Pathology in Practice

Antonio Carlos L. Câmara Veterinary Hospital, Universidade Federal Rural do Semi-Árido, Mossoró, RN 59625-900, Brazil.

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Paulo M. Lima Department of Animal Sciences, Universidade Federal Rural do Semi-Árido, Mossoró, RN 59625-900, Brazil.

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Jael S. Batista Department of Animal Sciences, Universidade Federal Rural do Semi-Árido, Mossoró, RN 59625-900, Brazil.

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Francisco M. C. Feijó Department of Animal Sciences, Universidade Federal Rural do Semi-Árido, Mossoró, RN 59625-900, Brazil.

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Benito Soto-Blanco Department of Animal Sciences, Universidade Federal Rural do Semi-Árido, Mossoró, RN 59625-900, Brazil.

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History

A 9-year-old 31.0-kg (68.3-lb) crossbred female Saanen goat was evaluated at the Large Animal Veterinary Hospital of the Universidade Federal Rural do Semi-Árido, Mossoró, RN, Brazil, because of paralysis of the hind limbs. The goat had been purchased recently and had arrived at the property 12 days earlier. On arrival, the goat's mental status and gait were considered normal, but the owner reported the presence of a scarred wound in the final stage of healing in the lumbar area over the vertebral column. On the fifth day on the farm, the goat developed ataxia and hind limb weakness. On the eighth day, hind limb paralysis was evident; the goat was no longer able to stand and assumed a dog-sitting position (Figure 1). The goat had been treated IM with dexamethasone (2 mg, q 24 h for 4 days) before referral to the hospital.

Figure 1—
Figure 1—

Photograph of a 9-year-old crossbred female Saanen goat that was evaluated because of progressive development of total paralysis of the hind limbs. On the fifth day after arrival at the farm, the goat developed ataxia and hind limb weakness; on the eighth day, the goat was no longer able to stand and had assumed a dog-sitting position.

Citation: Journal of the American Veterinary Medical Association 240, 3; 10.2460/javma.240.3.269

Clinical and Gross Findings

On physical examination, the goat's rectal temperature was 38.8°C (101.8°F), heart rate was 96 beats/min, and respiratory rate was 48 respiratory excursions/min. Gastrointestinal tract motility and appetite appeared normal. Neurologic examination revealed apparently normal mental status and cranial nerve function, but the goat had flaccid paralysis of the hind limbs. Sensory responses to gentle pricking of the skin along the dorsum were detectable, with the exception of responses of a lumbar segment between the L4 and L6 vertebral bodies. Tail tone and anal reflex were present. On the basis of the physical findings, a diagnosis of spinal cord disease was made and the lesions were assumed to be associated with the L4, L5, and L6 vertebrae. A CBC and analysis of a sample of CSF collected without anticoagulant from the lumbosacral space were performed on the eighth day. Because of the goat's condition and its difficulty ambulating and foraging, euthanasia was performed after the referral examination. During necropsy, multiple cavitations were detected in the thoracic and lumbar spinal cord regions; the cavitations ranged from 0.1 × 0.2 cm to 0.3 × 0.7 cm and contained yellowish-white material that had a granular appearance.

Formulate differential diagnosis from the history, clinical findings, and Figure 1—then turn page →

Cytologic, Histopathologic, and Microbiological Findings

A CBC (blood sample collected on the eighth day after arrival at the farm) revealed mild lymphopenia (1,450 cells/μL; reference range,1 2,000 to 9,000 cells/μL) that could have been attributable to stress. The CSF sample collected on the eighth day after arrival at the farm was grossly clear and colorless with presence of clots. The CSF total protein concentration was 48 mg/dL (reference range,2 24 to 40 mg/dL), and glucose concentration was 50 mg/dL (reference range,2 45 to 87 mg/dL). The nucleated cell count was 75 cells/μL (reference range,2 0 to 7 cells/μL), with predominance of mononuclear cells. In addition, there were 18 RBCs/μL of CSF; the pH was 8.0. Results of the CSF analysis were interpreted as evidence of an inflammatory reaction in the CNS. The presence of clots in the CSF sample could have affected the observed degree of pleocytosis.

Various tissues, including sections of cerebrum, cerebellum, pons, medulla oblongata, and cervical thoracic and lumbar regions of the spinal cord, were examined histologically. Histopathologic findings were indicative of severe meningitis characterized by a peri-vascular infiltrate of lymphocytes, plasmacytes, and macrophages that extended radially to the white matter. In the gray matter, multifocal areas contained microabscesses, which were composed of neutrophils and macrophages; areas of necrosis with neuropil vacuolization, gitter cells, and occasional axonal spheroids were also present (Figure 2).

Figure 2—
Figure 2—

Photomicrograph of a section of the thoracic portion of the spinal cord of the goat in Figure 1. Notice the multifocal areas of microabscess formation, which are composed of neutrophils and macrophages, and areas of necrosis with neuropil vacuolization, gitter cells, and occasional axonal spheroids. H&E stain; bar = 170 μm.

Citation: Journal of the American Veterinary Medical Association 240, 3; 10.2460/javma.240.3.269

Samples of the yellowish material inside the cavitations in the thoracic and lumbar regions of the spinal cord were collected for microbiological culture and biochemical analysis. Results indicated the presence of Listeria monocytogenes.

Morphologic Diagnosis

Listerial myelitis restricted to the spinal cord and without brainstem involvement.

Comments

Listeriosis is an infectious disease caused by L monocytogenes (a nonsporulating, facultative, anaerobic gram-positive rod), which affects a wide range of mammals, including ruminants, monogastric animals, and humans. In ruminants, the main clinical features are encephalitis, keratoconjunctivitis, uveitis, septicemia, abortion, mastitis, and gastroenteritis.3,4 A CNS form of the disease named listerial myelitis has been detected in sheep,5,6 cattle,7 and humans.8 This syndrome develops relatively rarely; the affected animals have normal mental status and cranial nerve function but develop flaccid paraparesis or hemiparesis, tetraparesis or tetraplegia, and recumbency.3,4 In goats, the only form described previously has been encephalitic listeriosis, which is characterized by unilateral or bilateral cranial nerve deficits.9,10

For the goat of this report, the definitive diagnosis was made on the basis of the clinical signs, pathological findings, and bacteriologic isolation of L monocytogenes. In countries of North America and Europe, listeriosis is often associated with ingestion of poorly fermented silage (pH > 5.0 to 5.5) that provides an excellent substrate for survival and possible multiplication of the microorganism.3 However, in northeastern Brazil, outbreaks of encephalitic listeriosis have not been linked to silage sources but to penetration of the mucosal barrier through injury or inflammation of the buccal or intestinal tract mucosa or to dental disease.11 Listerial myelitis is thought to result from hematogenous spread of bacteria or ascending bacterial infection along spinal nerves of affected spinal cord segments.5,6 In the goat of this report, the proximity of the wound to the spinal cord may have shortened the incubation period required for the encephalitic form to develop (4 to 6 weeks). Although this is the first report of this disease in a goat to our knowledge, practitioners should be aware that listerial myelitis can develop in this species and it should be considered as a differential diagnosis of spinal cord disease in goats.

References

  • 1.

    Kramer JW. Normal hematology of cattle, sheep, and goats. In: Feldman BF, Zinkl JG, Jain NC, eds. Schalm's veterinary hematology. 5th ed. Ames, Iowa: Blackwell Publishing, 2006;10751084.

    • Search Google Scholar
    • Export Citation
  • 2.

    Smith MO, George, LW. Cerebrospinal fluid. In: Smith BP, ed. Large animal internal medicine. 3rd ed. St Louis: Mosby, 2002;873875.

  • 3.

    Brugére-Picoux J. Ovine listeriosis. Small Rumin Res 2008; 76:1220.

  • 4.

    Francoz D. Cranial nerve abnormalities. In: Anderson DE, Rings DM, eds. Current veterinary therapy: food animal practice 5. St Louis: Saunders Elsevier, 2009;299306.

    • Search Google Scholar
    • Export Citation
  • 5.

    Gates GA, Blenden DC, Kintner LD. Listeric myelitis in sheep. J Am Vet Med Assoc 1967; 150:200204.

  • 6.

    Seaman JT, Carter GI, Carrigan MJ, et al. An outbreak of listerial myelitis in sheep. Aust Vet J 1990; 67:142143.

  • 7.

    Schweizer G, Fuhrer B, Braun U. Signs of spinal cord disease in two heifers caused by Listeria monocytogenes. Vet Rec 2004; 154:5455.

  • 8.

    Rossi FH, White J, Quisling R, et al. Listeria spinal cord abscess responsive to trimethoprim-sulfamethoxazole monotherapy. Can J Neurol Sci 2001; 28:354356.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9.

    Rissi DR, Rech RR, Barros RR, et al. Forma nervosa de listeriose em caprinos. Pesq Vet Bras 2006; 26:1420.

  • 10.

    Wood JS. Encephalitic listeriosis in a herd of goats. Can Vet J 1972; 13:8082.

  • 11.

    Schild AL. Listeriose. In: Riet-Correa F, Schild AL, Lemos RAA, et al, eds. Doenças de ruminantes e equideos. 3rd ed. Santa Maria, RS, Brazil: Palotti, 2007;352357.

    • Search Google Scholar
    • Export Citation
  • Figure 1—

    Photograph of a 9-year-old crossbred female Saanen goat that was evaluated because of progressive development of total paralysis of the hind limbs. On the fifth day after arrival at the farm, the goat developed ataxia and hind limb weakness; on the eighth day, the goat was no longer able to stand and had assumed a dog-sitting position.

  • Figure 2—

    Photomicrograph of a section of the thoracic portion of the spinal cord of the goat in Figure 1. Notice the multifocal areas of microabscess formation, which are composed of neutrophils and macrophages, and areas of necrosis with neuropil vacuolization, gitter cells, and occasional axonal spheroids. H&E stain; bar = 170 μm.

  • 1.

    Kramer JW. Normal hematology of cattle, sheep, and goats. In: Feldman BF, Zinkl JG, Jain NC, eds. Schalm's veterinary hematology. 5th ed. Ames, Iowa: Blackwell Publishing, 2006;10751084.

    • Search Google Scholar
    • Export Citation
  • 2.

    Smith MO, George, LW. Cerebrospinal fluid. In: Smith BP, ed. Large animal internal medicine. 3rd ed. St Louis: Mosby, 2002;873875.

  • 3.

    Brugére-Picoux J. Ovine listeriosis. Small Rumin Res 2008; 76:1220.

  • 4.

    Francoz D. Cranial nerve abnormalities. In: Anderson DE, Rings DM, eds. Current veterinary therapy: food animal practice 5. St Louis: Saunders Elsevier, 2009;299306.

    • Search Google Scholar
    • Export Citation
  • 5.

    Gates GA, Blenden DC, Kintner LD. Listeric myelitis in sheep. J Am Vet Med Assoc 1967; 150:200204.

  • 6.

    Seaman JT, Carter GI, Carrigan MJ, et al. An outbreak of listerial myelitis in sheep. Aust Vet J 1990; 67:142143.

  • 7.

    Schweizer G, Fuhrer B, Braun U. Signs of spinal cord disease in two heifers caused by Listeria monocytogenes. Vet Rec 2004; 154:5455.

  • 8.

    Rossi FH, White J, Quisling R, et al. Listeria spinal cord abscess responsive to trimethoprim-sulfamethoxazole monotherapy. Can J Neurol Sci 2001; 28:354356.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 9.

    Rissi DR, Rech RR, Barros RR, et al. Forma nervosa de listeriose em caprinos. Pesq Vet Bras 2006; 26:1420.

  • 10.

    Wood JS. Encephalitic listeriosis in a herd of goats. Can Vet J 1972; 13:8082.

  • 11.

    Schild AL. Listeriose. In: Riet-Correa F, Schild AL, Lemos RAA, et al, eds. Doenças de ruminantes e equideos. 3rd ed. Santa Maria, RS, Brazil: Palotti, 2007;352357.

    • Search Google Scholar
    • Export Citation

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