navigator!!

  • USA—west and east coasts are regions most affected
  • The disease has been diagnosed in Germany, Switzerland, Sweden, Norway, the UK, Denmark, Canada, Austria, Czech Republic, the Netherlands, France, Poland, and Italy, among other countries. Reports also exist from Asia and Africa

Signalment!!navigator!!

  • Primarily affects horses, but donkeys have been experimentally infected
  • No breed or sex predilections
  • Horses ≥4 years are most severely affected
  • Has been reported in a foal as young as 2.5 months

Signs!!navigator!!

Historical Findings

  • Lethargy
  • High fever
  • Anorexia
  • Limb edema
  • Tick exposure

Physical Examination Findings

  • Pyrexia
  • Anorexia
  • Depressed mentation
  • Limb edema (absent in young animals)
  • Mild petechiae and ecchymoses on mucous membranes and sclerae
  • Icterus
  • Ataxia
  • Reluctance to move, stiffness, myopathy
  • Arrhythmias (rare)
  • Recumbency (rare)

Causes!!navigator!!

  • A. phagocytophilum
  • Close antigenic and genetic similarity to the agent of HGE and to European tick-borne fever affecting ruminants

Risk Factors!!navigator!!

  • Geography
  • Exposure to Ixodes ricinus complex ticks
  • Age—horses ≥4 years are most severely affected
  • Immune status

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Viral encephalitis
  • Liver disease with hepatic encephalopathy
  • Purpura haemorrhagica
  • Equine infectious anemia
  • Equine viral arteritis

CBC/Biochemistry/Urinalysis!!navigator!!

  • Leukopenia with neutropenia
  • Less commonly leukocytosis
  • Thrombocytopenia
  • Increased icteric index
  • Anemia
  • Hyperfibrinogenemia
  • Hyperbilirubinemia (high unconjugated bilirubin)

Other Laboratory Tests!!navigator!!

  • Giemsa-, new methylene blue-, or Wright-stained peripheral blood smears show inclusion bodies (i.e. morula) within the cytoplasm of neutrophils and eosinophils. Inclusions are pleomorphic and blue-gray to dark blue in color, have a spoke-wheel appearance, and occur in 3–75% of circulating granulocytes within 2–6 days of the onset of fever
  • Buffy coat smears concentrate granulocytes and, therefore, increase the sensitivity of identifying inclusion bodies
  • Indirect fluorescent antibody tests are available for serology. A titer ≥1:10 suggests exposure which may not be acute. An increasing titer documents active infection but requires an acute and convalescent sample. A single sample with a cutoff value of 1:40 can be seen from prior subclinical infection and is not diagnostic for acute infection
  • PCR amplification of DNA from buffy coats of infected horses is a very sensitive diagnostic tool. PCR is positive before inclusion bodies are first observed in neutrophils and persists while the animal is febrile
  • Immunohistochemistry of tissues from postmortem examination can be used for diagnosis

Diagnostic Procedures!!navigator!!

See Other Laboratory Tests.

Pathologic Findings!!navigator!!

  • Mortality is rare, except for reasons of secondary complications. One recent report of mortality from the primary infection itself is thought to be due to severe vasculitis and DIC
  • Inflammation of small arteries and veins (vasculitis), hemorrhage, edema
  • Petechiae on mucous and serous membranes
  • Mild inflammatory, vascular, or interstitial lesions in the heart, CNS, kidneys, spleen, liver, and lung

Treatment ⬆ ⬇

Outline

TREATMENT

Appropriate Health Care!!navigator!!

Hospitalize horses with severe ataxia or secondary complications; otherwise, uncomplicated cases can be managed in the field. The infection is often self-limiting, with horses recovering fully within 1–2 weeks.

Nursing Care!!navigator!!

  • Supportive limb bandages for edema
  • NSAIDs for antipyretic purposes
  • Debilitated cases may benefit from IV fluid or electrolyte therapy
  • Corticosteroids may benefit horses with severe ataxia by reducing the severity of vasculitis

Activity!!navigator!!

Stall confinement for ataxic animals; otherwise, hand-walking may help to reduce edema.

Client Education!!navigator!!

When entering known Ixodes tick-infested areas, use tick repellents, and check horses closely for ticks upon return from these areas.

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • Oxytetracycline (7 mg/kg IV every 24 h for 3–7 days diluted and administered slowly in 0.9% saline (1 L for an average-sized horse)). With this treatment, a marked decrease in rectal temperature and improvement in appetite and attitude should be observed within 12–24 h of the first administered dose
  • Doxycycline (10 mg/kg PO every 12 h for 7–10 days) and minocycline (4 mg/kg PO every 12 h for 7–10 days) are alternatives used with success in field cases. For cases in which oxytetracycline is administered IV for 1–3 days, they can be switched to oral doxycycline or minocycline for a further 7 days
  • Short-term corticosteroids (dexamethasone) have been used to reduce inflammation and ataxia and have been safe to use in the experimental setting

Precautions!!navigator!!

  • Tetracyclines can retard fetal skeletal development and discolor deciduous teeth; therefore, use with caution and only for a short duration during the first half of gestation, then only when the benefits outweigh the fetal risks
  • Tetracyclines have been associated with enterocolitis, photosensitivity, and nephrotoxicity
  • IV oxytetracycline can result in perivascular swelling and phlebitis if administered perivascularly

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

  • Monitor temperature, attitude, and appetite for significant improvement within 12–24 h of treatment. In horses diagnosed in the very early stages of the disease and treatment administered for 5 days, relapses of the original infection have occurred
  • Evaluate serial buffy coat smear for inclusion bodies
  • Monitor hydration status and renal function while on oxytetracycline

Prevention/Avoidance!!navigator!!

  • Minimize exposure to Ixodes or other transmitting ticks through application of topical tick repellents when entering infested areas, and carefully examine horses for ticks on their return from such areas
  • Many horses may experience subclinical infections and develop subsequent immunity

Possible Complications!!navigator!!

  • Rare, secondary bacterial infections, especially bronchopneumonia
  • Horses with severe ataxia may suffer traumatic injury (e.g. fractures)
  • Cardiac arrhythmias, including ventricular tachycardia, may be associated with myocarditis
  • DIC—very rare
  • Recumbency
  • Immune-mediated myopathy (rare)

Expected Course and Prognosis!!navigator!!

  • Excellent prognosis in uncomplicated cases
  • Horses are immune to reinfection for at least 2 years; no carrier or latent state has been documented
  • With therapy, horses show rapid improvement—a decrease in rectal temperature, increase in appetite, and improvement in overall demeanor should be noted in 12–24 h; the ataxia should resolve within 2–3 days and the edema within several days
  • Left untreated, the disease is self-limiting in 2–3 weeks; however, affected horses exhibit more severe weight loss, edema, and ataxia and are at greater risk for secondary complications than horses treated with tetracycline. Laminitis is not associated with infection
  • Mortality due solely to acute infection is rare

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Age-Related Factors!!navigator!!

Severity of clinical signs is associated with age—horses <1 year generally do not show signs of infection or only slight lethargy and fever; 1–3 years of age show mild to moderate signs; and ≥4 years are affected most severely, with ataxia, icterus, edema, and petechial hemorrhages.

Zoonotic Potential!!navigator!!

  • The agent of HGE may represent 1 or more strains of the equine pathogen; however, horses are considered dead-end hosts and do not act as a source of human infection directly
  • Ticks are required as intermediate hosts

Pregnancy/Fertility/Breeding!!navigator!!

  • 2 pregnant mares are reported to have been naturally infected with A. phagocytophilum during gestation and to have subsequently delivered live foals at full term. Experimental infection in pregnant mares produces no abortion, and live foals have resulted
  • No abortions or congenital abnormalities have been described
  • Passive immunity is transferred to suckling foals but is short-lived in duration

Synonyms!!navigator!!

Equine ehrlichiosis

Abbreviations!!navigator!!

  • CNS = central nervous system
  • DIC = disseminated intravascular coagulation
  • HGE = human granulocytic ehrlichiosis
  • NSAID = nonsteroidal anti-inflammatory drug
  • PCR = polymerase chain reaction

Suggested Reading ⬆ ⬇

Dziegiel B, Adaszek L, Kalinowski M, Winiarczyk S. Equine granulocytic anaplasmosis. Res Vet Sci 2013;95:316–320.

Madigan JE, Gribble D. Equine ehrlichiosis in northern California: 49 cases (1968–1981). J Am Vet Med Assoc 1987;190:445–448.

Nolen-Walston RD, D'Oench SM, Hanelt LM, et al. Acute recumbency associated with Anaplasma phagocytophilum infection in a horse. J Am Vet Med Assoc 2004;224:1964–1966.

Reubel GH, Kimsey RB, Barlough JE, Madigan JE. Experimental transmission of Ehrlichia equi to horses through naturally infected ticks (Ixodes pacificus) from northern California. J Clin Microbiol 1998;36:2131–2134.

Author(s) ⬆

Authors: K. Gary Magdesian and John E. Madigan

Consulting Editor: Ashley G. Boyle