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PubMed1992

Nitric oxide synthase in ferret brain: localization and characterization.

1. In the present study, we have investigated the distribution of nitric oxide synthase in the ferret brain. Nitric oxide synthase was determined biochemically and immunochemically. 2. In the rat brain, the highest nitric oxide synthase activity has been detected in the cerebellum. However, in the ferret brain, the highest activity was found in the striatum and the lowest in the cerebellum and cerebral cortex. The enzymatic activity was localized predominantly in the cytosolic fractions, it was dependent on NADPH and Ca2+, and inhibited by NG-nitro-L-arginine or NG-methyl-L-arginine. 3. Western blot analysis revealed that all regions of the ferret brain contained a 160 kD protein crossreacting with an antibody to nitric oxide synthase purified from the rat cerebellum, and the levels of relative intensity of staining by the antibody correlated with the distribution of nitric oxide synthase activity. 4. These results indicate that the ferret brain contains a nitric oxide synthase similar to the rat brain, but the distribution of enzymatic activity in the ferret brain differs markedly from the rat brain.

Amino Acid Oxidoreductases↗
PubMedDate not supplied

Genetic diversity of Pneumocystis carinii derived from infected rats, mice, ferrets, and cell cultures.

The degree of strain and/or species diversity among Pneumocystis carinii isolates is unknown. As a first approach to the study of P. carinii genetic relatedness, we compared the pulsed field gel electrophoretic karyotypes of P. carinii derived from lung homogenates of three immunosuppressed host animals: rats transtracheally inoculated with P. carinii-infected mouse lung; and ferrets which developed reactivated latent P. carinii pneumonia. Rat P. carinii propagated on HEL299 cells was also examined. Karyotypes of P. carinii DNA from both rat lung homogenate and cell culture were identical (14 bands, 315-680 kb). In contrast, mouse and ferret P. carinii DNA karyotypes were each distinctly different from the rat P. carinii samples (mouse P. carinii 15 bands, 315-610 kb; ferret P. carinii nine bands, 410-760 kb). Three distinct rat P. carinii gene probes reacted with both Southern-transferred rat and mouse P. carinii DNA but not with ferret P. carinii DNA. Thus, P. carinii from rat, mouse, and ferret are genetically diverse. The results are consistent with recently reported antigenic and nucleic acid sequence differences among P. carinii isolates recovered from different hosts.

Animals↗
PubMed1988

Transmission of measles virus encephalitis to ferrets by intracardiac inoculation of a cell-associated SSPE virus strain.

Ferret fibroblasts infected with a cell-associated strain of subacute sclerosing panencephalitis virus were inoculated into the hearts of ferrets in order to study whether the virus can spread from the blood to the brain in this animal model. Five of 21 inoculated ferrets developed encephalitis 5-7 days later and were sacrificed. Sick animals showed inflammatory lesions in the brain, both perivascular cuffings and infiltration of inflammatory cells in the choroid plexus and meninges. Virus was isolated in cell cultures from various parts of the brain and virus antigen was found by immunostaining, particularly in the cortex. Virus was not detected in inflammatory cells by immunostaining but in situ hybridization with a cDNA probe demonstrated measles virus RNA in neurons and glia cells surrounding perivascular inflammatory cuffings and in a lymph node of one ferret. Ferrets inoculated into the heart with cell-associated SSPE virus seem to be a suitable animal model to study how the virus spreads from the blood to the brain.

Animals↗
PubMed1987

Intracellular pH in sheep Purkinje fibres and ferret papillary muscles during hypoxia and recovery.

1. The changes of intracellular pH (pHi) of papillary muscles from ferret and Purkinje fibres from sheep heart during hypoxia and recovery from hypoxia were recorded with pH-sensitive micro-electrodes filled with neutral H+ carrier. 2. Hypoxia was produced by replacement of O2 with N2 in the superfusing solutions. When oxidative phosphorylation was prevented, developed tension fell within 20 min to about 16 and 21% of its control value for papillary muscle and Purkinje fibres respectively. On restoration of O2, recovery of developed tension in ferret papillary muscle is preceded by a transient additional decrease. 3. In ferret papillary muscle, the pHi first increased by a mean value of 0.11 pH units after 3 min hypoxia, then decreased by about 0.24 pH units after 20 min. In sheep Purkinje fibres, the initial alkalosis was small or absent, and after 5-9 min, the pHi started to fall reaching 0.17 pH units after 20 min of hypoxia. On return to oxygenated solution, a transient additional intracellular acidification occurred. This acidification reached its peak of 0.31 pH units in papillary muscle and of 0.13 pH units in Purkinje fibres. In both preparations hypoxia was accompanied by a depolarization of a few millivolts. 4. The presence of cyanide (1-2 mM) or fluorodinitrobenzene (20-40 microM) prevented the additional intracellular acidification occurring on return to oxygenated solution. Removal of cyanide itself produced a transient but smaller and slower acidification. 5. On both preparations, exposure to a Tyrode solution containing 10 mM-L-lactate produced a transient intracellular acidification. After recovery from this acidification the acidification produced by hypoxia was increased without affecting the extra acidification on reintroduction of O2. 6. After reduction of the rate of glycolysis by removal of glucose and application of 2-deoxyglucose, the transient intracellular acidification, occurring on return to oxygenated solution after hypoxia, was inhibited in both preparations. In ferret papillary muscle, insulin (100 mU/ml) potentiated the changes of pHi occurring during hypoxia. 7. Using Na+-sensitive glass micro-electrodes it was found that the intracellular Na+ activity rose slightly during the later stages of hypoxia and rose transiently on readdition of O2. These results are consistent with a Na+-H+ exchange being stimulated by acidosis. 8. The origins of the pH changes during and after hypoxia are discussed as are the differences between the responses of sheep Purkinje fibres and ferret papillary muscle.

Animals↗
PubMed2003

Brain penetration of aprepitant, a substance P receptor antagonist, in ferrets.

The pharmacokinetics, metabolism, and brain penetration of the neurokinin 1 (NK1) receptor antagonist (substance P receptor antagonist), aprepitant (MK-0869), were examined in ferrets. This species exhibits human-type NK1receptor pharmacology and is of proven value in the identification of clinically useful drugs for the treatment of chemotherapy-induced nausea and vomiting in humans. After a single p.o. dose of aprepitant at 1 or 2 mg/kg, plasma levels of the compound were between approximately 200 and 270 ng/ml, 24 h after dosing. In the brain cortex, concentrations of aprepitant reached between approximately 80 and 150 ng/g of tissue 24 h after dosing. The predominant radioactive component present in the plasma and the brain of ferrets at 24 or 48 h after a single oral dose of [14C]aprepitant at 3 mg/kg was the parent compound itself. The slow plasma clearance of aprepitant ( approximately 1.5 ml/min/kg) and its abundance in ferret brain were in accord with its efficacy in blocking the retching and vomiting at 24 and 48 h postdose when ferrets were challenged with the emetic anticancer drug, cisplatin. When aprepitant and some of its metabolites were assessed for their in vitro binding affinity to the human NK1receptor, aprepitant demonstrated the highest affinity. Collectively, these data suggested that aprepitant, rather than its metabolites, was responsible, primarily, for the antiemetic activity of this compound in the male ferret.

Animals↗
PubMed1976

Influenza infection in ferrets: role of serum antibody in protection and recovery.

The passive administration of ferret antiserum to Ao (H0N1) influenza virus failed to protect the recipient ferrets from subsequent infection with homologous virus. This susceptibility to infection was observed even when the passively acquired serum hemagglutination inhibition (HI) titer was similar to peak convalescent titers. It is therefore concluded that serum antibody alone is probably not a major factor in the prevention of influenza infection. This does not rule out a possible role for serum antibody in prevention of illness. Subsequent to infection, ferrets that had received passive antisera failed to develop high levels of serum HI antibody. In fact, many had no detectable serum antibody (less than 1:8). These animals shed virus for periods of time quite similar to those of infected control animals, which did develope serum antibody. From these data it was concluded that detectable serum HI antibody does not play a significant role in the recovery of ferrets from influenza infection. Interferon was present in high concentrations in the secretions a few days prior to cessation of virus shedding, but it is not clear whether this was the cause of the recovery or merely a concomitant event. Twenty-one days after initial infection two-thirds of the ferrets that had received passive antibody and all control animals were immune to reinfection with the homologous influenza virus. Since the former group had little or no detectable serum HI antibody but most members were immune, there must be some other host mechanism to account for the immunity.

Administration, Intranasal↗
PubMed1988

Gastric colonization by Campylobacter pylori subsp. mustelae in ferrets.

Campylobacter pylori subsp. mustelae was cultured from both normal and inflamed gastric mucosa of ferrets. Examination of neonatal, juvenile, and adult ferrets established that the gastric mucosa in the majority of preweanling (age, less than 6 weeks) ferrets sampled were not colonized with C. pylori subsp. mustelae, whereas the gastric mucosa of 100% of adult ferrets were colonized with this gastric organism. C. pylori subsp. mustelae was isolated from the gastric mucosa on a sequential basis from nine ferrets during a several-month period, inferring either persistent colonization or frequent reinfection with C. pylori subsp. mustelae.

Age Factors↗
PubMed1994

Intracellular Campylobacter-like organism from ferrets and hamsters with proliferative bowel disease is a Desulfovibrio sp.

Proliferative bowel disease is an intestinal disorder of a variety of domestic animals associated with the presence of an intracellular Campylobacter-like organism (ICLO). We have identified the ICLO obtained from a ferret with proliferative colitis by 16S rRNA sequence analysis. In this ferret, proliferative bowel tissue containing the ICLO had translocated to the mesenteric lymph nodes, omentum, and liver. The 16S rRNA genes of the ICLO were amplified from an infected fragment of extraintestinal tissue by using universal prokaryotic primers. Approximately 1,480 bases of the amplified 16S rRNA gene were sequenced by cycle sequencing. Comparison of the sequence of the ICLO with those of over 400 bacteria in our data base indicated that the sequence of the ICLO was most closely related to that of Desulfovibrio desulfuricans (87.5% similarity). Phylogenetic analysis with 12 Desulfovibrio species and 20 species from related genera placed the ICLO in a subcluster within the genus Desulfovibrio with D. desulfuricans and 5 other Desulfovibrio species. We will refer to this organism as the intracellular Desulfovibrio organism (IDO). Specific primers were produced for PCR amplification of a 550-base fragment of the 16S rRNA gene of the IDO in proliferative intestinal tissue samples. This unique 550-base segment was amplified from samples of frozen intestinal tissue from nine ferrets and three hamsters with ICLO-associated disease but not in four intestinal tissue samples from animals without the ICLO-associated disease. The 550-base amplified products from the bowel tissues of one hamster and one ferret were fully sequenced. The ferret IDO partial sequence was identical to the previously determined 16S rRNA sequence over its length, and the hamster IDO sequence differed by a single base. The same intracellular organism has been identified in proliferative intestinal tissues of swine and that the organism has been successfully maintained in tissue culture. The availability of specific primers for PCR-based detection of this intracellular Desulfovibrio organism will aid in the determination of its role in the pathogenesis of proliferative bowel disease in a variety of infected hosts.

Animals↗
PubMed2002

Pathogenesis of avian influenza A (H5N1) viruses in ferrets.

Highly pathogenic avian influenza A H5N1 viruses caused outbreaks of disease in domestic poultry and humans in Hong Kong in 1997. Direct transmission of the H5N1 viruses from birds to humans resulted in 18 documented cases of respiratory illness, including six deaths. Here we evaluated two of the avian H5N1 viruses isolated from humans for their ability to replicate and cause disease in outbred ferrets. A/Hong Kong/483/97 virus was isolated from a fatal case and was highly pathogenic in the BALB/c mouse model, whereas A/Hong Kong/486/97 virus was isolated from a case with mild illness and exhibited a low-pathogenicity phenotype in mice. Ferrets infected intranasally with 10(7) 50% egg infectious doses (EID(50)) of either H5N1 virus exhibited severe lethargy, fever, weight loss, transient lymphopenia, and replication in the upper and lower respiratory tract, as well as multiple systemic organs, including the brain. Gastrointestinal symptoms were seen in some animals. In contrast, weight loss and severe lethargy were not noted in ferrets infected with 10(7) EID(50) of two recent human H3N2 viruses, although these viruses were also isolated from the brains, but not other extrapulmonary organs, of infected animals. The results demonstrate that both H5N1 viruses were highly virulent in the outbred ferret model, unlike the differential pathogenicity documented in inbred BALB/c mice. We propose the ferret as an alternative model system for the study of these highly pathogenic avian viruses.

Adolescent↗
PubMed2005

Lethality to ferrets of H5N1 influenza viruses isolated from humans and poultry in 2004.

The 2004 outbreaks of H5N1 influenza viruses in Vietnam and Thailand were highly lethal to humans and to poultry; therefore, newly emerging avian influenza A viruses pose a continued threat, not only to avian species but also to humans. We studied the pathogenicity of four human and nine avian H5N1/04 influenza viruses in ferrets (an excellent model for influenza studies). All four human isolates were fatal to intranasally inoculated ferrets. The human isolate A/Vietnam/1203/04 (H5N1) was the most pathogenic isolate; the severity of disease was associated with a broad tissue tropism and high virus titers in multiple organs, including the brain. High fever, weight loss, anorexia, extreme lethargy, and diarrhea were observed. Two avian H5N1/04 isolates were as pathogenic as the human viruses, causing lethal systemic infections in ferrets. Seven of nine H5N1/04 viruses isolated from avian species caused mild infections, with virus replication restricted to the upper respiratory tract. All chicken isolates were nonlethal to ferrets. A sequence analysis revealed polybasic amino acids in the hemagglutinin connecting peptides of all H5N1/04 viruses, indicating that multiple molecular differences in other genes are important for a high level of virulence. Interestingly, the human A/Vietnam/1203/04 isolate had a lysine substitution at position 627 of PB2 and had one to eight amino acid changes in all gene products except that of the M1 gene, unlike the A/chicken/Vietnam/C58/04 and A/quail/Vietnam/36/04 viruses. Our results indicate that viruses that are lethal to mammals are circulating among birds in Asia and suggest that pathogenicity in ferrets, and perhaps humans, reflects a complex combination of different residues rather than a single amino acid difference.

Animals↗
PubMed1990

Pulmonary arterial and venous constriction during hypoxia in 3- to 5-wk-old and adult ferrets.

We have determined the sites of hypoxic vasoconstriction in ferret lungs. Lungs of five 3- to 5-wk-old and five adult ferrets were isolated and perfused with blood. Blood flow was adjusted initially to keep pulmonary arterial pressure at 20 cmH2O and left atrial and airway pressures at 6 and 8 cmH2O, respectively (zone 3). Once adjusted, flow was kept constant throughout the experiment. In each lung, pressures were measured in subpleural 20- to 50-microns-diam arterioles and venules with the micropipette servo-nulling method during normoxia (PO2 approximately 100 Torr) and hypoxia (PO2 less than 50 Torr). In normoxic adult ferret lungs, approximately 40% of total vascular resistance was in arteries, approximately 40% was in microvessels, and approximately 20% was in veins. With hypoxia, the total arteriovenous pressure drop increased by 68%. Arterial and venous pressure drops increased by 92 and 132%, respectively, with no change in microvascular pressure drop. In 3- to 5-wk-old ferret lungs, the vascular pressure profile during normoxia and the response to hypoxia were similar to those in adult lungs. We conclude that, in ferret lungs, arterial and venous resistances increase equally during hypoxia, resulting in increased microvascular pressures for fluid filtration.

Aging↗
PubMed1997

Estimation of thickness of airway surface liquid in ferret trachea in vitro.

The tracheae of ferrets and rabbits were mounted in vitro in organ baths. While the tracheae were liquid filled, the permeability coefficient ( P) was determined, and then while the tracheae were air filled, the percent clearance for 99mTc-labeled diethylenetriaminepentaacetic acid (DTPA) was determined. The thickness of airway surface liquid (ASL) was estimated by three methods. 1) The initial concentration of 99mTc-DTPA and the total amount of 99mTc-DTPA (the sum of that entering the outside medium, that draining from the trachea, and that washed out at the end of 40 min) gave the initial volume of ASL and thus its thickness. Mean values were 45.7 micron for the ferret and 41.9 micron for the rabbit. 2) Estimates of ASL thickness at the end of the 40-min period, based on the final 99mTc-DTPA concentration and the amount in the washout, were 42.9 micron for ferret and 45.4 micron for rabbit. 3) The ratio of P to percent clearance gave mean ASL thickness values of 49.2 micron for the ferret and 40.3 micron for the rabbit. Thus three separate methods for determining ASL thickness give very similar results, with means in the range 40-49 micron. Administration of methacholine or atropine to ferret tracheae did not significantly change ASL thickness.

Animals↗
PubMed2003

Receptive fields and response properties of neurons in layer 4 of ferret visual cortex.

The ferret has become a model animal for studies exploring the development of the visual system. However, little is known about the receptive-field structure and response properties of neurons in the adult visual cortex of the ferret. We performed single-unit recordings from neurons in layer 4 of adult ferret primary visual cortex to determine the receptive-field structure and visual-response properties of individual neurons. In particular, we asked what is the spatiotemporal structure of receptive fields of layer 4 neurons and what is the orientation selectivity of layer 4 neurons? Receptive fields of layer 4 neurons were mapped using a white-noise stimulus; orientation selectivity was determined using drifting, sine-wave gratings. Our results show that most neurons (84%) within layer 4 are simple cells with elongated, spatially segregated, ON and OFF subregions. These neurons are also selective for stimulus orientation; peaks in orientation-tuning curves have, on average, a half-width at half-maximum response of 21.5 +/- 1.2 degrees (mean +/- SD). The remaining neurons in layer 4 (16%) lack orientation selectivity and have center/surround receptive fields. Although the organization of geniculate inputs to layer 4 differs substantially between ferret and cat, our results demonstrate that, like in the cat, most neurons in ferret layer 4 are orientation-selective simple cells.

Animals↗
PubMed2002

Anti-emetic activity of the novel nonpeptide tachykinin NK1 receptor antagonist ezlopitant (CJ-11,974) against acute and delayed cisplatin-induced emesis in the ferret.

The anti-emetic effects of a novel tachykinin NK(1) receptor antagonist, ezlopitant ((2S,3S-cis)-2-diphenylmethyl)- N-[(2-methoxy, 5-isopropylphenyl)methyl]-1-azabicyclo- [2.2.2]octan-3-amine), were investigated in ferrets. Ezlopitant inhibited [(3)H]substance P ([(3)H]SP) binding to the human, guinea pig, ferret and gerbil NK(1) receptors (K(i) = 0.2, 0.9. 0.6 and 0.5 nmol/l, respectively), but had no affinity to NK(2) and NK(3) receptors up to 1 micromol/l. Ezlopitant also inhibited SP-induced contraction of guinea pig trachea with a pA(2) value of 7.8, but had no effects on the baseline tension and maximum contractile response. In ferrets, ezlopitant, either orally (0.03-3 mg/kg) or subcutaneously (0.3-3 mg/kg), prevented acute retching and vomiting responses induced by intraperitoneal injection of cisplatin (10 mg/kg). In addition, repeated subcutaneous injection of ezlopitant significantly inhibited delayed retching and vomiting responses that occurred in ferrets treated with the lower dose of cisplatin (5 mg/kg, i.p.). Ezlopitant (0.1-1 mg/kg, s.c.) also produced a dose-dependent inhibition of hindpaw tapping induced by intracerebroventricular injection of [Sar(9),Met(O(2))(11)]SP in gerbils, which is known to be mediated by NK(1) receptors in the brain. These findings indicate that ezlopitant is a potent and selective NK(1) receptor antagonist, and that it inhibits both acute and delayed emetic reactions induced by cisplatin in ferrets via acting on NK(1) receptors in the central nervous system.

Animals↗
PubMed1998

Connexin 26 expression in human and ferret airways and lung during development.

Coordinated microscopic and molecular biological studies were used to document gap junction expression during postnatal development in ferret tracheal epithelium and lung and in fetal and adult human airway and lung. Expression of connexin 26 (Cx26) in the ferret airways was limited to the epithelial layer and was observed only during the newborn interval. In contrast, we found Cx26 expressed in the alveolar epithelium of the ferret lung by in situ hybridization, Northern blotting, RT-PCR amplification, and immunocytochemical labeling at all ages examined. This finding was further confirmed by documentation of gap junctional plaques upon ultrastructural examination of freeze-fracture replicas of adult ferret lung tissue. Parallel studies of developing human fetal lung and airway suggested connexin expression in the airways only in the first trimester but, as in the ferret, persistent expression was observed in both fetal and adult lung. These studies suggest that the transient expression of Cx26 is a reliable early indicator of airway epithelial development and differentiation in the airways. In contrast, Cx26 expression persists throughout life in the lung, suggesting that gap junctions serve more perennial intercellular communication functions in the peripheral lung.

Animals↗
PubMed2001

Laryngeal mask versus endotracheal tube in a ferret model.

Acquired subglottic stenosis in infants is a difficult iatrogenic problem with notable morbidity, primarily caused by prolonged endotracheal intubation. The laryngeal mask airway (LMA) is a recently developed, alternative airway device that does not contact the subglottis. To explore the possibility of preventing subglottic stenosis, we compared the endotracheal tube (ETT) and the LMA in terms of the incidence and severity of glottic and subglottic injury resulting from prolonged intubation in the adult ferret model of the infant airway. Ten adult ferrets were randomly intubated under inhalational anesthesia with either a 4.0 cuffless ETT or a size 1 LMA for a 24- to 48-hour period. Rigid laryngeal endoscopy was used to detect pharyngeal or glottic injury during the period of intubation and on a routine basis for 3 months after extubation. All 5 ferrets in the ETT group developed endoscopically evident glottic and subglottic injury; 2 of the 5 developed a symptomatic, mature subglottic stenosis. The 5 ferrets in the LMA group had endoscopically normal larynges. However, all ferrets in the LMA group developed significant tongue edema and cyanosis during the first 24 hours of intubation, and 3 of the 5 died of respiratory failure due to airway obstruction. In the 2 LMA survivors, evidence of oropharyngeal injury persisted until 6 weeks after extubation. We conclude that the LMA does not cause subglottic injury in this model. However, its prolonged use results in significant pharyngeal morbidity that raises serious doubt as to its potential routine use in infants requiring prolonged ventilatory support.

Animals↗
PubMed1993

Histopathologic features and post-surgical sequelae of 57 cutaneous neoplasms in ferrets (Mustela putorius furo L.).

The study of the signalment, histomorphologic features, and post-surgical clinical progress of 57 cutaneous neoplasms in 55 domestic ferrets (Mustela putorius furo L.) was based on diagnostic pathologic accessions (1987-1992) from 142 ferrets. Mean age of the group was 4.3 years; 31/54 (57%) were female and 23/54 (43%) were male. Thirty-three (58%) of the cutaneous neoplasms were basal cell tumors. The mean age of ferrets with basal cell tumor was 5.2 years, and 23/33 (70%) were female. Histologically, the basal cell tumors were composed of well-differentiated basaloid epithelial cells with various degrees of squamous and sebaceous differentiation, similar to those seen in basal cell neoplasms of dogs. Nine of the 57 (16%) cutaneous neoplasms were mastocytomas. The mean age of ferrets with mastocytoma was 4.1 years; four were male, four were female, and the sex of one was unrecorded. Histologically, the mastocytomas were composed of well-differentiated mast cells with few eosinophils, similar to cutaneous mastocytomas of domestic cats. The mast cells had a small number of metachromatic cytoplasmic granules, and in six of eight neoplasms the granules had an affinity for conjugated avidin-peroxidase. Six of the cutaneous neoplasms (11%) were fibromas. The mean age of ferrets with fibroma was 2.7 years; 5 (83%) were male. Two cutaneous hemangiomas (4%) were in females, which were 4 and 5 years of age. There was one each hemangiosarcoma, cutaneous polyp, anal gland adenocarcinoma, lymphosarcoma of the prepuce and inguinal lymph node, and adenocarcinoma of the prepuce.

Animals↗
PubMed2001

Nucleotide sequence and polymerase chain reaction/restriction fragment length polymorphism analyses of Aleutian disease virus in ferrets in Japan.

Two ferrets with spontaneous Aleutian disease (AD) were found in Japan. The diagnosis was verified by polymerase chain reaction (PCR) amplification of part of the capsid gene specific to AD virus (ADV). The nucleotide sequences (365 bp in length) of the amplified fragments from the 2 ferrets differed by a single nucleotide, producing an amino acid alteration. Compared with other types of ADV, these isolates had 96% sequence similarity to a published ferret ADV (FADV) in contrast to <91% homology to various types of mink ADV (MADV). The phylogenetic tree of ADVs indicates that these 2 isolates and the published FADV belong to the same genetic group and definitely are divergent from MADVs. The predicted amino acid sequence of the hypervariable segment in the capsid gene was conserved among the 3 types of FADV. These results indicated that the 2 isolates found in Japan were new DNA types of FADV and could have been derived from FADV(s). A restriction fragment length polymorphism (RFLP) method to distinguish the ferret types of ADV from the mink types of ADV was developed on the basis of differences in their nucleotide sequences. Digestion of the PCR products with Afal or ScaI provided different cleavage patterns for FADV and MADV. This PCR/RFLP analysis of the ADV capsid gene will be a valuable asset for diagnosis of this virus infection in ferrets.

Aleutian Mink Disease↗