Secondary phosphorus poisoning in dogs

Subsequent to a possum (Trichosurus vulpecula) poisoning operation purportedly using 1% phosphorus baits, six dogs with access to poisoned possums died of phosphorus poisoning. Two dogs survived, following treatment with oral copper sulphate and parenteral vitamin K. Clinical signs included depression, jaundice, vomiting and bloody diarrhoea. Post-mortem lesions included large areas of subcutaneous, interstitial and intermuscular haemorrhage, subserosal haemorrhage and liver degeneration. Free phosphorus was detected in the ingesta of three of the dogs which died up to 7 days after the last of the poison was laid. Analysis of two batches of baits used showed P levels of 1.17% and 1.24%.     

CHRONIC COPPER POISONING IN DAIRY COWS

SUMMARY Chronic copper poisoning in a dairy herd fed supplementary copper is recorded. Most cows received 11 g of copper sulphate per day but high milk producers received 22,0 g and within 6 months, 3 of them became ill and died. The signs shown by the 3 cows were anorexia, decreased milk production, frequent recumbency and jaundice. Within 4 days of showing signs, the cows died. The autopsy findings were dehydration, anaemia, jaundice, liver damage and intestinal haemorrhage. Liver copper values varied from 1,250 to 2,410 ppm DM.     

A randomised, blinded, placebo-controlled clinical trial with allopurinol in canine leishmaniosis.

A total of 45 non-uremic dogs, with clinical signs indicating leishmaniosis, entered the study. Diagnosis was confirmed by indirect immunofluorescence assay (IFA) on serum and polymerase chain reaction (PCR) on bone marrow samples. The dogs were randomly allocated into Group A (n=37) that received allopurinol (10mg/kg B.W., per os, twice daily) for 4 consecutive months, and Group B (n=8) that were placebo-treated. Clinical signs were scored just before and at monthly intervals throughout the study period, in a blinded and independent fashion. Complete blood count, serum biochemistry profile, urinalysis, lymph node and bone marrow parasitology, IFA and enzyme-linked immunosorbent assay (ELISA) serology and bone marrow PCR were carried out at the beginning and at the end of the trial. A total of three Group A and one Group B dogs died of end stage kidney disease that developed during the trial. In Group A animals that endured the trial there was a significant improvement in the general body condition, conjunctivitis, peripheral lymphadenopathy, splenomegaly, masticatory muscle atrophy, ulcerative stomatitis, epistaxis, exfoliative dermatitis, cutaneous ulcerations, blepharitis and nasodigital hyperkeratosis. The same observation was made for anemia, lymphopenia, hyperproteinemia, hyperglobulinemia, hyperphosphatemia, increased alkaline phosphatase activity and the low albumin/globulin ratio. By contrast, no improvement of any kind was seen in Group B dogs. Lymph node and bone marrow parasite numbers were significantly decreased in Group A animals. In Group B, that occurred only in the lymph nodes. Apart from remission of clinical signs and restoration to normal of clinicopathological abnormalities, allopurinol did not eliminate Leishmania organisms, as the PCR result on bone marrow was still positive in all the dogs that finished the trial.     

The use of propofol for induction of anaesthesia in dogs premedicated with acepromazine, butorphanol and acepromazine-butorphanol

Cardiovascular, pulmonary and anaesthetic-analgesic responses were evaluated in 18 male and female dogs to determine the effect of the injectable anaesthetic propofol used in conjuction with acepromazine and butorphanol. The dogs were randomly divided into three groups. Dogs in Group A were premeditated with 0.1 mg/kg of intramuscular acepromazine followed by an induction dose of 4.4 mg/kg of intravenous propofol; Group B received 0.2 mg/kg of intramuscular butorphanol and 4.4 mg/kg of intravenous propofol; dogs in Group AB were administered a premeditation combination of 0.1 mg/kg of intramuscular acepromazine and 0.2 mg/kg of intramuscular butorphanol, followed by induction with 3.3 mg/kg of intravenous propofol. The induction dose of propofol was given over a period of 30-60 seconds to determine responses and duration of anaesthesia. Observations recorded in the dogs included heart and respiratory rates, indirect arterial blood pressures (systolic, diastolic and mean), cardiac rhythm, end-tidal CO, tension, oxygen saturation, induction time, duration of anaesthesia, recovery time and adverse reactions. The depth of anaesthesia was assessed by the response to mechanical noxious stimuli (tail clamping), the degree of muscle relaxation and the strength of reflexes. Significant respiratory depression was seen after propofol induction in both groups receiving butorphanol with or without acepromazine. The incidence of apnea was 4/6 dogs in Group B, and 5/6 dogs in Group AB. The incidence of apnea was also correlated to the rate of propofol administration. Propofol-mediated decreases in arterial blood pressure were observed in all three groups. Moderate bradycardia (minimum value > 55 beats/min) was observed in both Groups B and AB. There were no cardiac dysrhythmias noted in any of the 18 dogs. The anaesthetic duration and recovery times were longer in dogs premeditated with acepromazine/butorphanol.     

Chronic active hepatitis in 26 Doberman pinschers

Chronic active hepatitis with increased hepatic copper concentration was diagnosed in 25 female and 1 male Doberman Pinscher dogs. Common clinical signs included polyuria/polydipsia, weight loss, anorexia, icterus, and ascites. Increased liver enzyme activities and abnormal liver function test results were the most consistent clinicopathologic changes. The dogs were assigned to 3 groups on the basis of clinical course of the disease. Group 1 dogs (n = 12) had clinical signs of advanced liver failure and died within one week. Group 2 dogs (n = 7) had less severe clinical signs of liver disease and died within one month. Group 3 dogs (n = 5) did not have clinical signs of illness or had mild clinical signs of liver disease and died 1 to 42 months after initial evaluation. One dog could not be reevaluated and another dog was alive 3 months after initial examination. Treatments consisted of supportive care for dogs in group 1, and dietary manipulations and corticosteroids for dogs in groups 2 and 3. The association of increased liver copper concentration and chronic active hepatitis is not known.     

Natural occurrence of grape poisoning in two dogs

Clinical grape poisoning in two dogs (a 1.6-year-old male Shih Tzu and a 5-year-old female Yorkshire Terrier) was described in the present study. Clinical signs included decreased urine output in the Shih Tzu and ataxia in the Yorkshire Terrier after grape ingestion. The Shih Tzu died 5 days post-grape ingestion, while the Yorkshire Terrier died 3 days post-grape ingestion. Erythematous serosae and mucosae, multifocal red small intestinal foci, and blood and grape seeds were identified in the intestinal lumen. Brownish-yellow crystals were bilaterally identified in the renal pelvis. The primary histological findings were acute tubular necrosis of the proximal convoluted tubules, severe necrosis, and mineralization in the renal cortical tubules. Blood urea nitrogen, creatinine, and alanine aminotransferase were increased in the dogs. Many Korean veterinary clinicians have suspected clinical grape poisoning. However, to our knowledge, grape poisoning has not been identified by pathologic and clinicopathologic basis until this writing in Korea. Education and knowledge about the risks of grape poisoning is necessary for the prevention of accidental exposures.     

Treatment of experimentally induced Theileria annulata infection in cross-bred calves with buparvaquone

Twenty cross-bred (Bos taurus X Bos indicus) calves, 7-21 days old, were infected by a ground-up tick supernate of Hyalomma anatolicum anatolicum infected with the Hisar isolate of Theileria annulata. Six calves acted as untreated controls and they all died of theileriosis within 17 days of infection. The remaining 14 calves were divided into Group A and B, each consisting of seven calves. All the calves of Groups A and B were treated intramuscularly with buparvaquone (BW 720C) on Day 11 post-infection, when clinical signs of theileriosis were apparent. Each calf received 2.5 mg BW 720 C kg-1 body weight as a single injection. In addition, each calf of Group B was given proprietary haematinics by intramuscular injection, daily for 12 days. In Group A, two calves died of cerebral theileriosis and five were clinically cured. However, four of these five calves later died of anaemia. In Group B, all the calves were clinically cured and none died during the observation period of 1 month. The parasitaemia declined to less than 1% within a fortnight of treatment. The initial declines in haemoglobin concentration and packed cell volume were halted and preinfection values were soon restored. No toxic signs attributable to treatment with buparvaquone were observed.     

Hypovolaemic shock after anthelmintic treatment of canine angio-strongylosis

Canine angiostrongylosis was diagnosed in a whippet with typical signs of respiratory and circulatory distress. Subclinical Angiostrongylus vasorum infections were also demonstrated in two other whippets belonging to the same owner. All three dogs were given standard anthelmintic levamisole treatment combined with corticosteroids. Two days after initiation of treatment, one of the subclinically infected dogs developed severe hypovolaemic shock that required intravenous fluid therapy and corticosteriods to save its life. The shock is believed to have been caused by an anaphylactic reaction triggered by the rapid release of a large amount of worm antigen in the blood due to the rapid death of adult worms by levamisole. Thus, dog owners should be instructed to monitor dogs undergoing levamisole treatment against A vasorum. Alternatives to levamisole treatment of canine angiostrongylosis should be considered.     

Effect of blood derivatives with immunomodulators on the immunoprotein profile in calves under clinical conditions

The data on the selected humoral and cellular parameters of the immuno-protein profile were evaluated in calves in a critical period of the availability of immunoglobulins (Ig), in dependence on the administration of the blood derivative with levamisole (group AL) and on the administration of levamisole solution (group L). The preparations were administered intramuscularly at a rate of 10 mg levamisole per 1 kg of live weight. No statistical significance was recorded in the comparison of the humoral parameters after repeated administration (interval of five days) of the Algalev (AL) and levamisole (L) preparations. During the same investigation, the administration of AL produced a significant increase in the T lymphocytes of the blood both in comparison with the T lymphocyte concentration before treatment (P less than 0.05 on the 5th, 7th, 11th, 14th and 20th day of experiment) and in comparison with the calves of group L (P less than 0.05 on the 7th, 11th, 14th, and 20th day); in the case of B lymphocytes an increase was recorded only in comparison with the initial value (P less than 0.01 on the 2nd, 5th and 7th day). Administration of levamisole alone led to a positive change in T lymphocyte concentration (P less than 0.05 on the 5th, 7th, 11th, 15th and 20th day) but not in the concentration of the B cells (P greater than 0.05). In another experiment, administration of the AL preparation (repeatedly after six days) led to a significant increase in the percentage of T lymphocytes (P less than 0.01 the 8th day and P less than 0.05 the 2nd, 6th, 15th, 21st and 35th day) and B lymphocytes (P less than 0.01 the 15th and 21st day), in comparison with their levels before administration as well as in comparison with the control (T lymph.: P less than 0.01 the 6th day and P les than 0.05 the 8th, 15th, 21st and 35th day; B lymph.: P less than 0.05 the 15th day). The maximum percent proportion of T lymphocytes after administration of the AL preparation was recorded on the seventh and eighth day after the first administration.     

Adverse reactions suggestive of type III hypersensitivity in six healthy dogs given human albumin

CASE DESCRIPTION:6 healthy dogs given human albumin solution as part of a study were examined following development of an immediate hypersensitivity reaction (1 dog) and signs suggestive of a type III hypersensitivity reaction (all 6 dogs). CLINICAL FINDINGS: All 6 dogs were healthy prior to administration of human albumin solution. One dog developed signs of an immediate hypersensitivity reaction, characterized by vomiting and facial edema, during administration of human albumin solution. All 6 dogs developed signs of a delayed adverse reaction 5 to 13 days after administration of human albumin solution. Initial clinical signs included lethargy, lameness, edema, cutaneous lesions indicative of vasculitis, vomiting, and inappetance. TREATMENT AND OUTCOME: In the dog with signs of immediate hypersensitivity, signs resolved after administration of human albumin solution was discontinued and diphenhydramine was administered. Supportive treatment was provided after dogs developed signs of a delayed adverse reaction. Four dogs recovered, but 2 dogs died despite treatment. All 6 dogs were found to have antihuman albumin antibodies. There was no evidence of contamination of the human albumin solution. CLINICAL RELEVANCE: Findings suggest that administration of human albumin solution in healthy dogs with normal serum albumin concentrations may result in signs of a type III hypersensitivity reaction.     

Serial monitoring of clinical, haematological and immunological parameters in canine autoimmune haemolytic anaemia

Clinical, haematological and immunological data are presented from 14 dogs with autoimmune haemolytic anaemia (AIHA) serially monitored for up to 945 days after initial presentation. At the time of diagnosis, all dogs had severe anaemia (mean packed cell volume [PCV] 17.6±7.1 per cent) with leucocytosis in seven cases and thrombocytopenia in four dogs. The Coombs' test was positive in all cases. Immunoglobulin G (IgG) autoantibody alone was identified in eight cases, a combination of IgG and IgM autoantibodies was recognised in three cases, and in two dogs only IgM autoantibody was recorded (complement fixing in one of these dogs). All dogs were treated with immunosuppressive doses of corticosteroids and some animals also received cyclophosphamide (four cases), azathio-prine (two cases), blood transfusion (four cases) or underwent splenectomy (two cases). Two dogs died during the initial episode of AIHA. In 12 dogs, the anaemia was resolved by an average of 36.3 ±16.0 days after initial presentation, but autoantibody titre often persisted after clinical improvement and normalisation of PCV. Four dogs had a clinical relapse 67 to 170 days after initial presentation and one of these dogs subsequently died from thromboembolic disease. One dog developed lymphocytic thyroiditis and serum antinuclear antibody at day 691 after initial presentation, and two cases developed disease consistent with autoimmune thrombocytopenia (AITP) at 365 and 618 days post initial presentation. In one of these dogs, AITP was concurrent with multicentric lymphoma. No correlation was recorded between haematological and immunological parameters at presentation and subsequent response to therapy or long-term clinical behaviour.     

Toxicoses associated with administration of mitoxantrone to dogs with malignant tumors

One hundred twenty-nine dogs with histologically confirmed malignant tumors were used in a prospective study to determine the toxicity of the new dihydroxyquinone derivative of anthracene, mitoxantrone, which was administered IV at 21-day intervals at dosages ranging from 2.5 to 5 mg/m2 body surface area. Each dog was evaluated for signs of toxicosis for 3 weeks after each dose was administered or until the dog died, whichever came first. The number of dogs in each evaluation period were as follows: 1 dose (n = 129), 2 doses (n = 82), 3 doses (n = 43), 4 doses (n = 26), 5 doses (n = 19), 6 doses (n = 9), 7 doses (n = 6), 8 doses (n = 5), 9 doses (n = 3), and 10 doses (n = 1). The most common signs of toxicosis were vomiting, diarrhea, anorexia, and sepsis secondary to myelosuppression. None of the dogs died of complications resulting from mitoxantrone treatment. Dogs with signs of toxicosis during the 21-day interval from administration of the first dose of mitoxantrone were 95 times (P = 0.003) more likely to develop signs of toxicosis during the 21-day interval from the second dose of mitoxantrone. Similarly, dogs that developed signs of toxicosis during the 21-day interval from the administration of the second dose were 34 times (P less than 0.001) more likely to develop signs of toxicosis during the 21-day interval from the administration of the third dose. With each 1 mg/m2 increase in mitoxantrone, the odds of developing signs of toxicosis increased by 5.9 fold (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical signs, clinicopathological findings, etiology, and outcome associated with hemoptysis in dogs: 36 cases (1990-1999)

Hemoptysis, the expectoration of blood or bloody mucus from the respiratory tract at or below the larynx, was retrospectively evaluated in 36 dogs. Cough, tachypnea, and dyspnea were common historical and physical examination signs. Anemia was documented in 11 dogs, but was severe in only one dog. Other clinicopathological findings reflected the underlying diseases. All thoracic radiographs obtained were abnormal; alveolar and interstitial patterns were most common. Diseases predisposing to hemoptysis included bacterial bronchopneumonia (n=7), neoplasia (n=5), trauma (n=5), immune-mediated thrombocytopenia (n=4), heartworm disease (n=4), rodenticide poisoning (n=3), lung-lobe torsion (n=1), left-sided congestive heart failure (n=1), pulmonary hypertension (n=1), and foreign-body pneumonia (n=1). Four additional dogs had more than one underlying disease process. Nine dogs were either euthanized or died in the hospital during the initial visit. While at least half of the 27 dogs discharged went on to completely recover, five dogs discharged were known to have either died or been euthanized as a result of their disease in <6 months.     

Evaluation of a constant rate infusion of lidocaine for balanced anesthesia in dogs undergoing surgery

This study assessed the intraoperative analgesic effects of intravenous lidocaine administered by a constant rate infusion (CRI) in surgical canine patients. A prospective, blinded, randomized study was designed with 2 treatment groups: A (lidocaine) and B (placebo), involving 41 dogs. All patients were premedicated with acepromazine and buprenorphine, induced with propofol and midazolam; anesthesia was maintained with isoflurane in oxygen. Group A received 2 mg/kg IV lidocaine immediately after induction, followed within 5 min by a CRI at 50 μg/kg/min. Group B received an equivalent volume of saline instead of lidocaine. Changes in heart rate and blood pressure during maintenance were treated by increasing CRI. Fentanyl was used as a supplemental analgesic when intraoperative nociceptive response was not controlled with the maximum dose of lidocaine infusion. There was a significantly lower use of supplemental intraoperative analgesia in the lidocaine than in the placebo group. Group B dogs had almost twice as high a risk of intraoperative nociceptive response as group A dogs.     

Risk factors associated with outcome in dogs with tetanus: 38 cases (1987-2005)

OBJECTIVE: To assess the clinical course of disease and risk factors associated with outcome in dogs with tetanus. DESIGN: Retrospective case series. ANIMALS: 38 dogs with tetanus. PROCEDURES: Data were collected from medical records of dogs with tetanus, including signalment; wound characteristics; initial clinical signs; severity of worst clinical signs; time to wound management, antimicrobial treatment, and antitoxin administration; and 28-day survival rate. Statistical analyses were performed to evaluate relationships between the potentially predictive variables and disease progression and outcome. RESULTS: The 28-day survival rate was 77% (among 35 uncensored dogs). The most common initial clinical signs in affected dogs were ocular (n = 18) and facial (11) abnormalities. Nineteen dogs progressed to recumbency with severe muscle spasms, and 14 dogs had high or low heart rate or blood pressure values. Eight dogs died or were euthanized because of complications of tetanus. There was a significant association between younger age and development of more severe clinical signs. Furthermore, a significant inverse relationship between development of severe clinical signs and survival was identified. There was no association between earlier initiation of wound management, antimicrobial administration, or antitoxin administration and either progression of signs or 28-day survival rate. Wound type was not associated with 28-day survival rate. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that younger dogs with tetanus may be more likely to develop severe clinical signs. The prognosis for survival in dogs with tetanus is good if abnormalities in heart rate or blood pressure values do not develop.     

Rheumatoid arthritis subsequent to Borrelia burgdorferi infection in two dogs

Two dogs with clinical signs of polyarthritis developed rheumatoid arthritis subsequent to Borrelia burgdorferi infection. In both dogs, the diagnosis of B burgdorferi infection was based on clinical signs of disease and high serum B burgdorferi titer. After antibiotic administration, both dogs had decreased B burgdorferi titer, but clinical response was temporary or was lacking. The dogs subsequently were rheumatoid factor-positive (antinuclear antibody- and anti-globulin-negative) and responded to anti-inflammatory drug administration. Development of rheumatoid arthritis in both dogs after B burgdorferi infection implicates the Borrelia organism as an infective agent leading to the development of rheumatoid arthritis in dogs. Dogs with clinical signs suggestive of B burgdorferi infection should have antiglobulin, anti-nuclear antibody rheumatoid factor, and B burgdorferi tests performed to aid definitive diagnosis.     

Efficacy of maropitant in the prevention of delayed vomiting associated with administration of doxorubicin to dogs

Background: Vomiting, nausea, inappetence, and diarrhea are common delayed adverse effects of doxorubicin. Maropitant, a neurokinin‐1 receptor antagonist, is known to prevent acute vomiting in dogs receiving cisplatin. Objective: To evaluate the efficacy of maropitant in preventing delayed vomiting after administration of doxorubicin to dogs. Animals: Fifty‐nine dogs with cancer. Methods: This randomized, double‐blind, placebo‐controlled study used a cross‐over design. Dogs were randomized into 1 of 2 treatment groups. Group A received maropitant after the 1st doxorubicin, and placebo after the 2nd. Group B received placebo first, and maropitant second. Maropitant (2 mg/kg) or placebo tablets were administered PO for 5 days after doxorubicin treatment. Owners completed visual analog scales based on Veterinary Cooperative Oncology Group‐Common Terminology Criteria for Adverse Events to grade their pet's clinical signs during the week after administration of doxorubicin. Statistical differences in gastrointestinal toxicosis and myelosuppression between maropitant and placebo treatments were evaluated. Results: Significantly fewer dogs had vomiting (P= .001) or diarrhea (P= .041), and the severity of vomiting (P < .001) and diarrhea (P= .024) was less the week after doxorubicin when receiving maropitant compared with placebo. No differences were found between maropitant and placebo for other gastrointestinal and bone marrow toxicoses. Conclusions and Clinical Importance: Maropitant is effective in preventing delayed vomiting induced by doxorubicin. Its prophylactic use might improve quality of life and decrease the need for dose reductions in certain dogs.     

Diagnosis of anatoxin-a poisoning in dogs from North America.

Anatoxin-a, a toxin produced by several genera of blue-green algae, is considered a potent neurotoxin. Ingestion of water contaminated with the toxin results in acute neurological signs and often death. This report describes fatal cases of anatoxin-a ingestion in 6 dogs, with confirmation of anatoxin-a exposure by liquid chromatography/tandem mass spectrometry (LC-MS/MS/MS). In 1 outbreak, 3 dogs developed seizures and died within an hour after swimming in a river in California, while the other outbreak involved 3 dogs that died within 1 hour after swimming in a pond in Ontario. Anatoxin-a poisoning is rarely reported in dogs as a cause of acute neurological signs and death. However, increased occurrences of blue-green algae blooms in North America make this neurotoxin an important consideration in the diagnosis of sudden death associated with environmental water exposure. This brief communication reports on the isolation and detection of anatoxin-a from environmental water sources and the stomach contents of North American dogs dying of acute neurotoxicosis. This demonstrates the first documented cases of anatoxin-a poisoning in dogs in North America and the importance of LC-MS/MS/MS in identifying neurotoxins responsible for sudden death in cases of suspected blue-green algae toxicosis; especially those cases showing no gross or histological lesions.     

Canine infectious tracheobronchitis: effects of an intranasal live canine parainfluenza-Bordetella bronchiseptica vaccine on viral shedding and clinical tracheobronchitis (kennel cough)

A modified-live intranasal (IN) canine parainfluenza (CPI)-virus Bordetella bronchiseptica vaccine was evaluated in dogs for efficacy against laboratory-induced canine infectious tracheobronchitis. The comparative efficacies of IN and parenteral administrations of the CPI virus fraction were also evaluated. The frequency and duration of clinical tracheobronchitis, blood serum agglutination titer, humoral antibody response, and duration of CPI virus and B bronchiseptica shedding were measured. Group A dogs were vaccinated subcutaneously or IM with an experimental CPI vaccine and challenge exposed with CPI virus. Group B dogs were vaccinated IN with avirulent CPI virus-B bronchiseptica live antigens and challenge exposed with virulent CPI virus and virulent B bronchiseptica. The IN vaccination (group B) significantly reduced (P less than or equal to 0.001) the occurrence of clinical tracheobronchitis by 96%. The combined challenge exposure of virulent CPI and virulent B bronchiseptica produced a synergistic enhancement of the clinical signs of kennel cough. The percentage of days after challenge exposure that virus shedding was detected for controls equaled 70% as compared with 50% and only 1% for parenterally and IN vaccinated dogs, respectively. Isolation of virulent B bronchiseptica microorganisms was reduced 89% in dogs vaccinated IN compared to controls. The geometric mean humoral antibody titers to CPI virus after 2 parenteral vaccinations and 1 IN vaccination were 1:43 and 1:34, respectively.     

Immunity against Babesia rossi infection in dogs vaccinated with antigens from culture supernatants

Soluble parasite antigens (SPA) from different Babesia species have been shown earlier to induce protective immunity when used as vaccine. However, initial attempts to produce such vaccine against Babesia rossi infection using SPA from B. rossi culture supernatants were not or only partially successful. Here we show that when dogs were vaccinated with a vaccine comprising SPA from B. rossi combined with SPA from Babesia canis protective immunity against experimental challenge infection was induced. Immunity was reflected in reduced clinical signs that resolved spontaneously, and reduction of parasitaemia and SPA in the blood. Not a single infected erythrocyte could be found in blood smears of dogs that had been repeatedly boosted (three vaccinations in total). In contrast, three out of four control dogs required chemotherapeutic treatment to prevent death. The fourth control dog showed a transient parasitaemia that resolved spontaneously. Vaccination did not prevent the development of a transient anaemia. It is concluded that a vaccine containing a mixture of SPA obtained from in vitro culture supernatants of B. rossi and B. canis induces protection in dogs against heterologous challenge infection with B. canis (as shown before) or B. rossi.