A total of 215 isolates from infections of dogs and cats, including 49 Enterococcus faecalis, 37 Enterococcus faecium, 59 Escherichia coli, 56 Pseudomonas aeruginosa, and 14 Acinetobacter baumannii, were investigated for their susceptibility to 27 (Gram-positive bacteria) or 20 (Gram-negative bacteria) antimicrobial agents/combinations of antimicrobial agents by broth microdilution according to the recommendations of the Clinical and Laboratory Standards Institute. Moreover, all isolates were analysed for their susceptibility to the biocides benzalkonium chloride, chlorhexidine, polyhexanide, and octenidine by a recently published broth microdilution biocide susceptibility testing method. While the E. faecalis isolates did not show expanded resistances, considerable numbers of the E. faecium isolates were resistant to penicillins, macrolides, tetracyclines, and fluoroquinolones. Even a single vancomycin-resistant isolate that carried the vanA gene cluster was detected. Expanded multiresistance phenotypes were also detected among the E. coli isolates, including a single carbapenem-resistant, bla_OXA-48-positive isolate. In addition, multiresistant A. baumannii isolates were detected. The minimal inhibitory concentrations of the biocides showed unimodal distributions but differed with respect to the biocide and the bacterial species investigated. Although there were no indications of a development of biocide resistance, some P. aeruginosa isolates exhibited benzalkonium MICs higher than the highest test concentration.

A total of 114 Staphylococcus isolates from various infections of companion animals, including 43 feline Staphylococcus aureus, 19 canine S. aureus, 11 feline Staphylococcus pseudintermedius and 41 canine S. pseudintermedius were investigated for (i) their susceptibility to 24 antimicrobial agents and three combinations of antimicrobial agents by broth microdilution following CLSI recommendations and (ii) the corresponding resistance genes. In addition, the isolates were tested for their susceptibility to the four biocides benzalkonium chloride, chlorhexidine, polyhexanide and octenidine by a recently developed biocide susceptibility testing protocol. Penicillin resistance via blaZ was the dominant resistance property in all four groups of isolates ranging between 76.7 and 90.9%. About one quarter of the isolates (25.4%) proved to be methicillin-resistant and carried the genes mecA or mecC. Macrolide resistance was the second most prevalent resistance property (27.2%) and all isolates harbored the resistance genes erm(A), erm(B), erm(C), erm(T) or msr(A), alone or in combinations. Fluoroquinolone resistance was detected in 21.1% of all isolates tested, whereas tetracycline resistance via tet(K) and/or tet(M) occurred in 19.3% of the isolates. Resistance to last resort antimicrobial agents in human medicine was seen only in single isolates, if at all. The minimal inhibitory concentrations (MICs) of the four biocides showed unimodal distributions and were very similar for the four groups of staphylococci. Because of the large number of (multi)resistant isolates, antimicrobial susceptibility testing of feline and canine S. aureus and S. pseudintermedius isolates is highly recommended before the start of an antimicrobial chemotherapy. Moreover, no hints towards the development of biocide resistance were detected.

Background: Vector-borne diseases are of increasing importance in Germany. Since 2015, autochthonous cases have been increasingly documented in Berlin/Brandenburg. Objectives: Describe autochthonous Babesia canis infection in the Berlin/Brandenburg region. Animals: Forty-nine dogs with autochthonous B. canis infection. Methods: Evaluation of history, clinical signs, laboratory abnormalities, treatment, and outcome. Results: Dogs were presented between March and August (9) and September and January (40) in the years 2015-2021. Historical and clinical findings were lethargy (100%), pale mucous membranes (63%), fever (50%), and pigmenturia (52%). Common clinicopathological findings were thrombocytopenia (100%), anemia (85%), intravascular hemolysis (52%), pancytopenia (41%), and systemic inflammatory response syndrome (SIRS; 37%). Babesia detection was based on blood smear evaluation (n = 40) and PCR targeting the 18S rRNA gene of piroplasms (n = 49). Sequencing indicated 99.47% to 100% identity to B. canis sequences from GenBank. All dogs were treated with imidocarb (2.4-6.3 mg/kg; median, 5 mg/kg); 8 dogs received 1, 35 received 2, and 1 dog each received 3, 4, or 5 injections, respectively. Continued PCR-positive results were detected in 7 dogs after the 1st, in 5 after the 2nd, in 2 after the 3rd, and in 1 28 days after the 4th injection. Four dogs were euthanized and 3 dogs died. Conclusions and Clinical Importance: Autochthonous B. canis infections in Berlin/Brandenburg were associated with severe clinicopathological changes, SIRS, and multiorgan involvement. Testing by PCR during and after treatment is advisable to monitor treatment success. Screening of blood donors in high-risk areas and year-round tick protection is strongly recommended.

Objectives: To describe the clinical features and outcome of dogs after chocolate ingestion.Material and Methods: Retrospective evaluation of clinical signs, clinical pathological findings, therapy and outcome of 156 dogs after chocolate ingestion. The concentration of methylxanthines (theobromine, caffeine) was calculated based on the type of chocolate and the amount ingested.Results: One hundred and twelve dogs had no clinical signs. Forty‐four dogs had clinical signs of chocolate intoxication. Twenty‐eight of these 44 dogs ingested dark and bitter chocolate. Reasons for presentation were agitation (33), tremor (22), vomiting (21), panting (11), polyuria/polydipsia (seven) and diarrhea (two). Common clinical findings were sinus tachycardia (28), tachypnea/panting (14), hyperthermia (10) and dehydration (seven). Clinical pathological findings in 34 of 44 dogs consisted of hyperlactataemia (23), hypokalaemia (16), mild hyperglycaemia (16) and mild alanine aminotransferase (ALT) and aspartate aminotransferase (AST) elevation (14). After decontamination (apomorphine, activated carbon) and symptomatic treatment (fluid therapy, esmolol, forced diuresis, sedatives), 43 of the 44 dogs survived.Clinical Significance: In dogs with potential chocolate intoxication, the type and amount of chocolate and the time of ingestion are important factors. Cardiovascular, neurological and gastrointestinal signs are the most common clinical signs. In this case series, the prognosis after decontamination and symptomatic therapy was good, with a mortality rate of less than 3%.

Objectives The objective of this study is to describe the course of disease of dogs with primary immune‐mediated haemolytic anaemia (pIMHA) with an observation period longer than 90 days in regard to clinical signs, laboratory results and treatment response. Material and methods Clinical records between January 2003 and December 2011 were reviewed. Diagnosis of pIMHA was based on the presence of haemolytic anaemia with a packed cell volume of <0.35 L/L, a positive Coombs' test and/or erythrocyte agglutination, spherocytosis and exclusion of an underlying disease. Included were dogs which could be monitored for more than 90 days after initial presentation. Results Sixty‐one dogs with pIMHA were included. The initial packed cell volume ranged from 0.08 to 0.30 L/L (median 0.16). Immunosuppressive treatment included prednisolone in all the cases; 32 dogs successively received cyclosporine (28), cyclophosphamide (5), leflunomide (2) or human intravenous immunoglobulins (2) in addition. In 33/61 dogs, the drugs were discontinued 67–3372 days (median 334) after beginning of therapy; in 28 dogs, the drug dosage was reduced, but not discontinued until the end of the study. Three dogs developed immune‐mediated thrombocytopenia (days 132, 156 and 680). The observation period ranged from 96 to 4147 days (median 628). A total of 22.9% (14/61) of the dogs developed a relapse after 94–3972 days (median 517). Five dogs were euthanased due to a relapse after 96–1188 days (median 628). Clinical significance Long‐term prognosis in dogs with pIMHA is favourable. However, a relapse can occur after many years. Relapse was the most common cause of death in dogs with pIMHA that survive more than 90 days.