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Cattle are susceptible to experimental infection with the Stetsonville isolate of the transmissible mink encephalopathy (TME) agent. To determine if they are susceptible to other TME isolates, two groups of calves were inoculated intracerebrally with homogenate of mink brain containing the Hayward isolate or the Blackfoot isolate. For comparison, a third group was inoculated with a brain homogenate from a steer infected with the Stetsonville isolate in its primary cattle passage and a fourth group was inoculated with a pool of brain homogenate from three cattle experimentally infected with a sheep and goat scrapie agent in its primary cattle passage. Clinical signs of neurological disease appeared in each steer of every group between 15 and 25 months after inoculation. An encephalopathy characterized by severe spongiform change and pronounced astrocytosis occurred in the three groups inoculated with the TME agent. In contrast, the neurohistological changes in the steers inoculated with the cattle-passaged scrapie agent were slight and subtle. Analysis of the octapeptide repeat region of the bovine protease-resistant protein (PrP) gene showed that variations in incubation period, clinical signs, and neurohistological changes were unrelated to the homozygous or heterozygous condition of six or six/five octapeptide repeats.

Development of control measures for the gammaherpesviral disease of cattle known as sheep-associated malignant catarrhal fever (SA-MCF) has been hampered by a lack of accurate diagnostic tests either for the causative virus or for antibody against that virus. A recently developed competitive-inhibition enzyme-linked immunosorbent assay (CI-ELISA) for the detection of antibody to malignant catarrhal fever (MCF) virus (MCFV) in ruminants based on a monoclonal antibody to a widely conserved epitope of MCFV (H. Li, D. T. Shen, D. P. Knowles, J. R. Gorham, and T. B. Crawford, J. Clin. Microbiol. 32:1674-1679, 1994) and a PCR assay based on previously reported primers (S. I. F. Baxter, I. Pow, A. Bridgen, and H. W. Reid, Arch. Virol. 132:145-159, 1993) were used to detect anti-MCFV antibody and SA-MCFV DNA in sheep and other ruminants. The PCR amplified a specific 238-bp SA-MCFV genomic DNA fragment from peripheral blood lymphocytes of adult sheep and other ruminants with clinical MCF. Of 144 samples from randomly selected healthy adult sheep, 143 (99%) were positive by PCR and 136 (94%) were positive by CI-ELISA. The agreement between the two assays exceeded 95%. Of nine samples collected from cattle and deer with clinical MCF of apparent sheep origin, seven were CI-ELISA positive and all 9 were PCR positive. Among 59 serum samples from presuckling lambs, none contained antibody detectable by CI-ELISA. After suckling, maternal anti-MCFV antibody was detectable for about 10 +/- 3 weeks. Although all colostrum and milk samples from infected ewes were strongly PCR positive, the appearance of detectable SA-MCFV DNA in lambs was correlated generally with antibody patterns, which suggests that the natural infection event in sheep may not occur during the perinatal period but occurs sometime later in life.

To determine whether the aetiological agent of bovine spongiform encephalopathy (BSE) is pathogenic for mink, standard dark mink were inoculated with coded homogenates of bovine brain from the U.K. Two homogenates were from cows affected with BSE. The third was from a cow that came from a farm with no history of having had BSE or having been fed ruminant-derived, rendered by-products, the proposed vehicle for introduction of the BSE agent. Each homogenate was inoculated intracerebrally into separate groups of mink and a pool of the three was fed to a fourth group. Signs of neurological disease appeared in mink an average of 12 months after intracerebral inoculation and 15 months after feeding. Decreased appetite, lethargy and mild to moderate pelvic limb ataxia were the predominant clinical signs, quite unlike the classic clinical picture of transmissible mink encephalopathy (TME). Microscopic changes in brain sections of most affected mink were those of a scrapie-like spongiform encephalopathy. Vacuolar change in grey matter neuropil was accompanied by prominent astrocytosis. Varying greatly in severity from one mink to another, the degenerative changes occurred in the cerebral cortex, dorsolateral gyri of the frontal lobe, corpus striatum, diencephalon and brainstem. Although resembling TME, the encephalopathy was distinguishable from it by less extensive changes in the cerebral cortex, by more severe changes in the caudal brainstem and by sparing of the hippocampus. The results of this study extend the experimental host range of the BSE agent and demonstrate for the first time the experimental oral infection of mink with a transmissible spongiform encephalopathy agent from a naturally infected ruminant species.

BALB/c and severe combined immunodeficiency (SCID) mice were inoculated intracerebrally or intraperitoneally with scrapie agent strain ME7 to examine the role of functional lymphocytes and follicular dendritic cells in splenic infectivity and PrPSc accumulation. Intracerebrally inoculated BALB/c and SCID mice developed the clinical signs and microscopic lesions characteristic of scrapie. Spleens from terminally affected BALB/c mice contained PrPSc which was detectable by immunoblot analysis; SCID mouse spleens did not contain detectable PrPSc. SCID mouse spleens collected during the first 90 days after intraperitoneal infection contained neither infectivity nor PrPSc.

Most estimates of the prevalence of anaplasmosis have been based on serologic data using the complement-fixation (CF) and/or card agglutination tests. Since these tests are considered to be only about 50 percent reliable for detecting carrier cattle in enzootically stable herds, the need for more sensitive diagnostic tests is widely recognized. The objective in the present study was to compare the sensitivity of the CF test with that of the indirect immunofluorescence (IIF) test and a recently developed DNA probe in determining the prevalence of Anaplasma marginale infection in cattle from an enzootic area. The study herd consisted of 52 8-month-old steers and 13 3-year-old cows of mixed beef breed. All cattle were initially tested for this comparative purpose. All but one animal (one that was a positive reactor as assessed by all three tests, and served as a positive control), were treated with long-acting oxytetracycline in an attempt to clear any carrier infections. Each animal was then retested at 1 month and 2 months post-treatment (PT), in an effort to determine if the DNA probe could be used to evaluate the effectiveness of the drug. Six of the 65 (9.2%) initial serum samples were CF positive. In contrast, 60 (92.3%) and 64 (98.5%) of the samples were positive as assessed with the IIF test and the DNA probe, respectively. The DNA hybridization reactions varied in intensity within the sample population indicating different individual levels of infection. The DNA probe hybridized with two samples taken at 1 month PT, and with two different samples taken at 2 months PT. The mean IIF titers were reduced at both the 1 month and 2 month sampling times. These results suggest that the drug did not eliminate infections in all cattle. Some may have been cleared, but, in any event, the drug did reduce the level of infections below the sensitivity of the DNA probe and interrupted continuity of stimulation of antibody. Therefore, the DNA probe and the IIF test appear to be considerably more sensitive in detecting carrier infections than the CF test, and should be considered in future epidemiologic studies.

The prevalence of infection with ovine progressive pneumonia (OPP) virus and its effects on ewe wool and lamb production were investigated in a flock of 2,976 ewes of 6 breed types (Rambouillet, Targhee, Columbia, Polypay, 1/4 cross Finnsheep, and 1/2 cross Finnsheep). Prevalence of seropositivity was significantly (P less than or equal to 0.01) lower among Rambouillet and Targhee breeds (44 and 42%, respectively), intermediate in Polypay, Columbia, and 1/4 cross Finnsheep (approximately 53%), and higher among 1/2 cross Finnsheep (62%). Seropositivity increased with age in all breed types from 11% at 1 year of age to 93% at greater than or equal to 7 years of age. Lateral disease transmission is indicated by linear increase of seropositivity prevalence with increasing age, including that in sheep greater than 6 years old. Subclinical infection with OPP virus had no apparent detrimental effect on number of lambs born, lamb viability, birth weight, number of lambs weaned, or growth rate of single and twin lambs, compared with findings for noninfected sheep in the same flock. Mature ewe body weight and grease fleece weight did not differ between subclinically infected seropositive and seronegative ewes. Subclinical infection with OPP virus does not appear to have an adverse economic effect on ewe wool and lamb production. Culling rate attributable to clinical manifestation of infection with OPP virus must be accurately determined before the true effects of virus infection on production can be determined and an eradication program can be recommended.

Groups of canine distemper virus (CDV)-susceptible ferrets were treated daily with 2·0 ml of normal goat serum (NGS) or goat anti-ferret platelet serum from 2 days before to 11 days after infection. Each group was subdivided into 2 and one subgroup of each was subsequently injected intraperitoneally with virulent R252-CDV. Ferrets were killed on days 2, 4, 6, 9 and 11 after infection and tissues from the central nervous system (CNS) were examined for histopathological lesions typical for CDV and also of CDV antigen by indirect immuno-fluorescence methods. In NGS-treated animals, a time course-dependent spread of CDV from CNS endothelium during days 2 to 4 after infection through choroid plexus epithelium was observed. In contrast, CDV-infected ferrets treated with anti-platelet antibody exhibited a delay in infection of CNS endothelium until 9 days after infection. The results of this study confirm vascular endothelium as the primary route of invasion of CNS tissues by CDV and implicate the circulating platelet in the initiation of this event.

The indirect hemagglutination method was used to determine the seroprevalence of Toxoplasma gondii in a random sample (250) of lambing ewes from a large (4,226 ewes) western range flock. Agglutination (greater than or equal to 2+) at the 1:64 serum dilution was considered a positive reaction; the seroprevalence was 20.8%. The neonatal mortality for lambs born to seropositive ewes was 30.7%, which was significantly greater than that for seronegative ewes (13.6%). The average age at death for lambs born to seropositive ewes was 24.8 hours, which was significantly less than that for lambs born to seronegative ewes (31.2 hours).

The desired response to vaccination is protection from clinical disease. This article presents several factors, related to both the host and the vaccine, which may result in inadequate protection from clinical disease following vaccination. Also presented is an overview of adverse reactions to vaccines and the response of young animals and pregnant animals to vaccination.

Newborn Saanen goats were orally infected with two distinct biologically cloned isolates of the caprine arthritis-encephalitis lentivirus (CAEV), designated CAEV(63) (Crawford TB, Adams DS, Cheevers WP, Cork LC: Science 207:997, 1980) and CAEV (Co) (Cork LC, Hadlow WJ, Crawford TB, Gorham JR, Piper RC: J Infect Dis 129:134, 1974; Narayan O, Clements JE, Strandberg JD, Cork LC, Griffin DE: J Gen Virol 50:69, 1980). All infected goats seroconverted for antibodies to CAEV, and there were no serologic reversions. Histologic lesions consisted of chronic inflammation of variable incidence and severity in joints and mammary gland. Clinical arthritis, estimated by enlargement of carpi, correlated with severe inflammation of radiocarpal synovium. Statistical evaluations of clinical and histologic parameters indicated that chronic joint disease was significantly more frequent and more severe in the group of goats infected with CAEV(63) than in the group infected with CAEV (Co). Thus, the severity of chronic arthritis is determined in part by the relative pathogenicity of individual CAEV isolates. Analysis of the temporal development of carpal arthritis during the first 3 years of infection indicated that (a) the extent of eventual chronic disease in individual joints was apparent relatively early after infection, (b) joints with severe chronic lesions were clinically enlarged at irregular intervals and (c) the pattern of recurrent arthritis was unique for each joint. Thus, chronic arthritis develops with a progressive course which may be promoted by recrudescent inflammation. Infectious virus was recovered 3 years after infection from selected tissues of 12 of 17 CAEV(63)-infected goats and 11 of 18 CAEV(Co)-infected goats. Virus recovery was independent of the virus isolate used for experimental infection and did not correlate with the severity of lesions.

Of 254 sheep examined for antibodies to the virus of ovine progressive pneumonia, 162 (63.8%) were seropositive. The mean age of the seropositive ewes was 4.9 +/- 1.8 years, which was significantly greater than that for the seronegative ewes (4.1 +/- 2.3 years). The age-specific prevalence increased with ewe age, from 25% among yearling ewes to 85% among 7-year-old ewes. Seropositive ewes produced more pounds of live lamb at birth than did seronegative ewes.

A prolonged mean template bleeding time of 13 minutes was present in nine Aleutian mink affected with Chediak-Higashi syndrome (CHS) compared with 4 minutes in dark control mink. The concentrations of blood platelets in normal and affected animals did not differ significantly. However, in mink with CHS, a marked disturbance of platelet response to collagen was present. Administration of aspirin and indomethacin completely blocked CH platelet response to collagen. Blood platelet adenosine triphosphate and adenosine diphosphate values from mink with CHS were significantly less than those of normal mink, and the platelet adenosine triphosphate/adenosine diphosphate ratios were 10.31 in affected mink and 2.74 in normal mink. These findings are consistent with our previous investigations in affectd cattle and persons and indicate that a "storage pool disease" of platelets exist in the mink with CHS.

Hcmatologic atad patltologic examination on thirty-live mink, clinically affectedwith gray diarrhea, were carried otut. Four had other recognizable diseases. Twenty-two1?ad microscopic stomach lesions, not described in other mink diseases. The lesions weremultifocal ancl consisted of loss of the ntiddle and basal layers c>f the mucosa, with neutro-phil and monont?c1ear cell infiltratiort. Fibrosis was observecl in the stomach lesions ofsome. Dircct ancl indirect fluorescent antibody tecltniques, tttilizing sera from affectedmink, failed to demonstrate an aul-oantibocly in them. Hematologic responses of aflecteclmink varied widely.

Clinical salmon poisoning disease (SPD), and survival of Neorickettsia helminthoeca and metacercariae of Nanophyetus salmincola in fish were evaluated experimentally in 12-wk-old coyotes (Canis latrans) to determine the potential of SPD for biological control of coyotes. Coyotes readily ate fish that contained metacercariae and rickettsiae. They developed diarrhea, anorexia and lethargy within 7 days after feeding. Infected coyotes lost 58% of their body weight when compared to uninfected controls. They died or became moribund and were euthanatized within 17 days after feeding. Rickettsiae were present in the macrophages of lymph nodes of all affected coyotes. Clinical disease occurred in coyotes fed fresh fish, but not in coyotes fed fish stored at 4 C for greater than or equal to 30 days or at -20 C for 14 days. Metacercariae in fish were viable after 60 days at 4 C. These trematodes developed in coyotes, but clinical SPD did not occur. This indicated survival of metacercariae, but not rickettsiae. Metacercariae were not viable after 14 days at -20 C.

A central nervous system disease of mink occurred in three unrelated fur farms in Oregon in September, 1981. Only kits four to five months old were affected. Clinical signs consisted of posterior ataxia progressing to complete posterior paralysis with loss of motor control and sensation. Complete or partial recovery occurred in approximately 1.5 months in most mink. Microscopic lesions consisted of severe nonsuppurative meningoencephalitis and meningomyelitis with vacuolation of the white matter of the brain and spinal cord. Canine distemper virus infection and other recognized causes were ruled out on the basis of clinical signs, history, lesions, or laboratory findings. Experimental inoculations of mink with brain and spinal cord specimens from affected mink failed to reproduce the disease.

An indirect ELISA for the detection of bovine immunoglobulin to bovine herpesvirus type 4 (BHV-4) was developed. Three methods of antigen preparation were compared. They included (1) BHV-4-infected Madin Darby bovine kidney (MDBK) cells treated with glycine and then frozen and thawed, (2) BHV-4-infected MDBK cells treated with glycine and then sonicated, and (3) BHV-4-infected MDBK cells treated with a detergent. The antigen preparation that gave the highest reactivity was the first method. We obtained serum samples from 178 cattle in the field and assayed the serum by ELISA and the complement-fixation (CF) test. Eighty-six percent (153) of the serum samples were positive by ELISA, and 70% (124) were positive by the CF test. The ELISA had a higher degree of sensitivity than did the CF test. Also, the ELISA was specific, and the prevalence of BHV-4-infection was more common in beef and dairy herds than previously recognized.

Ferrets experimentally infected by various routes with pseudorabies virus were examined for gross and microscopic lesions. Nonsuppurative meningoencephalomyelitis, as well as visceral lesions, occurred. The incubation period seemed related to the viral dose and to the distance between the inoculation site and the central nervous system. The distribution of the lesions in the central nervous system appeared to be closely related to the peripheral nerve pathways from the inoculation sites. Other findings indicated that the lymphohematogenous route could have a role in the dissemination of the virus in infected ferrets.

Epizootics of pneumonia in mink caused by Pseudomonas aeruginosa were investigated to characterize the serotype of organisms and to identify possible predisposing factors. Most epizootics were associated with P aeruginosa Fisher serotype 1, and a few were associated with 3 other serotypes. There were no predisposing factors identified that could be used to differentiate farms affected and those not affected with pseudomonas pneumonia. Cultural studies indicated that P aeruginosa was present in mink from affected and nonaffected herds. Organisms isolated included serotypes associated with naturally occurring disease. Serostudy results were similar among herds. A prospective field vaccination trial did not yield definitive results, since only slight losses occurred in both vaccinated and nonvaccinated mink. Significant levels of antibody were detected in mink 15 to 17 weeks after they were given a single dose of P aeruginosa lipopolysaccharide vaccine.

The administration of estrogen-induced severe bone marrow depression in 9 of 12 ferrets, independent of sex (male, female) or ovariohysterectomy. Resultant pancytopenia was manifested by subcutaneous petechiae, melena, hematomyelia, pale mucous membranes, pale bone marrow, centrilobular hepatic degeneration, hydrometra, and pyometra. These findings are compatible with the naturally occurring estrus-associated anemia seen in female ferrets.

Mink that were homozygous recessive for the Aleutian gene (aa) were inoculated with Aleutian disease virus (ADV) and simultaneously treated with cyclophosphamide (Cy). Control mink were inoculated with ADV. All mink were injected with bovine serum albumin (BSA) and their anti-BSA antibody response was measured to monitor the influence of drug therapy on the humoral antibody response. Formation of anti-BSA antibody was markedly suppressed and the hypergammaglobulinemia and development of AD lesions was inhibited in the Cy-treated mink. The non-Cy-treated control mink developed characteristic signs and lesions including glomerulonephritis and arteritis. The nontreated ADV-infected mink, but not the Cy-treated ADV-infected mink, had glomerular deposition of C3 and gamma globulin. Both groups had high titers of virus in their blood. These results indicate that the development of ADV lesions can be prevented by immunosuppressive treatment and further implicate host immune mechanisms in the pathogenesis of Aleutian disease.

ACCORDING to several reports, the prevalence of tonsillar carcinoma among dogs in London and Philadelphia is relatively high1–5. Because the prevalence in a rural population was never available for comparison, it was only speculation that the rate was higher for urban than for rural dogs. Carcinoma of the tonsil was the most common oral-pharyngeal tumour in both London and Philadelphia dogs. Withers5 estimated that the prevalence of tonsillar carcinoma in London dogs was 12 per 10,000. The prevalence was 9.1 per 10,000 in the Philadelphia study2. It has been proposed that an increased prevalence of carcinoma of the tonsil may be due to the presence of carcinogenic substances in the atmosphere of industrialized cities1.

Observations showed that the mosquito,Aedes fitchii (Felt andYoung), readily feeds on mink. Injection of homogenized mosquitoes, held for various periods after an infectious blood meal, into susceptible mink revealed that this mosquito retained Aleutian disease (AD) virus for 35 days. The virus in groundA. fitchii was titrated immediately and 15 days after infective feeding. The titer decreased from 104ID50/ml to 102ID50/ml during this time. Conversely, AD virus did not persist for six days inAedes aegypti (Linnaeus). Homogenized pools of heads combined with salivary glands ofA. fitchii 5, 10, and 15 days after infective feeding were injected into susceptible mink, viral infectivity was demonstrated in this region at 10 and 15 days after infective feeding but not at 5 days. This study suggests that replication of AD virus may occur inA. fitchii and a true vectorpathogen relationship exists between AD virus and certain arthropods.

Pathologic and virologic studies were conducted on 13 mature ewes with serum precipitin antibodies to progressive pneumonia virus (PPV). Pulmonary lesions of ovine progressive pneumonia were found in 4 sheep, a meningoencephalitis resembling visna in 1 sheep, chronic proliferative carpal arthritis in 2, and massive lymphoid proliferation in the mammary gland in 3. Virus producing cytopathic effect typical of PPV was isolated from the lungs, mediastinal lymph node, spleen, and choroid plexus of 4 sheep and from the carpal synovium of 2 sheep with chronic carpal arthritis. Three viral isolates selected for further study were antigenically related to visna virus by immunofluorescence and immunodiffusion, but these 3 isolates were not neutralized by antisera to reference strains of visna virus. Seemingly, infection of sheep by ovine retroviruses is common in the United States, and these viruses are capable of causing disease in more than 1 organ system.