Linda S. Jacobson

Effect of early enteral nutrition on intestinal permeability, intestinal protein loss, and outcome in dogs with severe parvoviral enteritis.

A randomized, controlled clinical trial investigated the effect of early enteral nutrition (EN) on intestinal permeability, intestinal protein loss, and outcome in parvoviral enteritis. Dogs were randomized into 2 groups: 15 dogs received no food until vomiting had ceased for 12 hours (mean 50 hours after admission; NPO group), and 15 dogs received early EN by nasoesophageal tube from 12 hours after admission (EEN group). All other treatments were identical. Intestinal permeability was assessed by 6‐hour urinary lactulose (L) and rhamnose (R) recoveries (%L, %R) and L/R recovery ratios. Intestinal protein loss was quantified by fecal α1‐proteinase inhibitor concentrations (α1‐PI). Median time to normalization of demeanor, appetite, vomiting, and diarrhea was 1 day shorter for the EEN group for each variable. Body weight increased insignificantly from admission in the NPO group (day 3: 2.5±2.8% day 6: 4.3±2.3% mean ± SE), whereas the EEN group exhibited significant weight gain (day 3: 8.1±2.7% day 6: 9.7 ± 2.1%). Mean urinary %L was increased, %R reduced, and L/R recovery ratios increased compared to reference values throughout the study for both groups. Percent lactulose recovery decreased in the EEN group (admission: 22.6±8.0% day 6: 17.9 ± 2.3%) and increased in the NPO group (admission: 11.0±2.6% day 6: 22.5 ± 4.6%, P= .035). Fecal α1‐PI was above reference values in both groups and declined progressively. No significant differences occurred for %R, L/R ratios, or α1‐PI between groups. Thirteen NPO dogs and all EEN dogs survived (P= .48). The EEN group showed earlier clinical improvement and significant weight gain. The significantly decreased %L in the EEN versus NPO group might reflect improved gut barrier function, which could limit bacterial or endotoxin translocation.

Feline Babesiosis in South Africa: A Review

Abstract: Babesia felis, originally identified in wild cats in the Sudan, was subsequently found to cause clinical disease in domestic cats. Although babesiosis in domestic cats has been reported sporadically from various countries, as a significant disease it appears to be a distinctly South African phenomenon. Apart from an inland focus, feline babesiosis is reported regularly only from coastal regions. The infection is assumed to be tick‐borne, but the vector has not been identified. Feline babesiosis tends to be an afebrile, chronic, low‐grade disease. The most frequently reported complaints by owners are anorexia and lethargy. The main clinical findings are anemia, depression, and occasionally icterus. Concurrent infections (e.g., Mycoplasma haemofelis, FeLV, FIV) may contribute to the clinical picture. Laboratory findings commonly include regenerative anemia, elevation of alanine transaminase (but not alkaline phosphatase) and total bilirubin concentrations, and a variety of electrolyte disturbances. Secondary immune‐mediated hemolytic anemia can be seen occasionally. Drugs effective against other Babesia species give variable and questionable results. The drug of choice is primaquine phosphate, which effects a clinical cure but does not sterilize the infection. Repeated or chronic therapy may be required.

Nitric oxide metabolites in naturally occurring canine babesiosis.

Babesiosis, caused by the virulent haemoprotozoan parasite Babesia canis rossi, is an important disease of dogs in South Africa. The nitric oxide metabolites, nitrate and nitrite (collectively termed reactive nitrogen intermediates or RNIs) were measured in admission sera from dogs in a babesiosis-endemic area. Five groups were prospectively studied: mild uncomplicated (n=9), severe uncomplicated (severe anaemia) (n=10) and complicated babesiosis (n=11); and two groups of healthy aparasitaemic dogs: endemic controls from the study area (n=10) and experimental dogs kept in tick-free conditions (n=10). Four measures of RNI production were studied: (i) serum RNI; (ii) serum RNI/creatinine ratio; (iii) fractional clearance of RNI (FC(RNI)); (iv) fractional excretion of RNI (FE(RNI)). Marked elevations of serum RNI occurred in only two dogs, both in the severe uncomplicated group. The highest concentration (log value 5.29 micromol/l) was in a dog that died, but concentrations in the other four dogs that died were unremarkable (0, 0.34, 1.66 and 2.64 micromol/l). Age, appetite and free serum haemoglobin were significant covariates for measures of RNI production. There were no significant differences among the babesiosis groups for serum RNI. Adjustment for creatinine had minor effects on the results. All babesiosis groups had significantly higher serum RNI and RNI/creatinine than the tick-free control group, but did not differ from the endemic controls except for the severe uncomplicated group, which had higher RNI/creatinine. The complicated group had significantly lower FC(RNI) and FE(RNI) than all other groups, except for the tick-free control group, which had similar FE(RNI). The results indicate that, in an endemic area, measures of RNI production are unlikely to be useful indicators of severity or outcome in canine babesiosis.