Vascular Encephalopathy Associated With Bacterial Endocarditis in Four Dogs
Vascular encephalopathy is a commonly encountered clinical complication of infectious endocarditis in humans, but it has been infrequently reported in dogs. A series of four dogs with bacterial endocarditis that subsequently developed acute onset of neurological deficits is described. Clinical signs, diagnostic test results, and outcomes for each case are presented and compared with the human clinical syndrome.
Introduction
The incidence of vascular encephalopathy in dogs is low in comparison to humans.1 As a clinical entity, vascular encephalopathy (more commonly referred to as cerebrovascular accident or stroke) is the third leading cause of death in humans.2 Causes of stroke in people are numerous, but the most common include atherosclerosis, heart disease, hypertension, and diabetes mellitus. Other causes include septic or metastatic embolization arising from extracranial foci.3 Reported causes of vascular encephalopathy in dogs include atherosclerosis associated with hypothyroidism, cerebrovascular anomalies, vasculitides, emboli from Dirofilaria immitis, sepsis, neoplasia, heart disease, cerebral hemorrhage from systemic hypertension, coagulopathies, trauma, other systemic illnesses, and idiopathic causes.1,4–7 Bacterial endocarditis in dogs and humans can cause thromboembolic disease affecting multiple organ systems.2,4 Vascular encephalopathy is seen in approximately one-third of all humans affected with bacterial endocarditis, and it is associated with a poor outcome.2 Acute onset of hemiplegia and hemi-inattention (i.e., loss of recognition of sensory input from one side of the body) are the presenting signs in half of all affected humans.2 In dogs, secondary embolization from bacterial endocarditis commonly occurs to the spleen and kidneys and less frequently to the lungs, liver, and heart.8 Central nervous system (CNS) thromboembolic disease secondary to bacterial endocarditis in dogs has been rarely reported.8–10 The purpose of this retrospective study is to describe the presentation, diagnosis, management, and outcome of four dogs with vascular encephalopathy associated with bacterial endocarditis.
Materials and Methods
Cases for this study were retrospectively identified from the population of dogs examined at the Texas A&M University Veterinary Medical Teaching Hospital (TAMU-VMTH) between 1993 and 2001. Dogs were included if they fit two selection criteria, including documentation of infectious endocarditis by echocardiography or necropsy findings and clinical signs of vascular encephalopathy. Signs of vascular encephalopathy included acute onset of focal brain dysfunction of a nonprogressive nature followed by a positive clinical response to medical therapy, or documentation of brain infarction by computed tomography or necropsy findings. Based on these criteria, four dogs were determined to have infectious endocarditis with concurrent evidence of vascular encephalopathy.
Case Reports
Case No. 1
A 6-year-old, 22.7-kg, male English bulldog was referred with a 1-month history of intermittent lethargy, fever, and episodes of abdominal discomfort. The dog developed a shifting leg lameness 1 week prior to presentation. The referring veterinarian reported a leukocytosis (white blood cell [WBC] count of 22,700/μL; reference range 6000 to 17,000/μL) and thrombocytopenia (77,000/μL; reference range 200,000 to 500,000/μL) on a complete blood count (CBC) 1 day prior to referral. In addition, elevations in blood urea nitrogen (BUN) (43 mg/dL; reference range 8 to 24 mg/dL), phosphorus (7.6 mg/dL; reference range 2.7 to 6.0 mg/dL), and alkaline phosphatase (330 IU/L; reference range 0 to 107 IU/L) were noted on biochemical panels. Urinalysis revealed isosthenuria, trace protein, positive hemoglobin, and 2 to 3 WBCs per high-power field (hpf) with many bacteria in the sediment. Coombs’ test and serology for Ehrlichia canis, Leptospira (L.) pomona, L. icterohemorragicae, L. canicola, L. grippotyphosa, and L. hardjo were negative. Initial treatments by the referring veterinarian included trimethoprim sulfadiazine,a oxytetracycline,b gentamicin,c and dexamethasone.d The owner noted transient improvement in the dog, followed by recurrence of clinical signs.
At presentation, the dog was lethargic and weak. Rectal temperature was 100.2°F (reference range 99.5° to 102.5°F); pulse rate was 150 beats per minute (bpm; reference range 80 to 120 bpm); and respiratory rate was 40 breaths per minute (reference range 15 to 30 breaths per minute). A grade 3/6 systolic murmur was ausculted over the left cardiac apex. The murmur was not previously noted by the referring veterinarian. The dog was moderately dehydrated, and the gait was stiff in all limbs. Multiple retinal hemorrhages were evident bilaterally on fundic examination. Blood pressure was not recorded.
A mature neutrophilic leukocytosis (WBCs 49,700/μL; absolute neutrophils 43,239/μL; reference range 3000 to 11,000/μL), mild thrombocytopenia (136,000/μL), and monocytosis (4970/μL; reference range 150 to 1350/μL) were evident on the CBC. Mild elevations in BUN (40 mg/dL) and serum alkaline phosphatase (341 IU/L) were noted on a biochemical panel. Isosthenuria was present on urinalysis. Urine culture was negative for bacterial growth after 72 hours. Mild right heart enlargement was seen on thoracic radiographs. Mitral valvular insufficiency, mild compensatory left ventricular dilatation, and left atrial enlargement were noted on echocardiography. Electrocardiography (ECG) demonstrated a sinus rhythm with a rate of 120 bpm and showed evidence of both left atrial and left ventricular enlargement. Abdominal ultrasonography revealed that the dorsolateral cortex of the right kidney was diffusely hyperechoic, and areas of mixed echogenicity with two hyperechoic nodules in the prostate were seen. Differential diagnoses for the prostatic changes included hemorrhage, inflammatory infiltrate (e.g., abscess), neoplastic infiltrate (i.e., primary or metastatic), or infarctions. Initial treatment included intravenous (IV) lactated Ringer’s solution for dehydration and enalaprile (0.25 mg/kg per os [PO] q 12 hours) for the mitral valve insufficiency.
Two days after hospital admission, the dog was more active and had a normal gait. The rectal temperature was slightly elevated (102.6°F) on the morning of day 3. On day 4, the dog developed mild large bowel diarrhea with hematochezia. The dog became lethargic with a depressed appetite and was reluctant to walk by day 5. Pain was identified on manipulation of the right stifle and tarsal joints, but no joint effusion was evident. A persistent neutrophilic leukocytosis (WBCs 26,000/μL; absolute neutrophils 23,140/μL), resolving monocytosis (1820/μL), and a severe thrombocytopenia (18,000/μL) were noted on CBC.
Arthrocentesis was performed on the right stifle, tarsal, and carpal joints. The synovial joint fluid was straw-colored and hazy. Results of cytological examination suggested suppurative inflammation with increased nondegenerate neutrophils (89.6 × 103/μL; reference range <3 × 103/μL), but no infectious agents were evident.9 Bacterial culture of the fluid yielded no growth after 72 hours. Infectious or immune-mediated polyarthritis and immune-mediated thrombocytopenia were suspected. Other differential diagnoses included rickettsial infections (e.g., Ehrlichia spp., Rocky Mountain spotted fever) and systemic lupus erythematosus. Treatment was initiated with prednisonef (2 mg/kg per day PO). On day 6 after admission, the dog was clinically improved but was still reluctant to walk and had persistent large bowel diarrhea with mild hematochezia. Oral petechiation was noted on physical examination.
The clinical signs worsened on days 7 and 8. A persistent neutrophilic leukocytosis (WBCs 33,200/μL; absolute neutrophils 29,548/μL), thrombocytopenia (36,000/μL), and a mild nonregenerative anemia (packed cell volume [PCV] 27%; reference range 35% to 45%; corrected reticulocyte count 0.1%) were noted on the CBC on day 8. Urinalysis revealed trace proteinuria and moderate hematuria with 2 to 5 WBCs/hpf and 2+ bacteria/hpf. A second urine sample was submitted for urine culture. Treatment was changed to ampicilling (30 mg/kg subcutaneously q 8 hours), cimetidineh (15 mg/kg PO q 8 hours), and sucralfatei (1 g PO q 8 hours). On day 9, the dog was markedly ataxic and exhibited head pressing. Severe miosis and absent menace response were noted in the left eye. Persistent neutrophilic leukocytosis (WBCs 35,100/μL; absolute neutrophils 32,643/μL) with occasional toxic change, severe thrombocytopenia (18,000/μL), and nonregenerative anemia (PCV 34%; corrected reticulocyte count 0.3%) were found on a CBC. Marginally decreased prothrombin time (6.2 seconds; reference range 6.5 to 7.6 seconds), normal partial thromboplastin time (15.6 seconds; reference range 13 to 16.5 seconds), and decreased antithrombin III (54% natural human protein; reference range 84% to 128%) were detected on a coagulation panel.
Because of the acute onset of neurological signs and deterioration in the dog’s physical status, he was euthanized. Necropsy revealed vegetative endocarditis of the left atrio-ventricular valve; chronic infarction of the right kidney, with multiple petechiae present; acute fibrinous polyarthritis involving all of the joints of the distal extremities; and a 1-cm infarction in the left dorsal cerebral hemisphere. Bacterial culture of the kidney yielded pure growth of Klebsiella pneumoniae.
Case No. 2
A 4-year-old, 27.7-kg, male German shepherd dog was referred with a history of acute onset of ataxia beginning 3 days earlier. The referring veterinarian treated the dog for suspected intoxication by inducing emesis and administering IV fluids, antibiotics, and corticosteroids. The dog’s condition did not improve.
On physical examination, the dog was lethargic; rectal temperature was elevated at 103.4°F; heart rate was 100 bpm; the dog was panting; and femoral arterial pulses were bounding. A grade 4/6 diastolic murmur with a 2/6 proto-systolic component (i.e., “to-and-fro” murmur) was ausculted loudest over the left heart base. A mildly enlarged, symmetrical, nonpainful prostate was palpated rectally. The dog had normal mentation but mild intention tremors, a head tilt to the right, and was falling to the left. Conscious proprioception was decreased in the left thoracic and both hind limbs. There was no menace response in the left eye, moderate anisocoria with left mydriasis, spontaneous nystagmus with a rotary component to the right, and decreased facial sensation on the left side of the face. Based on the neurological findings, a left cerebellomedullary angle lesion with a paradoxical component was suspected.
A mild neutrophilic leukocytosis (WBCs 18,300/μL; absolute neutrophils 15,738/μL) was evident on a CBC. Indirect blood pressure measurements were 133 mm Hg systolic, 69 mm Hg diastolic, with a mean arterial blood pressure of 87 mm Hg. Echocardiographic findings were consistent with moderate subaortic stenosis (transaortic gradient of 64 mm Hg), with severe endocarditis of the aortic valve and anterior mitral valve leaflet, resulting in severe aortic insufficiency and moderate mitral insufficiency. Because of the severity of the clinical signs and a poor prognosis, the dog was euthanized. Necropsy findings included congenital subaortic stenosis, aortic valvular endocarditis, and a focal area of necrosis and malacia on the left side of the cerebellum, consistent with a thromboembolic event. Cultures of the aortic valve lesions were not performed.
Case No. 3
A 14-year-old, 17.2-kg, castrated male, mixed-breed dog was referred with a history of acute-onset nonambulatory tetraparesis. Two days prior to referral, the referring veterinarian noted tetraparesis with proprioceptive deficits in all limbs, normal spinal reflexes, intention tremors, and spontaneous nystagmus. Complete blood count and serum biochemical profile were reported to be normal. The dog was treated with dexamethasone and hospitalized, but had two generalized seizures and was subsequently referred.
The dog had been diagnosed 15 months earlier with mitral valvular endocarditis and subsequent valvular insufficiency and congestive heart failure at TAMU-VMTH. Prior treatment for endocarditis consisted of amoxicillin-clavulanic acidj (14.5 mg/kg PO q 12 hours) and enrofloxacink (4 mg/kg PO q 12 hours). The congestive heart failure was managed with enalapril (0.5 mg/kg PO q 12 hours), furosemidel (2 to 4 mg/kg PO q 8 to 12 hours), spironolactonem (0.5 mg/kg PO q 12 hours), carvediloln (0.08 mg/kg PO q 12 hours), and pimobendano (2.5 mg/kg PO q 12 hours). Two months prior to admission for acute neurological signs, the dog developed mucosal petechiae, right pelvic limb lameness, pitting edema over the ventral and medial right thigh area, and absent femoral pulses. Thromboembolic disease and disseminated intravascular coagulation were suspected, and the dog was hospitalized for 6 days and treated with Imipenemp (4.7 mg/kg IV q 8 hours for 6 days) and heparin (100 IU/kg subcutaneously q 8 hours). The dog was discharged with enrofloxacin (4 mg/kg PO q 12 hours). Six weeks later, the edema and lameness had resolved, and heparin and antibiotic therapy were discontinued.
At presentation, the dog was quiet, alert, and responsive. Rectal temperature was 100.2°F; pulse rate was 110 bpm; and respirations were 42 breaths per minute. A grade 4/6 pansystolic murmur was ausculted over the left cardiac apex. Pulses were not palpable in the right femoral artery. Neurological examination revealed severe tetraparesis with the right side more severely affected than the left. Proprioception was absent in all limbs. Spinal reflexes were intact. Menace responses and palpebral reflexes were decreased bilaterally. A spontaneous vertical nystagmus was present bilaterally. Neurological deficits were compatible with multifocal disease affecting the forebrain and cerebellomedullary angle, especially on the right side. Differential diagnoses included vascular encephalopathy secondary to endocarditis, CNS infectious/inflammatory disease, CNS hemorrhage, or neoplasia.
A neutrophilic leukocytosis (WBCs 22,200/μL; absolute neutrophils 19,536/μL) was found on a CBC. A persistent mild elevation in BUN (39 mg/dL) was detected and unchanged over the previous 15 months. Marked, generalized cardiomegaly was evident on thoracic radiographs. Indirect systolic and diastolic blood pressure measurements were 127 mm Hg and 75 mm Hg, respectively. The owners declined computed tomography (CT) of the brain and cerebrospinal fluid analysis, and conservative management was elected. Therapy was continued with amoxicillin/clavulanic acid (14.5 mg/kg PO q 12 hours) for previously diagnosed endocarditis. Over the next 5 days of hospitalization, the dog’s neurological status improved. The dog became ambulatory without assistance, the nystagmus resolved, and there was no evidence of seizure activity. The dog was discharged on day 7. The acute onset and rapid resolution of neurological signs were compatible with a cerebrovascular accident secondary to endocarditis.
The dog remained neurologically normal for approximately 1 year. Thirteen months after presentation for neurological signs, the dog was diagnosed with severe bilateral jugular venous thrombosis, chylothorax, and acute renal failure, and was euthanized. Necropsy confirmed severe endocarditis involving the mitral valve, with prominent subendocardial fibrosis of the left atrium (“jet lesion”). Culture of the mitral valve leaflets yielded Escherichia coli (E. coli). In the kidneys, severe, diffuse, membranous glomerulonephritis was seen, as well as interstitial fibrosis and multifocal, interstitial, lymphoplasmacytic infiltrates. Mixed growth of E. coli and Enterococcus spp. were obtained from cultures of the kidney. Multiple areas of gliosis of the white matter in the cerebrum and spongiosis of the brain stem were also found. These latter changes were nonspecific but may have indicated a prior thromboembolic episode.
Case No. 4
A 4-year-old, castrated male Labrador retriever was referred with a 1-month history of lethargy and lameness, sudden onset of ataxia, excessive salivation, and stupor of 1-day duration. The referring veterinarian initiated treatment including IV fluids, corticosteroids, ceftiofur,q and tetracycline.r
On presentation, the dog was depressed but responsive and circling to the left. Rectal temperature was 103.1°F; pulse rate was 80 bpm; and the dog was panting. No cardiac murmur was ausculted. A left-sided hemi-inattention was noted on neurological examination. Postural reactions were decreased in all limbs but were more severely affected on the right side. Depressed facial sensation, partial facial droop on the right side, and anisocoria with miosis of the left pupil were noted. A left-sided forebrain lesion was suspected. A mild neutrophilic leukocytosis (WBCs 19,000/μL; absolute neutrophils 13,680/μL) was evident on a CBC. Serum biochemical panel and urinalysis results were within the reference ranges. Thoracic radiographs were normal. Brain CT identified a hyperintense, mildly contrast-enhanced lesion of the left temporal lobe of the cerebral cortex. The lesion compressed the left lateral ventricle [Figures 1A, 1B] and was surrounded by mild edema. Differential diagnosis was probable neoplasm or focal inflammatory disease.
Because of a poor prognosis, the dog was euthanized. Necropsy revealed severe, suppurative, and lymphoplasmacytic, vegetative, aortic endocarditis with numerous intralesional gram-negative coccobacilli. No bacterial culture was performed. Focal, chronic, arterial thrombosis with severe, locally extensive, parenchymal hemorrhage and necrosis were present in the left temporal cortex where the lesion was identified on CT.
Discussion
The four cases reported here had vascular encephalopathy and concurrent endocarditis. Although uncommonly reported in dogs, neurological complications related to bacterial endocarditis in humans have been recognized since 1885, when the triad of fever, heart murmur, and hemiplegia was described.3 Thromboembolic disease is commonly seen in affected people, with 65% of all emboli involving the brain.2,3 In people, thromboembolism occurs most commonly at the middle cerebral artery.2,3 The middle cerebral artery supplies the lateral cerebral hemisphere, including the motor cortex, thalamus, and basal nuclei. Thromboembolism occluding the blood supply results in brain ischemia. If ischemia is mild, focal brain dysfunction is transient, and signs typically resolve within minutes to hours. This clinical syndrome in humans is known as a transient ischemic attack.10 If ischemia persists, ischemic necrosis may occur. Abscess formation or mycotic aneurysm formation secondary to spread of infection through the vessel wall may also cause neurological symptoms.2 Neurological signs are often the first symptoms to develop. In one report, a focal neurological deficit, hemiparesis or a hemisensory deficit, altered mentation, or a headache was the chief complaint in up to 28% of patients affected with bacterial endocarditis.2
As previously described in people, the middle cerebral arteries are also the most commonly affected sites in the CNS of dogs.10 Unilateral forebrain signs predominate in many cases, but the cerebellum and brain stem may also be involved if other vessels are occluded.10 Unlike affected humans, dogs with bacterial endocarditis have not been at high risk for CNS complications. In one report of aortic valvular endocarditis, one of 20 dogs had evidence of embolization of the brain.11 In another study, two of 35 dogs had brain involvement.4 In a case report of bacterial endocarditis in a Doberman pinscher, acute onset of central vestibular signs was noted, possibly from thromboembolic disease.12 In another case report of bacterial endocarditis in a Labrador retriever without overt neurological dysfunction, thromboembolism involving multiple organ systems (including cerebral microinfarcts) were identified on necropsy.13
The signalment of the dogs in this report was consistent with that described for bacterial endocarditis, where large-breed (e.g., German shepherd dogs, boxers) male dogs tend to be overrepresented.4,11 Three of the four dogs reported here were presented with vascular encephalopathy as their first sign of illness. Two of the dogs had signs of forebrain involvement, and two had central vestibular signs.
It has been reported that as many as 26% of dogs with bacterial endocarditis may not have auscultable murmurs.11 One of the dogs in this study (case no. 4) had no murmur reported, and cardiovascular disease was not identified until necropsy examination. Because cardiac disease was not suspected, an undetected murmur could not be ruled out. Fever has been reported in 80% to 90% of dogs with bacterial endocarditis.11 Two of the dogs reported here were febrile on presentation.
Aortic and mitral valvular endocarditis was documented in the dogs of this study, which was compatible with prior reports of bacterial endocarditis in dogs.8,11–14 In humans, mitral and aortic valvular bacterial endocarditis has been linked to cerebrovascular complications.15 Echocardiography may identify valvular insufficiency and/or vegetative lesions on affected valve leaflets in dogs with bacterial endocarditis [Figure 2].
A positive blood culture is considered the best method to diagnose bacterial endocarditis in dogs, and susceptibility results can guide the therapy chosen.2,11,14 Commonly implicated organisms in canine endocarditis include Streptococcus spp., Staphylococcus spp., and E. coli.14 In the study reported here, none of the dogs had blood cultures performed. Commonly cultured organisms in affected people are Staphylococcus aureus, Enterobacteriaceae, E. coli, and Streptococcus pneumoniae, and the risk of neurological complications increases with bacterial virulence.16 Staphylococcus aureus endocarditis results in neurological disease (67% of affected people in one report) more often than Streptococcus viridans (22%) infections.15,17
Thromboembolism may be more likely with rapid development of large, friable vegetations in acute bacterial endocarditis rather than the slowly progressive lesions that occur with subacute bacterial endocarditis. In addition, a strong immune response produces circulating immune complexes that may lead to vasculitis, which in turn may predispose to thrombosis.2,3 In humans, vegetations identified on two-dimensional echocardiography that are >10 mm in size are associated with a higher risk of embolization.2,16
A presumptive diagnosis of vascular encephalopathy was made in case no. 3 based upon the acute onset of brain dysfunction that subsequently resolved with antimicrobial therapy administered for bacterial endocarditis. The diagnosis was confirmed on postmortem examination of three dogs. In people, the diagnosis of vascular encephalopathy depends largely on a history of acute-onset, nonprogressive CNS signs that may slowly improve over time.17 Onset of neurological signs usually occurs early (within 48 hours of presentation), before bacterial infections are controlled. Though signs typically are nonprogressive, neurological status may deteriorate over the first few days secondary to brain edema or hemorrhage associated with the infarction.3 In dogs and humans, cerebrospinal fluid analysis may be normal, have elevated protein levels, hemorrhage, xanthochromia, or neutrophilic or mononuclear pleocytosis.3,15–17 Imaging studies such as CT or magnetic resonance imaging (MRI) in dogs may help to rule out other causes of focal brain disease, to identify hemorrhage, and to evaluate the extent of disease.18,19 Cerebral angiography has been used to diagnose vascular encephalopathy in people; but it is no longer recommended, because CT and MRI are less invasive and provide more specific information.16,17,20–22 Angiography is not used in dogs because of its high morbidity.10 Brain scintigraphy may identify focal infarctions or hemorrhage, but it lacks sensitivity in distinguishing such lesions from other focal brain diseases.3
Complete resolution of neurological signs occurred in case no. 3 with empirical antimicrobial therapy. Therapy for thromboembolic events includes supportive care and treatment of bacterial endocarditis. Appropriate control of the infection is necessary to reduce the risk of bacterial embolization. Therapy is usually continued for at least 6 to 8 weeks because of the low antimicrobial penetrance of vegetative lesions. In many cases, antimicrobial therapy may be needed long term, and some dogs require antibiotics indefinitely.14 In people, proper antimicrobial therapy has been shown to dramatically decrease the risk of embolization.2,20,23 The rate of embolic events drops more than tenfold in the first 2 weeks of therapy.2
Anticoagulant therapy was advocated in the past for people to improve penetration of vegetations by reducing platelet aggregation, but it has been linked to an increased risk of intracranial hemorrhage and has not been proven to be protective against thromboembolic disease.2,20–25 Valve replacement surgery is employed in 20% to 25% of human bacterial endocarditis cases and has been shown to reduce the risk of major embolic events, especially if performed early in the course of disease.2,20–25 Valve replacement surgery has not been performed in dogs with bacterial endocarditis; but with the increasing availability of cardiopulmonary bypass procedures, the use of surgical intervention for these dogs warrants evaluation.
Prognosis for survival in affected humans with vascular encephalopathy is dramatically worse, with a 1.6 to 3.2 times greater mortality than for patients without neurological complications.2,20 Vascular encephalopathies in dogs tend to be less devastating than those in humans, and some dogs improve with supportive therapy.10 The major motor tracts (corticospinal tracts) in humans are interrupted with embolization of the middle cerebral artery, while the major motor tracts in dogs (rubrospinal tracts) run through the brain stem and are therefore less commonly affected. As a result, severe paresis occurs in more human stroke victims than in dogs.6
Overall mortality rates for bacterial endocarditis in dogs range from 47% to 80%.11–14 The most favorable prognosis reported in dogs occurred when only the mitral valve was involved (47% survived). In comparison, there was a >70% mortality rate in dogs with septic embolization.11 In the study reported here, three dogs were euthanized because of neurological deterioration; therefore, it appears that the development of neurological sequelae in dogs with endocarditis is a poor prognostic event.
Conclusion
Four dogs developed vascular encephalopathy secondary to bacterial endocarditis. The dogs were predominately large breeds, sometimes had fevers, and recently described cardiac murmurs. Three of the dogs were euthanized for progressive neurological signs, despite antibacterial therapy for endocarditis.
Tribrissen; Coopers Agropharm, Inc., Mundelein, IL 60060
Oxytetracycline; Fermenta Animal Health Co., Kansas City, MO 64153
Gentocin; Schering-Plough Animal Health, Kenilworth, NJ 07033
Azium; Schering-Plough Animal Health, Kenilworth, NJ 07033
Enacard; Merck, Rahway, NJ 07065
Prednisone Rx; West-ward Pharmaceutical Corp., Eatontown, NJ 07724
Amp-Equine; SmithKline Beecham, King of Prussia, PA 19406
Tagamet; GlaxoSmithKline, Pittsburgh, PA 15230
Carafate; Marion Merrell Dow, Inc., Kansas City, MO 64137
Clavamox; GlaxoSmithKline, Research Triangle Park, NC 27709
Baytril; Bayer, Shawnee Mission, KS 66201
Lasix; Fermenta Animal Health, Kansas City, MO 64153
Aldactone; Searle, Chicago, IL 60680
Coreg; GlaxoSmithKline, Research Triangle Park, NC 27709
Vetmedin; Boehringer Ingelheim, St. Joseph, MO 64506
Primaxin; Merck, West Point, PA 19486
Naxcel; Pharmacia & Upjohn, Kalamazoo, MI 49001
Panmycin; Pharmacia & Upjohn, Kalamazoo, MI 49001
Citation: Journal of the American Animal Hospital Association 41, 4; 10.5326/0410252
Citation: Journal of the American Animal Hospital Association 41, 4; 10.5326/0410252
Transverse computed tomographic images of the brain of case no. 4 without (A) and with (B) intravenous contrast administration. A hyperintense, well-defined mass is present in the region of the left piriform lobe (arrows). Minimal, uniform contrast enhancement is noted (B). There is also mild compression of the left lateral ventricle from the mass. R=right.
Two-dimensional echocardiogram. Right parasternal long-axis view of the aortic outflow tract. The aortic valve is thickened, has increased echogenicity, and there is a portion of the aortic valve that prolapses into the left ventricular outflow tract (arrows). These findings are consistent with aortic endocarditis. LV=left ventricle; LA=left atrium.
