Veterinary Research Communications, 27 Suppl. 1 (2003) 767–770 © 2003 Kluwer Academic Publishers. Printed in the Netherlands
Clinical Findings Associated with Borrelia burgdorferi Infection in the Dog E. Giudice1*, F. Domina1, D. Britti2, S. Di Pietro1 and A. Pugliese1 1Department of Veterinary Medical Sciences, University of Messina; 2Department of Veterinary Clinical Sciences, University of T eramo, Italy *Correspondence: Dipartimento di Scienze Mediche Veterinarie, Universita` degli Studi di Messina, Polo Universitario SS. Annunziata, 98168 Messina, Italy E-mail:
[email protected] Keywords: antibiotic treatment, Borrelia burgdorferi, case report, dog
INTRODUCTION Borrelia burgdorferi, the aetiological agent of Lyme disease, is transmitted to humans and animals by Ixodes ticks during the blood meal. In dogs the micro-organism is known to induce a variety of clinical symptoms, particularly acute and chronic skin lesions, polyarthritis, pericarditis and inflammation of the central and peripheral nervous systems. The diagnosis of borreliosis is made on the basis of a history of tick exposure, symptomatology, micro-biological and serological examinations and treatment response (Straubinger, 2000). The course of the disease may be asymptomatic, although the serological tests are often positive, with high antibody titres possibly indicating a previous disease or premunition (Burrascano, 2000). In this paper we report the course, the clinical features and the therapeutic protocol in a Pitbull seropositive for B. burgdorferi.
CASE REPORT A 10-month-old, female Pitbull from Catania (Sicily, Italy). Past medical history reported that the dog had been examined by another veterinarian at 4 months of age for disorexia, movement difficulty and diffuse pain. At that time it also had a fever, and a tick had been detected on the withers. Medication with amoxicillin and clavulanic acid (15 mg/kg PO q 12 h) for 5 days was started and no other investigations were performed after clinical recovery. Recent history reported that at the end of the first oestrus, the dog showed the same symptomatology and was treated with amoxicillin (15 mg/kg PO q 12 h) and prednisone (0.5 mg/kg per day) for 7 days. However there was a rapid regression of symptoms that reappeared 4 weeks later. The animal was treated first with betamethasone (0.05 mg/kg per day IM) and then with paracetamol (10 mg/kg every 6 hours) associated with sulphamethoxazole-trimethoprim (30 767
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and 6 mg/kg per day respectively SC). Despite anti-inflammatory treatment, the dog’s body temperature persisted over 40°C (range 40.5–41.7°C) for 80 hours. On the fourth day of illness, the dog was brought to our clinic. On general examination it presented high sensory depression, diffuse pain upon palpation, especially of the sternal region, fever (T 42°C), and presence of a cold, painless, hard-elastic, intradermal nodule on the withers. No other abnormalities were noted. Neurological evaluation, haematological and haematochemical exams, radiological examination of the thorax, bone marrow biopsy, an indirect fluorescent antibody test (IFAT) for L eishmania infantum and for Ehrlichia canis were performed. No abnormalities were noted, with the exception of a leukocytosis (17,800 WBC/ml, reference range 5200 to 13,900 WBC/ml). The differential count indicated neutrophilia with a right shift and monocytosis. Imidocarb dipropinate (6.6 mg/kg SC) was administered while the dog was in our clinic and 2 hours later there was a progressive reduction of the body temperature. It was then sent home on sulphadimethoxine-trimethoprim (30 and 6 mg/kg per day respectively SC) for 15 days. On control examination the dog showed low sensory depression, no fever, intercostal pain on palpation, no modification of the nodule. Examination of the respiratory system showed light dyspnoea and dry cough. Wheezes were auscultated in left lung fields and on the pulmonary apexes. Thoracic radiographs were taken and showed an increase in the radio-opacity of the pulmonary diaphragmatic lobes. Cytological examination of the nodule showed a lymphoplasmacellular infiltration, numerous MPS and Langhans cells. Imidocarb dipropinate administration was repeated and then ceftriaxone (35 mg/kg per day IM), betamethasone (0.05 mg/kg per day IM) and N-acetylcysteine (5 mg/kg b.i.d. OS) were prescribed for 15 days. On control examination the clinician decided to continue the treatment for a further 15 days, after which clinical recovery was obtained. A month later the dog presented a transient lameness first in the thoracic left limb and then in the contralateral limb. No abnormalities were noted on physical examination. Haematochemical and haematological examinations and urinalysis showed no alteration. Radiographs of both thoracic limbs were taken and showed no modification. Four weeks later the dog was presented to our attention for a relapse of the previous symptomatology with the exception of the lameness. Blood tests were performed. The results were unremarkable except for a leukocytosis (19,700 WBC/ml, reference range 5200 to 13,900 WBC/ml). It was decided to submit the sera for: rheumatoid factor test (negative), ANA test (negative) and IFAT for Rickettsia rickettsii (negative), while the specimens from the two previous control examinations were found to be IFAT positive for B. burgdorferi (title 1:200 and 1:100 respectively) and the last was negative. Ceftriaxone (35 mg/kg IM) twice a day for 14 days and once a day for 7 more days was prescribed. Imidocarb was used again and repeated after 15 days. One month later, 1 week after the beginning of oestrus, the dog had a relapse. On general examination it presented severe prostration, diffuse pain on palpation which was more evident on the thorax, fever (T 40,1°C), and the nodule on the withers was once again evident. No other abnormalities were noted. The blood tests
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showed only a moderate leukocytosis (15,400 WBC/ml, reference range 5200 to 13,900 WBC/ml). Doxycycline treatment was started (10 mg/kg per day OS, for 30 days) and caused a regression of symptomatology. Three months later an ovariohysterectomy was performed by the referring veterinarian and three days after surgery there was a worsening of the clinical conditions and the dog was hospitalized. Betamethasone (0.05 mg/kg per day IM), ceftriaxone (30 mg/kg b.i.d. IV) and paracetamol (10 mg/kg b.i.d.) were administered. The fever persisted for 72 hours and then the dog was transferred to our clinic. On general examination the dog showed sensory depression, mild weight loss, diffuse pain upon palpation, and the nodule on the withers was about 10 cm in diameter. As recommended for long-standing and relapsing clinical cases of borreliosis in humans, amoxicillin (35 mg/kg b.i.d. IV) treatment was started (Burrascano, 2000). Topical meclocycline was administered twice a day on the nodule. On the second day of therapy, an improvement in symptomatology was observed. Five days later, clinical signs disappeared and the nodule was diminished but still evident. Amoxicillin therapy was continued. On the 37th day the drug was administered orally at the same dosage. On the 54th day the dosage was reduced (25 mg/kg b.i.d.) and was continued until the 70th day. Throughout the therapy only a mild dermatitis appeared. Over the following 18 months the dog had no relapse and remained serum-negative.
DISCUSSION The history of tick exposure, the cyclic clinical pattern (about every 4 weeks), the seropositivity and the response to antibiotics ‘of choice’ are the most relevant clinical keys to a diagnosis of borreliosis (Burrascano, 2000; Straubinger, 2000). An important update in the biology of Borrelia burgdorferi is the discovery of three forms of the bacterium: spirochaetal, spheroplastic and cystic. Only the spirochaetal form can be killed by beta-lactamic antibiotics; spheroplasts seem to be susceptible to tetracyclines and erythromycin, and the cysts have been proven to only be susceptible to metronidazole, losing the surface antigens after contact with other antibiotics (Preac-Mursic et al., 1996; Burrascano, 2000; Straubinger, 2000). This circumstance could explain the decrease in antibody levels after treatment and, as we observed, the seronegativity that occurs in patients with chronic disease (Preac-Mursic et al., 1996; Burrascano, 2000; Straubinger, 2000). This case report confirms that, during an infectious disease, immune system immaturity or conditions such as stress or steroid administration that interfere with the immunological response are associated with clinical manifestation or worsening of the clinical signs. The clinical improvement following imidocarb treatment could confirm the suspicion that ‘Lyme disease’ is probably a mixed infection, explaining the difference between experimental and natural infection (Burrascano, 2000). Moreover, this case report suggests that B. burgdorferi infection should be considered in differential diagnosis if a tick bite is suspected.
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REFERENCES Burrascano, J.J.Jr, 2000. Advanced topics in Lyme disease. Lyme Net, http://www2.lymenet.org Preac-Mursic, V., Wanner, G., Reinhardt, S., Wilske, B., Busch, U. and Marget, W., 1996. Formation and cultivation of Borrelia burgdorferi spheroplast-L-form variants. Infection, 24, 218–226 Straubinger, R.K., 2000. PCR-based quantification of Borrelia burgdorferi organism in canine tissues over a 500-day postinfection period. Journal of Clinical Microbiology, 38, 2191–2199
