Tongue nodules in canine leishmaniosis — a case report

Viegas, Carlos; Requicha, João Filipe; Albuquerque, Carlos; Sargo, Teresa; Machado, João Firmino; Dias, Isabel; Pires, M.A.; Campino, Lenea; Cardoso, Luı́s

doi:10.1186/1756-3305-5-120

Cited by 17 publications

(19 citation statements)

References 21 publications

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“…An important diagnostic finding pertaining to the canine leishmaniosis‐associated lingual lesions in all the published cases, including the present dog, was the cytologic and histopathologic/immunohistologic evidence of Leishmania spp. amastigotes and the presence of a granulomatous inflammation, ruling out other potential differential diagnoses including neoplastic disease and eosinophilic granuloma …”

Section: Discussionmentioning

confidence: 99%

Nodular granulomatous glossitis as the sole clinical sign in canine leishmaniosis

Tangalidi

Oikonomidis

Psalla

et al. 2016

Veterinary Clinical Pathol

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A 5.5-year-old, intact male Rottweiler dog was admitted with a history of multifocal nodular tongue lesions which progressively deteriorated during the previous year. Physical examination revealed several reddish nodules with central depression on the surface of the tongue in an otherwise healthy dog. Clinicopathologic abnormalities included eosinophilia and hyperproteinemia. Lingual nodule cytopathology, histopathology, and immunohistochemistry revealed Leishmania spp. amastigotes and a severe granulomatous glossitis. The dog was also seroreactive to L infantum antigens by an indirect immunofluorescence assay. Clinical reevaluation 3 months after the institution of treatment with allopurinol and miltefosine indicated that the nodular lesions had completely regressed. In endemic areas, lingual nodular lesions may rarely be the sole clinical sign of canine leishmaniosis. Standard medical treatment may provide an excellent prognosis.

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Section: Discussionmentioning

confidence: 99%

Nodular granulomatous glossitis as the sole clinical sign in canine leishmaniosis

Tangalidi

Oikonomidis

Psalla

et al. 2016

Veterinary Clinical Pathol

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“…The interpretation of clinicopathologic, serologic, and molecular tests should take into account the history (eg, exposure to phlebotomine vectors), signalment (male dogs > 2 years are at high risk), and clinical presentation. The latter is characterized by a wide spectrum of clinical presentations, ranging from infections characterized by the absence of overt clinical findings in the presence of obvious laboratory abnormalities, to more or less marked clinical and laboratory abnormalities that may require hospitalization, especially in cases with severe life‐threatening complications …”

Section: Clinical Signs Of Canine Leishmaniasismentioning

confidence: 99%

Laboratory tests for diagnosing and monitoring canine leishmaniasis

Paltrinieri

Gradoni

Roura

et al. 2016

Veterinary Clinical Pathol

141

232

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Although several reviews on canine leishmaniasis have been published, none thoroughly described clinicopathologic abnormalities and their clinical usefulness. The aim of this review was to provide information concerning current diagnostic tests relevant for clinical pathologists and from a practical perspective. Specifically, in canine leishmaniasis, nonregenerative normocytic normochromic anemia, thrombocytopenia, or leukogram changes may be present. Clinical chemistry and urinalysis may indicate renal dysfunction (azotemia, decreased urine specific gravity, proteinuria) and an inflammatory/immune response (increased acute phase proteins [APP] or α - and/or γ-globulins). Although a potential gammopathy is usually polyclonal, it may also appear oligo- or monoclonal, especially in dogs coinfected by other vector-borne pathogens. When lesions are accessible to fine-needle aspiration (lymphoadenomegaly, nodular lesions, joint swelling), cytology is strongly advised, as the presence of Leishmania amastigotes in a pattern of pyogranulomatous inflammation or lymphoplasmacytic hyperplasia is diagnostic. If the cytologic pattern is inconclusive, the parasite should be identified by histology/immunohistochemistry or PCR on surgical biopsies. Alternatively, cytology and PCR may be performed on bone marrow samples where amastigotes, along with erythroid hypoplasia, myeloid hyperplasia, plasmacytosis, or secondary dysmyelopoiesis can be observed. Dogs with overt leishmaniasis generally have high antibody titers, while low titers predominate in immunologically resistant infected dogs or in exposed dogs with no parasite confirmation. Quantitative serology is recommended in clinically suspect dogs as high-titer antibodies titers may confirm the clinical diagnosis. In confirmed and treated dogs, renal function and inflammatory/immune response variables should be periodically monitored.

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“…These lesions have been attributed to the migration of infected macrophages to sites of microtrauma in the oral mucosa or to accidental chewing on infected sandflies. 49,75,108,149 Digestive disease in CanL is an uncommon to rare cause to admit leishmanial dogs and is mainly expressed as chronic hepatitis or chronic colitis, the subclinical form of which far outnumbers the clinical one. 3,46,120 In the liver, chronic granulomatous inflammation may involve the sinusoids, portal area, or capsule or become diffuse along with the presence of parasites that may also be seen within Kupffer cells and hepatocytes.…”

Section: General Pathomechanismsmentioning

confidence: 99%

Pathologic Mechanisms Underlying the Clinical Findings in Canine Leishmaniosis due to Leishmaniainfantum/chagasi

Koutinas¹,

2014

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In dogs with symptomatic or asymptomatic leishmaniosis, Leishmania infantum appears to induce a mixed Th1/Th2 immune response that in the sick dog may eventually result in tissue damage via different pathomechanisms, notably granulomatous inflammation (eg, nodular dermatitis, osteomyelitis), immune complex deposition (eg, glomerulonephritis), and/or autoantibody production (eg, polymyositis). This is a compensatory but detrimental mechanism generated mainly because of the insufficient killing capacity of macrophages against the parasite in the susceptible dog. Clinical disease is typically exemplified as exfoliative and/or ulcerative dermatitis, with or without nasodigital hyperkeratosis and onychogryphosis, glomerulonephritis, atrophic myositis of masticatory muscles, anterior uveitis, keratoconjunctivitis sicca, epistaxis, and/or polyarthritis, appearing alone or in various combinations. The pathogenesis of these clinical conditions has recently been highlighted, to a greater or lesser extent. The usually subclinical conditions expressed as chronic colitis, chronic hepatitis, vasculitis, myocarditis, osteomyelitis, orchiepididymitis, and meningoencephalomyelitis, though uncommon, are of pathologic importance from a differential point of view. The leading cause of death among canine leishmaniosis patients is chronic proteinuric nephritis that may progress to end-stage kidney disease, nephrotic syndrome, and/or systemic hypertension. However, even the asymptomatic proteinuria, when profuse, may be a serious problem because it predisposes to arterial thromboembolism and eventually contributes to the deterioration of the body condition.

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Tongue nodules in canine leishmaniosis — a case report

Cited by 17 publications

References 21 publications

Nodular granulomatous glossitis as the sole clinical sign in canine leishmaniosis

Nodular granulomatous glossitis as the sole clinical sign in canine leishmaniosis

Laboratory tests for diagnosing and monitoring canine leishmaniasis

Pathologic Mechanisms Underlying the Clinical Findings in Canine Leishmaniosis due to Leishmaniainfantum/chagasi

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