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Echinococcosis
BASIC INFORMATION
DEFINITION
• Cestode (tapeworm) infection with larval stages (hydatid cysts) that causes hydatid disease, primarily in humans:
• Hydatid cyst disease refers to the clinical condition in which intermediate hosts have multiple, often large intraparenchymal cysts containing brood capsules that in turn contain protoscolices in serous fluid.
EPIDEMIOLOGY
SPECIES, AGE, SEX
• E. granulosus definitive hosts are dogs and other canids; intermediate hosts are sheep, goats, swine, cattle, horses, camels, and humans.
• E. multilocularis definitive hosts are foxes and less frequently dogs, cats, coyotes, and wolves. Intermediate hosts are small rodents.
RISK FACTORS
Exposure and ingestion of intermediate hosts (rodents, cattle, sheep) harboring the hydatid cysts
CONTAGION & ZOONOSIS
• Humans (and other suitable intermediate hosts) become infected by ingestion of eggs from the feces of definitive hosts.
CLINICAL PRESENTATION
HISTORY, CHIEF COMPLAINT
• Clinical signs of hydatid disease in domesticated animals are uncommon; humans are most commonly affected by disease.
• Intermediate host’s signs relate to location and size of cyst and the species of Echinococcus infecting the host.
ETIOLOGY AND PATHOPHYSIOLOGY
• E. granulosus adults reside in the small intestine of the definitive host (dogs, coyotes, wolves).
• Eggs are passed into the feces where they are ingested by an intermediate host (e.g., cattle, sheep, horses).
• In the intermediate host, the organism invades the small intestine and spreads through the circulatory system, entering organs of predilection. The organism develops into a thick-walled unilocular (single compartment) cyst that gradually enlarges.
• Definitive host becomes infected by ingestion of raw hydatid cyst within the visceral organs of intermediate hosts.
• E. multilocularis larval growth remains in the proliferative stage, resulting in invasion of surrounding tissues. The liver is primarily affected, with occasional metastasis to the brain and lungs. The organism develops into a thin-walled multilocular (demonstrating many compartments) cyst that easily spreads, thus overtaking the affected organs.
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
Other taeniids, to include many tapeworms within the genera Taenia and Multiceps.
TREATMENT
TREATMENT
• Hydatids require surgical removal from humans who serve as intermediate hosts. The thick-walled unilocular cysts of E. granulosus are less difficult to remove, but the thin-walled multilocular cysts of E. multilocularis are quite invasive and almost impossible to remove. The organs infected by the hydatid cyst will also affect the prognosis.
PEARLS & CONSIDERATIONS
PREVENTION
• Hygiene, to avoid human acquisition of the infection through fecal-oral contamination from dogs and cats
Eckert J, Thompson RC, Bucklar H, Bilger B, Deplazes P. Efficacy evaluation of epsiprantel (Cestex) against Echinococcus multilocularis in dogs and cats. Berl Munc Tierarztl Wochenchr. 2001;114(3–4):121-126.
Jenkins DJ, Romig T. Milbemycin oxime in a new formulation, combined with praziquantel, does not reduce the efficacy of praziquantel against E. multilocularis in cats. J Helminthol. 2003;77(4):367-370.
Eclampsia 
BASIC INFORMATION 
EPIDEMIOLOGY
GENETICS & BREED PREDISPOSITION
More likely to occur in small-breed dogs, although any lactating bitch may be affected
CLINICAL PRESENTATION
HISTORY, CHIEF COMPLAINT
Lactating bitch with signs of aberrant behavior, ataxia, muscle tremors, seizures, and/or tetany
TREATMENT 
ACUTE GENERAL TREATMENT
• Intravenous (IV) administration of a 10% calcium gluconate or calcium borogluconate solution slowly, at a rate of 1-1.5 mL/kg over 10-30 minutes or until resolution of clinical signs.
○ Calcium chloride solutions are not recommended; risk of perivascular corrosive effects if the solution extravasates.
• IV calcium gluconate administration may be repeated in the event of a relapse; refractory cases should be reevaluated for hypoglycemia.
• The IV dose of calcium gluconate required to resolve clinical signs can be diluted 1:1 in saline for subcutaneous administration in 3 equal doses over 24-48 hours to prevent immediate relapse.
CHRONIC TREATMENT
• Remove puppies for 24-36 hours to reduce maternal calcium loss through lactation; in the event of recurrence, remove puppies permanently.
• Puppies can be fed milk replacer every other day to decrease lactation demand on the bitch until weaning at age 3 weeks.
NUTRITION/DIET
PROGNOSIS AND OUTCOME 
Prognosis is good to excellent with immediate treatment and subsequent management.
PEARLS & CONSIDERATIONS 
COMMENTS
• Preventive prepartum calcium supplementation is not recommended, as it may promote the development of eclampsia.
• Preventative postpartum calcium supplementation is recommended, as it may prevent recurrence during a subsequent lactation.
Edema, Subcutaneous
BASIC INFORMATION 
SYNONYMS
Peripheral edema (edema of the paws and legs), anasarca (generalized, massive subcutaneous edema)
CLINICAL PRESENTATION
HISTORY, CHIEF COMPLAINT
Limb swelling or a swollen appearance may be historical findings suggestive of subcutaneous edema.
PHYSICAL EXAM FINDINGS
• The hock with its lateral saphenous vein, the Achilles tendons, and the bony prominence of the mandible are useful to evaluate for subcutaneous edema; these areas are well defined even in obese animals.
• Edema is by definition nonpainful and neither very warm nor very cool to the touch unless secondary infection is present.
• Edema tends to accumulate where gravity draws it, where lymphatic obstruction or insufficiency is greatest, or a combination of both. Therefore, the pattern of edema distribution can be variable.
• It may be possible to “pit” edema: digital pressure exerted on edematous skin may leave a depression, or pit, for several seconds after the pressure is released. Pitting edema represents interstitial fluid accumulation, whereas nonpitting edema is formed by intra-cellular swelling (e.g., a wheal). In dogs and cats, pitting edema is more common than nonpitting edema.
• Hyperemia, or the reddening of the subcutaneous tissue due to engorgement of oxygenated blood, indicates an active process causing arteriolar dilation. Congestion, or the cyanotic (“blue-red”) appearance of the subcutaneous tissue, is a passive process that occurs as worsening congestion leads to accumulation of deoxygenated hemoglobin. Capillary bleeding can occur uncommonly as a result of chronic congestion and may appear as petechiae, purpura, ecchymosis, or hematoma.
TREATMENT 
ACUTE AND CHRONIC TREATMENT
• Management of subcutaneous edema is typically nonemergent and is primarily achieved by treatment of the underlying condition while considering specific therapies to restore water balance within the body.
• Patients with decreased oncotic pressure (hypoproteinemia), decreased osmotic balance (anemia), or increased endothelial permeability (inflammation) may benefit from plasma products, hetastarch, or dextran 70 to increase intravascular volume and favor water retention within the vasculature.
• Patients with increased hydrostatic pressure secondary to severe right-sided heart failure can benefit from potent loop diuretics such as furosemide. Furosemide causes increased sodium excretion by the kidneys, with resultant water loss and edema mobilization from the interstitial tissues.
PROGNOSIS AND OUTCOME 
The prognosis for patients with subcutaneous edema depends on the underlying condition and the ability to treat and resolve this primary disease. Edema due to inflammation or infection, congestive heart failure, or hypoproteinemia can often be successfully managed or resolved. Treatment response for lymphatic obstruction is variable; lymph-edema (see p. 667) can be challenging to manage long term, and there is no curative therapy.
Mathews KA. Monitoring fluid therapy and complications of fluid therapy. In: Dibartola SP, editor. Fluid, electrolyte, and acid-base disorders in small animal practice. ed 3. St Louis: Elsevier Saunders; 2006:385.
Raffe MR, Roberts J. Edema. In: Ettinger SJ, Feldman EC, editors. Veterinary internal medicine. ed 6. St Louis: Elsevier Saunders; 2005:70.
Ehrlichiosis, Canine Monocytic
BASIC INFORMATION 
EPIDEMIOLOGY
GENETICS & BREED PREDISPOSITION
German shepherd dogs have a more fulminant illness, owing to reduced cellular immune response.
CLINICAL PRESENTATION
DISEASE FORMS/SUBTYPES
HISTORY, CHIEF COMPLAINT
• Overt signs: depression, anorexia, weight loss, ocular or nasal discharge, bleeding tendencies, lameness.
PHYSICAL EXAM FINDINGS
• Bleeding disorders: cutaneous and/or mucosal petechiae, ecchymoses, unilateral or bilateral epistaxis, melena, retinal hemorrhage, hyphema
• Signs of uveitis: blepharospasm, photophobia, excessive lacrimation, hyperemia of scleral vessels, and decreased intraocular pressure. Blindness due to retinal detachment can occur.
• Neurologic signs: ataxia, seizures, vestibular signs, anisocoria, and hyperesthesia (severe cases)
ETIOLOGY AND PATHOPHYSIOLOGY
• Ticks acquire the organism by feeding as either larvae or nymphs on infected animals. No transovarial transmission occurs in the tick (i.e., life cycle requires the mammal).
• When an infected tick ingests a blood meal, the organism is transmitted via saliva to the vertebrate host.
• Infection leads to multiplication in mononuclear cells and tissues (spleen, liver, and lymph nodes).
• Infected cells attach to vascular endothelium in lungs, kidneys, joints, myocardium, and meninges, leading to vasculitis and subendothelial tissue infection and the acute phase of disease initially.
• Thrombocytopenia occurs secondary to increased platelet consumption and decreased platelet half-life, as a result of antiplatelet antibodies production, platelet migration-inhibition factor production, and splenic sequestration.
• Dysfunction of remaining platelets (thrombocytopathy) may occur secondary to antiplatelet antibodies binding to platelet receptors.
• Systemic inflammation may occur, with varying degrees of thrombosis, hyperviscosity, and red cell destruction.
DIAGNOSIS 
INITIAL DATABASE
• CBC, serum biochemistry profile, urinalysis
○ Thrombocytopenia (mild to severe) is the typical finding in all stages of illness, but absence does not rule out ehrlichiosis.
○ Neutropenia, nonregenerative anemia, lymphocytosis (sometimes marked), monocytosis, and eosinophilia may be observed.
○ Hyperglobulinemia is common; polyclonal gammopathy is typical, but in rare cases a monoclonal gammopathy is present.
• Arthrocentesis and limb radiography if signs of polyarthritis. Sterile, nonerosive polyarthritis with predominance of nondegenerate neutrophils may occur.
ADVANCED OR CONFIRMATORY TESTING
• Buffy coat, blood smear evaluation: rarely identify morulae in mononuclear cells (many false-negative results)
• Serologic titers: IFA or ELISA (antibody tests):
○ Negative results may occur in acute cases. Confirmation with a convalescent titer (2–4 weeks later; ≥fourfold increase) is necessary for definitive diagnosis.
○ Positive results suggest exposure, not infection. Antibody titers can persist from months to more than a year.
• PCR amplification: may be applied to tissue or whole blood. It provides definitive diagnosis, since it can differentiate between A. phagocytophilum, A. platys, E. canis, E. chaffeensis, E. ewingii, and other bacteria from the Anaplasmataceae family. False-negative PCR tests can occur if low numbers of circulating organisms.
TREATMENT 
TREATMENT OVERVIEW
• The treatment of choice for both E.canis and E. chaffeensis infection is doxycycline or tetracycline, with rapid clinical improvement (beginning within 24-48 hours) in the majority of cases. Dogs with slow or partial recovery might be coinfected with other tickborne organisms. There is no consensus whether or not the antibiotic therapy clears these organisms from infected dogs, and chronic subclinical infections may be possible. Some manifestations such as glomerulonephritis may persist after treatment, but progression should be halted.
ACUTE GENERAL TREATMENT
• Supportive care depends on clinical manifestation (i.e., transfusions for anemia, analgesics for polyarthritis pain).
• The authors do not routinely use corticosteroids for the treatment of ehrlichiosis. Reduction of ehrlichial antigens through appropriate antibiotic therapy should reduce secondary immune-mediated pathology. Despite being controversial, some clinicians have used corticosteroids at immunosuppressive doses (e.g., prednisone, 2–4 mg/kg PO q 24 h during first 2–7 days of acute stage).
DRUG INTERACTIONS
• Tetracycline derivatives should not be used in the last half of pregnancy. Oral doxycycline should be given with food to avoid GI effects (nausea and vomiting). Tetracycline derivatives should not be given concomitant with oral antacids, cathartics, or other GI products containing cations (aluminum, calcium, magnesium, zinc, or bismuth).
PROGNOSIS AND OUTCOME 
• Good prognosis with quick improvement in acute and mild chronic cases. Expect dramatic positive response to doxycycline or tetracycline beginning within 24-48 hours.
PEARLS & CONSIDERATIONS 
COMMENTS
• E. canis infection occurs in some cats, with clinical signs resembling acute canine monocytic ehrlichiosis.
• E. canis has been detected in at least six sick humans in Venezuela. Human E. canis cases have not been described from other countries.
• E. chaffeensis is the most frequent Anaplasma/Ehrlichia infection in humans in the United States, with 1137 cases reported in 2008.
Eisenmenger’s Syndrome
BASIC INFORMATION
SYNONYMS
• Eisenmenger’s complex (large, nonrestrictive ventricular septal defect [VSD] plus pulmonary hypertension causing right-to-left shunting with or without dextroposition of the aorta)
EPIDEMIOLOGY
GENETICS & BREED PREDISPOSITION
Dependent on the underlying cause:
• PDA: quasi-continuous or threshold trait with high degree of heritability. Miniature and toy poodles, collie, Pomeranian, Shetland sheepdog, American cocker spaniel, German shepherd, Maltese, keeshond, Yorkshire terrier.
ETIOLOGY AND PATHOPHYSIOLOGY
• Size of the defect and severity of pulmonary hypertension determine the degree of shunting and thus the occurrence and extent of clinical signs.
○ Hypoxemia from shunting of venous blood into the arterial circulation leads to erythropoietin production and polycythemia.
• Acquired:
○ Large systemic-pulmonary communication (left-to-right shunt) offers minimal resistance to systolic flow.
○ Prolonged pulmonary hypertension leads to pulmonary vascular disease, an abnormal maturation of the pulmonary vasculature, and right ventricular hypertrophy.
○ Pulmonary arterial histologic features: medial muscular hypertrophy, laminar intimal fibrosis, necrotizing arteritis, plexiform lesions.
DIAGNOSIS
INITIAL DATABASE
• Thoracic radiographs: right heart enlargement, enlarged main pulmonary artery, normal to mildly enlarged pulmonary vasculature
• Systemic arterial blood pressure measurement: hypotension contraindicates performing phlebotomy without fluid replacement
• Electrocardiogram: tall P waves in lead II, deep S waves in lead II, right axis deviation; arrhythmias are uncommon
• Echocardiogram:
○ 2D: right ventricular hypertrophy, enlarged main pulmonary artery, identification of structural defects
○ M mode: right ventricular free wall and septal hypertrophy, septal flattening, paradoxical septal motion
○ Color flow Doppler: aliased or laminar flow across the congeni-tal defect, tricuspid regurgitation (uncommon)
○ Spectral Doppler: tricuspid regurgitant velocity > 3.5 m/s, pulmonic insufficiency velocity > 3 m/s, reversed E/A ratio of mitral valve inflow profile, midsystolic notching of the pulmonary flow profile (severe cases)
TREATMENT
ACUTE GENERAL TREATMENT
• Phlebotomy: if PVC > 60%. Withdrawal of 10%-20% of circulating blood volume (= 1-2 mL/kg) with or without intravenous fluid replacement. Repeated as needed (typically every several weeks) based on recurrence of clinical signs.
CHRONIC TREATMENT
• Hydroxyurea, 20-25 mg/kg PO q 12-24 h until hematocrit is lower; then 25-50 mg/kg PO q 48 h as needed to maintain stable hematocrit. Recommended when patient requires frequent phlebotomies.
• Diuretics, ACE inhibitors, and antiarrhythmics following the treatment guidelines. See Heart Failure, Acute/ Decompensated, 468; Heart Failure, Chronic, 470; Ventricular Arrhythmias (Premature Ventricular Complexes, Ventricular Tachycardia), 1165.
BEHAVIOR/EXERCISE
Restrict exercise and excitement in patients with collapsing or syncopal episodes.
PROGNOSIS AND OUTCOME
Long-term prognosis is guarded to poor, depending on severity of pulmonary hypertension.
