Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has affected millions of people globally since its first detection in late 2019. Besides humans, cats and, to some extent, dogs were shown to be susceptible to SARS-CoV-2, highlighting the need for surveillance in a One Health context. Seven veterinary clinics from regions with high incidences of coronavirus disease (COVID-19) were recruited during the early pandemic (March to July 2020) for the screening of patients. A total of 2257 oropharyngeal and nasal swab specimen from 877 dogs and 260 cats (including 18 animals from COVID-19-affected households and 92 animals with signs of respiratory disease) were analyzed for the presence of SARS-CoV-2 RNA using reverse transcriptase real-time polymerase chain reaction (RT-qPCR) targeting the viral envelope (E) and RNA dependent RNA polymerase (RdRp) genes. One oropharyngeal swab from an Italian cat, living in a COVID-19-affected household in Piedmont, tested positive in RT-qPCR (1/260; 0.38%, 95% CI: 0.01–2.1%), and SARS-CoV-2 infection of the animal was serologically confirmed six months later. One oropharyngeal swab from a dog was potentially positive (1/877; 0.1%, 95% CI: 0.002–0.63%), but the result was not confirmed in a reference laboratory. Analyses of convenience sera from 118 animals identified one dog (1/94; 1.1%; 95% CI: 0.02–5.7%) from Lombardy, but no cats (0/24), as positive for anti-SARS-CoV-2 receptor binding domain (RBD) antibodies and neutralizing activity. These findings support the hypothesis that the prevalence of SARS-CoV-2 infection in pet cat and dog populations, and hence, the risk of zoonotic transmission to veterinary staff, was low during the first wave of the pandemic, even in hotspot areas.

The diagnostic accuracy of a smartphone electrocardiograph (ECG) in evaluating heart rhythm and ECG measurements was evaluated in 166 dogs. A standard 6-lead ECG was acquired for 1 min in each dog. A smartphone ECG tracing was simultaneously recorded using a single-lead bipolar ECG recorder. All ECGs were reviewed by one blinded operator, who judged if tracings were acceptable for interpretation and assigned an electrocardiographic diagnosis. Agreement between smartphone and standard ECG in the interpretation of tracings was evaluated. Sensitivity and specificity for the detection of arrhythmia were calculated for the smartphone ECG. Smartphone ECG tracings were interpretable in 162/166 (97.6%) tracings. A perfect agreement between the smartphone and standard ECG was found in detecting bradycardia, tachycardia, ectopic beats and atrioventricular blocks. A very good agreement was found in detecting sinus rhythm versus non-sinus rhythm (100% sensitivity and 97.9% specificity). The smartphone ECG provided tracings that were adequate for analysis in most dogs, with an accurate assessment of heart rate, rhythm and common arrhythmias. The smartphone ECG represents an additional tool in the diagnosis of arrhythmias in dogs, but is not a substitute for a 6-lead ECG. Arrhythmias identified by the smartphone ECG should be followed up with a standard ECG before making clinical decisions. The study was not supported by a grant. Abbreviations: HR, heart rate; App HR, heart rate automatically measured by the 19 smartphone application; AVB, atrioventricular block; QTc, corrected QT interval. evaluating heart rhythm and ECG measurements in dogs. 24Design-Prospective, multicenter, single-blind study. 25Animals-166 client-owned dogs. 26Procedures-A standard 6-lead ECG was acquired for 1 minute in each dog. A smartphone 27 ECG tracing was simultaneously recorded using a single-lead bipolar ECG recorder. All was found in detecting arrhythmias, with a 100% sensitivity and 97.9% specificity. 36Conclusions and clinical relevance-The smartphone ECG provides tracings that are 37 adequate for analysis in most dogs with a reliable assessment of heart rate, heart rhythm,

OBJECTIVE To determine survival estimates and outcome predictors for shelter cats with feline panleukopenia virus (FPV) infection. DESIGN Retrospective cohort study. ANIMALS 177 shelter cats with FPV infection. PROCEDURES Medical records of cats treated for FPV infection from 2011 through 2013 were reviewed to collect information pertaining to signalment; history; results of physical examination, CBC, serum biochemical analysis, and blood gas analysis; and treatments (antimicrobials, antiparasitics, antivirals, antiemetics, analgesics, crystalloid or colloid solutions, and blood products). Survival time and outcome predictors were determined by means of Kaplan-Meier estimation, logistic regression, and mixed-model ANOVA. RESULTS Median survival time after hospital admission was 3 days; 20.3% (36/177) of cats survived to discharge from the hospital. Risk of nonsurvival was greater in cats with (vs without) signs of lethargy, rectal temperature < 37.9°C (I00.2°F), or low body weight at hospital admission. Lower (vs higher) leukocyte count on days 3,4, and 7 of hospitalization, but not at admission, was associated with nonsurvival. Amoxicillin-clavulanic acid, antiparasitics, and maropitant but not interferon-ω were associated with survival, whereas glucose infusion was associated with nonsurvival. CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that FPV infection carried a poor prognosis for shelter cats. Several variables measured at admission or during hospitalization were associated with outcome. Remarkably and contrary to the existing literature, leukopenia at admission had no association with outcome, possibly owing to early prevention of complications.

Systemic AA-amyloidosis is a protein-misfolding disease that is characterized by fibril deposition of serum amyloid-A protein (SAA) in several organs in humans and many animal species. Fibril deposits originate from abnormally high serum levels of SAA during chronic inflammation. In domestic short-hair cats, AA-amyloidosis has only been anecdotally reported and is considered a rare disease. Here we report that an astonishing 57-73% of early deceased short-hair cats kept in three independent shelters suffer from amyloid deposition in the liver, spleen, or kidney. Histopathology and mass spectrometry of post-mortem extracted deposits identified SAA as the major protein source. The duration of stay in the shelters was positively associated with a histological score of AA-amyloidosis (B=0.026, CI95%=0.007-0.046; p=0.010). Presence of SAA fragments in bile secretions raises the possibility of fecal-oral transmission of the disease.

Systemic AA-amyloidosis is a protein-misfolding disease characterized by fibril deposition of serum amyloid-A protein (SAA) in several organs in humans and many animal species. Fibril deposits originate from abnormally high serum levels of SAA during chronic inflammation. A high prevalence of AA-amyloidosis has been reported in captive cheetahs and a horizontal transmission has been proposed. In domestic cats, AA-amyloidosis has been mainly described in predisposed breeds but only rarely reported in domestic short-hair cats. Aims of the study were to determine AA-amyloidosis prevalence in dead shelter cats. Liver, kidney, spleen and bile were collected at death in cats from 3 shelters. AA-amyloidosis was scored. Shedding of amyloid fibrils was investigated with western blot in bile and scored. Descriptive statistics were calculated. In the three shelters investigated, prevalence of AA-amyloidosis was 57.1% (16/28 cats), 73.0% (19/26) and 52.0% (13/25), respectively. In 72.9% of cats (35 in total) three organs were affected concurrently. Histopathology and immunofluorescence of post-mortem extracted deposits identified SAA as the major protein source. The duration of stay in the shelters was positively associated with a histological score of AA-amyloidosis (B = 0.026, CI95% = 0.007–0.046; p = 0.010). AA-amyloidosis was very frequent in shelter cats. Presence of SAA fragments in bile secretions raises the possibility of fecal-oral transmission of the disease. In conclusion, AA-amyloidosis was very frequent in shelter cats and those staying longer had more deposits. The cat may represent a natural model of AA-amyloidosis.