Objective—To investigate the contribution of gyrA mutation and efflux pumps to fluoroquinolone resistance and multidrug resistance among Escherichia coli isolates from dogs and cats.
Sample Population—536 clinical isolates of E coli.
Procedures—Minimum inhibitory concentrations (MICs) were determined for enrofloxacin and 6 other drug classes by use of broth microdilution techniques. Real-time PCR assay was used to determine the mutation in gyrA; Phe-Arg-β-naphthylamide, an efflux pump inhibitor, was used to examine the contribution of efflux pump overexpression.
Results—The MIC for fluoroquinolones increased in a stepwise fashion and was lowest in the absence of mutations, higher with a single point mutation, and highest with 2 point mutations. Level of resistance in the latter category was high (8 times the breakpoint), but this was associated with expression of the AcrAB efflux pump. Inhibition of the efflux pump resulted in a reduction in the MIC to less than the susceptible breakpoint for isolates with an MIC ≤ 4 mg/L, regardless of the presence of a mutation. The greatest magnitude in MIC decrease (MIC was decreased by a factor of > 67 fold) was for isolates with a single mutation but the greatest absolute decrease in MIC (124 mg/L) was for isolates with 2 mutations. Inhibition of the AcrAB efflux pump in isolates characterized by multidrug resistance decreased the MIC of drugs structurally unrelated to fluoroquinolone.
Conclusions and Clinical Relevance—Fluoroquinolone resistance in E coli appeared to be a stepwise phenomenon, with MIC increasing as the number of point mutations in gyrA increased, but high-level resistance and multidrug resistance associated with fluoroquinolone resistance reflected overexpression of the AcrAB efflux pump.
Objective—To determine the prevalence and severity
of pulmonary arterial lesions in cats seropositive for
heartworms (Dirofilaria immitis) but lacking adult
heartworms in the heart and lungs during necropsy.
Animals—630 adult cats from an animal control shelter
Procedure—Cats were tested for adult heartworms
in the heart and pulmonary arteries and antibody
against heartworms in the serum. Histologic examination
was conducted on the right caudal lung lobe of
24 heartworm- and antibody-positive cats; 24 heartworm-negative and antibody-positive cats; and 24
heartworm-, antibody-, and antigen-negative cats.
Wall areas of 10 small to medium-sized pulmonary
arteries of each cat were measured and expressed as
a proportion of total cross-sectional area.
Results—Heartworm infection or seropositive status
was significantly and strongly associated with severity
of medial hypertrophy of pulmonary arterial walls.
Heartworm- and antibody-positive cats and heartworm-negative and antibody-positive cats had a significant
increase in wall thickness, compared with
wall thickness for heartworm- and antibody-negative
cats. Heartworm- and antibody-positive cats had the
most severe hypertrophy. The proportion with occlusive
medial hypertrophy was significantly higher in
heartworm- and antibody-positive cats (19/24 [79%])
and heartworm-negative and antibody-positive cats
(12/24 [50%]), compared with heartworm- and antibody-negative cats (3/24 [13%]).
Conclusions and Clinical Relevance—Cats with
serologic evidence of exposure to heartworms,
including those without adult heartworms in the lungs
and heart, have a greater prevalence of pulmonary
arterial lesions than heartworm-negative cats without
serologic evidence of exposure. Additional studies are
needed to define the pathogenesis, specificity, and
clinical importance of these lesions. (Am J Vet Res
Case Description—A 21-month-old spayed female Border Collie was examined because of progressive right forelimb lameness, signs of pain, and subcutaneous edema. The dog lived in a fenced yard in Tampa, Fla, that contained a small area of marshy terrain.
Clinical Findings—The subcutis and intermuscular fascia contained multiple cystic cavities filled with larval cestodes (plerocercoids or spargana) and cloudy red fluid. Parasites were identified morphologically and by DNA sequence analysis as pseudophyllidean cestodes, most likely Sparganum proliferum. The dog developed a progressively worsening fever, dyspnea, mature neutrophilia, and hypoproteinemia. Septic pleuritis and peritonitis complicated the later stages of the disease.
Treatment and Outcome—Treatment with praziquantel, fenbendazole, and nitazoxanide failed to control the proliferation and dissemination of larval cestodes. The dog was euthanatized after 133 days of treatment. At necropsy, numerous parasitic tissue cysts were present in the subcutis and intermuscular fascia; these cysts were most abundant in the soft tissues of the forelimbs and cervical musculature. The pleural and peritoneal cavities contained multiple larval cestodes and were characterized by neutrophilic inflammation and secondary bacterial infection.
Clinical Relevance—Findings indicated that clinical signs associated with proliferative sparganosis in dogs may be rapidly progressive and that the condition may be refractory to antiparasitic treatment. Veterinarians should be aware of this zoonotic, water-borne agent.