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Hepatozoon canis (Apicomplexa, Adeleorina, Hepatozooidae) is a tickborne pathogen that belongs to a diverse group of parasites which includes approximately. WE wish to share with our colleagues the details of a case of Hepatozoon canis in a two-year-old female spaniel imported from Cyprus two days before. Find details on Hepatozoon canis in dogs including diagnosis and symptoms, active forms, resting forms, clinical effects, treatment and more. All information is.

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American canine bepatozoon ACH is a debilitating disease caused by Hepatozoon americanum and transmitted by ingestion of oocyst-containing Amblyomma maculatum ticks. A history of incomplete response to common antibiotics, together with physical findings of fever and muscle wasting and laboratory findings of leukocytosis and periosteal proliferation, hepatozokn prompt testing for ACH.

Muscle biopsy and whole-blood polymerase chain reaction are currently the most reliable methods of diagnosis. Treatment consists of a 2-week course of trimethoprim-sulfonamide, clindamycin, and pyrimethamine, followed by a 2-year course of decoquinate.

Relapses are common, but prognosis is fair overall. Canine hepatozoonosis was first recognized in North America in in Texas. Molecular evidence separating H.

This tick, which was once confined to the Texas Gulf Coasthas now expanded its range as far north as southern Kansas and Kentucky. For example, Hurricane Katrina has broadened the distribution of ACH as dogs from the Gulf Coast region were moved throughout the country. Therefore, a thorough history is imperative in establishing the potential for exposure ccanis ACH.

Hepatozoon – Wikipedia

Under natural conditions, the host range of larval and nymphal Gulf Coast ticks includes birds and small mammals, making these species potential reservoir hosts.

The definitive host and vector for H. Repeated attempts to achieve infection of R. There is one report of transmission via R.

Further research is required to determine whether these ticks can transmit the hepatozoon organism. Transmission to intermediate hosts, including the domestic dog and the coyote, is by ingestion of H. Following ingestion, sporocysts are quickly released from the fragile-walled oocysts. The latter is a structure unique to, and diagnostic for, ACH. At completion of merogony, the meront ruptures, releasing numerous merozoites and inducing a severe, localized pyogranulomatous reaction as well as systemic illness.

A sexual stage of reproduction followed by asexual multiplication in the tick gut epithelium produces oocysts that contain hundreds of sporocysts, each of which holds 10 to 26 sporozoites. The occurrence of ACH is seasonal, peaking in the warmer months or early fall when dogs are most likely to be exposed to ticks. However, infected dogs may exhibit clinical signs throughout the year as the cycles of asexual reproduction and pyogranulomatous inflammation are repeated.

The first evidence of ACH appears as early as 3 weeks postexposure, consists of a large zoite-containing macrophage situated between muscle fibers, and is clinically silent. The inflammatory response to the infection is very limited while the organism is encysted, but when the cyst ruptures, an acute inflammatory response occurs, followed by pyogranulomatous inflammation and clinical illness.

Clinical evidence of disease, such as lethargy, bone pain, and ocular discharge, occurs shortly thereafter. Gamonts have been observed in peripheral blood leukocytes 4 weeks after exposure. Continued reproduction of the organism and release of merozoites lead to waxing and waning clinical signs and relapses after treatment. Chronic infections cause persistent antigenic stimulation and secondary complications, including vasculitis, glomerulonephritis, and amyloid deposition in various organs.

Prolonged infections commonly result in progressive weight loss and muscle wasting, with death occurring within 12 months after ingestion. Common clinical signs of H. Gait problems include stiffness, generalized weakness, hindlimb paresis and ataxia, and inability or unwillingness to rise. Hyperesthesia attributed to pyogranulomatous myositis and possibly periosteal reaction may be generalized or localized to the cervical, back, or joint regions.


Dogs may have a history of polydipsia and concurrent polyuria due to secondary glomerulonephritis or renal amyloidosis in the chronic stage of the disease. Transient bloody diarrhea, abnormal lung sounds, cough, and lymphadenomegaly are less common.

Many dogs continue to eat despite severe fever but exhibit progressive weight loss and muscle wasting due to increased caloric demands associated with the prolonged inflammatory state.

Although affected dogs may also exhibit variable minor clinical signs, there should be a strong index of suspicion for ACH when a dog in an endemic area presents with fever, hyperesthesia, poor response to antibiotic therapy, and muscle wasting.

These salient clinical signs, coupled with mature neutrophilic leukocytosis and periosteal proliferation, can be considered initially diagnostic for ACH. Marked leukocytosis with few signs of systemic illness should likewise raise the suspicion of ACH in dogs with potential exposure.

Platelet numbers are usually normal to slightly elevated, 17,25 but marked thrombocytosis has been reported secondary to chronic inflammation.

Common serum biochemistry abnormalities are elevations in alkaline phosphatase levels, hypoglycemia, and hypoalbuminemia. Hypoalbuminemia is attributed to decreased protein intake, chronic inflammation, or protein-losing nephropathy secondary to glomerulonephritis or renal amyloidosis. Serum blood urea nitrogen BUN values may be decreased unless significant secondary renal disease is present, causing azotemia.

Hypoglycemia, hypoalbuminemia, and a low BUN level mimic liver disease biochemically, but serum bile acid assays are usually normal or only slightly elevated in dogs with ACH. Despite significant myositis, creatinine phosphokinase values are typically normal.

Hyperglobulinemia is uncommon, chronic inflammation notwithstanding. Urinalysis may reveal proteinuria, with an elevated urine protein: Other diagnostic tests and subsequent findings include electromyography revealing changes consistent with generalized polymyopathy, lymph node aspirates consistent with reactive hyperplasia, and bone marrow cytology findings that include granulocytic hyperplasia and erythroid hypoplasia with a high myeloid: Dogs with ACH may have minimal bone abnormalities or significant changes consisting of disseminated, symmetric, periosteal new bone formation that most frequently involves the diaphyses of the proximal long bones of the limbs 17,26 FIGURE 5.

Flat and irregular bones are less commonly affected. The pathogenesis of these lesions is unknown, but the disseminated and symmetric distribution of proliferation is more likely attributable to stimulation by humoral factors than to stimulation by local factors. The gross and microscopic bone lesions of ACH are very similar to those seen with hypertrophic osteopathy.

In both conditions, the periosteal reaction occurs without cortical destruction, and the lesions primarily affect the diaphyses of long bones.

With ACH, the onset and progression are faster and usually occur in the proximal bones of the limbs. With hypertrophic osteopathy, the proliferation tends to begin in the metacarpals and metatarsals and is typically associated with a primary pulmonary lesion.

The pathogenesis of the bone lesions in both conditions is incompletely understood. Scintigraphy has been used to study the onset and distribution of the early skeletal lesions of ACH. Lesions are bilaterally symmetrical, have high intensity, and occur primarily proximal to the carpus or tarsus on the axial skeleton. These lesions were detected as early as day 67 postinfection, suggesting that bone scintigraphy may be a useful method for identifying ACH bone lesions.

Gamonts appear within the cytoplasm of leukocytes as pale blue to clear oblong capsules measuring approximately 8.

American Canine Hepatozoonosis

Because peripheral blood smears rarely demonstrate the hepatozokn, buffy coat smears may be conducted to caniis the chance of detecting gamonts. He;atozoon biopsy is the most reliable method of confirming the diagnosis of ACH.


Evaluation of multiple biopsy samples can increase the likelihood of diagnosis. It also distinguishes H. The test is conducted on blood samples treated with EDTA, and the samples can be shipped by regular mail. At necropsy, cachexia and muscle atrophy are consistent gross findings in dogs chronically infected with ACH, along with thickened, roughened bone surfaces.

Pyogranulomas may appear as 1- to 2-mm, white to tan foci scattered throughout muscle and other tissues. Pyogranulomas, cysts, and meronts can be visualized microscopically in skeletal and cardiac muscle and may be found in adipose tissue, lymph nodes, intestinal smooth muscle, and spleen, skin, kidney, salivary gland, liver, pancreas, and lung tissue. Renal lesions are common, including focal pyogranulomatous inflammation with mild glomerulonephritis, lymphoplasmacytic interstitial nephritis, mesangioproliferative glomerulonephritis, and, occasionally, amyloidosis.

The spleen, lymph nodes, small intestine, and liver may also contain hepatozoln deposits. Pulmonary congestion, splenic coagulative necrosis, lymphadenomegaly, and congestion of the gastric mucosa are less common.

Remission of clinical signs can be achieved quickly in most cases by initiating treatment with trimethoprim”sulfonamide, clindamycin, and canjs TCP combination for 14 days TABLE 2. Although the clinical response to treatment can be striking, relapse often occurs in 2 to 6 months when this treatment is used alone.

It is ineffective in resolving active disease but can arrest the development of merozoites as they are released from mature meronts. Dogs with ACH that experience relapse should be treated with the TCP combination for 14 days, after which decoquinate should be reinstituted. The optimum duration of decoquinate treatment is debatable, and current recommendations include conducting whole-blood PCR testing every 3 to 6 months and discontinuing the drug once the test result is negative.

The powder can be mixed into moist food at a dose of 0. Treatment of ACH can be discouraging because no therapy can eliminate yepatozoon tissue stages of the organism. Relapses are frequent, and the disease’s natural relapsing-remitting cycle can make treatment success difficult hpatozoon evaluate. Relapses result from continued release of merozoites into muscle and other tissues as meronts undergo replication and development. Current treatments cannot penetrate host cells to arrest the development hepatlzoon encysted meronts.

Relapses increase the likelihood of long-term complications such as glomerulonephropathy, amyloidosis, vasculitis, and chronic cachexia. In the past, the hepatozokn for dogs with ACH was considered guarded to poor.

Many dogs died or were euthanized due to the severity of their clinical signs.

Hepatozoon canis

The use of TCP combination therapy followed by daily decoquinate administration has markedly improved this picture. Relapses are now less severe and less frequent, with a lower occurrence of glomerulonephritis and amyloidosis. Tick control is the mainstay of prevention for ACH and should consist of effective preventive and acaricidal treatments and regular examination to remove ticks.

Environmental control of ticks is also necessary, so yards and outdoor kennels should be sprayed routinely.

It is also prudent to refrain from feeding dogs raw meat or organs of wildlife from endemic areas. Although this route of infection has not been documented for ACH, it can occur with other species of Hepatozoon. With dogs being redistributed throughout the United States as a result of recent hurricanes, canls is incumbent on clinicians to maintain a high index of suspicion for ACH, regardless of where they practice.

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