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  • Author or Editor: Jeanne W. George x
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SUMMARY

Iron status, as determined by hematologic values, serum iron concentration, total iron-binding capacity, and zinc protoporphyrin concentration, was determined in 2 groups of 6 nonpregnant monkeys. Monkeys of groups 1 and 2 had 10 and 5%, respectively, of their blood volume withdrawn per week for up to 10 weeks or until blood hemoglobin concentration was ≤ 10 g/dl. A third group of 6 monkeys served as controls.

The majority (8/12) of the monkeys became anemic (hemoglobin concentration, ≤ 10 g/dl) after approximately 30 to 70% (mean, 49%) of their blood volume was removed. Anemia was accompanied by decrease in serum iron concentration and percentage of transferrin saturation. Microcytosis, hypochromasia, and increased zinc protoporphyrin concentration, all hematologic characteristics of iron deficiency, developed later. The calculated iron stores ranged from 1 to 133 mg, with mean value of 51 mg. Iron-depleted monkeys had mean calculated available iron store of 20.8 mg, whereas iron-replete monkeys had mean available iron store of 114.0 mg. Changes were not observed in monkeys of the control group during the study period.

None of the baseline hematologic or biochemical analytes measured were good predictors of iron stores. The diet used at the research center did not provide sufficient iron to prevent iron deficiency in most of the monkeys from which a total amount of 30 to 70% of blood volume at 5 or 10%/week was withdrawn. Studies requiring that much blood may need to be modified to include iron supplementation, reduction of sample volume, or iron replacement after termination of projects.

Free access
in American Journal of Veterinary Research

Summary

Serum electrolyte values from 100 rhesus monkeys with diarrhea were reviewed. The most frequent finding was hyponatremia (88%), with hypochloremia next most frequently detected (80%). Metabolic acidosis was less common (59%) and usually associated with high anion gap values. Associations between electrolyte abnormalities and age, housing, or case outcome were not found. Bacteriologic culturing was performed on fecal specimens from 90 monkeys. Campylobacter coli or C jejuni alone was isolated from 42 (46.7%) specimens, C coli and Shigella flexneri were isolated from 25 (27.8%) specimens, and S flexneri alone was isolated from 6 (6.7%) specimens. A pathogen was not isolated from 17 (18.9%) specimens. Hyponatremia, hypochloremia, acidosis, and high anion gap values were most severe in monkeys infected with Campylobacter sp, either alone or with concurrent S flexneri infection. Serum sodium concentrations < 132 mEq/L and serum Cl concentrations < 93 mEq/L were consistently associated with Campylobacter sp infection.

Free access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To characterize serum biochemical abnormalities in goats with uroliths.

Design—Retrospective case-control series.

Animals—107 male goats with uroliths and 94 male goats with various nonrenal diseases (controls).

Procedures—For male goats, results of serum biochemical analyses collected from 1992 through 2003 were retrieved from computerized records, as were signalment, clinical diagnoses, and discharge status. Results of analyses for BUN, creatinine, phosphorus, calcium, Na, K, Cl, total CO2, anion gap, and glucose were compared between goats with uroliths and control goats.

Results—Goats with uroliths had higher mean BUN, creatinine, total CO2, K, and glucose concentrations and lower mean phosphorus, Na, and Cl concentrations than control goats, with no difference in mean calcium concentration and anion gap. Goats with uroliths had higher frequency of azotemia, hypophosphatemia, hypochloridemia, and increased total CO2 and lower frequency of decreased total CO2 than control goats. Urolithiasis occurred more frequently in castrated males than in sexually intact males and in dwarf African breeds than in other breeds.

Conclusions and Clinical Relevance—Goats with uroliths often had hypophosphatemia at admission. Hypochloridemic metabolic alkalosis was the most common acid-base disorder. Rupture in the urinary tract system was associated with increased prevalence of hyponatremia and hyperkalemia. Clinicians should be aware of these abnormalities when determining fluid therapy.

Full access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To investigate the effects of preexisting FeLV infection or FeLV and feline immunodeficiency (FIV) coinfection on the pathogenicity of the small variant of Haemobartonella felis (Hfsm, California variant) in cats.

Animals—20 FeLV infected, 5 FeLV-FIV coinfected, and 19 retrovirus-free cats.

Procedure—A client-owned cat, coinfected with FeLV and Hfsm, was the source for Hfsm. Inoculum 1 (FeLV free) was obtained by passage of source Hfsm through 4 FeLV-resistant cats. Inoculum 2 was obtained by further passage of Hfsm (inoculum 1) through 2 specific pathogenfree cats.

Results—A mild-to-moderate anemia started 21 days after inoculation, with its nadir occurring at 35 to 42 days after inoculation. Infection with Hfsm induced greater decrease in hemoglobin concentration in FeLV infected cats, compared with retrovirus free cats. Reticulocytosis, macrocytosis, and polychromasia of erythrocytes developed in anemic cats regardless of retrovirus infection status. Mean neutrophil counts decreased during the hemolytic episode. For most cats, the anemia was transient. Four FeLV infected cats, 1 of which was also FIV infected, developed fatal FeLV-associated myeloproliferative diseases. Of the surviving cats, 8 died over the next 24 months from other FeLV-related diseases. Hemolysis did not recur after the initial episode. Inoculum 1 induced more severe anemia than inoculum 2.

Conclusions and Clinical Relevance—Our results support the clinical observation that cats coinfected with FeLV and H felis develop more severe anemia than cats infected with H felis alone. Infection with Hfsm may induce myeloproliferative disease in FeLV infected cats. The small variant of H felis may lose pathogenicity by passage through FeLV-free cats. (Am J Vet Res 2002;63:1172–1178)

Full access
in American Journal of Veterinary Research