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Brief Communication |
Correspondence: 1Corresponding Author: Uneeda K Bryant, University of Kentucky, Livestock Disease Diagnostic Center, PO Box 14125, Lexington, KY 40512
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Abstract |
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Key Words: Cerebellum • Halicephalobus gingivalis • meningoencephalitis • Thoroughbred foal
A 13-week-old Thoroughbred colt developed an acute onset of ataxia, blindness, and head tremors. The foal had been normal at birth and did not exhibit signs of illness until this event. The neurologic examination showed no further specific cranial nerve deficits other than blindness and poor menace response. The foal was afebrile, depressed, and had intention tremors of the head and neck and ataxia involving all 4 limbs. During the next 12 hours, the condition progressed to severe ataxia, leaning to the right, and, within 24 hours, to recumbency and seizures. A complete blood count revealed a leukocytosis (17.7 K/µl, normal 5–12.6 K/µl) with a differential demonstrating a neutrophilia (90.1%, normal 55–65%) and lymphopenia (9.4%, normal 35–45%). Biochemistry panel values were within normal limits, and a blood culture was not obtained. Radiographs were obtained from the foal in a standing position and under light sedation with xyzaline.a Lateral and dorsoventral views of the cervical spinal column and cranium revealed a suspected occipital fracture. The cerebrospinal fluid (CSF) obtained from the atlanto-occipital joint space was clear with a white blood cell count of 14 cells/µl (normal 0–5 cells/µl) and a red blood cell count of 10 cells/µl (normal 0–5 cells/µl). There was a mixed pleocytosis (42% eosinophils, 54% mononuclear cells, and 4% neutrophils) with a mild elevation in protein levels detected at 66.7 mg/dl (normal 10–60 mg/dl). No growth was obtained during a culture of the CSF. Differential diagnoses included head trauma with subsequent cranial fracture and metabolic and inflammatory conditions such as meningitis (bacterial, fungal, viral, or parasitic etiologies). The treatment regimen included balanced electrolyte fluidsb (1 liter BID) containing dimethyl sulfoxidec (1 gm/kg) as well as dexamethasoned (1 mg/kg, IV, BID), trimethoprim-sulfamethaxozolee (15 mg/kg PO, BID), vitamin Ef (10,000 units, PO, SID), and flunixin meglumineg (1.1 mg/kg, IV, BID). Despite treatment, the colt's condition did not improve, and humane euthanasia was elected. The colt was submitted to the Livestock Disease Diagnostic Center, University of Kentucky, on August 10, 2005, for necropsy.
Gross examination at necropsy revealed a colt in good postmortem preservation with no cranial or cervical vertebral fractures and no gross findings in the brain or internal organs. Sections of brain, cervical spinal cord, spleen, liver, kidney, lung, heart, diaphragm, and small and large intestines were obtained during necropsy and placed in 10% buffered formalin. Half of the brain was removed and frozen. Tissues placed in formalin were embedded in paraffin blocks, sectioned into 5-µm sections, and stained with hematoxylin and eosin for routine histopathologic examination.
Histopathologic findings within the brain were consistent with a verminous meningoencephalitis, predominantly affecting the cerebellum. Randomly distributed regions within the neuropil of the cerebellum, cerebrum, and the meninges or dura mater of the brainstem contained cross and longitudinal sections of nematodes within a granulomatous inflammatory reaction. Moderate numbers of eosinophils were within vascular lumens and occasionally extended into perivascular spaces and the adjacent tissues (Fig. 1). Low to moderate numbers of macrophages, multinucleated giant cells, eosinophils, and lymphocytes frequently formed perivascular cuffs and surrounded partially phagocytized nematodes (Fig. 2). Several randomly distributed nematodes were dispersed throughout the neuropil without an inflammatory response. Morphologic features of the nematodes included: 1) smooth and thin cuticle; 2) rhabditiform esophagus composed of an isthmus, bulb, and corpus (Fig. 3); 3) platymyarian-meromyarian musculature; 4) a solitary genital tract/uterus containing a single uninucleate ovum; 5) a tapered tail; and 6) characteristic and distinguishable positioning of the reproductive tract. The ovaries of the nematodes were dorsoflexed, and the vulva was ventroflexed (Fig. 4).2–5 This unique reproductive tract definitively identifies the nematodes as Halicephalobus gingivalis and differentiates them from other species of Halicephalobus as well as other parasites that can cause central nervous systems signs, symptoms, and lesions such as Hypoderma sp., Angiostrongylus cantonensis, Setaria sp., Strongylus vulgaris, and Draschia megastoma. 3,6 Additional microscopic alterations included scattered regions of neuropil rarefaction, marked depletion of lymphocytes within the white pulp of the spleen, and gut-associated lymphoid tissue of the colon. The remaining internal organs. including the spinal cord, spleen, liver, lungs, heart, diaphragm, intestines, and kidneys. were unremarkable.
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In a Petri dish, 12 small, nonviable nematodes were observed in the final washings from the cerebellum. The vast majority of the nematodes were found in the 200-mesh sieve washings. Examination of the extracted nematodes with the use of a compound microscope revealed them to be H. gingivalis formerly known as Micronema deletrix.1,7,8,10 Morphologically, the nematodes were very small. Total lengths of 8 of 12 extracted nematodes were 395.0, 379.2, 347.6, 347.6, 331.8, 363.4, 379.2, and 379.2 µm, respectively. Identical procedures performed on the cerebellum were executed on the cerebrum and midbrain for the extraction of nematodes but no parasites were recovered.
No bacteria were isolated from the lung, liver, and brain during bacteriologic examination. The fluorescent antibody testing for equine rhinopneumonitis virus was negative.
Several cases of H. gingivalis has been reported in horses and less frequently in humans.1,6 Nematodes in the genus Halicephalobus are free-living, saprophytic, and opportunistic parasites commonly found in organic matter such as soil and manure.4–7,9 H. gingivalis has the ability to produce destructive lesions and extensive tissue damage because of its migratory behavior. The ability of these nematodes to reproduce parthenogenetically within the host results in massive numbers occurring in various tissues, thereby setting up the probability of killing the host.6,7 Reports of parasiticides effective against H. gingivalis are limited.7
Organs commonly affected by H. gingivalis in horses include brain, kidneys, lymph nodes, spinal cord, adrenal glands, and oral and nasal cavities.3,6 Additional organs reported to be affected to a lesser degree include heart, stomach, liver, ganglia, and bones.3,6,7 H. gingivalis also has been recovered from the semen and urine of 2 horses.6 The literature has been reviewed extensively by one group of researchers1 on the taxonomy, life history, and detrimental effects caused by these parasites. Speculation concerning the tendency of H. gingivalis to develop in equine feces has been raised. Ingestion of plant material acting as mechanical vectors for H. gingivalis and accompanying bacteria has been speculated by researchers to cause mandibular/gingival lesions in horses.1 Furthermore, these authors surmise that the nematodes may enter the bloodstream and disseminate throughout the body of the host, including the central nervous system.
Other investigators,3,5,9 reviewing the literature and their own conjectures, have considered the possibilities of acquired infections of H. gingivalis derived from gingival or cutaneous penetration, central nervous system infections via the hematogenous route, or pulmonary infections from inhalation of the nematodes. Other theories concerning the transmission of H. gingivalis involve probable colostral transfer to foals during nursing, as described in one report involving a Thoroughbred mare with mastitis and a nursing foal with encephalitis.10
Considering all proposed hypotheses concerning the pathogenesis of an infection caused by H. gingivalis, an oronasal route, via ingestion, inhalation, or both, are highly suggestive in this reported case. Rhabditiform nematodes are infamous for their migratory capabilities. Inhalation of these parasites may lead to migration through the cribiform plate of the ethmoid bone resulting in an intracranial infection. A hematogenous route of transmission would coincide with the disseminated nature of the parasites within previously reported cases where multiple organ systems were involved. 6,8–10 The nematodes present within this reported case were restricted to the brain. A hematogenous route is questionable because of the absence of parasites within other organs. Nonetheless, a hematogenous route cannot be completely ruled out since adult nematodes and larvae were predominantly in perivascular regions. Hematogenous dissemination frequently is suggested because worms have been reported free within vascular lumens of the brain.6 This foal demonstrated marked lymphoid depletion of splenic lymphoid follicles, as well as the colonic gut-associated lymphoid tissue, which may suggest that a compromised immune system may have played a susceptibility role in acquiring an infection caused by H. gingivalis.
In conclusion, several nematodes were extracted from frozen brain tissue of this 13-week-old Thoroughbred colt 5 weeks after the initial postmortem examination. The parasites were definitively identified as H. gingivalis based on characteristic morphologic features of the reproductive tract. These characteristic features of the reproductive tract include a dorsoflexed ovary and ventroflexed vulva. The high pathogenicity of H. gingivalis is demonstrated in this reported case as well as previously documented occurrences. Although uncommon, H. gingivalis should be considered as a differential diagnosis when eosinophilic pleocytosis in CSF is present and clinical signs suggestive of central nervous system dysfunction are present.
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TOPSources and manufacturersAbstractReferences |
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a. Rompun, Bayer AG, Leverkusen, Germany.
b. Normosol-R, Abbott Laboratories, Abbott Park, IL.
c. DMSO, W. A. Butler Company, Dublin, OH.
d. Dexamethasone, Schering-Plough Animal Health Corporation, Branchburg, NJ.
e. Trimethoprim-sulfamethaxozole, Schering-Plough Animal Health Corporation, Branchburg, NJ.
f. Elevate, Kentucky Performance Products, Versailles, KY.
g. Banamine, Schering-Plough Animal Health Corporation, Branchburg, NJ.
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