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Paraparesis Caused by Vertebral Canal Leishmaniotic Granuloma in a Dog


Corresponding author: Alberto Cauduro, DVM, via Maestri del Lavoro 29, 20025 Legnano, Milano, Italy; e-mail: alberto.cau@libero.it.

A 7-year-old male Shih Tzu was examined because of acute onset of abnormal gait in pelvic limbs. Physical examination revealed pain at the level of the lumbar spine, paraparesis, ataxia, and decreased postural reactions in pelvic limbs. Muscle tone was normal. Normal patellar and cranial tibial reflexes were normal but flexor reflex was mildly reduced in the left pelvic limb. The neuroanatomic diagnosis was a focal or diffuse lesion between T3–L3. Hematologic and serum biochemical analysis revealed severe anemia (RBC 3.9, ref. 5.5–7.9; HB, 9.9 ref. 12–18 g/dL; HCT 27.5, ref. 37–55%), and on the following day paraparesis and ataxia increased.

Bone marrow biopsy performed under general anesthesia at the level of humerus head revealed a leishmaniasis infection, with a high presence of amastigotes. Bone marrow plasmacytosis was present and numerous histiocytes containing Leishmania spp. were evident. Leishmania spp. were detected extracellulary microscopically. IFA titre for Leishmania was >320. PCR for Ehrlichia and Borrelia spp. were negative.

An MRI study was performed with an open permanent magnet operating in 0.2 T (ESAOTE). The study included T1-weighted spin echo (SE) sequences [800/26/3; repetition time (TR) echo time (TE)], T2-weighted SE sequences (3000/100/1; TR/TE), gadolinium-dimeglumide (0.5 mmol/mL, GE Healthcare Omniscan, Paderno Dugnano, Milan, Italy) enhanced T1-weighted SE sequences (gadolinium chelate dose was 0.1 mmol/kg, IV), in the 3 orthogonal planes, and Gradient echo STIR sequences (1490/25/1; TR/TE/IR).

The MRI revealed the presence of an extradural mass ventral to the spinal cord and lateralized to the left localized on the L4–L5 intervertebral disk to the midbody of L5, displacing the spinal cord. The lesion was hyperintense on T1-weighted, T2-weighted, and STIR images, and had heterogeneous postconstrast enhancement (Fig 1).

Figure 1.

 Magnetic resonance imaging. Transverse images at the level of L5 reveal an extradural mass, ventral and on left side (arrow) and shows heterogeneous postcontrast enhancement.

As neurological signs were rapidly progressing, surgery was performed to decompress the spinal cord by means of a left L4–L5 hemilaminectomy, an ill-defined extradural mass, located ventrolaterally, was identified. The mass was yellow and hardly distinguishable from the epidural fat, neither encapsulated nor adhesive and with friable appearance. The diseased tissue was then removed and fixed in 10% buffered formalin.

After surgery, cephalosporine (20 mg/kg PO q12h for 10 days) and prednisolone (0.5 mg/kg PO q12h for 5 days) were administered.

The surgically removed tissue consisted of epidural fat tissue heavily infiltrated by macrophages, lymphocytes, plasma cells, and neutrophils. Proliferation of capillaries and scattered hemorrhages were also seen. The cytoplasm of many foamy macrophages contained multiple Leishmania amastigotes (Fig 2). The parasites were also identified free within the interstitium. The organisms were strongly labeled by immunohistochemical staining by the streptavidin-biotin immunohistochemical method with canine hyperimmune serum as the primary antibody.1

Figure 2.

 Excised epidural tissue. Granulomatous inflammation with infiltrates of macrophages containing Leishmania amastigotes (Hematoxylin and eosin, × 500). Inset, parasites are positively labeled with streptavidin-biotin immunohistochemistry.

There was a polyclonal gammopathy (total protein 7.07 g/dL; albumin 23.2%; α1 1; α2 9.6%; β 14.7%; and γ 51.4%).

The diagnosis was myelopathy induced by an extradural inflammatory granuloma caused by Leishmania spp.

The dog was then treated for leishmaniosis with N-methyl-glucamine antimoniate 100 mg/kg PO q24h for 1-month period and allopurinol 10 mg/kg PO q12h for a 6-month period. On the follow-up at 8 months the dog was clinically normal and in good health and ELISA test for Leishmania was negative. At 12 months the dog remained clinically normal.

Leishmania spp. are intracellular protozoa parasites of macrophages in man, dog, and a wide variety of wild animals. The related clinical manifestations are both cutaneous and visceral.2–3 The vector is a blood-sucking sand fly in which the parasites undergo morphological transformation and multiplication. Three species of Leishmania spp. infect dogs: L. tropica, L. donovani, and L. braziliensis. The dog is a natural host and reservoir of infection for some strains of leishmaniosis,4 which can infect humans.

It can take months to years for infected dogs to develop clinical signs, so the disease might become clinically evident long after having left endemic areas, and the clinical course can be characterized by remitting and relapsing of clinical signs. Diagnosis depends on the demonstration of the amastigote parasites in smears or scrapings from affected skin tissue or from lymph node or marrow biopsies.2,3,5

In the nervous system, typical phenotypic features of granulomatous meningitis have been observed in naturally infected dogs, with important lympho-plasma–cellular infiltrates and the presence of large numbers of parasites inside and outside macrophages.6 The cerebrospinal fluid contained a large number of protein bands (anti-Leishmania IgGs). A failure of the blood-cerebrospinal barrier has been demonstrated.6,7

In the present report, we describe thoracolumbar neurological signs because of a Leishmania spp. inflammatory granuloma affecting the vertebral column with extension into the epidural space where it caused compression of the spinal cord. Systemic infection might also have been present.

Although evaluation of the proteinogram and hemogram could have suggested the presence of a leishmaniasis infection,8 this was not first considered on the differential diagnosis because the dog was born and lived in the north of Italy. Leishmaniasis is not endemic in this area, where the blood-sucking sand flies are wrongly thought to be absent.

Furthermore, it would have been hazardous to hypothesize the vertebral column localization of a Leishmania granuloma, as to the authors' knowledge, it has not been described although there are reports of postmortem diagnosis of Leishmania granuloma.6,7 Histopathological examination revealed the existence of ependymal cells, scattered lymphocytes, and macrophages packed with amastigotes, which were also observed outside the cytoplasm, in the central nervous system.

Although the lesions were of a granulomatous type,7 a well-defined granuloma or giant multinucleated cells were not observed.

Leishmaniosis causes neurological disease in both humans and animals with studies of both experimental infection9–11 and natural infection.6–8,12

In the present case, the lesion was macroscopically detectable as a granuloma. Histological examination showed free amastigotes inside the granuloma and many macrophages infected with leishmania amastigotes were well recognizable. The histological aspect was very similar to those described in literature; however, clinically important vertebral canal granuloma is not reported in animals or humans.