Spatial social polarization and birth outcomes: preterm birth and infant mortality - New York City, 2010-14.

AIMS: This study assessed the relationship between spatial social polarization measured by the index of the concentration of the extremes (ICE) and preterm birth (PTB) and infant mortality (IM) in New York City. A secondary aim was to examine the ICE measure in comparison to neighborhood poverty. METHODS: The sample included singleton births to adult women in New York City, 2010-2014 ( n=532,806). Three ICE measures were employed at the census tract level: ICE - Income (persons in households in the bottom vs top 20th percentile of US annual household income), ICE -Race/Ethnicity (black non-Hispanic vs white non-Hispanic populations), and ICE - Income + Race/Ethnicity combined. Preterm birth was defined as birth before 37 weeks' gestation. Infant mortality was defined as a death before one year of age. A two-level generalized linear model with random intercept was utilized adjusting for individual-level covariates. RESULTS: Preterm birth prevalence was 7.1% and infant mortality rate was 3.4 per 1000 live births. Women who lived in areas with the least privilege were more likely to have a preterm birth or infant mortality as compared to women living in areas with the most privilege. After adjusting for covariates, this association remained for preterm birth (ICE - Income: Adjusted Odds Ratio (AOR) 1.16 (1.10-1.21); ICE - Race/Ethnicity: AOR 1.41 (1.34-1.49); ICE - Income + Race/Ethnicity: AOR 1.36 (1.29-1.43)) and IM (ICE - Race/Ethnicity (AOR 1.80 (1.43-2.28) and ICE - Income + Race/Ethnicity (AOR 1.54 (1.23-1.94)). High neighborhood poverty was associated with PTB only (AOR 1.09 (1.04-1.14). CONCLUSIONS: These results provide preliminary evidence for the use of the ICE measure in examining structural barriers to healthy birth outcomes.

Syntrophomonas wolfei Uses an NADH-Dependent, Ferredoxin-Independent [FeFe]-Hydrogenase To Reoxidize NADH.

Syntrophomonas wolfei syntrophically oxidizes short-chain fatty acids (four to eight carbons in length) when grown in coculture with a hydrogen- and/or formate-using methanogen. The oxidation of 3-hydroxybutyryl-coenzyme A (CoA), formed during butyrate metabolism, results in the production of NADH. The enzyme systems involved in NADH reoxidation in S. wolfei are not well understood. The genome of S. wolfei contains a multimeric [FeFe]-hydrogenase that may be a mechanism for NADH reoxidation. The S. wolfei genes for the multimeric [FeFe]-hydrogenase (hyd1ABC; SWOL_RS05165, SWOL_RS05170, SWOL_RS05175) and [FeFe]-hydrogenase maturation proteins (SWOL_RS05180, SWOL_RS05190, SWOL_RS01625) were coexpressed in Escherichia coli, and the recombinant Hyd1ABC was purified and characterized. The purified recombinant Hyd1ABC was a heterotrimer with an αßγ configuration and a molecular mass of 115 kDa. Hyd1ABC contained 29.2 ± 1.49 mol of Fe and 0.7 mol of flavin mononucleotide (FMN) per mole enzyme. The purified, recombinant Hyd1ABC reduced NAD+ and oxidized NADH without the presence of ferredoxin. The HydB subunit of the S. wolfei multimeric [FeFe]-hydrogenase lacks two iron-sulfur centers that are present in known confurcating NADH- and ferredoxin-dependent [FeFe]-hydrogenases. Hyd1ABC is a NADH-dependent hydrogenase that produces hydrogen from NADH without the need of reduced ferredoxin, which differs from confurcating [FeFe]-hydrogenases. Hyd1ABC provides a mechanism by which S. wolfei can reoxidize NADH produced during syntrophic butyrate oxidation when low hydrogen partial pressures are maintained by a hydrogen-consuming microorganism.IMPORTANCE Our work provides mechanistic understanding of the obligate metabolic coupling that occurs between hydrogen-producing fatty and aromatic acid-degrading microorganisms and their hydrogen-consuming partners in the process called syntrophy (feeding together). The multimeric [FeFe]-hydrogenase used NADH without the involvement of reduced ferredoxin. The multimeric [FeFe]-hydrogenase would produce hydrogen from NADH only when hydrogen concentrations were low. Hydrogen production from NADH by Syntrophomonas wolfei would likely cease before any detectable amount of cell growth occurred. Thus, continual hydrogen production requires the presence of a hydrogen-consuming partner to keep hydrogen concentrations low and explains, in part, the obligate requirement that S. wolfei has for a hydrogen-consuming partner organism during growth on butyrate. We have successfully expressed genes encoding a multimeric [FeFe]-hydrogenase in E. coli, demonstrating that such an approach can be advantageous to characterize complex redox proteins from difficult-to-culture microorganisms.

Two pathways for glutamate biosynthesis in the syntrophic bacterium Syntrophus aciditrophicus.

The anaerobic metabolism of crotonate, benzoate, and cyclohexane carboxylate by Syntrophus aciditrophicus grown syntrophically with Methanospirillum hungatei provides a model to study syntrophic cooperation. Recent studies revealed that S. aciditrophicus contains Re-citrate synthase but lacks the common Si-citrate synthase. To establish whether the Re-citrate synthase is involved in glutamate synthesis via the oxidative branch of the Krebs cycle, we have used [1-(13)C]acetate and [1-(14)C]acetate as well as [(13)C]bicarbonate as additional carbon sources during axenic growth of S. aciditrophicus on crotonate. Our analyses showed that labeled carbons were detected in at least 14 amino acids, indicating the global utilization of acetate and bicarbonate. The labeling patterns of alanine and aspartate verified that pyruvate and oxaloacetate were synthesized by consecutive carboxylations of acetyl coenzyme A (acetyl-CoA). The isotopomer profile and (13)C nuclear magnetic resonance (NMR) spectroscopy of the obtained [(13)C]glutamate, as well as decarboxylation of [(14)C]glutamate, revealed that this amino acid was synthesized by two pathways. Unexpectedly, only the minor route used Re-citrate synthase (30 to 40%), whereas the majority of glutamate was synthesized via the reductive carboxylation of succinate. This symmetrical intermediate could have been formed from two acetates via hydration of crotonyl-CoA to 4-hydroxybutyryl-CoA. 4-Hydroxybutyrate was detected in the medium of S. aciditrophicus when grown on crotonate, but an active hydratase could not be measured in cell extracts, and the annotated 4-hydroxybutyryl-CoA dehydratase (SYN_02445) lacks key amino acids needed to catalyze the hydration of crotonyl-CoA. Besides Clostridium kluyveri, this study reveals the second example of a microbial species to employ two pathways for glutamate synthesis.

The importance of hydrogen and formate transfer for syntrophic fatty, aromatic and alicyclic metabolism.

We used a combination of genomic, transcriptional and enzymatic analyses to determine the mechanism of interspecies electron transfer by two model syntrophic microorganisms, Syntrophomonas wolfei and Syntrophus aciditrophicus. Both organisms contain multiple hydrogenase and formate dehydrogenase genes, but lack genes for outer membrane cytochromes and nanowire formation. Syntrophically grown cells and cell-free extracts of S. aciditrophicus and S. wolfei had both hydrogenase and formate dehydrogenase activities. Butyrate metabolism and CH4 production by washed cell suspensions of S. wolfei and Methanospirillum hungatei were inhibited by hydrogenase inhibitors (cyanide and carbon monoxide), but not by a formate dehydrogenase inhibitor (hypophosphite). Syntrophic benzoate oxidation and CH4 production by washed cell suspensions of S. aciditrophicus and M. hungatei were inhibited by hypophosphite, but not cyanide and carbon monoxide. All three inhibitors halted syntrophic cyclohexane-1-carboxylate metabolism. Two hydrogenase genes, hydA1 and hydA2, were more highly expressed when S. wolfei was grown syntrophically. S. aciditrophicus expressed multiple hydrogenase and formate dehydrogenase genes during syntrophic benzoate and cyclohexane-1-carboxylate growth, one of which (fdhA2) was highly differentially expressed during syntrophic benzoate growth. Thus, these syntrophic microorganisms have flexible metabolisms that allow them to use either H2 or formate transfer depending on the substrate involved.

Gentrification and preterm birth in New York City, 2008­2010.

Adverse birth outcomes have been linked to neighborhood level socioeconomic status. However, little work has examined the influence of social and economic change over time (i.e., gentrification) on health. This study aims to assess the association between gentrification and preterm birth (PTB) while examining the modifying effect of maternal race/ethnicity and educational attainment. New York City births, 2008­2010, (n=126,165) were linked to a measure of gentrification at the community district level (n=59). The gentrification measure was calculated using percent change in education level, poverty level, and median household income (MHI) between the 2005­2009 American Community Survey and the 1990 Census. PTB was defined as clinical gestational age less than 37 weeks. Generalized estimating equations were utilized to examine the association. Gentrification (i.e., increase in residents with a college education, increase in MHI, and decrease in residents living below the poverty line) was not associated with PTB. However, among Non-Hispanic Blacks, very high gentrification was adversely associated with PTB (AOR, 1.16; 95 % CI, 1.01­1.33) as compared to those who lived in a very low gentrified neighborhood. Among non- Hispanic Whites, living in a very high gentrified neighborhood was protective as compared to living in a very low gentrified neighborhood (AOR, 0.78; 95 % CI, 0.64­ 0.94). Although there is a need to develop a more nuanced measure of gentrification, these results indicate that changes in the economic character of a neighborhood may have a significant influence on birth outcomes.

Identification and characterization of the first cholesterol-dependent cytolysins from Gram-negative bacteria.

The cholesterol-dependent cytolysins (CDCs) are pore-forming toxins that have been exclusively associated with a wide variety of bacterial pathogens and opportunistic pathogens from the Firmicutes and Actinobacteria, which exhibit a Gram-positive type of cell structure. We have characterized the first CDCs from Gram-negative bacterial species, which include Desulfobulbus propionicus type species Widdel 1981 (DSM 2032) (desulfolysin [DLY]) and Enterobacter lignolyticus (formerly Enterobacter cloacae) SCF1 (enterolysin [ELY]). The DLY and ELY primary structures show that they maintain the signature motifs of the CDCs but lack an obvious secretion signal. Recombinant, purified DLY (rDLY) and ELY (rELY) exhibited cholesterol-dependent binding and cytolytic activity and formed the typical large CDC membrane oligomeric pore complex. Unlike the CDCs from Gram-positive species, which are human- and animal-opportunistic pathogens, neither D. propionicus nor E. lignolyticus is known to be a pathogen or commensal of humans or animals: the habitats of both organisms appear to be restricted to anaerobic soils and/or sediments. These studies reveal for the first time that the genes for functional CDCs are present in bacterial species that exhibit a Gram-negative cell structure. These are also the first bacterial species containing a CDC gene that are not known to inhabit or cause disease in humans or animals, which suggests a role of these CDCs in the defense against eukaryote bacterial predators.

HS3ST2 expression induces the cell autonomous aggregation of tau.

Heparan sulfates have long been known to intracellularly accumulate in Alzheimer's disease neurons, where they colocalize with neurofibrillary tangles made of abnormally phosphorylated and aggregated tau protein. However, the reasons and consequences of the heparan sulfates accumulation in the Alzheimer's cells are not yet well understood. Previously, we showed that the neural heparan sulfate 3-O-sulfotransferase HS3ST2 is critical for the abnormal phosphorylation of tau in Alzheimer's disease-related tauopathy. Using cell models of tauopathy we showed that intracellular 3-O-sulfatated heparan sulfates interact with tau inducing its abnormal phosphorylation. However, it is unknown whether HS3ST2 expression induces the intracellular aggregation of tau in cells. Here, by using replicative pEBV plasmids, we engineered HEK293 cells to stably express HS3ST2 together with human tau carrying or not the P301S mutation. We show that HS3ST2 gain of function induces the cell autonomous aggregation of tau not only in cells expressing tauP301S, but also in cells expressing the wild type tau. Our engineered cells mimicked both the HS intracellular accumulation observed in neurons of Alzheimer's disease and the tau aggregation characteristic of tauopathy development and evolution. These results give evidence that the neural HS3ST2 plays a critical role in the cell autonomous self-aggregation of tau.

Promegapoietin, a family of chimeric growth factors, supports megakaryocyte development through activation of IL-3 and c-Mpl ligand signaling pathways.

OBJECTIVE: The signaling pathways induced by promegapoietin (PMP), a family of chimeric growth factors that activate the human IL-3 and c-Mpl receptors, were investigated. METHODS: The biological activity of PMP was examined by receptor binding, cell proliferation, ex vivo expansion of hematopoietic progenitor cells, and in vivo production of platelets. The activation of signaling pathways was examined by Western blot and Northern blot analyses. RESULTS: Two PMP molecules, PMP-1 and PMP-1a, induced proliferation of cells expressing the IL-3 receptor, c-Mpl, or both receptors and bound to the IL-3 receptor and c-Mpl with high affinity. Ex vivo expansion assays using human bone marrow CD34(+) cells suggested that PMP-1 induced greater total cellular expansion as well as expansion of CD41(+) megakaryocytic precursor cells than IL-3 or c-Mpl ligand alone. Subcutaneous administration of 50 microg/kg of PMP-1 for 10 days to rhesus monkeys resulted in increased platelet production in vivo from a baseline of 357 +/- 45 x 10(3) cells/mL to 1376 +/- 151 x 10(3) cell/mL. PMP-1 induced phosphorylation of the beta(c) subunit of IL-3 receptor and c-Mpl, JAK2, and STAT5b, but not STAT3. PMP-1 induced greater expression of Pim-1, c-Myc, and cyclin D2 than did either an IL-3 receptor agonist or c-Mpl receptor agonist alone. The magnitude of induction of early response genes was similar for PMP and the coaddition of IL-3 receptor agonist and c-Mpl receptor agonist. CONCLUSION: PMP combines the biological activities of IL-3 and c-Mpl ligand in a single molecule that can simultaneously activate signaling pathways induced by both these ligands.

Formation and Reactivity of the Osmium(IV)-Cyanoimido Complex [Os(IV) (bpy)(Cl)3 (NCN)](-).

Oxo-like reactivity exists for a new series of osmium complexes such as [Os(IV) (bpy)(Cl)3 (NCN)](-) (bpy=2,2'-bipyridine, see structure) containing the cyanoimido ligand. This ligand is formed directly at the metal center by the reaction of Os(VI) -nitrido precursors with tetraethylammonium cyanide. In the cyanoimido complexes there is an extensive electron-transfer chemistry at the metal center and an extensive functional-group chemistry based on the ligand.

Steroid-sensitive gene-1 is an androgen-regulated gene expressed in prostatic smooth muscle cells in vivo.

Steroid-sensitive gene-1 (SSG1) is a novel gene we cloned, found regulated by 17beta-estradiol in the rat uterus and mammary gland, and over-expressed in 7,12-dimethylbenz(a)anthracene-induced rat mammary tumors. We show here that SSG1 mRNA and protein expression are regulated by androgens in the rat ventral prostate. Increases in SSG1 mRNA levels were detected by Northern blotting after 24 h and reached a 27-fold peak 96 h following castration, relative to SSG1 mRNA expression in sham-operated rats. Dihydrotestosterone or testosterone supplementation of castrated rats prevented this rise in SSG1 mRNA. In contrast with SSG1 mRNA expression, SSG1 protein was decreased 16-fold 2 weeks following castration but was at control levels in the prostates of castrated rats receiving dihydrotestosterone or testosterone. Although SSG1 is regulated by androgens in vivo, treatment of LnCap cells with dihydrotestosterone, cyproterone acetate or flutamide did not result in the regulation of SSG1 protein levels in vitro. Immunofluorescence studies show that SSG1 is mainly expressed in prostatic smooth muscle cells. These results indicate that SSG1 is an androgen-regulated gene that is expressed in the smooth muscle component of the rat ventral prostate in vivo.

High dietary retinoic acid inhibits tumor promotion and malignant conversion in a two-stage skin carcinogenesis protocol using 7,12-dimethylbenz[a]anthracene as the initiator and mezerein as the tumor promoter in female SENCAR mice.

We studied the effect of dietary retinoic acid (RA) in a two-stage protocol of skin carcinogenesis in female SENCAR mice. At 3 weeks of age mice were initiated with 7,12-dimethylbenz[a]anthracene (DMBA, 20 micrograms) and promoted with either 12-O-tetradecanoylphorbol-13-acetate (TPA, 2 micrograms) once per week or mezerein (MEZ, 4 micrograms) twice per week for 20 weeks. At the week of DMBA initiation mice were also put on a purified diet containing either 3 (physiological dose) or 30 micrograms (pharmacological dose) of RA/g of diet. High dietary RA significantly inhibited papilloma yield but not incidence in the MEZ-promoted group. Papilloma incidence and yield were also lower in the MEZ- than in the TPA-treated groups. Cumulative carcinoma incidence and yield, and conversion efficiency (= (carcinomas/maximal papillomas) x 100%), were all decreased by high dietary RA in both MEZ- and TPA-treated groups. These results demonstrate that high dietary RA inhibited skin carcinogenesis in MEZ-promoted mice at the stages of tumor promotion and malignant conversion, while this inhibition occurred only at the malignant conversion stage in TPA-promoted mice.

Evaluation of the somatogenic activity of bovine placental lactogen with cell lines transfected with the bovine somatotropin receptor.

Studies have shown that bovine placental lactogen (bPL) has partial somatogenic activity in vivo even though binding results clearly indicate bPL does not cause homodimerization of the bovine somatotropin receptor (bST-R). To help understand the receptor binding versus biological activity of bovine somatotropin (bST) and bPL we have developed a homologous model system. Full length bST-R was stably transfected into a murine lymphoid cell line, Ba/F3 and a hamster kidney cell line, BHK. From both transfected cell lines, clones were isolated (Ba/F3-C1 and BHK-24) which demonstrated specific binding of bST and, or bPL. Bovine ST stimulated proliferation of the Ba/F3-C1 clonal line over a dose range of 10 to 3000 pM with an EC50 of 100 pM. A bST variant (des 1-4 bST) and porcine ST (pST) which both have approximately 10% of the binding affinity for bST-R as native bST were 1 and 10% as potent as bST in this bioassay, respectively. This suggests that affinity and biological activity are correlated for this system. Proliferation was initiated through the bST-R because addition of a monoclonal antibody which recognizes the extracellular domain of bST-R and inhibits binding of bST to its receptor, inhibited bST-stimulated mitosis. However, even though the affinity of bPL for the bST-R is similar to that of bST, bPL antagonized the proliferative action of bST with an IC50 of 1 nM. Components of the somatogenic signal transduction pathway were also evaluated in both cell lines. Addition of bST to the cell cultures increased phosphorylation of JAK2 in Ba/F3-C1 and BHK-24 cells in a dose-responsive manner but bPL failed to increase phosphorylation of JAK2 in either cell line. In summary, these data support the hypothesis that ST-R homodimerization is necessary for bioactivity in this model system but fail to explain apparent somatogenic activity of bPL in vivo.

Nursing students' blood pressure measurement following CD-ROM and conventional classroom instruction: a pilot study.

This paper describes a pilot investigation of first year nursing students' adherence to the recommended auscultatory blood pressure measurement procedure following three different forms of instruction; conventional classroom demonstration of the technique, a self instructional CD-ROM tutorial program, and a combination of both methods. This investigation was carried out over a 5-day time period using 27 students during normal teaching time. Students' adherence to the procedure was determined by observation using a performance checklist. Results suggest that the CD-ROM is no substitute for real life, hands on experience, although when used as an adjunct to traditional teaching methods, it can enhance learning.

Universal newborn hearing screening: feasibility in a community hospital.

BACKGROUND: The National Institutes of Health and the Joint Committee on Infant Hearing have recommended universal newborn hearing screening. The feasibility of universal newborn hearing screening in a community hospital, however, has not been demonstrated. We initiated a universal newborn hearing screening program using transient evoked otoacoustic emissions (TEOAE) at a community hospital to assess the feasibility of universal hearing screening in this setting. METHODS: A screening team composed of a family practice physician, family medicine resident, audiologist, and four technicians was developed. The study compared testing time between the technicians and the audiologist and assessed whether the technicians were able to perform hearing testing accurately and reliably. RESULTS: A total of 627 infants were screened. Of those, 11 (1.8%) failed TEOAE screening and were referred to a tertiary care center for further evaluation. Six of the 11 referrals were found to have a hearing impairment. Trained technicians were found to be capable of performing the screening accurately and reliably. CONCLUSIONS: Universal newborn hearing screening using transient evoked otoacoustic emissions is feasible in a community hospital.

Modeling SSI financial eligibility and simulating the effect of policy options.

This article simulates eligibility for Supplemental Security Income (SSI) among the elderly, analyzes factors affecting participation, and looks at the potential effects of various options to modify financial eligibility standards for the federal SSI program. We find that in the estimated noninstitutional elderly population of 30.2 million in the United States in 1991, approximately 2 million individuals aged 65 or older were eligible for SSI (a 6.6 percent rate of eligibility). Our overall estimate of the rate of participation among eligible elderly is approximately 63 percent, suggesting that more than a third of those who are eligible do not participate in the program. The results of our analysis of factors affecting participation among the eligible elderly show that expected SSI benefits and a number of demographic and socioeconomic variables are associated with the probability of participation. We also simulate the effects of various policy options on the poverty rate, poverty gap, annual program cost, the number of participants, and the average estimated benefits among participants. The simulations consider the potential effects of five policy alternatives: Increase the general income exclusion (GIE) from $20 to $80. Increase the earned income exclusion (EIE) from $65 to $260. Increase the federal benefit rate (FBR) by $50 for individuals and $75 for couples and eliminate the GIE. Increase the asset threshold to $3,000 for individuals and $4,500 for couples. Increase the asset threshold to $6,000 for individuals and $9,000 for couples. Using 1991 microdata from the Survey of Income and Program Participation (SIPP) matched to Social Security Administration administrative records and making adjustments reflecting aggregate program statistics, we present the results of our simulations for December 1999. The results show substantial variation in the simulated effects of the five policy alternatives along the various outcome dimensions considered. The simulated effects on the poverty gap of the elderly population range from a 7.9 percent reduction ("Increase the GIE from $20 to $80") to a 0.1 percent reduction ("Increase the EIE from $65 to $260"). All simulated interventions are expected to increase the rate of SSI participation among the elderly from a high of 20.3 percent ("Increase the GIE from $20 to $80") to a low of 0.5 percent ("Increase the EIE from $65 to $260"). We also find that the interventions that have greater estimated effects in terms of increased participation and reduced poverty tend to cost more. At the high end, we estimate that increasing the GIE from $20 to $80 could raise annual federal SSI cash benefit outlays by about 46 percent, compared with only 0.9 percent for increasing the EIE from $65 to $260. Similar to the EIE intervention, raising the resource thresholds by 50 percent would reduce the overall poverty gap of the elderly by only 0.2 percent, would increase SSI participation only modestly (by 1.3 percent), but would entail slightly higher program costs (by 1.4 percent). Increasing the asset threshold by 200 percent would have higher estimated effects on all three outcomes, but it would still be associated with relatively low increases in both costs and benefits. Finally, the simulated effects on the three key outcomes of increasing the FBR by $50 for individuals and $75 for couples, combined with eliminating the GIE, are relatively large but are clearly less substantial than increasing the GIE from $20 to $80. This work relies on data from the SIPP matched to administrative data on federal SSI benefits that provide a more accurate picture of SSI participation than has been feasible for previous studies. We simulate eligibility for federal SSI benefits by applying the program rules to detailed information on the characteristics of individuals and couples based on the rich array of demographic and socioeconomic data in the SIPP, particularly the comprehensive information SIPP provides on assets and monthly income. A probit model is estimated to analyze factors affecting participation among the eligible elderly. Finally, we conduct the policy simulations using altered program rules represented by the policy alternatives and predicted participation probabilities to estimate outcomes under simulated program rules. We compare those simulated outcomes to observed outcomes under current program rules. The results of our simulations are conditional on the characteristics of participants and eligibles in 1991, but they also reflect aggregate adjustments capturing substantial changes in overall participation and program benefit levels between 1991 and 1999.

Brainstem auditory-evoked response (BAER) in client-owned pet ferrets with normal hearing.

The objective of this study was to evaluate the feasibility of brainstem auditory-evoked response (BAER) testing in pet ferrets in a clinical setting, and to describe a routine method and baseline data for normal hearing ferrets for future investigation of deafness in this species. Twenty-eight clinically normal client-owned ferrets were included. BAER measurements were recorded under general anaesthesia (isoflurane delivered by mask), from subcutaneously placed needle electrodes. A 'click' stimulus applied by insert earphone with an intensity of 90 dB sound pressure level (SPL) was used. The final BAER waveform represents an average of 500 successive responses. Morphology of the waveform was studied; amplitude and latency measures were determined and means were calculated. The BAER waveform of the normal ferret included 4 reproducible waves named I, II, III and V, as previously described in dogs and cats. Measurements of latencies are consistent with previous laboratory research using experimental ferrets. In the present study, a reliable routine protocol for clinical evaluation of the hearing function in the pet ferret was established. This procedure can be easily and safely performed in a clinical setting in ferrets as young as eight weeks of age. The prevalence of congenital deafness in ferrets is currently unknown but may be an important consideration, especially in ferrets with a white coat. BAER test is a useful screening for congenital deafness in this species.

Disseminated Mycobacterium genavense infection in a chinchilla (Chinchilla lanigera).

A 1-year-old neutered male chinchilla (Chinchilla lanigera) was presented with emaciation and a 1-month history of progressive weight loss. The animal was bright and responsive on clinical examination, but had poor body condition. Serum biochemical analysis revealed elevated alanine amino transferase and alkaline phosphatase. Ultrasound examination was unremarkable. Thoracic radiography showed changes consistent with bullous emphysema and severe pneumonia. Antibiotic therapy was initiated, but the chinchilla died 6 weeks later. Necropsy examination revealed granulomatous lesions in the lungs and liver. Numerous acid-fast bacilli were present in the cytoplasm of macrophages. Sequencing of genetic material isolated from fixed tissue classified the pathogen as Mycobacterium genavense.