1ST EDITION AUTHOR: DOUGLASS K. MACINTIRE

BASIC INFORMATION

DEFINITION

Canine babesiosis is a tickborne disease caused by a hemoprotozoan parasite that infects red blood cells of dogs causing hemolytic anemia and thrombocytopenia. Two primary species have been identified: Babesia canis (large Babesia) and Babesia gibsoni (small Babesia).

EPIDEMIOLOGY

DIAGNOSIS

DIAGNOSTIC OVERVIEW

Most dogs with babesiosis have one or more of the following abnormalities: thrombocytopenia, anemia, hyperglobu linemia or splenomegaly. PCR assays have become the primary means of accurately diagnosing Babesia infections.

TREATMENT

TREATMENT OVERVIEW

It may not be possible to completely eradicate the parasite in all cases, but clinical signs usually improve with supportive care and antiparasitic therapy. The treatment of choice is dependent upon which Babesia species is identified. Currently, most data are available for treatment of B. canis and B. gibsoni.

ACUTE GENERAL TREATMENT

Supportive treatment may require blood transfusion or hemoglobin polymer (e.g., Oxyglobin) for animals that are anemic:

• IV fluids may be required in animals that are febrile and dehydrated.

• Imidocarb diproprionate (6.6 mg/kg IM once, repeat in 7-14 days). Pretreatment with atropine (0.04 mg/kg IM or SQ 30 minutes before imidocarb injection) may reduce cholinergic side effects. This drug appears to reduce morbidity and mortality for nearly all Babesia spp. but is not effective for the clearance of B. gibsoni. It is the treatment of choice for B. canis vogeli.

• Atovaquone (13.5 mg/kg PO q 8 h with fatty meal for 10 days) plus azithromycin (10 mg/kg PO q 24 h for 10 days) is the treatment of choice for B. gibsoni. Results in elimination or reduction of the parasite below the limit of detection of PCR testing in ≈82% of cases. Resistance to atovaquone has been identified.

• Clindamycin (25 mg/kg PO BID for 14 days) has been associated with clinical improvement but not clearance of B. gibsoni.

• A combination of clindamycin (25 mg/kg PO BID), metronidazole (15 mg/kg PO BID), and doxycycline (5 mg/kg PO BID) had been associated with elimination or reduction of the parasite below the limit of detection of PCR testing. Unfortunately, a well-defined treatment course has not been established, with treatment times ranging from 24-92 days.

• Concurrent immune suppression should be avoided whenever possible, as it may reduce the ability to clear the infection with antiprotozoal drugs.

CHRONIC TREATMENT

• Vector control: topical acaricide (e.g., fipronil) plus flea/tick collar

• Dogs with positive Babesia titers or PCR should not be used as blood donors.

POSSIBLE COMPLICATIONS

Prolonged immunosuppressive therapy before specific antibabesial treatment can worsen outcome and should not be used in sick, hospitalized dogs.

RECOMMENDED MONITORING

• Monitor hematocrit and platelet count daily until improvement is seen and then every 1-3 weeks until anemia and thrombocytopenia resolve.

• PCR should be negative 60 and 90 days post treatment if the parasite has been successfully eradicated.

BASIC INFORMATION

DEFINITION

Pain localized to the thoracolumbar spinal column

SYNONYMS

Spinal hyperesthesia, spinal hyperpathia

DIAGNOSIS

DIAGNOSTIC OVERVIEW

Back pain often presents nonspecific physical signs (or absence of any observable deficits) and gentle, thorough physical manipulations during the physical examination are used for eliciting signs of back pain. Diagnostic imaging and specific techniques then help to elucidate the source of the pain.

INITIAL DATABASE

• Neurologic examination (see p. 1311)

• CBC, serum biochemistry, urinalysis: often unremarkable unless systemic disease or infection present

• Radiographs: bone lysis or proliferation (neoplasia, osteomyelitis), vertebral fracture or luxation (trauma), intervertebral disk mineralization, disk space narrowing, wedging or displacement (IVDD), vertebral endplate lysis or proliferation (diskospondylitis), articular facet sclerosis and malformation, spondylosis

ADVANCED OR CONFIRMATORY TESTING

Selection based on history, clinical signs, and results of initial database:

• Cerebrospinal fluid tap: cytologic evaluation, culture, serologic testing for immunoglobulin A (IgA) or infectious agents

• Myelogram: identify and discern between extradural compression (IVDD), intradural/extramedullary lesion (meningioma), or intramedullary lesion (other neoplasia or cord swelling [e.g., due to FCE])

• Urine culture (diskospondylitis)

• Blood culture and sensitivity (discospondylitis, osteomyelitis, bacterial meningitis)

• Needle aspirate of intervertebral disk (diskospondylitis)

• Serology: Brucella canis (discospondylitis), rickettsial diseases (polyarthritis, meningitis)

• Arthrocentesis: cytology (polyarthritis), culture (septic polyarthritis or meningitis)

• Advanced imaging: CT or MRI if lesion is suspected but not identified on myelogram

• Biopsy of vertebral bone (neoplasia, osteomyelitis)

TREATMENT

CHRONIC TREATMENT

• Degenerative joint disease may require persistent or recurrent nonsteroidal antiinflammatory drug (NSAID) administration.

• Chronic intervertebral disk disease or immune-mediated disease may require intermittent or persistent corticosteroid treatment.

• Antibiotic therapy for diskospondylitis (see p. 312) or vertebral osteomyelitis continued for 6 weeks beyond resolution of clinical signs.

DRUG INTERACTIONS

Corticosteroids and NSAIDs must not be administered concurrently, owing to the risk of severe gastrointestinal ulceration.

POSSIBLE COMPLICATIONS

• Worsening or recurrence of signs

• Progression of spinal cord lesions

• Myelomalacia

• Valvular endocarditis, for infectious conditions

RECOMMENDED MONITORING

• Repeat physical and neurologic examination within 12 to 24 hours of treatment

• Follow-up examination and radiographs as needed

PROGNOSIS AND OUTCOME

Variable, depending on underlying cause

BASIC INFORMATION

DEFINITION

Syndrome developing following the ingestion of one of several centrally-acting skeletal muscle relaxants (SMR) and characterized mainly by central nervous system (CNS) depression.

SYNONYMS

Generic Name	Trade Name(s)
Baclofen	Lioresal, Kemstro
Carisoprodol	Soma
Chlorphenesin carbamate	Maolate
Chlorzoxazone	Parafon Forte
Cyclobenzaprine	Flexeril
Guaifenesin	Gecolate
Metaxalone	Skelaxin
Methocarbamol	Robaxin, Robaxin-V
Orphenadrine	Norflex
Tizanidine	Zanaflex

CLINICAL PRESENTATION

HISTORY, CHIEF COMPLAINT

History of exposure to muscle relaxants or presence of drugs in environment (see Table).

Drug	Chief Complaint
Baclofen	Onset of signs within 15 minutes to 7 hours following ingestion Dogs: vomiting, ataxia, hypersalivation, depression, vocalization, disorientation/agitation, recumbency, coma, seizure Cats: vomiting, depression, ataxia, weakness, hypothermia, recumbency, coma, mydriasis, diarrhea
Cyclobenzaprine	Onset within 30 minutes to several hours Depression, ataxia, vomiting, weakness, mydriasis, tachycardia, vocalization, agitation, tremors, seizures
Orphenadrine	Onset within 30 minutes to several hours Weakness, vomiting, tachycardia, agitation, seizures
Tizanidine	Onset within 30 minutes to 4 hours Lethargy, somnolence, bradycardia, hypotension, recumbency, weakness, vocalization, urinary retention, collapse, coma
Other SMRs: carisoprodol, chlorphenesin carbamate, chlorzoxazone, metaxalone, methocarbamol, and guaifenesin	Stupor, hypotension, coma, respiratory depression, seizures (rare)

PHYSICAL EXAM FINDINGS

• Tizanidine

○ Depression, weakness, ataxia

○ Hypotension, bradycardia

○ Pale mucous membranes, prolonged capillary refill time

○ Hypothermia

• Other SMR

○ Depression, somnolence, weakness

○ Hypoventilation, cyanosis

○ Tachycardia, hypotension

○ Hypothermia (if recumbent), hyperthermia (if seizuring)

ETIOLOGY AND PATHOPHYSIOLOGY

Source

• Most centrally acting SMRs are used for controlling spasticity in humans with neuromuscular disorders. May also be prescribed for relief of musculoskeletal pain.

Mechanism of Toxicosis

• Baclofen: Mimics gamma-aminobutyric acid (GABA) within the spinal cord, blocking excitatory responses to sensory input and causing flaccid paralysis. Baclofen-induced seizures may be due to interference with GABA release from presynaptic neurons, resulting in excessive postsynaptic nerve firing.

• Cyclobenzaprine: Structurally and functionally related to tricyclic antidepressants. Skeletal muscle relaxation may be related to sedative effects as well as inhibition of brainstem and spinal cord gamma and alpha motor neurons. In overdose situations, anticholinergic and antihistaminic effects become exaggerated.

• Tizanidine has a mechanism of action similar to that of xylazine and clonidine, in that it stimulates alpha-adrenoreceptors in the brainstem, causing decreased vascular resistance, heart rate, and blood pressure. At therapeutic levels, skeletal muscle effects predominate, but in overdose situations, pronounced cardiovascular effects occur.

• Orphenadrine has pronounced anticholinergic and antihistaminic effects.

• Chlorphenesin carbamate, guaifenesin, and methocarbamol may act by blocking nerve impulse transmission within the brainstem, spinal cord, and subcortical levels of the brain. Some of the skeletal muscle relaxant effect is due to sedation.

• Carisoprodol causes skeletal muscle relaxation via depression of postsynaptic spinal reflexes. Some of the skeletal muscle relaxant effect is due to sedation.

• Chlorzoxazone and metaxalone have no direct effect on skeletal muscles; muscle relaxant properties are likely due to sedative effects.

DIAGNOSIS

DIAGNOSTIC OVERVIEW

Diagnosis is based on history of exposure or presence of drugs in animal’s environment along with appropriate clinical signs (ataxia, depression, coma, vocalization).

INITIAL DATABASE

• CBC, serum biochemistry profile: minimal alterations expected from SMR (identify preexisting liver or kidney dysfunction that may interfere with drug elimination)

○ Orphenadrine overdose in humans has been associated with hypokalemia, hypoglycemia, liver enzyme elevations, and bleeding disorder.

TREATMENT

TREATMENT OVERVIEW

Treatment is aimed at early decontamination of the patient (emesis induction then administration of activated charcoal) when clinical signs are absent, and supportive care to address overt signs when they are present.

ACUTE GENERAL TREATMENT

• Stabilize patient

○ Maintain respiration: endotracheal intubation and positive-pressure mechanical ventilatory support may be required.

○ Control seizures: diazepam (0.5-1 mg/kg slow IV, to effect); propofol or isoflurane may be considered in cases refractory to diazepam (induce, keep anesthetized 5-10 minutes, then recover). Barbiturates should be considered a last resort, as their use may result in severe exacerbation of CNS depression; diazepam also generally useful for managing agitation.

• Manage cardiovascular abnormalities: most arrhythmias and blood pressure irregularities resolve during supportive care. Nitroprusside constant-rate IV infusion (1-2 mcg/kg/min [dogs] or 0.5 mcg/kg/min [cats], increased incrementally q 3-5 min until target BP is obtained) has been successfully used to manage baclofen-induced hypertension in dogs. Use of atropine to manage bradycardia is contraindicated in orphenadrine or cyclobenzaprine toxicosis, because it exacerbates anticholinergic effects.

• Supportive care:

○ Intravenous fluid therapy: as needed for hypotension/hypovolemia and to promote urine formation; may enhance excretion of baclofen

○ Atipamezole (50 mcg/kg, give ¼ to ⅓ of dose IV, remainder IM) or yohimbine (0.025 mg/kg slow IV) can be helpful to reverse hypotension from tizanidine.

○ Cyproheptadine (1.1 mg/kg PO or per rectum q 6 h) has been helpful in reducing vocalization in dogs.

○ Thermoregulation is essential, especially in comatose or recumbent animals.

• Decontamination of patient (no clinical signs):

○ Emesis (see p. 1364): Because of the potential for rapid onset of clinical signs, induction of emesis is best done under veterinary supervision (hydrogen peroxide 3%: 0.25-0.5 mL/kg PO once [dogs] or xylazine hydrochloride 0.44 mg/kg IM [cats]). Emesis is contraindicated in animals showing overt clinical signs.

○ Gastric lavage (see p. 1281): Consider for large ingestions (many tablets); protect airway with cuffed endotracheal tube.

○ Activated charcoal (see p. 1322): dose according to packaging label of product (e.g., 10 mL/kg of activated charcoal suspension PO made from 2 g activated charcoal suspended in 10 mL kg tap-water). Repeated doses of activated charcoal q 8 h × 24 h and a cathartic, given every 3rd charcoal dose, are recommended for cyclobenzaprine and orphenadrine; single doses are recommended for all other SMRs.