QUARTERLY BEAT
OCTOBER 2026
JULY 15, 2026
Protein-Losing Enteropathy in Dogs: Diagnostic and Management Strategies Dr. Laura Rayhel , MS, DACVIM (SAIM) • PLE is not a diagnosis; it is a sequela, reflecting excessive protein loss across disease or dysfunctional enteric mucosa, and can result from functional, infectious, inflammatory, or neoplastic primary causes. • Inflammatory bowel disease (IBD) terminology is out, and Chronic Inflammatory Enteropathy (CIE) is in, often with categorization based on treatment response including: food-responsive, microbiota- related modulation-responsive, immunosuppressant- responsive, or non-responsive disease. • A good initial PLE workup starts by ruling out extra- GI mimics and infectious causes. Consider CBC/ chemistry/urinalysis, abdominal ultrasound, fecal parasite testing or empirical deworming, bile acids, resting cortisol, urine protein:creatinine ratio, and a GI panel, with targeted infectious testing based on regional and exposure risks. • With evidence supporting success rates of around 80% and at least a partial clinical response often expected within 1–2 weeks, one or more therapeutic diet trials may be worth attempting before escalating to GI biopsy, unless the patient is severely ill or there is heightened concern for neoplasia or infectious disease. • If disease has progressed to PLE, assume lymphatic dysfunction is probably part of the problem. That means fat restriction is often key, with low-fat diets typically around 1.6–2.5 g fat/100 kcal and ultra-low- fat diets below 1.5 g fat/100 kcal. • Before reaching for glucocorticoids, or definitely before adding a second immunomodulatory drug, ask: have we really tried all the diets? Empirical steroids can be accessible, but they may mask lymphoma, complicate Addison’s diagnosis, or worsen an underlying infectious disease.
JULY 13, 2026
Leptospirosis in the Real World - Diagnosis, Treatment, & Clarifying Confusion Dr. Alison Manchester, PhD, DACVIM (SAIM) • Cats are more resistant to developing clinical
illness from leptospirosis, but exposure and urinary shedding have been documented. • Reported clinical signs in cats are similar to those reported for dogs including PU/PD, lethargy, reduced appetite, vomiting, diarrhea, fever, azotemia, isosthenuria with or without glucosuria, icterus, thrombocytopenia with or without bleeding, and possible thoracic radiographic abnormalities; however, there is no proven causality between leptospirosis and chronic kidney disease or uveitis in cats. • Leptospirosis diagnostics require clinical context. Point-of-care antibody tests may be useful for early detection but are not perfectly sensitive, and recently vaccinated dogs may test positive. • Blood and urine PCR can support a diagnosis, but timing matters. Blood PCR is preferred within the first 10 days of illness, while urine PCR is preferred after the first 7 days. • Antimicrobial therapy may dampen diagnostic results of PCR testing, so collect samples before antibiotics when possible. • Watch closely for severe complications, including oliguric to anuric AKI and leptospiral pulmonary hemorrhage syndrome. Overall, 80–90% of dogs with acute leptospirosis survive, but pulmonary hemorrhage syndrome is associated with reported death rates up to 70%. • Treatment includes antimicrobial therapy and careful supportive care. Initial IV ampicillin can be followed by doxycycline, or oral doxycycline can be started initially if the dog is eating well. • Natural infection with leptospirosis does not provide lifelong immunity, so dogs should still be vaccinated against leptospirosis after recovery. • Leptospirosis vaccines are safe and effective. Dogs should be vaccinated yearly for this preventable, life-threatening disease.
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