A randomized multicenter trial of Crotalidae polyvalent immune Fab antivenom for the treatment of rattlesnake envenomation in dogs

Objective – To determine clinical efficacy of the Crotalidae polyvalent immune F_ab (ovine) antivenom (OPCA) against progressive crotalid envenomation in the dog as reflected in stabilization or improvement of snakebite severity scores (SSS). Additionally, due to the potential decreased half‐life of the F_ab antibodies in dogs we compared SSS between dogs receiving 2 different dosing regimes. Design – Prospective, clinical trial. Setting – Five veterinary emergency and critical care facilities. Animals – One hundred and fifteen client‐owned Crotalid (rattlesnake) snake bitten dogs in whom worsening of the envenomation syndrome was observed before OPCA treatment. Interventions – In a multicenter randomized clinical trial a single dose (1 vial) of OPCA alone was compared with 2 doses (1/2 vial each) administered 6 hours apart. Standard supportive care was provided in all cases. Measurements and Main Results – Data were available for 115 patients, 9 of which were fatalities. All patients' clinical condition was documented with a standardized SSS system accounting for each major body system. Each fatality received maximum severity scores of 20. The mean severity score of the 115 patients decreased from 4.19 to 3.29 points and there was no difference between the 2 treatment groups. The mean severity score of the 107 patients without fatalities decreased from 4.16 to 2.15. Antivenin‐related acute reactions occurred in 6 dogs (6%), and no serum sickness occurred within the 95 cases contacted at the 2‐week posttreatment follow‐up. Conclusions – In the first randomized trial in dogs of antivenin in the United States, OPCA effectively stabilized or terminated venom effects. There were no statistical differences detected between treatment groups within the study time frame.     

Clinical findings associated with prairie rattlesnake bites in dogs: 100 cases (1989-1998)

OBJECTIVE: To identify clinically relevant variables and treatments for dogs bitten by prairie rattlesnakes (Crotalus viridis viridis). DESIGN: Retrospective study. ANIMALS: 100 client-owned dogs. PROCEDURE: Records of dogs evaluated for rattlesnake envenomation from 1989 to 1998 were reviewed. Analysis was performed to test for significant associations among clinical variables or treatments and cell counts, costs, and duration of hospitalization. RESULTS: Most prairie rattlesnake bites occurred between May and September. Dogs were 3 months to 12 years old (median, 3.7 years); most were bitten on the head in the late afternoon. There was no sex predilection. Median time to evaluation was 1 hour (range, 15 minutes to 13 hours). Swelling in the area of the bite was the primary physical abnormality. Principal initial laboratory findings were echinocytosis, thrombocytopenia, leukocytosis, and prolonged activated clotting time. Ninety-four dogs were hospitalized; 48 were discharged the following day. Antimicrobials and crystalloid fluids, glucocorticoids, antihistamines, and antivenin administered i.v. were the most commonly used treatments. One dog died, and small dogs were hospitalized longer than large dogs. Antivenin administration was not significantly associated with duration of hospitalization but was associated with higher platelet counts after treatment and higher total hospital costs. CONCLUSIONS AND CLINICAL RELEVANCE: Prairie rattlesnake envenomation in dogs is associated with high morbidity rate but low mortality rate. The efficacy of administration of antivenin for dogs with bites from this snake species is questionable.     

Effect of antivenin dose on outcome from crotalid envenomation: 218 dogs (1988–2006)

Objective – To determine whether the dose of antivenin administered is associated with a difference in survival of crotalid‐envenomated dogs. A secondary objective was to determine whether other covariables affect survival. Design – Retrospective study (1988–2006). Setting – Private referral center and university small animal teaching hospital. Animals – Two hundred and eighteen dogs with evidence of crotalid envenomation and treatment with equine‐derived antivenin. Interventions – Administration of antivenin. Measurements and Main Results – Patient signalment, physical and clinicopathologic data at time of presentation, treatments, complications of antivenin therapy, length and cost of hospitalization, and outcome were recorded. Confidence intervals were determined for the difference in median number of vials administered and for median dosage for patients that lived versus died. Penalized logistic regression was performed to evaluate the effect of other covariables on survival. The median age of affected dogs was 3 years (range 6 w–12 y) with a median weight of 25.7 kg (range 1.95–86.4 kg). The median number of antivenin vials administered was 1.0 (range 1.0–10.0). Acute and chronic reactions were reported in 7% (16/218) and 0.9% (2/218) of dogs, respectively. Nine of 218 dogs (4.1%) died. The median number of vials administered to the nonsurvivors and survivors were 2.0 (range 1–5 vials) and 1.0 (range 1–10 vials), respectively. The median number of vials received was significantly different in dogs that died versus those that lived (P<0.05). Increased heart rate (P=0.02) and petechiation (P=0.04) were associated with decreased likelihood of survival, while diphenhydramine (P=0.02) and fluoroquinolone (P=0.046) administration was associated with increased likelihood of survival. The median duration of hospitalization was 1.0 day (range 2 h–22 d). The median cost of hospitalization was US$1592.00 (range US$267.20–US$6738.00). Conclusion – The administration of more vials of antivenin is potentially associated with negative outcome; however, a causal relationship has not been established. Controlled, prospective studies are needed to optimize antivenin administration.     

Baclofen intoxication in a dog successfully treated with hemodialysis and hemoperfusion coupled with intensive supportive care

Objective: To describe a case of confirmed baclofen intoxication in a dog that was successfully treated with hemodialysis and hemoperfusion (HD/HP) and to report the serum baclofen kinetics. Case summary: A 2.5‐year‐old, 23 kg, spayed female Brittany Spaniel‐mix was treated after ingesting 21‐52 mg/kg of baclofen. The dog was comatose and was receiving manual ventilation at the time of presentation. Extracorporeal HD/HP was started 10 hours after admission. Within 3 hours of starting HD/HP the dog began initiating breaths and was extubated 18 hours after admission. Serial serum samples that were obtained during the first 24 hours of hospitalization were later analyzed for baclofen concentrations. The dog had elevated creatine phosphokinase and liver enzymes that correlated with an agitated recovery period. The dog had thrombocytopenia that resolved by 10 days after presentation. New or unique information provided: HD/HP shortened the baclofen serum elimination half‐life from 5 to 1.5 hours in the initial 2 hours of treatment. The intrinsic elimination rate constant (K_intr) for this dog was 0.138/hour and the total elimination rate constant (K_tot) during the first 2 hours of HD/HP treatment was 0.458/hour. In this dog, HD/HP was an effective method for rapidly decreasing serum baclofen concentration after an acute overdose.     

Electroretinographic changes after intravenous lipid emulsion therapy in a dog and a foal with ivermectin toxicosis

This case report describes ivermectin‐induced blindness in a dog and a foal with normal ophthalmic fundic examinations and attenuated electroretinography (ERG). Subsequent recovery in ERG was noted following intravenous lipid emulsion (ILE) therapy. A dog and a foal were evaluated for ivermectin‐induced blindness. Clinical signs included dull mentation, absent pupillary light reflexes (PLRs), and absent menace on presentation. The animals had normal fundoscopic examinations; however, in both cases ERG was consistent with neurosensory retinal dysfunction. Following ILE therapy for ivermectin toxicosis, return of menace, PLRs, and normal mentation were noted, as was improvement in ERG and serum ivermectin levels. These are the first documented cases of ivermectin‐induced blindness in a dog and a foal with normal fundic examinations and attenuated ERG. ERG improved in both animals after ILE therapy. ERG may assist in the diagnosis of ivermectin toxicosis in dogs and horses. ILE therapy may hasten recovery in treatment of ivermectin‐induced blindness.     

Abdominal compartment syndrome in a dog with babesiosis

Objective: To describe a case of abdominal compartment syndrome in a dog with babesiosis. Case summary: A 9‐year‐old female Bull Terrier presented with complicated babesiosis. Additional findings including respiratory distress, abdominal distension, and a decrease in urine output associated with an elevated abdominal pressure (23.5–25 cmH₂O) led to a further diagnosis of abdominal compartment syndrome. This case report describes the clinical course of both conditions through resolution. New information provided: Abdominal compartment syndrome is not well described in the veterinary literature, but clinicians should be aware of this potential complication in critically ill patients. The pathophysiology and veterinary literature of abdominal compartment syndrome are reviewed.     

Successful treatment of severe salt intoxication in a dog

Objective: To report successful treatment of severe salt intoxication and hypernatremia in a dog. Case summary: A 5‐year‐old intact female Doberman Pinscher was admitted to the intensive care unit with a history of seizures and coma. The owner had administered approximately 100 g of cooking salt to induce vomiting following ingestion of a nontoxic dose (10 g) of chocolate. Upon admission, the dog was comatose with intermittent seizures and vomiting. Diagnostic tests confirmed salt intoxication (Na: 200 mEq/L, Cl: 180 mEq/L) and metabolic acidosis (pH: 7.18; pCO₂: 39 mmHg; HCO₃: 14.3 mmol/L). Immediate treatment included intravenous fluid therapy, an anticonvulsant, antiemetic, diuretic, low molecular weight heparin, and supplemental oxygen. A fluid therapy protocol was initiated to decrease serum sodium concentration by approximately 2 mEq/L/hr. After 24 hours of intensive care, the patient regained consciousness and volume and acid‐base abnormalities improved. The patient developed a variety of abnormal clinical signs as a result of the severe hypernatremia. After 5 days of treatment, the serum sodium concentration returned to the established reference range. The patient recovered completely in 10 days. New information provided: Severe hypernatremia due to salt ingestion is a rare condition in dogs. All dogs in previous case reports of salt intoxication have died. This case report is the first to report survival of a dog with severe salt intoxication.     

Canine Trypanosoma evansi infection introduced into Germany

A 9‐year‐old male Jack Russell Terrier with a history of travel to Thailand was presented with chronic lethargy, weight loss, unilateral anterior uveitis, pancytopenia, hyperglobulinemia, and proteinuria. Numerous trypomastigotes were found on a blood smear, and using molecular methods the parasite was identified as Trypanosoma evansi. After initial response to treatment, the dog experienced a relapse with central neurologic signs 88 days after initial presentation and died. Antibodies to T evansi were detected in both serum and cerebrospinal fluid (CSF) using a card agglutination test (CATT/T evansi), and PCR analysis of CSF for T evansi was positive. Findings at necropsy included marked non‐purulent meningoencephalitis. Chronic infection with T evansi in a dog that returned to Germany following international travel highlights the risk associated with introduction of foreign animal diseases to Europe and the possibility of these infections becoming endemic. Detection of chronic infection and curative therapy of trypanosomiasis are challenging, and infection is usually fatal in the dog.     

Brain abscess and bacterial endocarditis in a Kerry Blue Terrier with a history of immune-mediated thrombocytopenia

Objective: To describe a case of multifocal brain abscessation as a sequela from bacterial endocarditis in a dog with a 4‐month history of immune‐mediated thrombocytopenia (ITP) and treatment with immunosuppressive therapies. Case summary: An 8‐year‐old spayed female Kerry Blue Terrier weighing 13 kg was presented for evaluation of progressive neurologic deficits after a 4‐month history of immunosuppressive treatment of ITP. Brain magnetic resonance imaging revealed lesions consistent with multiple central nervous system abscesses and rupture of an abscess into an adjacent ventricle. Staphylococcus species were cultured from blood and cerebral spinal fluid and a vegetative lesion of the mitral valve was identified by echocardiographic examination. Intensive care, intravenous antibiotics, and supportive therapy led to resolution of clinical signs. Resolution of the vegetative lesion on the mitral valve was documented by serial echocardiographic examination. The dog was clinically normal 11 months after treatment. New or unique information provided: Bacterial endocarditis can be an occult infection and difficult to diagnose. Emboli from endocarditis are common, but those that affect the spleen and kidneys are often clinically silent in dogs. This case represents the first report of multifocal brain abscessation (documented with magnetic resonance imaging) as a sequela from bacterial endocarditis.     

Temporary transvenous cardiac pacing in a dog with diltiazem intoxication

Objective: This case report presents the clinical findings of a dog with diltiazem intoxication and the utilization of temporary transvenous pacing for management of high‐grade second‐degree atrioventricular (AV) block with associated bradycardia and hypotension. Case summary: A nine‐year‐old spayed female Basset Hound, who ingested between 95 and 109 mg/kg of sustained‐release diltiazem exhibited clinical signs of cardiac arrhythmias, bradycardia, hypotension, mental depression and gastrointestinal (GI) upset. Bradycardia was present initially, then was followed by high‐grade second‐degree AV block with ventricular escape. Traditional medications to treat calcium channel blocker (CCB) intoxication, including atropine, calcium gluconate, dopamine and glucagon were initially successful in managing the cardiac rhythm disturbances and hypotension. Twenty‐two hours post‐ingestion, however, the dog became refractory to these medications following sedation for GI decontamination and a temporary transvenous pacemaker was placed. The dog was paced for 19 hours. Transvenous pacing effectively increased heart rate, which increased blood pressure into an acceptable range. The dog was successfully discharged from the hospital following treatment. New or unique information provided: The use of a temporary pacemaker should be considered an acceptable treatment for bradycardia, AV block and hypotension associated with CCB intoxication when conventional medical therapy fails.     

First record of autochthonous canine ehrlichiosis caused by Ehrlichia canis in Romania

This case study describes the first genetically confirmed and clinically manifested autochthonous Ehrlichia canis infection in a 9‐year‐old female mixed‐breed dog from Romania. Health screening of the dog included clinical examination, evaluation of stained peripheral blood smear and hematologic variables, as well as serologic testing and molecular analysis. Clinical signs included fever, apathy, dehydration, pale mucous membranes, and weakness. The microscopic examination of the blood smear and immunologic assays for Borrelia burgdorferi, Anaplasma phagocytophilum, and E canis antibodies, and for Dirofilaria immitis antigen yielded negative results. Hematologic abnormalities included moderate nonregenerative anemia, leucopenia with neutropenia, and moderate thrombocytopenia. The biochemical abnormalities identified were hypoalbuminemia, and mildly increased serum enzyme activities of AST and ALT. In addition, increased urea and creatinine levels associated with low urine specific gravity and proteinuria were also present. Nested PCR amplification of the partial E canis 16S rRNA gene demonstrated the presence of this rickettsial pathogen in the dog's blood, which subsequently was confirmed through sequencing based on the 100% homology with GenBank deposited E canis isolates. After specific treatment with doxycycline (10 mg/kg, orally, SID) for one month, the proteinuria, and hematologic and serum biochemical abnormalities with the exception of mild azotemia resolved. This report supports the geographical expansion of canine ehrlichiosis caused by E canis in nonendemic regions of Europe.     

Hypocalcemia in a critically ill patient

Objective: To present a case of clinical hypocalcemia in a critically ill septic dog. Case summary: A 12‐year old, female spayed English sheepdog presented in septic shock 5 days following hemilaminectomy surgery. Streptococcus canis was cultured from the incision site. Seven days after surgery, muscle tremors were noted and a subsequent low serum ionized calcium level was measured and treated. Intensive monitoring, fluid therapy, and antibiotic treatment were continued because of the sepsis and hypocalcemia, but the dog was euthanized 2 weeks after surgery. New or unique information provided: Low serum ionized calcium levels are a common finding in critically ill human patients, especially in cases of sepsis, pancreatitis, and rhabdomyolysis. In veterinary patients, sepsis or streptococcal infections are not commonly thought of as a contributing factor for hypocalcemia. Potential mechanisms of low serum ionized calcium levels in critically ill patients include intracellular accumulation of calcium ions, altered sensitivity and function of the parathyroid gland, alterations in Vitamin D levels or activity, renal loss of calcium, and severe hypomagnesemia. Pro‐inflammatory cytokines and calcitonin have also been proposed to contribute to low ionized calcium in the critically ill. Many veterinarians rely on total calcium levels instead of serum ionized calcium levels to assess critical patients and may be missing the development of hypocalcemia. Serum ionized calcium levels are recommended over total calcium levels to evaluate critically ill veterinary patients.     

Treatment of unresectable hepatocellular adenoma in dogs with transarterial iodized oil and chemotherapy with and without an embolic agent: A report of two cases

Transarterial iodized oil with chemotherapy was evaluated in two dogs with large, surgically unresectable hepatocellular adenoma. A single cycle of therapy was used in each dog. Chemoembolic mixtures varied: doxorubicin emulsified with iodized oil radiographic contrast (case 1), doxorubicin and mitomycin C emulsified with iodized oil radiographic contrast (case 2). In addition, dog 2 underwent arterial embolization with polyvinyl alcohol granules. Response was assessed by computed tomography at 1 and 3 months after treatment. Superselective catheterization of the hepatic arterial branch supplying the tumour was not achieved in either case. In the immediate post‐operative period, both dogs developed mild clinical signs that may have been consistent with post‐embolization syndrome, but neutropenia and reduced liver function were not observed. Tumour response was minimal: stable disease at 1 month and progressive disease at 3 months was observed in both cases.     

Rauwolfia serpentina toxicity in a dog

Objective– To describe the clinical manifestations and treatment of Rauwolfia serpentina toxicity in a dog. Case Summary– A 9‐month‐old intact male mixed breed dog was presented following ingestion of an antihypertensive medication containing alkaloids from R. serpentina. R. serpentina alkaloids cause depletion of the biologic amines: norepinephrine, dopamine, and serotonin. The dog experienced hypotension, mental depression, bradycardia, diarrhea, bronchoconstriction, and gastrointestinal ulceration similar to the adverse effects reported in humans. The dog was released from the hospital after 4 days of supportive care. New Information Provided– This is the first case of accidental R. serpentina toxicity in a dog reported in the literature. This case had a good clinical outcome with supportive care and monitoring of all the subsequent adverse effects.     

Canine leishmaniasis with nephrotic syndrome and aortic and caudal vena cava thromboembolism

Objective – To describe a case of leishmaniasis associated with nephrotic syndrome and aortic and caudal vena cava thrombosis in a dog. Case Summary – A 3‐year‐old male Boxer was referred to the Faculty of Veterinary Medicine, Lisbon, with vomiting, polyuria, polydipsia, lethargy, anorexia, and weight loss. On admission, the dog was thin, quiet, and dehydrated. Initial laboratory abnormalities were compatible with a diagnosis of leishmaniasis (confirmed by serology and bone marrow aspirate), and nephrotic syndrome. Three days later, the animal developed lumbar pain, paraparesis, and absent femoral pulses. Coagulation tests showed a marked reduction in antithrombin (AT) and a mild increase in serum fibrinogen concentration. A diagnosis of thromboembolism was made. In spite of treatment aimed at controlling the primary condition and decreasing further thrombus formation, necrosis developed in the distal right pelvic limb and the nail beds of the left pelvic limb. Against medical advice, medication was stopped and, 15 days later, the dog returned to the hospital, showing extensive necrosis of both pelvic limb extremities. Euthanasia was performed at the owner's request. Necropsy showed a thrombus localized at the distal aorta and extending into the right iliac artery, and an additional thrombus extending from both femoral veins onto the caudal vena cava. New or Unique Information Provided – Thromboembolic disease is rare in dogs with leishmaniasis with nephrotic syndrome. This case suggests that a marked decrease in AT and a mild increase in serum fibrinogen may elicit a hypercoagulable state in these patients.     

Successful treatment of intra‐abdominal eumycotic mycetoma caused by Penicillium duponti in a dog

A 2‐year‐old female neutered golden retriever was presented for investigation of an intra‐abdominal mass. Computed tomography revealed a mass associated with the caudal pole of the right kidney. Incisional biopsy findings were consistent with eumycotic mycetoma. The mass was subsequently removed in conjunction with right ureteronephrectomy. Two years later, the dog re‐presented with a splenic mass and fungal plaques located throughout the peritoneum. Splenectomy was performed and the mass was diagnosed as eumycotic mycetoma caused by Penicillium duponti. Indefinite systemic treatment with 10 mg/kg itraconazole orally once a day was initiated. Thirty‐two months after the last surgery, there were no clinical signs apart from mild polydipsia. Haematology and biochemistry results were unremarkable. To the authors’ knowledge, this is the first report of successful treatment of intra‐abdominal eumycotic mycetoma with a combination of surgery and systemic antifungal therapy in the dog. Penicillium duponti has not apparently been reported to cause disease in animals or humans.     

Emergency presentations of 4 dogs with suspected neurologic toxoplasmosis

Objective: To review the signalment, clinical signs, abnormal laboratory data, therapeutics, and response to therapy of dogs with clinical signs consistent with toxoplasmosis infection. Series summary: A retrospective review was performed on the records of 4 dogs presented to the Animal Emergency Center between January 1998 and February 2000 exhibiting neurologic signs and having elevated titers for Toxoplasma gondii. A tentative diagnosis of toxoplasmosis was based upon one of the following criteria: (1) a serial 4‐fold or greater change in serum T. gondii IgG titers; 2) serially decreasing serum T. gondii IgM titers with concurrent increasing serum T. gondii IgG titers; or 3) positive cerebrospinal fluid (CSF) T. gondii titers. In addition, inclusion of cases was limited to dogs that showed improvement of neurologic signs following treatment with antiprotozoal drugs. Trimethoprim–sulfamethoxazole treatment was associated with successful elimination of clinical signs in all of the dogs. Two of the dogs developed side effects potentially attributed to the trimethoprim–sulfamethoxazole (TMS), and antiprotozoal treatment was continued using clindamycin. Unique information presented: Toxoplasmosis is an important differential diagnosis in any dog that presents as an emergency with central or peripheral neurologic signs. Affected dogs need not be immunocompromised for clinical signs of toxoplasmosis to occur. Appropriate treatment with TMS or clindamycin can lead to resolution of clinical signs.     

Amanita muscaria toxicosis in two dogs

Objective: To report the manifestations, history, and pathophysiologic basis of disease in 2 dogs with Amanita muscaria toxicosis. Case summaries: Two dogs were evaluated for an acute onset of gastroenteritis and seizures. A. muscaria toxicosis was suspected in each dog after confirmation of environmental exposure and visualization of ingested mushrooms in vomitus. The diagnosis was confirmed following identification of toxic Amanita metabolites in the urine and serum of each dog. Administration of supportive and symptomatic therapies resulted in the complete recovery of each animal. Unique information provided: Ingestion of the mushroom, A. muscaria, by dogs can result in acute gastrointestinal distress that precedes a potentially life‐threatening central neurologic syndrome characterized by seizures, tremors, and somnolence. Central nervous system dysfunction results primarily from the actions of ibotenic acid and its decarboxylation product, muscimol, which are analogues of the neurotransmitters glutamate and γ‐aminobutyric acid (GABA), respectively. Identification of these toxins in the urine and serum of affected dogs using high‐performance liquid chromatography (HPLC) provides a definitive diagnosis.     

Hepatic fungal infection in a young beagle with unrecognised hereditary cobalamin deficiency (Imerslund‐Gräsbeck syndrome)

A 12‐month‐old beagle presented for anorexia, pyrexia and vomiting. The dog had been treated intermittently with antibiotics and corticosteroids for inappetence and lethargy since five months of age. Previous laboratory abnormalities included macrocytosis and neutropenia. At presentation, the dog was lethargic, febrile and thin. Laboratory examination findings included anaemia, a left shift, thrombocytopenia, hypoglycaemia and hyperbilirubinaemia. Multiple, small, hypoechoic, round hepatic lesions were observed on abdominal ultrasound. Cytological examination of hepatic fine needle aspirates revealed a fungal infection and associated pyogranulomatous inflammation. The dog's general condition deteriorated despite supportive measures and treatment with fluconazole, and owners opted for euthanasia before hypocobalaminaemia was identified. Subsequent genomic analysis revealed a CUBN:c.786delC mutation in a homozygous state, confirming hereditary cobalamin malabsorption (Imerslund‐Gräsbeck syndrome). Similar to human infants, dogs with Imerslund‐Gräsbeck syndrome may rarely be presented for infectious diseases, distracting focus from the underlying primary disorder.     

Listeria monocytogenes septicemia in an immunocompromised dog

An 11‐year‐old, male castrated, Boston Terrier was presented to the North Carolina State University College of Veterinary Medicine Small Animal Emergency Service with a 2‐day history of progressive ataxia, left‐sided head tilt, and anorexia. The dog had previously been diagnosed with chronic lymphoid leukemia and suspected immune‐mediated destruction of his bone marrow precursor cells, possibly due to therapy with immunosuppressive dosages of prednisone and azathioprine. During the physical examination, abnormal findings included an increased body temperature and horizontal nystagmus. Diagnostic investigations included a computed tomography (CT) scan, which confirmed bilateral otitis media, and a blood culture, which was positive for Listeria monocytogenes serotype 4b (epidemic clone 1). Upon treatment with ampicillin/sulbactam, enrofloxacin, and minocycline, the dog became normothermic and the neurologic signs improved. L monocytogenes serotype 4b (epidemic clone 1) has been associated with outbreaks of human listeriosis originating from food contamination. Although rare case reports of Listeria spp. infection in dogs exist, an actual infection with the epidemic clone 1 strain has never before been reported in a dog. It should be included in the differential diagnoses in immunocompromised dogs with clinical signs of septicemia.