Retrospective Survival Analysis of Cats with Feline Infectious Peritonitis Treated with Polyprenyl Immunostimulant That Survived over 365 Days.

Feline infectious peritonitis (FIP) remains a major diagnostic and treatment challenge in feline medicine. An ineffective immune response is an important component of FIP pathophysiology; hence treatment with an immune stimulant such as Polyprenyl Immunostimulant™ (PI), which enhances cell-mediated immunity by upregulating the innate immune response via Toll-like receptors, is a rational approach. Records of cats with FIP treated with PI orally for over 365 days were retrospectively studied. Of these cats (n = 174), records were obtained for n = 103 cats with appropriate clinical signs and clinical pathology. Of these, n = 29 had FIP confirmed by immunohistochemistry (IHC) or reverse transcription polymerase-chain-reaction (RT-PCR). Most of the cats (25/29; 86%) had non-effusive FIP, and only 4/29 cats (14%) had effusive FIP. The mean survival time (MST) was 2927 days (eight years); with 55% of the cats (16/29) still being alive at the time data collection, and 45% (13/29) having died. A persistently low hematocrit plus low albumin:globulin (A:G) ratio, despite treatment, was a negative prognostic indicator. It took a mean of ~182 days and ~375 days, respectively, for anemia and low A:G ratio to resolve in the cats that presented with these laboratory changes. This study shows that PI is beneficial in the treatment of FIP, and more studies are needed to establish the best protocols of use.

Utility of admission lactate concentration, lactate variables, and shock index in outcome assessment in dogs diagnosed with shock.

OBJECTIVE: To determine whether admission venous plasma lactate concentration, calculated lactate variables, or shock index (SI) could discriminate hospital survivors from nonsurvivors in dogs admitted with shock. DESIGN: Prospective investigation performed over a 19-month period. SETTING: Large urban private teaching hospital. ANIMALS: Twenty-three dogs consecutively admitted to the ICU from January 2008 to July 2009 with initial peripheral venous plasma lactate concentration >2 mmol/L (18.0 mg/dL) and clinical and hemodynamic parameters consistent with shock. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Heart rate, systolic blood pressure, and venous plasma lactate concentrations were serially recorded at predefined time points and used to calculate SI (SI = heart rate/systolic blood pressure) and lactate variables, including lactime (time lactate > 2.0 mmol/L), lactate clearance ([lactateinitial - lactatedelayed ]/lactateinitial × 100), and LACAREA (area under the lactate concentration versus time curve). Primary outcome was survival to discharge. Overall survival rate was 61%. Admission venous plasma lactate concentration did not differ between groups (P = 0.2). Lactime was shorter in survivors versus nonsurvivors (P = 0.02). Lactate clearance at 1, 10, 16, 24, and 36 hours, and final lactate clearance were greater in survivors versus nonsurvivors (P < 0.05). LACAREA at time intervals 0-1, 1-4, 4-10, 10-16, 16-24, 24-30, and 30-36 hours was larger in nonsurvivors versus survivors (P < 0.05). Total LACAREA did not differ between groups (P = 0.09). Admission SI and time to normalize SI (SI < 0.9) were not different between survivors and nonsurvivors (P > 0.05). CONCLUSIONS: While admission venous plasma lactate concentration could not discriminate between hospital survivors and nonsurvivors, lactate variables showed clinical utility to predict outcome in dogs with shock. Further studies are needed to determine SI reference ranges and optimal SI cut-off values to improve its prognostic ability in sick dogs.

Clinical management of canine babesiosis.

OBJECTIVE: To review and summarize current information regarding epidemiology, pathogenesis, and pathophysiology leading to the various clinical syndromes associated with canine babesiosis. Diagnosis, treatment, preventative strategies, and zoonotic implications are discussed. ETIOLOGY: Babesiosis is caused by hemoprotozoa of the genus Babesia. Numerous species of Babesia exist worldwide. An increased incidence of babesiosis is described, especially in North America. The babesial organism spends the majority of its life cycle within the erythrocyte of the definitive host, resulting in hemolysis, with or without systemic complications. DIAGNOSIS: Definitive diagnosis depends on direct visualization of the organism on blood smear or polymerase chain reaction. A positive serologic antibody test indicates exposure with or without active infection. THERAPY: Antiprotozoal drugs, antimicrobials, and supportive care are the mainstays of babesiosis therapy. PROGNOSIS: Prognosis depends on the severity of disease, which in turn depends on both organism and host factors. Clinical syndromes associated with a poorer prognosis include red biliary syndrome, acute renal failure, acute respiratory distress syndrome, neurologic dysfunction, acute pancreatitis, cardiac dysfunction, and hypoglycemia.

Feline babesiosis.

OBJECTIVE: To review and summarize current information regarding the etiology, clinical presentation, diagnosis, treatment, and prognosis of feline babesiosis, especially with regard to features distinct from canine babesiosis. ETIOLOGY: Babesiosis is caused by hemoprotozoa of the genus Babesia. Numerous species of Babesia exist worldwide. The babesial organism spends the majority of its life cycle within the erythrocyte of the definitive host, resulting in hemolysis, with or without systemic complications. DIAGNOSIS: Definitive diagnosis depends on direct visualization of the organism on blood smear or a positive polymerase chain reaction. Positive serologic tests indicate only exposure, with or without active infection. THERAPY: Antiprotozoal drugs and supportive care are the mainstays of therapy. Primaquine phosphate is considered the treatment of choice in cats. PROGNOSIS: Prognosis depends on the severity of disease, which in turn depends on both organism and host factors. Mortality rates of 15-20% are reported.