PCR detection of Anaplasma platys in blood and tissue of dogs during acute phase of experimental infection.

Four dogs were experimentally infected with Anaplasma platys to determine changes in real-time TaqMan PCR detection in blood and tissue, microscopically detectable parasitemia, and platelet concentrations during the first 28 days of infection. Buffy-coat blood cells were PCR positive for A. platys DNA at 4 days after inoculation and remained positive in all dogs until day 14. Marked thrombocytopenia and low parasitemia occurred in dogs during that initial period. During 17 and 28 days post-inoculation, the PCR results on buffy-coat blood cells were intermittently negative in each dog with marked thrombocytopenia and no microscopic evidence of parasitemia. Bone marrow and splenic aspirates collected from the A. platys-infected dogs were tested by real-time TaqMan PCR. Two dogs were PCR positive in spleen and marrow at 28 days post-inoculation, when PCR results for buffy-coat blood cells were negative. Spleen and/or bone marrow samples should be considered as additional samples for PCR testing of dogs, particularly when blood samples are PCR negative during the acute phase of A. platys infection.

Doxycycline clearance of experimentally induced chronic Ehrlichia canis infection in dogs.

BACKGROUND: Ineffective clearance of Ehrlichia canis after doxycycline administration has been reported despite the fact that the recommended treatment for canine ehrlichiosis is doxycycline. The effectiveness of doxycycline in clearing E canis infection from the blood and tissues of dogs requires additional evaluation. HYPOTHESIS: Doxycycline (5 mg/kg PO q12h), administered for 4 weeks, will eliminate E canis infection from the blood and tissues of experimentally infected dogs. ANIMALS: Fifteen Walker hound-mixed breed dogs were inoculated subcutaneously with E canis-infected canine histiocytic cells 4 months before doxycycline treatment. METHODS: Four dogs were treated with doxycycline (5 mg/kg PO q12h for 3 weeks), 5 dogs were treated with doxycycline at the same dosage for 4 weeks, and 5 control dogs were not treated. Dexamethasone (0.4 mg/kg i.v.) was given after treatment to precipitate recrudescence of any remaining E canis organisms. Platelet counts, anti-E canis immunofluorescent antibodies, and polymerase chain reaction (PCR) detection of E canis deoxyribonucleic acid (DNA) in blood and tissues were evaluated. RESULTS: E canis DNA was not detected in the blood and tissues of doxycycline-treated dogs after treatment. Platelet counts were within reference intervals, and E canis antibodies decreased. Spontaneous clearance of E canis infection occurred in 2 of 5 control dogs. Three control dogs had E canis DNA detected in blood and tissues, platelet counts remained low or within the reference interval, and E canis antibodies remained high. CONCLUSIONS AND CLINICAL IMPORTANCE: As administered in this study, doxycycline cleared E canis from the blood and tissues of experimentally infected dogs.

Failure of imidocarb dipropionate to clear experimentally induced Ehrlichia canis infection in dogs.

The recommended treatment for canine ehrlichiosis is tetracycline or its analog doxycycline, although recent reports have documented ineffective clearing of Erchlichia canis after doxycycline administration. Imidocarb dipropionate is used as an alternative treatment to tetracycline or is used in conjunction with doxycycline. The effectiveness of imidocarb dipropionate in clearing Ehrlichia species from the blood and tissues of dogs with E. canis infection has not been thoroughly evaluated. Fifteen dogs were experimentally infected with E. canis. Ten dogs were treated with imidocarb dipropionate (6.6 mg/kg, IM, 2 injections given 2 weeks apart). Five infected control dogs were not treated. Blood samples from all 15 dogs were E. canis DNA positive by PCR assay by 3 weeks after inoculation (PI), and E. canis antibodies were detected by IFA assay by 1 week PI. Blood platelet counts in all dogs were below the reference interval by 4 weeks PI. E. canis DNA was detected in bone marrow and splenic aspirates by PCR assay 4 weeks PI but not before infection. Bone marrow aspirates were E. canis DNA positive by PCR assay in 14/15 dogs, and splenic aspirates were E. canis DNA positive by PCR assay in 13/15 dogs. Blood samples from all treated and control dogs remained positive for E. canis DNA by PCR assay, and platelet counts remained below preinoculation values 13 weeks PI (6 weeks after 2nd treatment). As administered in this study, imidocarb dipropionate did not clear experimental E. canis infection in dogs.

Consensus statement on ehrlichial disease of small animals from the infectious disease study group of the ACVIM. American College of Veterinary Internal Medicine.

Within the past several decades, the number of Ehrlichia spp. recognized to infect cats, dogs, and human beings has expanded substantially. The recent application of advanced techniques in molecular biology has changed how ehrlichiosis is diagnosed and has provided new tools for the assessment of treatment. As these techniques are applied, the numerous questions that relate to the management of dogs and cats with ehrlichiosis ultimately will be answered. We hope this consensus statement will assist veterinarians in the management of their patients.

Familial cerebellar ataxia with hydrocephalus in bull mastiffs.

Familial cerebellar ataxia with concurrent hydrocephalus has previously been described in a family of bull mastiff pups, and recently has been identified in a litter from Louisiana. The 4 affected pups had ataxia, hypermetria, conscious proprioceptive deficits, behavioral abnormalities, and a visual deficit. In magnetic resonance imaging of the brain of two of the pups, there were symmetric hydrocephalus and two focal areas of increased signal intensity within the central nuclei of the cerebellum. Histopathologically there was vacuolization and mild astrogliosis within the deep cerebellar nuclei (dentate, interpositus, fastigial), caudal colliculi, and lateral vestibular nuclei. Although the postmortem results were not exactly the same as in the previously published report, the clinical features and histopathologic findings strongly support the diagnosis. This disorder is most likely inherited in an autosomal recessive manner.

Ototoxicity assessment of a gentamicin sulfate otic preparation in dogs.

Vestibulotoxic and ototoxic effects often are seen after long-term, high-dose systemic treatment with gentamicin, but toxic effects after topical use have not been reported in animals, to the authors' knowledge. Vestibular and auditory effects of twice daily otic gentamicin treatment for 21 days were evaluated in 10 dogs with intact tympanic membranes and in the same 10 dogs after experimental bilateral myringotomy. Each dog served as its own control; 7 drops of gentamicin sulfate (3 mg/ml in a buffered aqueous vehicle) were placed in 1 ear, and 7 drops of vehicle were placed in the opposite ear. Treatment and control ears were reversed after myringotomy. Vestibular function was evaluated daily by neurologic examination and behavioral assessment. Auditory function was evaluated twice weekly by determination of brain stem auditory evoked potentials. Gentamicin sulfate placed in the ear of clinically normal dogs with intact or ruptured tympanic membranes, in the quantities used in this study, did not induce detectable alteration of cochlear or vestibular function. Serum gentamicin concentration after 21 days of treatment was detectable in only 2 dogs and was an order of magnitude below documented toxic concentrations.

Leucoencephalomalacia and cerebral white matter vacuolar degeneration in two related Labrador retriever puppies.

Two Labrador Retriever dogs from a common dam had similar neurological deficits consisting of cortical blindness, dullness, and loss of previously learned habits. Both were examined at 5 months of age, and histopathological examination revealed leucoencephalomalacia and vacuolar degeneration of the cerebral white matter. Histopathologic findings in these 2 dogs differed from those reported previously in Labrador Retrievers with spongy degeneration of central nervous system white matter. A nonlittermate full sibling to 1 of these dogs was examined at 1.5 years of age for similar clinical signs that did not progress for the next 25 months.

Ivermectin toxicosis in a kitten.

A 4-month-old female kitten developed generalized ataxia, mild tremors, weakness, incoordination, and miosis after receiving an injection of ivermectin (0.3 mg/kg of body weight, SC) for treatment of ear mite infestation. The kitten became comatose within 12 hours, and despite supportive treatment, died 7 days after administration of ivermectin. Caution should be exercised when this drug is administered parenterally to kittens.

Fibrocartilaginous emboli.

Fibrocartilaginous embolism (FCE) is an acute ischemic myelopathy, primarily of large or giant breed dogs, which results from occlusion of blood vessels within the spinal cord parenchyma or the adjacent leptomeninges by masses of fibrocartilage. Lateralizing and asymmetric neurologic deficits are very suggestive of spinal cord infarction. The diagnosis of FCE is made by eliminating causes of acute compressive myelopathy such as trauma and intervertebral disc herniation. Patients with lower motor neuron deficits secondary to FCE have a more guarded prognosis than those with upper motor neuron deficits. In most instances, if recovery is to occur, improvement will be evident within the first 10 days after the onset of clinical signs.

Hypoprothrombinemia secondary to administration of sulfaquinoxaline to dogs in a kennel setting.

Sulfaquinoxaline, a coccidiostat readily available to the public, was mixed in the drinking water for this purpose by the owner. Secondary to its use, a bleeding disorder attributable to hypoprothrombinemia developed in several dogs. Clinical signs of bleeding ceased 24 hours after institution of vitamin K1 and discontinuation of sulfaquinoxaline in the drinking water. This report should remind veterinarians that drugs and medications readily available to the public may have adverse effects in animals, and such problems should be investigated whenever multiple dogs in a common setting are affected with the same clinical problem.

A review of disorders of the gallbladder and extrahepatic biliary tract in the dog and cat.

Disorders of the gallbladder and extrahepatic biliary tract in the dog and cat can easily be confused with other intra-abdominal disorders. This confusion results because many times the clinical course and signs of biliary tract disease are similar to these other intra-abdominal disorders. This review discusses the normal anatomy and physiology of the gallbladder, bile duct, and bile in the dog and cat and then summarizes the historic, physical examination, clinicopathologic, diagnostic, histologic and therapeutic aspects of all the cases of extrahepatic biliary tract disease reported in the veterinary literature.

Recurring tetraparesis attributable to a heartworm in the epidural space of a dog.

Recurring nonambulatory tetraparesis caused by a heartworm in the epidural space was diagnosed in a dog. On myelography and digital subtraction imaging, the parasite appeared as a large extradural mass. Surgical removal of a mature, female Dirofilaria immitis resulted in resolution of the neurologic signs.

Cervical spinal cord astrocytoma in a dog.

An astrocytoma of the cervical spinal cord was diagnosed in a 3-year-old Siberian Husky. The dog had an 8-week history of progressive neurologic deficits that finally resulted in nonambulatory tetraparesis. Neurologic examination, CSF analysis, myelography, exploratory laminectomy and histopathologic examination were performed. Intramedullary spinal cord tumors such as astrocytomas are rare, and this case illustrates the manner in which spinal cord tumors may be confused with other nervous system diseases, both from a clinical and clinicopathologic standpoint.

Clinical failure of streptokinase due to an unsuspected high titer of antistreptokinase antibody.

Neutralization of streptokinase by an unsuspected high titer of antistreptokinase antibody prevented activation of the fibrinolytic system and induction of a lytic state in a 62 year old man with an acute inferior myocardial infarction. There was no decrease in serum fibrinogen, minimal decrease in serum plasminogen and only a small increase in serum fibrin degradation products after intravenous administration of 1.5 million units of streptokinase. A high titer of antistreptokinase antibody, sufficient to neutralize 1.5 million units of streptokinase, was demonstrated by semiquantitative counterelectrophoresis . There was no clinical evidence of coronary artery reperfusion, and coronary angiography confirmed complete occlusion of the left circumflex artery.