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in Journal of the American Veterinary Medical Association

Abstract

Objective

To examine shedding of cell-free and cell-associated feline immunodeficiency virus (FIV) in semen of domestic cats during acute infection.

Animals

7 specific-pathogen-free sexually intact male cats.

Procedure

6 cats were inoculated IV with 5 × 106 50% tissue culture infective doses of FIV-NCSU1, and 1 cat served as an uninfected (control) cat. Infection was confirmed in the 6 cats. Periodically for up to 16 weeks after inoculation, cats were anesthetized and ejaculates obtained by use of electroejaculation. Virus was isolated from filtered seminal plasma and washed seminal cells by co-cultivation with a feline CD4+ T-cell line. Seminal cell lysates were also examined for a 582-base pair segment of FIV gag provirus DNA, using a nested polymerase chain reaction amplification.

Results

During the acute phase of FIV infection, virus was evident in semen of 5 inoculated cats. Five cats had virus-positive seminal plasma and 3 had virus-positive cellular constituents during the study. Virus was isolated from 8/22 (36%) seminal plasma samples and 2/17 (18%) seminal cell specimens. Provirus DNA was detected in 5/24 (21%) seminal cell lysates. Cell-free virus was isolated as early as 6 weeks after inoculation, whereas cell-associated virus was isolated as early as 12 weeks after inoculation. Provirus DNA was detected in seminal cells from one cat as early as 1 week after inoculation.

Conclusions and Clinical Relevance

Cell-free and cell-associated FIV are shed in semen of cats early during the course of infection. Samples obtained before seroconversion may contain virus. Virus shedding in ejaculates varies between and within cats during acute infection. (Am J Vet Res 1999;60:211-215.)

Free access
in American Journal of Veterinary Research

SUMMARY

Microcytosis is a common laboratory finding in dogs with congenital portosystemic shunt (pss), although its pathogenesis is not yet understood. Because the most common cause of microcytosis in dogs is absolute or relative iron deficiency, iron status was evaluated in 12 young dogs with pss. Complete blood counting was done before surgical correction in all dogs, and in 5 dogs after surgery, by use of an automated hematology analyzer. Serum iron concentration and total iron-binding capacity (tibc) were determined coulometrically, and percentage of transferrin saturation was calculated. Erythrocyte protoporphyrin content was quantified by use of front-face fluorometry. Serum ferritin concentration was measured by use of elisa. Serum ceruloplasmin content was determined colorimetrically (with p-phenylene-diamine dihydrochloride as substrate) as an indirect indicator of subclinical inflammation, which may result in impaired iron utilization. Special stains were applied to liver (10 dogs; Gomori's) and bone marrow aspiration biopsy (7 dogs; Prussian blue) specimens for qualitative assessment of tissue iron content. Nonpaired Student's t-tests were used to compare serum iron concentration, tibc, percentage of transferrin saturation, and erythrocyte protoporphyrin, ferritin, and ceruloplasmin concentrations in dogs with pss with those in clinically normal dogs. All dogs had microcytosis before surgery; microcytosis resolved in 3 dogs after surgical correction. Serum iron concentration and tibc were significantly lower in pss-affected dogs than in clinically normal dogs. Erythrocyte protoporphyrin, ferritin, and ceruloplasmin concentrations in pss-affected dogs were not significantly different from those in healthy dogs. Excess iron was not detected consistently in liver or bone marrow samples. These results suggest that relative iron deficiency, perhaps associated with altered iron transport and not absolute iron deficiency, is related to microcytosis in dogs with pss.

Free access
in American Journal of Veterinary Research