Rare case of disseminated rhinosporidiosis with chronic osteomyelitis of the calcaneum treated by a simple technique of negative pressure wound therapy.

Occurrence of nasal, cutaneous and disseminated rhinosporidiosis in the same patient is uncommon and involvement of calcaneum is rare. Rhinosporidial osteomyelitis is treated surgically, but multiple recurrences and local spread are common. Many a times, surgical ablation or amputation of the involved area of the limb is carried out to prevent recurrences. We present a case of rhinosporidial osteomyelitis of the calcaneum with a chronic discharging sinus and large lytic lesion in the calcaneum treated by an alternative surgical option in the form of debridement and negative pressure wound therapy.

Balantidium coli: an unrecognized cause of vertebral osteomyelitis and myelopathy.

Balantidium coli is a ciliated protozoan parasite that primarily infects primates and pigs. It is the largest protozoan to infect humans and is a well-known cause of diarrhea and dysentery. Extraintestinal disease is uncommon, and extraintestinal spread to the peritoneal cavity, appendix, genitourinary tract, and lung has rarely been reported. The authors describe a case of vertebral osteomyelitis with secondary cervical cord compression caused by B. coli. The patient was a 60-year-old immunocompetent man presenting with quadriplegia of short duration. Magnetic resonance imaging of the cervical spine showed extradural and prevertebral abscess at the C3-4 level. Drainage of the abscess, C3-4 discectomy, and iliac bone grafting were performed. Histologically B. coli was confirmed in an abscess sample. To the best of the authors' knowledge, involvement of bone by B. coli has never been reported, and this case is the first documented instance of cervical cord compression due to B. coli osteomyelitis of the spine in the literature.

Atypical trichinellosis without eosinophilia associated with osteomyelitis.

Human trichinellosis is an important food-borne zoonosis caused by a nematode worm, Trichinella. The symptoms of the disease vary widely depending on the infection load, stage of infection and host immunity and include nausea, vomiting, abdominal pain, fever, facial edema and muscle pain. The disease is usually characterized by moderate to high eosinophilia. We hereby discuss an atypical case of trichinellosis, which presented with myositis of the thigh muscles but had no eosinophilia and no facial or periorbital edema and was associated with osteomyelitis of the femur. The diagnosis was made by the demonstration of anti-trichinella antibodies and later confirmed by the presence of larvae of Trichinella in the digested muscle biopsy. Physicians must be aware of trichinosis and should include it in their differential diagnosis when examining patients with fever and myositis with or without eosinophilia.

Neutropenia associated with osteomyelitis due to Hepatozoon canis infection in a dog.

A 4-year-old, intact male Shiba dog was referred to Yamaguchi University Animal Medical Center, Yamaguchi, Japan, for the following complaints: anorexia, lethargy, intermittent fever, gingival bleeding and abdominal purpura. The dog presented with persistent neutropenia. Histopathological examination of a bone marrow sample revealed round to oval structures that resembled Hepatozoon micromerozoites and formed a "wheel-spoke" pattern. Furthermore, mature neutrophils were observed around these structures. PCR and sequencing using bone marrow aspirate confirmed Hepatozoon canis (H. canis) infection. These findings suggest that the neutropenia observed in this case was associated with osteomyelitis due to H. canis infection. This is the first report of neutropenia associated with H. canis infection. H. canis infection can be included in the differential diagnosis in canine cases of neutropenia in areas where the disease is endemic.

Hepatozoonosis in a dog with skeletal involvement and meningoencephalomyelitis.

A 15-month-old, female mongrel dog was presented with a 6-week history of inappetence, weight loss, and tetraparesis. Physical examination revealed weakness, poor body condition, mild fever, pale mucous membranes, and diffuse muscle atrophy. The right hind limb was painful and edematous, with large ecchymoses. The femur was irregular on palpation and moderate popliteal lymphadenopathy was evident. Results of a CBC showed severe anemia with mild regeneration, an inflammatory leukogram with 90% of neutrophils parasitized by Hepatozoon sp. gamonts, and moderate thrombocytopenia. A bone marrow aspirate had myeloid hyperplasia and contained a few extracellular Hepatozoon meronts and a few intracellular gamonts within neutrophils. Serum chemistry abnormalities included hypoalbuminemia, hyperglobulinemia, hypoglycemia, hypercalcemia, hyperphosphatemia, and elevated alkaline phosphatase activity. Radiologic findings of the right femur included periosteal bone proliferation and lesions compatible with osteomyelitis. A fine needle aspirate specimen from the bone lesion had neutrophilic inflammation; 36% of the neutrophils contained Hepatozoon gamonts. Results of cerebrospinal fluid analysis included a protein concentration of 37 mg/dL and marked mononuclear pleocytosis (243 cell/microL) with a predominance of lymphocytes. An ELISA was positive for Hepatozoon canis and PCR results with DNA sequencing confirmed infection with this organism. A diagnosis of hepatozoonosis with skeletal involvement and meningoencephalomyelitis was made. The dog recovered almost completely neurologically and had no gamonts in the blood after 60 days of therapy with imidocarb dipropionate and prednisone. This is an unusual case of canine hepatozoonosis involving neurologic signs and a periosteal reaction more typical of H. americanum infection and rarely reported in dogs infected with H. canis.

Unsuccessful treatment of a horse with mandibular granulomatous osteomyelitis due to Halicephalobus gingivalis.

An 8-year-old horse was presented with a submandibular swelling. Biopsy of the lesion indicated granulomatous osteomyelitis due to Halicephalobus gingivalis. In the absence of evidence of involvement of the central nervous system at the time of diagnosis, the horse was treated with ivermectin. Unfortunately, the horse did not survive.

Experimental model of chronic osteomyelitis caused by Leishmania (L) amazonensis.

Experimental animal models have been used for the study of the physiopathogenesis of leishmaniasis, on some occasions with success, while in other situations such as bone alterations that accompany tegumentary leishmaniasis, especially in diffuse cutaneous form (DCL), the mechanisms are still unknown. In the present study, we determined these alterations in an animal model susceptible to Leishmania (L) amazonensis. Amastigotes of L. (L) amazonensis isolated from patients with diffuse cutaneous leishmaniasis (DCL) were inoculated into the hind paws of eight BALB/c mice, macroscopic and histopathological aspects were analyzed. After 90 and 120 days of evolution, histopathological analysis demonstrated a mononuclear cell infiltrate rich in plasma cells and intense parasitism of intra- and extra-medullary macrophages, with areas of bone necrosis and discrete involvement of cartilaginous tissue. The results show that the inflammatory process developed during L. (L) amazonensis infection might cause bone tissue destruction and secondarily affect the joints.

Osteolytic osteomyelitis associated with visceral leishmaniasis in a dog.

A dog was examined with a history of weight loss and lameness of the left hind limb. A painful response to examination of the left hip joint, and lymphadenopathy were noted. Amastigote forms of Leishmania sp. were observed by cytology in samples from the popliteus lymph node, and anti-Leishmania sp. antibodies at a titer of 1:640 were detected in serum by indirect immunofluorescence. Radiological changes included osteolysis and a periosteal proliferative reaction in the left femoral greater trochanter. These changes were histologically characterized as an osteolytic granulomatous osteomyelitis associated with amastigotes within macrophages. Non-decalcified fragments of the periosteum were processed for immunohistochemistry, observed with prominent immunolabelling of amastigotes of Leishmania sp. within macrophages. The diagnosis was further confirmed by positive PCR for Leishmania sp., belonging to the Leishmania donovani complex.

Disseminated Halicephalobus deletrix infection in a horse.

A 13-year-old Quarter Horse gelding was referred for evaluation of a draining tract and fracture of the right hemimandible of 4 weeks' duration. Two days prior to admission, the horse had developed pigmenturia. Radiography of the mandible revealed a fracture of the vertical ramus of the right hemimandible, loss of the right lower second premolar, and osteomyelitis involving an extensive portion of the hemimandible. Ultrasonography of the left kidney revealed loss of normal renal architecture. Histologic examination of tissue obtained from the right hemimandible revealed granulomatous osteomyelitis and multiple metazoan parasites identified as Halicephalobus deletrix. The horse was treated with antimicrobial and deworming agents, and the mandible was surgically debrided. The horse became atactic 8 days after surgery and was euthanatized. Necropsy identified parasitic migration in the right hemimandible, kidneys, and CNS.