Central nervous signs, blindness and cerebral vermicosis in free-ranging peregrine falcons (Falco peregrinus) associated with aberrant larval migrations.

Four free-ranging peregrine falcons (Falco peregrinus) were submitted with a history of unilateral or bilateral blindness and central nervous signs to a veterinary clinic in Germany. There were no indications of trauma or ocular disease. Likewise, other differential diagnoses for CNS signs were ruled out within the diagnostic process. The clinical diagnostic panel in live falcons included general examination, radiography, endoscopy, hematology, ophthalmoscopy and parasitological examination of the feces, blood gas analysis and blood chemistry as well as computed tomography, and magnetic resonance imaging (MRI). A complete pathological and histopathological examination was performed post-mortem. The only common finding in all birds was an infection with the nematode parasite Serratospiculum tendo. The parasite was confirmed morphologically and via PCR. In two falcons intracerebral vermicoses was suspected in MRI and confirmed in subsequent histopathology, but molecular biological identification of the parasite species failed from brain tissue. Until today, S. tendo had been reported to affect the respiratory system, the liver and different parts of the gastrointestinal tract and to cause cachexia, inappetence, regurgitation, dyspnea and general signs of illness such as lethargy, poor plumage, and reduced reproduction. Our findings indicate that aberrant migration should be considered as cause for CNS signs in falcons. As S. tendo might be a possible cause for this, CNS signs might be included in the list of clinical signs of serratospiculiasis in falcons.

Angiostrongylus cantonensis central nervous system infection in captive callitrichids in Texas.

Angiostrongylus cantonensis is a tropical lungworm of rats known for central nervous system migration in aberrant primate hosts. Here, we describe A. cantonensis infection in three captive callitrichids from a Texas zoo. The affected animals included a Goeldi's monkey (Callimico goeldii), a cotton-top tamarin (Saguinus oedipus), and a pied tamarin (Saguinus bicolor) that ranged from 8 to 18 years old. Clinical signs included lethargy, ataxia, and seizures. Histologically, these animals had an eosinophilic meningoencephalitis to myelitis and some areas had abundant macrophages and parasite migration tracts. All cases had intralesional metastrongyle parasites, and nematodes were extracted from the formalin-fixed brain specimen in one case. This extracted parasite was identified as Angiostrongylus cantonensis based on morphologic features and diagnosis was confirmed with PCR. These cases represent the first report of this parasite in non-human primates in Texas, highlighting the western spread of A. cantonensis in the continental United States.

Baylisascaris procyonis Central Nervous System Infection in a Four-Month-Old Gordon Setter Dog.

A 16 wk old intact female Gordon setter was examined for a 2 wk history of progressive cerebellovestibular ataxia. Eosinophilia was found on complete blood count, and the remaining blood work was normal. A trial treatment with clindamycin and anti-inflammatory prednisone did not result in improvement of clinical signs; therefore, the dog was euthanized. On histopathologic examination, cross sections of a 75 µm wide nematode larva with a 5 µm cuticle, prominent lateral cords, lateral alae, and coeloemyelian musculature were identified in a focally extensive region of cerebellar necrosis. The size and morphology of the parasites was most consistent with Baylisascaris procyonis. This case highlights a rare but important zoonotic disease that should be considered as a differential diagnosis in any dog exhibiting acute, progressive central nervous system signs, and peripheral eosinophilia. The index of suspicion should be elevated in dogs with an unknown deworming history and known or suspected exposure to raccoons. Because most anthelminthics have been shown to be effective against B. procyonis, annual deworming is recommended in the at-risk population to reduce the likelihood of aberrant migration and zoonosis.

GRANULOMATOUS FILARIAL ENCEPHALOMYELITIS CAUSED BY CHANDLERELLA QUISCALI IN A NORTHERN CRESTED CARACARA (CARACARA CHERIWAY).

A northern crested caracara (Caracara cheriway) was presented after being found nonambulatory in a field. On physical examination, the bird had severe hind-limb paresis. The bird did not improve after 10 days of hospitalization and was euthanized. Histologic examination of the cerebrum and spinal cord revealed multiple adult filarial nematodes surrounded by granulomatous inflammation with several multinucleated giant cells. These parasites were confirmed to be Chandlerella quiscali with polymerase chain reaction. This is the first report of C. quiscali in a bird of prey.

Behavioral changes caused by Austrodiplostomum spp. in Hoplias malabaricus from the São Francisco River, Brazil.

Traira (Hoplias malabaricus) is a neotropical fish that is widely distributed in freshwater environments in South America. In the present study, we documented the occurrence of metacercariae of Austrodiplostomum spp. (Diplostomidae) in the eyes and cranial cavity of H. malabaricus and described parasite-induced behavioral changes in the host. The fish were collected from the upper São Francisco River, in the Serra da Canastra mountain range, Minas Gerais, transported alive to the laboratory, observed for 2 weeks, and subsequently examined for parasites. Of the 35 fish examined, 28 (80 %) had free metacercariae in the vitreous humor (mean intensity=95.4; mean abundance=76.3), and 24 (68.57 %) had free metacercariae in the cranial cavity, mainly concentrated below the floor of the brain, at the height of the ophthalmic lobe (mean intensity=12.91; mean abundance=8.85). Specimens of H. malabaricus with a high intensity of infection in the brain displayed changes in swimming behavior.

Acute neurological signs as the predominant clinical manifestation in four dogs with Angiostrongylus vasorum infections in Denmark.

Four dogs with acute neurological signs caused by haemorrhages in the central nervous system were diagnosed with Angiostrongylus vasorum infection as the underlying aetiology. Two dogs presented with brain lesions, one dog with spinal cord lesions and one with lesions in both the brain and spinal cord. Only one dog presented with concurrent signs of classical pulmonary angiostrongylosis (respiratory distress, cough), and only two dogs displayed overt clinical signs of haemorrhages. Results of coagulation assays were inconsistent. Neurological signs reflected the site of pathology and included seizures, various cranial nerve deficits, vestibular signs, proprioceptive deficits, ataxia and paraplegia. One dog died and three were euthanised due to lack of improvement despite medical treatment. This emphasises canine angiostrongylosis as a potential cause of fatal lesions of the central nervous system and the importance of including A. vasorum as a differential diagnosis in young dogs with acute neurological signs in Denmark.

Elaphostrongylus cervi in a population of red deer (Cervus elaphus) and evidence of cerebrospinal nematodiasis in small ruminants in the province of Varese, Italy.

Thirty-one faecal samples were collected from red deer in the northern area of Varese, in the Italian region of Lombardy, between August and October 2008. The animals had either been hunted or accidently killed. Examination for internal parasites showed a prevalence of 45.2% for Elaphostrongylus cervi larvae and species identification was confirmed by polymerase chain reaction (PCR). Ninety-seven faecal samples were also collected from two goat flocks grazing in the same area between December 2007 and May 2008. These showed a prevalence of 74.7% for lungworms. Furthermore, the central nervous systems from five goats and one sheep from this area with a history of neurologically related lameness were examined. Histopathology confirmed E. cervi cerebro-spinal nematodiasis in five cases out of six. This study demonstrates E. cervi transmission from wild to domestic ruminants when the animals graze in the same area, and the possible occurrence of clinical disease in infected goats and sheep associated with high prevalence in deer.

[Case report of Elaphostrongylus cervi in a goat in north Italy]. / Segnalazione di Elaphostrongylus cervi in una capra in nord-Italia.

A case of cerebral nematodiasis in a goat from Lombardy (north Italy) is described. Clinical signs, histopathological lesions and the finding of a nematode in cerebral tissue sections of the affected animal confirmed the diagnosis of infection with Elaphostrongylus cervi.

[Cerebrospinal nematodosis in sheep in Switzerland]. / Zerebrospinale Nematodose beim Schaf in der Schweiz.

In December 2005 three sheep, originating from Canton Tessin, were presented with cerebrospinal nematodosis. The animals had a history of progressive pelvic limb ataxia and recumbency. The most important clinical findings were an abnormal gait (wide stance, pelvic limb paresis) and decreased sensitivity of the pelvic limbs. The general condition was slightly or moderately disturbed, appetite was normal. Examination of the cerebrospinal fluid revealed mononuclear cells and eosinophils, suggesting a helminthic infection of the central nervous system. Postmortem findings confirmed the clinical diagnosis in one animal as parts of a nematode were found in the thoracic spinal cord. Even though the nematode could not be identified, infection with Elaphostrongylus cervi seems very likely, as the sheep are in close contact with deer on the pastures and the parasite is known to infect goats in Switzerland. This is the first description of cerebrospinal nematodosis in sheep in Switzerland.

[Bilateral bone perforation caused by Coenurus cerebralis in a sheep: case report]. / Bir koyunda Coenurus cerebralis'in neden oldugu bilateral kemik perforasyonu: olgu sunumu.

Coenurus cerebralis is a cestode located in the brain and spinal cord of sheep that causes atrophy and perforation of the brain. In this study, a skull perforation caused by Coenurus cerebralis was reported in a sheep.

Epidemiology of cerebrospinal Elaphostrongylus cervi infection in red deer in central Spain.

Elaphostrongylus cervi produces a subclinical cerebrospinal disease in many wild and domestic ruminants from Europe, North America and New Zealand and has recently been described in Spain. To determine some aspects of its epidemiology, 121 red deer (Cervus elaphus) from central Spain were sampled during 2000. The prevalence (7%) and mean worm burden (3.8 worms per brain) were similar to the values previously recorded in other European areas. The infection was only detected in young deer during the winter. The estimation of larval production in the faeces was not a reliable method of diagnosing E. cervi infection.

Establishment of adult Parelaphostrongylus tenuis, patent infections, and acquired immunity after experimental infection of white-tailed deer (Odocoileus virginianus) and red deer (Cervus elaphus elaphus).

Experimental Parelaphostrongylus tenuis infections were established in white-tailed deer (Odocoileus virginianus) and an atypical host, red deer (Cervus elaphus elaphus). Groups of deer were fed 10, 25, or 100 third-stage larvae (L3) of P. tenuis and received a single equivalent challenge exposure at varying intervals. Infections were monitored up to 6 yr in white-tailed deer and up to 2.8 yr in red deer. The prepatent period in white-tailed deer varied from 91 to 1,072 days (381 +/- 374) and in red deer from 105 to 358 days (167 +/- 77). Adult worms lived for up to 6 yr in white-tailed deer. Although most had patent infections until necropsy, latent periods were observed regardless of season. Adult worms lived for up to 2.8 yr in red deer, and patent infections persisted for 20-363 days (152 +/- 106). Patent infections were correlated with the presence of adult worms in blood vessels and sinuses of both deer species. Worms were restricted to the subdural space in all deer with latent and occult infections. Adult worm recovery in white-tailed deer fed 10 or 25 L3 corresponded to the mean intensities reported in natural infections of white-tailed deer Recovery from deer fed 100 L3 was not typical of natural infection intensities. Adult P. tenuis established in all groups of red deer, but neurologic disease was restricted to animals fed 100 L3. Acute neurologic disease was associated with subdural hemorrhage and occurred at 11 mo postinfection in 2 red deer. The absence of postchallenge patent periods and the persistence of occult infections indicated that challenge exposures did not establish. These data indicate that acquired immunity to P. tenuis was established by 6 mo postinfection in both white-tailed and red deer. Latent periods in white-tailed deer and latent infections in red deer reinforce the need for a reliable diagnostic assay.

Antemortem diagnosis of canine neural angiostrongylosis using ELISA.

A 5-month-old female Kelpie developed paraparesis, hind limb ataxia and spinal hyperaesthesia 4 days after ovariohysterectomy. Neurological examination demonstrated upper motor neuron signs in the pelvic limbs with lower motor neuron signs in the tail. Cerebrospinal fluid analysis demonstrated an increased protein concentration and marked eosinophilic pleocytosis. The dog was known to have eaten rats, snails and slugs. A tentative diagnosis of neural angiostrongylosis was made and later confirmed using an ELISA based on soluble antigens obtained from larval 4 Angiostrongylus cantonensis. Antibody titres from the patient's serum and CSF were 800 and 6400, respectively. The dog was treated successfully with prednisolone. ELISA testing of serum may provide a non-invasive means for diagnosing neural angiostrongylosis in dogs.

Neurotropic behaviour of Trichobilharzia regenti in ducks and mice.

The bird nasal schistosome Trichobilharzia regenti is a new agent of cercarial dermatitis. Cercariae are able to penetrate the skin of birds and mammals including man. The parasite then attacks the central nervous system. The present study has shown that schistosomula avoid penetration of blood capillaries and enter the peripheral nerves of the legs of mice and ducks as early as 1 day post-infection (p.i.) and 1.5 days p.i., respectively. These peripheral nerves are used as a route to the spinal cord. In the specific host (duck) schistosomula were found in the spinal cord from 2 days p.i. until 15 days p.i. and in the brain from 12 days p.i. until 18 days p.i. In non-specific hosts (mice; inbred strains BALB/c, hr/hr, SCID) living schistosomula were found in the spinal cord from 2 days p.i. until 21 or 24 days p.i. (depending on the mouse strain) and in the brain of two (BALB/c, SCID) of three inbred strains from 3 days p.i. until 24 days p.i. No correlation was found between the infection dose and clinical status of the experimental hosts. A high affinity of schistosomula for the peripheral nerves was also proved in vitro, suggesting a new type of migratory behaviour in schistosomatids.

Histopathology of CNS and nasal infections caused by Trichobilharzia regenti in vertebrates.

In bird infections caused by Trichobilharzia regenti, the central nervous system (CNS) represents probably the main route to the nasal cavity, where maturation of the parasite occurs. However, in an abnormal mouse host, development is incomplete and is accompanied by a strong affinity of the parasite to the CNS. In order to explain pathological changes caused by the parasite, a histological study of cross-sections from the CNS and nasal cavity was performed. In the CNS of duck and mouse, immature flukes were found. Cross-sections showed parasites located either in meninges or in matter of various parts of the spinal cord and brain. In the spinal cord, the submeningeal location led to a strong inflammatory reaction around the schistosomula and resulted in eosinophilic meningitis. In the white and gray matter of the spinal cord and in the white matter of the brain, a cellular infiltration of spongy tissue surrounded the immature parasites; and we observed dystrophic and necrotic changes of neurons, perivascular eosinophilic inflammation in the spinal cord and brain, and cell infiltration around the central canal of the spinal cord. T. regenti adults and eggs were detected in the nasal mucosa of infected ducklings; and aging of the eggs resulted in various host reactions, ranging from focal accumulation of cells to the formation of granulomas. Histopathological changes may explain symptoms described previously for prepatent and patent phases of infections caused by T. regenti, i.e., neuromotor abnormalities in birds and mammals and hemorrhages/petechiae in birds, respectively.

Trichobilharzia regenti, a pathogen of the avian and mammalian central nervous systems.

The development of nasal avian schistosomes of the genus Trichobilharzia in their final host is poorly known. Therefore, an experimental infection of ducklings (Anas platyrhynchos f. dom.) by T. regenti was performed. The infection resulted in leg paralysis and orientation/balance disorders of birds. The examination of the duck's spinal cord and brain confirmed the presence of developing parasites in pre-patent as well as patent periods. The absence of the worms in other tissues strongly supports our hypothesis that the parasite migrates through the central nervous system (CNS) to its final location in bird nasal mucosa. The injury level is probably dependent on number of parasites as well as yet unknown host factors. The affinity to the CNS seems to be high; also by exposure of experimental animals to low cercarial doses the growing worms in the CNS were found. In addition to the generally accepted view that bird schistosomes may cause cercarial dermatitis of mammals (including man), there is evidence of a partial development of T. regenti in mouse CNS; in certain cases leg paralysis was also recorded. Therefore, the pathogenesis spectrum caused by bird schistosomes in birds/mammals needs to be reconsidered.

Cerebral coenurosis in a wild sheep (Ovis ammon).

Cerebral coenurosis is described in a 2 year-old wild sheep (Ovis ammon). Diagnosis was based on clinical signs and pathology.