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CASE REPORT Neospora caninum infection in three dogs C. Knowler and S. J. Wheeler Department of Small Animal Medicine and Surgery, Royal Veterinary College, Hawkshead Lane, North Mymms, Hert- fordshire AL9 7TA Journal of Small Animal Practice (1995) 36, 172-177 ABSTRACT Infection with Neospora caninum in three young dogs is described. The predominant clini- cal signs were lower motor neuron deficits of the pelvic limbs, bladder and rectum. In two cases there was liver infection and dysfunction. The younger dogs had an acute onset rapidly progres- sive syndrome. The older dog had a similar but more chronic course. The diagnosis was con- firmed by an immunofluorescence antibody test. The parasite is sensitive to clindamycin and trimethoprim/sulphonamide preparations, how- ever the prognosis for return to function is poor especially if muscle contracture has occurred. INTRODUCTION Neospora caninum is a newly recognised fatal apicomplexan protozoal infection of dogs and other animals. It is structurally similar to Toxo- plasma gondii, but it is immunologically distinct. Until 1988, infections had been misdiagnosed as toxoplasmosis. The disease was first described in a litter of boxer dogs in Norway by Bjerkas and others (1984). Dubey and others (1988 a,b) isolated the parasite and named it N caninum. Retrospective studies have identified the parasite in cases as early as 1957 (Dubey and others 1988a). It was first recognised in Britain in 1990 (Dubey and others 1990b) and should be suspected in any immature dog presenting with neurological signs, especially if progressive pelvic limb paresis is present. CASE HISTORIES Case 1 A 15-week-old female labrador retriever was presented with paraplegia (Fig 1). The owner had noticed seven days previously that the right pelvic limb was dragging, and there was a rapid progression to a loss of voluntary movement of the pelvic limbs and the tail. On presentation, the puppy was clinically depressed with an increased respiratory rate and effort (60 breaths per minute). Rectal temper- ature was 393°C with a pulse rate of 158 beats per minute. Abdominal palpation suggested FIG 1. pelvic limb hyperextension Neospora caninum infection with paraplegia and 72

Neospora caninum infection in three dogs

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Page 1: Neospora caninum infection in three dogs

CASE REPORT

Neospora caninum infection in three dogs C. Knowler and S. J. Wheeler

Department of Small Animal Medicine and Surgery, Royal Veterinary College, Hawkshead Lane, North Mymms, Hert- fordshire AL9 7TA

Journal of Small Animal Practice (1995) 36, 172-177

ABSTRACT Infection with Neospora caninum in three

young dogs is described. The predominant clini- cal signs were lower motor neuron deficits of the pelvic limbs, bladder and rectum. In two cases there was liver infection and dysfunction. The younger dogs had an acute onset rapidly progres- sive syndrome. The older dog had a similar but more chronic course. The diagnosis was con- firmed by an immunofluorescence antibody test. The parasite is sensitive to clindamycin and trimethoprim/sulphonamide preparations, how- ever the prognosis for return to function is poor especially if muscle contracture has occurred.

INTRODUCTION Neospora caninum is a newly recognised fatal

apicomplexan protozoal infection of dogs and other animals. It is structurally similar to Toxo- plasma gondii, but it is immunologically distinct. Until 1988, infections had been misdiagnosed as toxoplasmosis.

The disease was first described in a litter of boxer dogs in Norway by Bjerkas and others (1984). Dubey and others (1988 a,b) isolated the parasite and named it N caninum. Retrospective studies have identified the parasite in cases as early as 1957 (Dubey and others 1988a). It was first recognised in Britain in 1990 (Dubey and others 1990b) and should be suspected in any immature dog presenting with neurological signs, especially if progressive pelvic limb paresis is present.

CASE HISTORIES Case 1

A 15-week-old female labrador retriever was presented with paraplegia (Fig 1). The owner had noticed seven days previously that the right pelvic limb was dragging, and there was a rapid progression to a loss of voluntary movement of the pelvic limbs and the tail.

On presentation, the puppy was clinically depressed with an increased respiratory rate and effort (60 breaths per minute). Rectal temper- ature was 393°C with a pulse rate of 158 beats per minute. Abdominal palpation suggested

FIG 1. pelvic limb hyperextension

Neospora caninum infection with paraplegia and

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Neospora caninuni infection in three dogs

hepatomegaly. The puppy was paraplegic with a rigid extension of the pelvic limbs due to muscle contracture. The quadriceps and gracilis muscles were most affected; the stifles could not be man- ually flexed and the limbs could not be abducted. The pelvic limbs had a complete loss of con- scious proprioception with absent tendon reflex- es. There was diffuse muscular pain and atrophy. The bladder was distended with urinary over- flow. It could not be manually expressed. The anus was flaccid and dilated; there was no per- ineal reflex. There was a mixed autonomic lesion of the right eye. Partial mydriasis with reduced direct and consensual pupillary light responses suggested a lesion of the parasympathetic fibres of the oculomotor nerve. There was also ptosis, enophthalmus and nictating membrane protru- sion indicative of a Homer’s syndrome. There were no other cranial nerve lesions.

Radiography confirmed hepatomegaly and revealed an interstitial infiltrate of the dorsal lung fields consistent with an early pneumonia. Routine serum biochemistry indicated liver disease with an alanine aminotransferase level of 487 U/litre (normal, 20 to 100 U/litre); other liver parameters were within normal limits.

Haematological parameters were normal with the exception of a slight eosinophilia at 1.4 x 103/mm7 (normal, 0.1 to 1 .2 X 103/mm7). Analysis of cerebral spinal fluid (CSF) did not reveal any abnormalities; there were no nucleated blood cells in a centrifuged sample. A CSF distemper titre was negative. Survey spinal radiographs and a myelogram were normal.

A protozoal infection was suspected due to the multisystemic clinical signs of myelitis, myositis, hepatitis and pneumonia. Serum was submitted for antibody titres against N caninum and T gondii. Treatment was initiated with clin- damycin (Antirobe; Upjohn) at 10 mg/kg three times daily and trimethoprim sulphonamide (Trimabac 80; BK Veterinary Products) at 15 mg/kg twice daily. Phenoxybenzamine (Dibeny- line; SmithKline & French Laboratories) at 10 mg once daily was administered during the first three days to aid bladder expression. Intraven- ous fluid therapy (Compound Sodium Lactade; Ivex Pharmaceuticals) was initiated to correct dehydration.

During the next three days there was no change in the puppy’s neurological condition. The muscle dysfunction had progressed. The puppy resented being handled as a result of diffuse muscle pain and there was continued muscle atrophy, including the masticatory muscles. Physiotherapy was initiated in an attempt to prevent permanent muscle contracture.

The N caninum antibody titre was positive at a dilution of 1/3200 in an indirect immunofluores- cent antibody test (IFAT) (performed by the Liv-

erpool School of Tropical Medicine, University of Liverpool [Trees and others 19931). Clinical infection is suggested by a positive result at a dilution of 1/800 or more. The T gondii antibody titre was less than 1/16 in an indirect latex agglu- tination test (Toxoreagent; Eiken).

Two weeks following presentation, voluntary movement was regained in the pelvic limbs such that the puppy was able to walk if supported with a sling. There was still a complete loss of conscious proprioception, and faecal and urinary incontinence. There was no muscle pain although the muscle contraction had persisted. The trimethoprim1sulphonamide was discontin- ued after a two-week course; the clindamycin was continued at 10 mg/kg three times daily. The N caninum antibody IFAT titre was unchanged at 1/3200. The dam of the puppy was tested and was positive for N caninurn at a dilution of 1/200 and also for T gondii at a dilution of 1/540 in a direct agglutination text (Toxo-Screen DA; bioMerieux). There is no immunological cross reactivity between the indirect fluorescent anti- body tests for N caninum and T gondii (Dubey and others 1988b). Two female littermates were tested - one was positive for N caninurn.

Over the following four weeks, locomotor abil- ity of the puppy improved to the extent that she was able to walk unassisted, although she ‘bunny hopped’ and fell frequently. She was able to rise unassisted, although the persistent quadriceps and gracilis contracture made this difficult. Con- scious proprioception had improved although there were still deficits. Faecal and urinary conti- nence had returned. The autonomic lesion of the right eye was unchanged. Clindamycin therapy was discontinued.

Three months later the owner reported that the puppy had improved although there were still proprioceptive deficits of the right pelvic limb and persistent muscle contracture. When the dog was 11 months old she was re-examined. Although of good body condition, she had not achieved her full growth potential. There was severe muscle atrophy of the pelvic limbs. Her gait had deteriorated due to genu recurvatum and joint deformities, which had occurred as a result of the muscle contracture (Fig 2). The dog was able to walk but could only manage short distances and the persistent proprioceptive deficits of the right pelvic limb meant that exco- riation of the dorsum of the hock was a prob- lem. The N caninurn antibody titre had dropped to 11200.

Case 2

An 18-month-old female boxer dog presented with pelvic limb ataxia, and faecal and urinary incontinence. The gait abnormalities were first noticed six months previously. The urinary and

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C. KNOWLER AND S. J. WHEELER

FIG 2. muscle contracture post Neospora caninurn infection

Joint deformities and genu recurvatum secondary to

FIG 3. lar cortex

Tissue cyst of Neospora caninurn within the cerebel-

faecal incontinence were first noted by the own- ers two months before presentation. The dog had progressively deteriorated over that time.

The dog was stunted and of poor body condi- tion. There was an ataxic gait with propriocep- tive deficits and muscle atrophy of the pelvic limbs. Patellar hyperreflexia with a poor with- drawal reflex suggested a sciatic nerve lesion. The dog dribbled urine and had a reduced perineal reflex. There was no evidence of muscu- loskeletal pain. The cranial nerves were normal.

Routine serum biochemistry provided evid- ence of hepatic dysfunction with an increased serum bile acid concentration at 27.2 pmol/litre (normal, 0 to 15 pmol/litre), alanine aminotrans- ferase at 1336 U/litre (normal, 20 to 100 U/litre) and alkaline phosphatase at 833 U/litre (normal, 10 to 300 U/litre). Ultrasonographically, the liver had a diffuse heterogenous echotexture suggest- ing liver disease. Survey radiographs and a myel- ogram did not reveal any abnormalities. Cisternal CSF had a slightly raised nucleated cell count at 13 cells/mm3 (normal, less than 5 cells/mm3) and total protein of 0.29 g/litre (normal, 0.1 to 0.25 g/litre). Electromyography demonstrated fib- rillation potentials in the intraosseous, quadri-

FIG 4. tendinosus muscle

Tachyzoites of Neospora caninum within the semi-

FIG 5. nantly mononuclear cellular infiltrate

Myositis of the quadriceps muscle with a predomi-

ceps and gluteal muscles of the left pelvic limb and intraosseus, cranial tibialis and semitendi- nosus muscles of the right pelvic limb. The changes in the intraosseus muscle were consid- ered significant as the dog was less than five years old. No abnormalities were detected in the tho- racic limbs. The electromyographic changes were consistent with primary muscular disease or den- ervation (Niederhauser and Holliday 1989).

The owner elected to have the dog euthanased. A N caninurn IFAT antibody titre was positive at 1/12,800. Post mortem examination confirmed protozoal inflammatory disease. Tissue cysts were found in the white matter of the cervical spinal cord and within the cerebellar cortex (Fig 3). In the spinal cord they were associated with considerable granulomatous reaction. Intracellu- lar tachyzoites were found in the right semitendi- nosus muscle and in the cerebellum (Fig 4). In the lumbar spinal cord and cauda equina there was perivascular lymphocytic cuffing and degen- eration of the white matter. There was a diffuse infiltration of mononuclear cells throughout the meninges of the spinal cord and brain. The myelin sheaths of the sciatic nerves were vacuo- lated. All the muscles examined, including those of the oesophagus, displayed evidence of myosi- tis with mainly a mononuclear cellular infiltrate (Fig 5). An unusual finding was gross muscular

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Neospora caninum infection in three dogs

hypertrophy of the caudal oesophagus. There was diffuse bile duct hyperplasia and periportal fibrosis of the liver, Incidental findings were renal dysplasia and the absence of a gall bladder.

Case 3

A five-week-old female boxer dog presented with paraplegia and pelvic limb hyperextension. Clinical signs were first noticed 10 days previ- ously, initially with proprioceptive deficits which rapidly progressed to paraplegia. Tendon reflexes were absent, the bladder was flaccid and dilated and the puppy dribbled urine. Routine serum biochemistry and haematology was nor- mal. Survey radiographs and a myelogram were normal. A N caninum IFAT antibody titre was positive at 1/3200. Therapy with clindamycin was initiated, however there was no improve- ment and the puppy was euthanased one week later. Post mortem examination was not permit- ted, however N caninum infection was con- firmed by immunoperoxidase staining of a biopsy of the biceps femoris muscle. The dam was clinically normal and had a N caninum IFAT titre of 1/800. Sera from the littermates were negative in the N caninum IFAT.

DISCUSSION The life cycle and source of infection of N can-

inum have not been determined. Tachyzoites and tissue cysts containing bradyzoites are the only known stages. Tissue cysts have only been found in the central nervous system. Sexual intestinal stages and the definitive host have not been identified. Affected dogs do not appear to shed oocytes in the faeces (Dubey and others 1988b).

Transplacental infection is the only proven route of transmission (Dubey and Lindsay 1989). The bitch remains asymptomatic. Not all litter- mates develop an antibody response to N can- inum or develop clinical neosporosis (Dubey and Lindsay 1989a). Unlike toxoplasmosis, exposure of animals prior to pregnancy fails to prevent transplacental infection during subsequent pregnancies (Bjerkas and others 1984, Dubey and others 1988b, 199Oc, Barr and others 1993). Treatment of a dam during pregnancy with trimethoprim/sulphonamide was not effective in preventing N caninum infection of the puppies (Mayhew and others 1991).

The dams of cases 1 and 3 in this series had titres of 1/200 and 1/800, respectively, suggesting a subclinical infection and transplacental or neonatal infection of the puppy. A littermate of case 1 had also developed antibodies to N can- inum but was asymptomatic.

The age of affected dogs ranges from five weeks

to 15 years, however the majority of patients are less than one year old. It is with these cases that the disease is most severe. The characteristic clinical signs of neonatal neosporosis are propri- oceptive deficits which progress to paraplegia within a week. The pelvic limbs are held in rigid hyperextension due to contracture of the quadri- ceps and gracilis muscles. The cause of the con- tracture is not understood. Faecal and urinary incontinence are also present. Affected dogs may have clinical signs of pneumonia or hepatic involvement. Cranial nerve dysfunction or multi- focal neurological disease may also be present. The paralysis ascends rapidly causing quadriple- gia, cervical weakness and dysphagia (Cummings and others 1988, Dubey and others 1988a). The causes of death are usually myocarditis, respira- tory disease or hepatic dysfunction (Dubey and others 1988a, Dubey 1992). Affected puppies may also present with primary polymyositis (Dubey and others 1988a). Gross pathological lesions include necrosis and mineralisation of the muscles, and malacia of the central nervous system (CNS). Occasionally granulomatous nod- ules are found in the body cavities or within the CNS (Dubey and others 1988a, Dubey 1992). The predominant histological findings are non-sup- purative encephalomyelitis, polyradiculoneuri- tis, myocarditis, hepatitis and myositis.

Older dogs may have a range of clinical signs including lethargy, focal or multifocal CNS dis- ease, polymyositis, dermatitis, and necrotising pancreatitis (Dubey and others 1988a, Dubey 1992). Lesions have also be found histologically in the adrenal cortex in both neonatal and adult infected dogs (Dubey and others 1988a).

Infection with N caninum in the UK was first reported by Dubey and others (1990b). Trees and others (1993) found that 16.6 per cent of clinical- ly normal English dogs have a positive serum antibody titre to N caninum at a dilution of 1/50 or more. This is a higher prevalence than in stud- ies of American dogs where a 2.2 per cent preval- ence was suggested (Lindsay and others 1990). A study of dogs presenting at The Royal Veterinary College suggested a prevalence of 4.8 per cent (C. L. Lathe, personal communication). There was no association between the subclinically infected dogs and age, sex, breed, feeding offal or fresh meat, vaccination status or other pets in the household (Trees and others 1993).

N caninum infection is an important cause of bovine abortion in Britain (Trees and others 1994), USA (Anderson and others 1991), Aus- tralia (Barr and others 1993), New Zealand (Thornton and others 1991) and the Netherlands (Nietfield and others 1-992). The main lesions in the aborted fetuses were encephalitis and myocarditis (Barr and others 1990, Anderson and others 1991). N caninum infection can also cause

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C. KNOWLER AND S. J. WHEELER

paraplegia in neonatal calves (Parish and others 1987, Dubey 1989, Dubey and others 1989, Gun- ning and others 1994). Natural infection has also been demonstrated in horses causing abortion (Dubey and Porterfield 1990) and sheep causing abortion and encephalomyelitis of lambs (Dubey and others 1990a). Experimentally, infection can be induced in immunosuppressed cats (Dubey and Lindsay 1989b,c, Dubey and others 1990d), mice (Lindsay and Dubey 1989) and rats (Dubey 1990). There has been no evidence of naturally occurring feline neosporosis in the UK (J. Barber, personal communication) or in the USA (Dubey 1992).

Treatment of neosporosis appears more likely to be successful if initiated before pelvic limb hyperextension has occurred. The combination therapy of clindamycin and trimethopriml sulphonamide has not been reported before although it has been successfully used by one of the authors (C.K.) for treating feline toxoplasmo- sis. Clindamycin was successful in treating polymyositis, which in retrospect was likely due to N caninum (Greene and others 1985). Howev- er, clindamycin was unsuccessful in reversing neosporosis in a dog with CNS defects, paralysis and muscle contracture (Hay and others 1990).

Dosage rates of clindamycin are recommended at 10 to 40 mg/kg orally, divided two or three times daily (Murtaugh 1988). Therapeutic con- centrations are achieved in most tissues (Panzer and others 1972), however there is poorer pene- tration into the CNS. Drug concentrations may achieve 40 per cent of the serum concentration if the meninges are inflamed (Plumb 1990). Howev- er, in human patients with meningitis, therapeu- tic CSF concentrations are not achieved (Klaine 1987, Harari and Lincoln 1989).

Adverse effects reported with this drug include gastroenteritis, which usually resolves when the drug is discontinued (Greene and others 1985, Plumb 1990). In a small percentage of humans it causes a fatal pseudomembranous colitis which may be caused by a toxin secreted by drug res- istant strains of Clostridium difficile (Klaine 1987). In case 1 of this series, there were no side effects except for mild gastroenteritis on the last two days of therapy.

Trimethoprim/sulphonamide has been used successfully to treat toxoplasmosis for many years. Drug concentrations in the CSF may achieve 50 per cent of the serum concentration if the meninges are inflamed (Plumb 1990). A dosage rate of 15 mg/kg orally two to three times daily is recommended (Murtaugh 1988). Possible side effects include keratoconjunctivitis sicca, hepatitis, gastrointestinal effects, polyarthritis, haemolytic anaemia and other blood dyscrasias (Plumb 1990). As side effects are more common with trimethoprim/sulphonamide preparations,

therapy with this drug was discontinued in case 1 of this series after 14 days.

In a suspected case of neosporosis with mild clinical signs, McGlennon and others (1990) suc- cessfully used a combination of trimethoprim/ sulphonamide (Tribissen 20; Coopers Pitman- Moore) at 15 mg/kg twice daily and oral pyrimethamine at 1 mg/kg/day (Daraprim; Bur- roughs Wellcome). A folic acid supplement was also given. This regimen was also used by May- hew and others (1991) in a litter of puppies with ataxia and pelvic limb proprioceptive defects whose dam had a history of a previous litter with clinical neosporosis.

N caninum infection requires early recognition and diagnosis so that therapy with an appropri- ate antibiotic may be initiated. This is especially important with neonatal cases where the disease is rapidly progressive and resulting muscle con- tracture appears unresponsive to therapy.

ACKNOWLEDGEMENTS The authors gratefully acknowledge the sup-

port of the Liverpool School of Tropical Medicine who provided the immunofluorescence antibody testing service. Dr J. B. A. Smyth, Pathology Department, Royal Veterinary College, performed the gross and histopathological exami- nation of case 2. C. K. is the BSAVA/Petsavers Resident in Neurology; this support is gratefully acknowledged.

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ABSTRACT Intracardiac thyroid tumour in a dog: Diagnosis and surgical removal

A THIRTEEN-year-old mongrel had had two episodes of syncope in three months, tired easily and over three days suffered collapse during excitement or activity. The only abnormality found on physical examination was a 4/6 systolic murmur between the left apical and basilar areas, radiating caudally and to the right. Two-dimen- sional echocardiography demonstrated right ven- tricular hypertrophy and dilatation. A well- demarcated soft tissue mass was visible in the right ventricular outflow tract. This obstructed the pulmonary valve during systole and was attached to the interventricular septum. During the examination, the dog had paroxysms of ven- tricular tachycardia. His condition deteriorated over three weeks and surgical removal of the mass was attempted. This was performed with the use of hypothermia and occlusion of the venous inflow. The histopathological diagnosis of the mass was ectopic thyroid tumour. The dog was alive and well two years afterwards.

WARE, W. A., MERKLEY, D. F. & RIEDESEL, D. H. (1994) Journal of the American Animal Hospital Association 30, 20-23

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