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A Poland

Publications and source records attributed to A Poland.

At least 19 recordsLinked to original sources
PubMed2003

An epizootic of highly virulent feline calicivirus disease in a hospital setting in New England.

This article reports an outbreak of 24 cases of an unusually virulent feline calicivirus (FCV) infection in a small animal hospital. The circumstances and disease signs were very similar to those recently described in an outbreak of FCV hemorrhagic disease in Northern California (Vet. Microbiol. 73 (2000) 281). The virus entered the facility through shelter cats showing upper respiratory signs. Affected cats manifested high fever, anorexia, labored respirations, oral ulceration, facial and limb edema, icterus, and pancreatitis. The infection spread rapidly among the patients by contaminated animal caretakers and hospital equipment. One case of fomite transmission from an employee to a housecat was documented. Prior vaccination, even with multiple doses of FCV-F9-based live calicivirus vaccine, was not protective. Affected cats often required extensive supportive care for 7-10 days, and the overall mortality from death and euthanasia was 32%. The strain of FCV responsible for this outbreak was genetically and serologically distinct from the FCV strain responsible for a similar epizootic and the FCV-F9 strain contained in most vaccines. Outbreaks of this type are being reported with increasing frequency, and are often associated with the practice of treating sick shelter cats in private practices. Similar to the present epizootic, outbreaks of FCV hemorrhagic disease have been self-limiting, but require prompt application of strict quarantine, isolation, personnel sanitation, and disinfection procedures.

Animals↗
PubMed2002

Clinical, microscopic, and molecular aspects of canine leproid granuloma in the United States.

Leproid granulomas from seven dogs in the United States were evaluated. Gross characteristics included nodular and ulcerated dermal and subcutaneous lesions primarily on the caudal aspects of the pinnae and to a lesser extent on the muzzle, face, and forelimbs. In all except one dog, there was complete regression of the lesions within 6 months, either with no therapy or after surgical resection. Cytology or histopathology revealed pyogranulomatous inflammation with few to many acid-fast mycobacterial bacilli within macrophages. The organisms could not be cultivated in vitro. DNA sequencing of part of the 16S ribosomal RNA gene region revealed 99-100% homology among fragments from five of these dogs and fragments from dogs in the south Pacific. This syndrome occurs in dogs in North America and the prognosis is excellent, in contrast to the prognosis for rapid-growing or tuberculous mycobacteriosis.

Animals↗
PubMed2000

Binding of aryl hydrocarbon receptor (AhR) to AhR-interacting protein. The role of hsp90.

The aryl hydrocarbon receptor (AhR) has been shown to interact with an immunophilin-like molecule known as AhR-interacting protein (AIP) and to enhance AhR function. We show here that AIP associates with AhR homologues from mouse and fish, which can bind ligands such as dioxin, but nonligand binding homologues from Caenorhabditis elegans or Drosophila do not bind to AIP. However, a minimal ligand-binding domain of the AhR is incapable of binding AIP. The binding of AIP to AhR in reticulocyte lysate shows several of the characteristics of an hsp90-dependent process, including sensitivity to geldanamycin and temperature and a requirement for ATP or nonhydrolyzable analogues. Purified AIP binds to the C terminus of hsp90, and mutation of a conserved basic residue in the tetratricopeptide repeats of AIP (K266A, analogous to K97A in protein phosphatase 5) abolishes binding to hsp90. Mutation of K266A in AIP reduces binding to AhR by 75-80%; the geldanamycin sensitivity of this complex shows that AhR stabilizes the AIP-hsp90-AhR complex. The alpha-helical C terminus of AIP, which is outside the tetratricopeptide repeat domain, is absolutely required for binding to AhR as shown by deletions of the C-terminal 5 amino acids or alanine-scanning mutagenesis, but it is not required for binding of AIP to hsp90. The data support a model where 1) AIP binds to both hsp90 and AhR; 2) hsp90 is required for AhR-AIP binding; and 3) the binding of AhR to AIP stabilizes the AIP-hsp90-AhR complex.

Amino Acid Sequence↗
PubMed2000

An isolated epizootic of hemorrhagic-like fever in cats caused by a novel and highly virulent strain of feline calicivirus.

An isolated epizootic of a highly fatal feline calicivirus (FCV) infection, manifested in its severest form by a systemic hemorrhagic-like fever, occurred over a 1-month period among six cats owned by two different employees and a client of a private veterinary practice. The infection may have started with an unowned shelter kitten that was hospitalized during this same period for a severe atypical upper respiratory infection. The causative agent was isolated from blood and nasal swabs from two cats; the electron microscopic appearance was typical for FCV and capsid gene sequencing showed it to be genetically similar to other less pathogenic field strains. An identical disease syndrome was recreated in laboratory cats through oral inoculation with tissue culture grown virus. During the course of transmission studies in experimental cats, the agent was inadvertently spread by caretakers to an adjoining room containing a group of four normal adult cats. One of the four older cats was found dead and a second was moribund within 48-72h in spite of symptomatic treatment; lesions in these animals were similar to those of the field cats but with the added feature of severe pancreatitis. The mortality in field cats, deliberately infected laboratory cats, and inadvertently infected laboratory cats ranged from 33-50%. This new isolate of calicivirus, named FCV-Ari, was neutralized at negligible to low titer by antiserum against the universal FCV-F9 vaccine strain. Cats orally immunized with FCV-F9, and then challenge-exposed shortly thereafter with FCV-Ari, developed a milder self-limiting form of disease, indicating partial protection. However, all of the field cats, including the three that died, had been previously immunized with parenteral FCV-F9 vaccine. FCV-Ari caused a disease that was reminiscent of Rabbit Hemorrhagic Disease, a highly fatal calicivirus infection of older rabbits.

Animals↗
PubMed1999

Outbreak of fatal salmonellosis in cats following use of a high-titer modified-live panleukopenia virus vaccine.

A 14-week-old kitten from a private cattery was examined because of an acute onset of recumbency and epistaxis 10 days after receiving a high-titer modified-live virus vaccine containing panleukopenia virus, calicivirus, and herpesvirus components. The kitten died the following day, and intestinal crypt necrosis; hepatic, splenic, and lymph node inflammation and necrosis; and pneumonia were seen at necropsy. Salmonella typhimurium was isolated from mesenteric lymph nodes and the spleen. The breeder reported that 4 other kittens had died in the previous month, each within 1 to 2 weeks after being vaccinated with the same modified-live virus vaccine. Carcasses of 3 kittens were available for examination, and Salmonella sp was isolated from mesenteric lymph nodes of all 3. Villus crypt necrosis and secondary fibrosis were also found. Three of the remaining 12 kittens in the cattery were also found to be shedding Salmonella sp in their feces. Clinical and pathologic findings in these kittens were likely attributable to salmonellosis and panleukopenia, and suggest that mild immunosuppression induced by vaccination could have facilitated development of fatal salmonellosis in subclinical carrier kittens. However, we cannot prove that vaccination actually played any role.

Animals↗
PubMed1999

The trouble with TEFs.

Comments on Van den Berg, et al. Toxic equivalency factors (TEFs) for PCBs, PCDDs, PCDFs for humans and wildlife. Environ Health Perspect 106:775-792 (1998)

Animals↗
PubMed1998

Feline infectious peritonitis viruses arise by mutation from endemic feline enteric coronaviruses.

Feline infectious peritonitis virus (FIPV) strains from six cats and three different geographic areas were compared genetically with feline enteric coronavirus (FECV) isolates obtained from cats inhabiting the same environments. Sequence comparisons were made from 1.2- to 8.9-kb segments on the 3' end of the genome. FECV/FIPV pairs from the same catteries or shelters were 97.3-99.5% related but were genetically distinct from FIPV and FECV strains obtained from cats living in geographically distinct environments. The high genetic similarity between FECVs and FIPVs from the same environment strongly suggested a common ancestry. Based on the presence of deletion mutations in the FIPVs and not in the FECVs, it was concluded that FIPVs evolved as mutants of FECVs. The mutations are deletions in the FIPVs and not insertions in the FECVs since similar sequences are present in other strains that have segregated earlier from a common ancestor. Therefore, the order of descent is form FECV to FIPV. Mutations unique to FIPVs were found in open reading frames (ORFs) 3c in 4 of 6 isolates and/or 7b in 3 of 6 isolates. When the study was extended to include 7 additional FIPV isolates, 11/13 of the FIPVs sequenced were found to have mutated 3c ORFs.

Amino Acid Sequence↗
PubMed1998

Ehrlichia spp. in cervids from California.

Blood samples from six mule deer (Odocoileus hemionus hemionus), 15 black-tailed deer (O. hemionus columbianus), and 29 elk (Cervus elaphus nannodes) were assayed for human monocytic and human granulocytic ehrlichiosis (HGE) by polymerase chain reaction (PCR), DNA sequencing, and serology to determine whether or not cervids are involved in the maintenance of these potential human pathogens in California (USA). The deer were sampled in August to October 1992-95. The 29 tule elk from Point Reyes National Seashore were sampled in August 1997. All deer were seronegative for antibodies to HGE/Ehrlichia equi, while the E. equi seroprevalence among elk was 17%. The 16S rDNA PCR prevalence in deer was 38% (in mule deer and black-tailed deer) for Ehrlichia-like sp. of white-tailed deer, 5% (one black-tailed deer only) for E. equi, and 0% for E. chaffeensis. The PCR prevalence in elk was 0% for Ehrlichia-like sp. of white-tailed deer, 31% for E. equi, and 0% for E. chaffeensis. The E. equi from two positive elk samples was successfully propagated in HL-60 cell cultures. DNA sequencing confirmed that the Ehrlichia-like sp. sequences from deer in California were closely related to sequences reported from white-tailed deer from Oklahoma and Georgia. The E. equi strain from deer and elk resembled other E. equi strains from California. These results suggest that cervids may be important in the natural maintenance of E. equi in California.

Animals↗
PubMed1998

Molecular, clinical, and pathologic comparison of two distinct strains of Haemobartonella felis in domestic cats.

OBJECTIVE: To characterize 2 strains of Haemobartonella felis by use of molecular techniques. ANIMALS: 35 specific-pathogen-free cats, 6 months to 4 years old. PROCEDURE: Intraperitoneal or IV inoculation with blood containing H felis small form (Hfsm, 18 cats) or H felis large form (Hflg, 11 cats); 6 cats were uninfected controls. Hfsm was evaluated for capability to cross-protect against the more virulent Hflg. Morphology of both strains was compared by light microscopy of Wright-Giemsa-stained blood smears, and the 16S rRNA genes were sequenced. RESULTS: Infection with Hflg induced signs of depression, fever, and severe macrocytic normochromic anemia with nucleated erythrocytes. More than 95% of erythrocytes were parasitized. Inoculation with Hfsm and uninfected control blood induced mild or no clinical signs and no hematologic abnormalities. Anti-H felis IgG was first detected on postinoculation day (PID) 21, and increased to maximal titer of 400 by PID 28. Reactivated infection was observed in 8 of 29 cats (4 Hfsm and 4 Hflg), with 5% parasitized erythrocytes during the later attack. On PID 8, Hflg-inoculated cats had positive results of polymerase chain reaction analysis (PCR) that persisted until cats were treated with doxycycline or oxytetracycline; Hfsm-inoculated cats had positive PCR results that persisted for duration of observation (3 months). CONCLUSIONS: Genetically and morphologically distinct strains of H felis infect cats in the field. The level of genetic difference suggested that these strains may be different species or genera. CLINICAL RELEVANCE: PCR is a critical diagnostic aid to detect occult Haemobartonella spp infection, as well as response to treatment and clearance of the organism.

Anaplasmataceae↗
PubMed1997

Patterns of feline coronavirus infection and fecal shedding from cats in multiple-cat environments.

OBJECTIVE: To determine, by use of a reverse transcriptase-polymerase chain reaction (RT-PCR) test, patterns of fecal shedding of feline coronavirus among cats. DESIGN: Prospective observational study. ANIMALS: 275 purebred cats from 6 private catteries and 40 specific-pathogen-free (SPF) laboratory-reared cats. PROCEDURE: 40 SPF cats were experimentally inoculated with crude fecal extract containing feline enteric coronavirus (FECV). Fecal and plasma samples were collected every 4 days and evaluated by use of RT-PCR and indirect immunofluorescence assays, respectively, to correlate RT-PCR results with fecal infectivity and to determine patterns of FECV shedding and anti-FECV IgG production in acutely infected cats. The 275 cats in private catteries were monitored for 1 year. Fecal and blood samples were collected every 1 to 3 months and assayed by use of RT-PCR and serologic tests to determine patterns of coronavirus shedding and cofactors for high frequency shedding. RESULTS: Results of the RT-PCR test in SPF cats were directly correlated with fecal extract infectivity. Overall, 370 of 894 (41%) fecal samples collected from cattery and shelter cats contained infectious levels of coronavirus. Of 121 cats from which multiple samples were collected, 11 never shed virus and 35, 65, and 10, respectively, shed virus with low, moderate, and high frequency. High frequency shedding was associated with age and cattery of origin, but not with sex or concurrent disease. Stress associated with parturition and lactation did not induce shedding in queens. Kittens did not shed coronavirus before they were 10 weeks old, even when nursed by shedding mothers. CLINICAL IMPLICATIONS: A large proportion of cats in multiple-cat environments shed coronavirus at any given time, but most undergo cycles of infection and shedding, recovery, and reinfection. Infection is acquired from chronically shedding cats and from infectious cats undergoing transient primary infection. Chronically shedding cats cannot be identified on the basis of antibody titer or signalment, but must be identified on the basis of the results of serial fecal RT-PCR tests.

Animals↗
PubMed1997

Risk factors for feline infectious peritonitis among cats in multiple-cat environments with endemic feline enteric coronavirus.

OBJECTIVE: To determine what risk factors, other than genetic predisposition, contribute to the incidence of feline infectious peritonitis (FIP) in private breeding catteries and animal shelters. DESIGN: Cats from 7 catteries and a shelter were observed monthly for 1 year. At each visit, cats were examined, fecal samples were collected for determination of feline coronavirus shedding, and blood samples were collected for determination of coronavirus antibody titers. Diagnostic tests were performed on all cats that died of FIP. ANIMALS: 275 purebred or random-bred cats that were kept by private breeder-owners in homes. RESULTS: 24 cats died of FIP during the study. Development of FIP was not associated with cattery, mean cat number, mean age, sex, cattery median coronavirus antibody titer, husbandry and quarantine practices, caging and breeding practices, or prevalence of concurrent diseases. However, risk factors for FIP included individual cat age individual cat coronavirus titer, overall frequency of fecal coronarvirus shedding, and the proportion of cats in the cattery that were chronic coronavirus shedders. Deaths from FIP were more frequent in fall and winter, and on the basis of analysis of cattery records, the number of deaths varied yearly. Epidemics (> 10% mortality rate) were reported at least once in 5 years in 4 catteries. CLINICAL IMPLICATIONS: Elimination of FIP from a cattery is only possible by total elimination of endemic feline enteric coronavirus (FECV) infection. The most important procedure to reduce FECV from catteries is elimination of chronic FECV shedders.

Age Factors↗
PubMed1994

Photoaffinity labeling of the Ah receptor: phylogenetic survey of diverse vertebrate and invertebrate species.

The mammalian aromatic hydrocarbon (Ah) receptor is a soluble protein involved in the regulation of gene expression by halogenated aromatic hydrocarbons such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Little is known, however, about the presence and properties of this receptor in nonmammalian species. In these studies, we sought evidence for an Ah receptor in the liver or liver-equivalent of diverse species of invertebrate and vertebrate animals. Velocity sedimentation analysis of hepatic cytosol labeled with [3H]TCDD gave equivocal results with three species of marine fish. In subsequent studies, photoaffinity labeling with 2-azido-3-[125I]iodo-7,8-dibromodibenzo-p-dioxin was used to identify the Ah receptor. Specific labeling (labeling that could be displaced by an excess of unlabeled ligand) was observed in seven species of teleost and elasmobranch fish, including winter flounder (Pleuronectes americanus), killifish (Fundulus heteroclitus), scup (Stenotomus chrysops), rainbow trout (Oncorhynchus mykiss), brown trout (Salmo trutta), and dogfish (Mustelus canis and Squalus acanthias). Specific labeling was also found in cytosolic fractions prepared from PLHC-1 fish hepatoma cells and livers of a turtle (Chrysemys picta) and a cetacean, the beluga whale Delphinapterus leucas. The fish Ah receptor was sensitive to conditions of tissue preparation; inclusion of proteinase inhibitors in the homogenization buffer stabilized the receptor in some species. There was heterogeneity in the apparent molecular mass of the largest specifically labeled band in each species; these ranged from 105 to 146 kDa, slightly larger on average than mammalian Ah receptors (95-130 kDa). In contrast to the results obtained with teleost and elasmobranch fish, no specifically labeled polypeptides were detectable in cytosol from two agnathan fish species (hagfish Myxine glutinosa and sea lamprey Petromyzon marinus), the tunicate Ciona intestinalis, or any of nine other invertebrate species representing eight classes in four phyla. Overall these results suggest that the Ah receptor evolved at least 450 million years ago, prior to the divergence of bony and cartilaginous fishes. Although the exact relationship between receptor presence and dioxin responsiveness in these species is uncertain, our data predict that the invertebrate species examined in this study, which appear to lack an Ah receptor protein like that seen in mammals and fish, may be less sensitive than vertebrates to the effects of environmental contaminants that act through this transcriptional regulator.

Affinity Labels↗
PubMed1994

Analysis of the four alleles of the murine aryl hydrocarbon receptor.

The cDNAs for the four murine aryl hydrocarbon (Ah) receptor alleles were cloned and sequenced, and the deduced amino acid sequences were compared. The Ahb-1 allele encodes a protein of 805 amino acids, the Ahd and Ahb-2 alleles encode proteins of 848 amino acids, and the Ahb-3 allele encodes a protein of 883 amino acids. The alleles differ by eight point mutations in the common open reading frame (the initial 805 amino acids) and by additional sequences at the carboxyl end. The amino halves of the proteins, containing a spliced leader sequence, a basic helix-loop-helix motif, and two 50-amino acid repeats (PAAS), have identical sequences except for a single amino acid change in the second PAAS box. The Ahd allele, which has a lower ligand binding affinity, differs from the Ahb-2 receptor by only two amino acids. Mutagenesis experiments with these cloned cDNAs, using in vitro transcription and translation and 2-[125I]iodo-7,8-dibromodibenzo-p-dioxin binding, indicate that the low ligand binding affinity of the Ahd allele is attributable to a valine at residue 375; changing this amino acid to an alanine, as in the Ahb-2 protein, enhances the affinity 4-fold. For in vitro translated Ahb-1 and Ahb-2 alleles the Kd values were approximately 6-10 pM and for Ahd the Kd value was approximately 37 pM. Using 5' truncation and mutations to produce 3' translation truncation sites, we mapped the ligand binding region for the Ahb-1 allele.

Alleles↗
PubMed1994

The aryl hydrocarbon receptor and aryl hydrocarbon receptor nuclear translocator protein show distinct subcellular localizations in Hepa 1c1c7 cells by immunofluorescence microscopy.

The aryl hydrocarbon receptor (AhR) and AhR nuclear translocator (Arnt) protein were evaluated in the Hepa 1c1c7 (Hepa-1) cell line by indirect immunofluorescence microscopy and Western blot analysis. Wild-type (WT) Hepa-1 cells stained for AhR show intense cytoplasmic fluorescence with minimal nuclear reactivity. WT cells treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) show a time-dependent decrease in cytoplasmic AhR staining and a concomitant increase in nuclear fluorescence. WT cells stained for Arnt show nuclear fluorescence with minimal cytoplasmic reactivity, a pattern unchanged after TCDD treatment. Hepa-1 type II variants express normal levels of AhR but are defective in TCDD-mediated induction of cytochrome P4501A1. Type II variants stained for Arnt show reduced nuclear fluorescence, compared with WT cells, and express minimal levels of Arnt protein, as determined by Western blot analysis. Type II variants stained for the AhR show intense cytoplasmic fluorescence that becomes nuclear after TCDD treatment. Detailed evaluation by immunoelectron microscopy of the AhR and Arnt present in the nuclear compartment of WT cells shows that both proteins are uniformly distributed and do not appear to be associated with nuclear pores, membranes, or nucleoli. Western blot analysis of nuclei isolated from WT Hepa-1 cells fractionated with Nonidet P-40 shows that minimal levels of AhR or Arnt are retained in the nuclear fraction after TCDD treatment. Collectively, these results indicate that the unliganded AhR resides in the cytoplasm, Arnt is localized to the nucleus, and Hepa-1 cells defective in Arnt expression exhibit TCDD-mediated nuclear accumulation of the AhR.

Amino Acid Sequence↗
PubMed1993

Physiological and genetic analyses of inbred mouse strains with a type I iodothyronine 5' deiodinase deficiency.

Inbred mouse strains differ in their capacity to deiodinate iododioxin and iodothyronines, with strains segregating into high or low activity groups. Metabolism of iododioxin occurs via the type I iodothyronine 5'deiodinase (5'DI), one of two enzymes that metabolize thyroxine (T4) to 3,5,3'-triiodothyronine (T3). Recombinant inbred strains derived from crosses between high and low activity strains exhibit segregation characteristic of a single allele difference. Hepatic and renal 5'DI mRNA in a high (C57BL/6J) and low (C3H/HeJ) strain paralleled enzyme activity and concentration, in agreement with a recent report. 5'DI-deficient mice had twofold higher serum free T4 but normal free T3 and thyrotropin. Brown adipose tissue 5'DII was invariant between the two strains. Southern analyses using a 5'DI probe identified a restriction fragment length variant that segregated with 5'DI activity in 33 of 35 recombinant inbred strains derived from four different pairs of high and low activity parental strains. Recombination frequencies using previously mapped loci allowed assignment of the 5'DI gene to mouse chromosome 4 and identified its approximate chromosomal position. We propose the symbol Dio1 to denote the mouse 5'DI gene. Conserved linkage between this segment of mouse chromosome 4 and human HSA1p predicts this location for human Dio1.

Animals↗
PubMed1993

Impairment of the selenoenzyme type I iodothyronine deiodinase in C3H/He mice.

Type I iodothyronine deiodinase (ID-I) activity is impaired in C3H/He (C3H) mice compared with BALB/c and C57BL/6N (C57) mice. In this study we compared ID-I activity and protein labeling with N-bromoacetyl(-)[125I]T3 (BrAc[125I]T3) or 75Se in liver microsomes of C3H and C57 mice. Hepatic ID-I activity in C3H mice was highly variable with a median of only 18% of that in C57 mice. However, C3H mice had normal serum T4 and T3 levels, although serum reverse T3 was increased. The 28-kilodalton (kDa) ID-I protein was identified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis of BrAc[125I]T3-labeled microsomes. Labeling of this protein was virtually undetectable in C3H samples with low enzyme activity. ID-I activity in liver microsomes was strongly decreased in Se-deficient mice, which was paralleled by a drastic decrease in BrAc[125I]T3-labeling of the 28-kDa band compared with control mice. Labeling of ID-I with 75Se was demonstrated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis of liver microsomes of [75Se]selenite-injected mice. 75Se labeling of the 28-kDa band was markedly higher in Se-deficient than in control mice and was also markedly higher in C57 than in C3H mice. Finally, liver ID-I messenger RNA (mRNA) was measured on Northern blots using a rat ID-I complementary DNA probe. Messenger RNA levels correlated strongly with ID-I activity, showing a significant decrease in C3H mice. We conclude that in mice, like in rats and humans, ID-I is a selenoprotein. ID-I activity is impaired in C3H mice because of decreased transcription of the ID-I gene or reduced stability of the mRNA.

Animals↗