An outbreak of neurofilariosis in young goats

Veterinary Parasitology 120 (2004) 151–156 Short communication An outbreak of neurofilariosis in young goats O.M. Mahmoud∗ , E.M. Haroun, O.H. Omer Department of Veterinary Medicine, King Saud University, P.O. Box 1482, Buraydah, Qassim, Saudi Arabia Received 17 April 2003; received in revised form 11 September 2003; accepted 22 October 2003 Abstract An outbreak of cerebrospinal microfilariosis in 23 kids, representing a whole kid crop, occurred on a farm in Qassim, Central Saudi Arabia. The morbidity and mortality rates were 100%. Clinical signs, in kids from the fourth to sixth week of age, manifested as weakness in the hind legs followed by incoordination of movement and feet dragging. Seven to ten days later, the hind legs were completely paralyzed, and within a week the front legs were also paralyzed. The animals continued to feed, drink and suckle normally, and were in good health. Paralyzed kids were helped to suckle by the farm attendants. With time, loss of control of motor functions occurred and the ability to hold the head in upright position was lost, ability to eat or drink was lost. The infected kids health deteriorated and they eventually died. Two dead kids were postmortemed. With the exception of a meningeal haemorrhage seen in one kid, no obvious macroscopic lesions were seen in any of the autopsied animals. Histopathological examination of the spinal cord and brain showed different microfilaria of different sizes between the meninges and the nervous tissue. This indicated that development of the parasite occurred in the nervous tissue. The larger microfilaria contained black deposits, most likely to be digested blood, in their guts. It is likely that the parasites are haematophagus. The main lesions caused by the microfilaria were migratory traumatic haemorrhagic tracts in the spinal cord and the brain. These sometimes contained parts of the microfilariae. In the brain malacic lesions and sporadic aggregates of lymphocytes were also noted. © 2003 Published by Elsevier B.V. Keywords: Setaria digitata; Goat neurofilariasis; Saudi Arabia 1. Introduction Cerebrospinal microfilariosis is a serious and fatal disease in goat kids (Mahmoud et al., 1994). Juvenile filaria migrate through the nervous tissue causing severe damage, this is initially manifested clinically by disturbed gait and finally by paralysis (Jones et al., 1997). ∗ Corresponding author. Tel.: +966-6-3800050; fax: +966-6-3801360. E-mail address: qagrvit@ksu.edu.sa (O.M. Mahmoud). 0304-4017/$ – see front matter © 2003 Published by Elsevier B.V. doi:10.1016/j.vetpar.2003.10.003 152 O.M. Mahmoud et al. / Veterinary Parasitology 120 (2004) 151–156 Setaria digitata, a filarial worm that usually inhabits the peritoneal cavity of cattle, has been incriminated in the etiology of cerebrospinal filariosis in aberrant infections (Jones et al., 1997). The parasite has been found in the peritoneal cavity of healthy adult goats in Saudi Arabia (El-Azazy and Ahmed, 1999). We have described an outbreak of cerebrospinal microfilariosis in which all lamb crop died (Mahmoud et al., 1994). In this paper, we report a second outbreak of cerebrospinal microfilariosis in which the entire kid crop on the farm died. 2. Materials and methods The disease occurred during the months of November and December 2002 at Gassim (latitude: 26◦ 18′ 28′′ N, longitude: 43◦ 46′ 03′′ E). The average rainfall for both months were 47.2 mm. The average maximum and minimum temperatures for both months were 22.1 and 10.2 ◦ C, respectively (source Gassim Metrological Station, Meterology and Environmental Protection Administration, Kingdom of Saudi Arabia). Two paralyzed kids approximately 2–3 months of age, were sacrificed and autopsied. Samples collected from different regions of the spinal cord and the brain were fixed in 10% formal saline. These were processed and stained with H&E for routine histopathology. 3. Results The goat herd consisted of 23 kids, 16 adult females and 2 breeding males. The kids were between 1 and 4 months old. They are fed on alfalfa (Medicago sativa) and a locally made concentrate diet. There is free access to drinking water. Pregnancy was normal, the kids were born in good health and developed normally until the age of 4–6 weeks when the symptoms first appeared. Initially the kids showed an unsteady gait and weakness of the hindlimbs which deteriorated over time. Their hind legs were completely paralyzed within 7–10 days of the appearance of symptoms (Fig. 1). With time, paralysis spread to the forelimbs after which the kids became completely paralyzed. The kids continued to feed and drink normally and were otherwise in good health. About 1 month from infection, motor control of the head was lost and the kids could no longer feed and drink. They all eventually died. No adult goats showed clinical symptoms. Suspicions of copper and selenium deficiencies have delayed proper diagnosis. Single doses of commercial preparations containing Vitamin E and selenium and copper as copper methionate were injected to adult goats and kids in the farm. The disease was unresponsive to injections containing these minerals. The last two surviving paralyzed kids were brought to the University clinic for investigation. With the exception of meningeal haemorrhage seen on the brain (Fig. 2), postmortem examination revealed no visible macroscopic lesions. Histopathological examination of the brain and the spinal cord revealed different sizes of microfilariae between the nervous tissue and the meninges. The larger microfilariae contained blackish material in their guts (Fig. 3a and b). The parasites burrowed cavities into the nervous tissue, the boundaries of which were haemorrhagic (Fig. 4). Some contained parts of the microfilariae. In some instances O.M. Mahmoud et al. / Veterinary Parasitology 120 (2004) 151–156 153 Fig. 1. Hindlimb paralysis. Note the good health of affected kids. Fig. 2. Haemorrhage in the brain meninges. malacic lesions without haemorrhages were seen in the nervous (Fig. 5). Focal aggregates of lymphocytes were seen in the brain of one of the kids (Fig. 6). 4. Discussion The lesions caused by the microfilariae in the brain and spinal cord were severe and do accounted for the paralysis seen in the involved kids. It appears that the microfilariae gained 154 O.M. Mahmoud et al. / Veterinary Parasitology 120 (2004) 151–156 Fig. 3. (a) Microfilaria between spinal meninges: H&E 400×. (b) More developed microfilaria in the spinal cord meninges. Note longer and larger body and gut containing black digested blood: H&E 125×. entrance to the nervous tissue from the posterior part of the spinal cord and then moved forward, which explains the forward progressive paralysis, which started in the hindlimbs and moved anteriorly. We were unable to identify the causative filarial worm, but S. digitata has been reported in the peritoneal cavity of healthy goats in the western region of Saudi Arabia (El-Azazy and Ahmed, 1999). Having seen only microfilariae in the tissues, no adult worm species could be identified. The microfilaria existed in different sizes, and this means the juvenile parasites were able to develop in the nervous tissue of the kids. Developed microfilaria had O.M. Mahmoud et al. / Veterinary Parasitology 120 (2004) 151–156 155 Fig. 4. Trauma and haemorrhage in the migratory track of a microfilaria in the spinal cord. blackish deposits in their guts, which indicates that they had a blood meal. Nervous tissue is made of lipids and fibres and the black deposits could, therefore, only be digested blood. The search for blood by the smaller microfilariae explains the haemorrhages seen in the meninges as well as the malacic lesions of the nervous tissue. Microfilariae are likely to occlude small blood vessels resulting in malacic infarcts of those areas supplied by these blood vessels. Cerebrospinal filariosis is usually an aberrant infection involving few animals in a flock (Jones et al., 1997). This is the second outbreak we have witnessed in Qassim region where the morbidity and mortality in young kids were 100% (Mahmoud et al., 1994). It is possible that other outbreaks have not been diagnosed because diagnosis depends on a thorough pathological investigation including the examination of large number of serial sections of Fig. 5. Malacic lesion in the spinal cord: H&E 125×. 156 O.M. Mahmoud et al. / Veterinary Parasitology 120 (2004) 151–156 Fig. 6. Focal aggregates of lymphocytes in the brain tissue. the spinal cord and brain. Currently the mode of transmission of this disease is unknown although Culex mosquitoes and Stomoxys flies, both of which are haematophagus, are found in the area. Since certain cerebral filariasis might be zoonotic (Orithel, 1973), verification of its epidemiology and identification of the adult worm needs urgent attention. References El-Azazy, O.M., Ahmed, Y.F., 1999. Patent infection with Setaria digitata in goats in Saudi Arabia. Vet. Parasitol. 82, 161–166. Jones, T.C., Hunt, R.D., King, N.W., 1997. Cerebrospinal nematodiasis. In: Veterinary Pathology, 6th ed. Williams and Wilkins, Philadelphia, London, Paris, pp. 626–628. Mahmoud, O.M., Sulman, A., Haroun, E.M., Abdel-Magied, E.M., Hameid, Y.M., Ibrahim, I.A., 1994. Ivermectin treatment of an outbreak of cerebrospinal microfialriosis in goats in Saudi Arabia. Trop. Anim. Hlth. Prod. 26, 177–179. Orithel, T.C., 1973. Cerebral filariasis in Rhodesia—a zoonotic infection? Am. J. Trop. Med. Hgy. 22, 596–599.