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Effect of ethanol on human colon carcinoma CaCo-2 and HT-29 cell lines during the maturation process.

The aim of the study was to ascertain whether the exposure to ethanol of human colon carcinoma CaCo-2 and HT-29 cell lines affects the differentiation process. As an index of enterocytic differentiation, the expression of sucrase, alkaline phosphatase, alpha 2,6-sialyltransferase toward the N-acetyllactosaminic sequence, and beta 1,4-N-acetylgalactosaminyltransferase (beta 1,4GalNAc-transferase) was examined. The latter enzyme is responsible for the biosynthesis of Sda carbohydrate histo-blood antigen, which mainly occurs in human colonic cells; its expression in CaCo-2 cells depends strictly on the enterocytic differentiation. The addition of ethanol in the culture medium resulted in a significant increment of sucrase and alpha 2,6-sialyltransferase activities in both cell lines, as well as the beta 1,4GalNAc-transferase activity in CaCo-2 cells and alkaline phosphatase activity in HT-29 cells. The increment was dose-dependent in the range between 50 and 200 mM ethanol and evident after 2 days of exposure in both cell systems. These results support the notion that, as occurs for cell lines of different origin, the ethanol in vitro positively affects the differentiation of intestinal cells, namely along the enterocytic lineage. The putative mechanism by which ethanol interferes with the maturation process of colonic cells is discussed.

Cell Differentiation↗

The role of cognition in the risk--benefit and safety analysis of antipsychotic medication.

Conventional neuroleptics can further reduce cognitive function, which is already impaired in most patients with schizophrenia. Although some areas of cognition may remain relatively well preserved in schizophrenia, it has been suggested that the origins of a neurocognitive decline in schizophrenia may be related to a reduction in dopamine activity in the prefrontal cortex. If this is the case, dopamine D2 blockade would be expected to impair some aspects of neurocognitive function further. The level of neurocognitive function in schizophrenia is related to vocational and social ability, and the course of cognitive decline appears to be consistent with a static encephalopathy, rather than progressive dementia. Intensive cognitive retraining in patients with schizophrenia may improve, but not normalize, some aspects of cognitive performance. Most cognitive deficits remain stable, even when improvements in symptoms are obtained with antipsychotic treatment. Drugs such as risperidone, one of the newer serotonin-dopamine antagonists (SDAs), have a better effect on cognitive function than conventional antidopaminergic neuroleptics, and are therefore more likely to enable the patient to benefit from cognitive and other forms of training. Anticholinergic drugs used to treat EPS, or drugs with anticholinergic activity, also impair cognitive function. Consequently, because the need to use anticholinergic drugs is less with the SDA antipsychotics, the cognitive function of patients treated with drugs such as risperidone is likely to be better than it would be if they took a conventional neuroleptic.

Antipsychotic Agents↗

Spontaneous and drug-induced movement disorders in schizophrenia.

The extrapyramidal side-effects (EPS) of conventional neuroleptics are widely recognized. However, a substantial number of drug-naïve patients exhibit movement disorders which could be mistaken for EPS if drug therapy were started without a careful baseline assessment. Patients' experience of EPS during their first exposure to antipsychotic medication can have lasting effects on their attitudes to medication and compliance. Unmedicated, approximately 60% of patients will relapse in the first year after resolution of an acute psychotic episode, whereas prophylactic medication can reduce the relapse rate to less than 20%. The conventional neuroleptics produce antipsychotic effects at doses which differ little from those that induce EPS, and although anticholinergic medication helps to reduce the severity of EPS, it also causes side-effects, e.g. constipation, blurred vision, retention of urine, dry mouth and disturbances of sexual function. More importantly, anticholinergic drugs may worsen the psychosis and impair memory. Low or intermittent dose strategies with conventional neuroleptics may give patients relief from EPS, but they increase the relapse risk, and may also increase the risk of tardive dyskinesia. The serotonin-dopamine antagonist (SDA) antipsychotics, such as risperidone, produce both significant antipsychotic effects at doses which are lower than those that cause EPS, and also a lower level of EPS compared with conventional drugs. Clinical trials have shown that risperidone is effective in first-episode schizophrenia. In these trials the same doses were used as in chronic patients. However, clinical experience in Canada since the drug became generally available in 1993 suggests that first-episode patients require lower doses of risperidone than chronically ill patients who have had several acute psychotic episodes. More than 3 years of use has made it clear that risperidone should be seriously considered in first-episode patients, as it offers an opportunity to treat psychosis with minimal EPS. This in turn should lead to better compliance and a lower long-term relapse rate.

Antipsychotic Agents↗

Increase in alfalfa nodulation, nitrogen fixation, and plant growth by specific DNA amplification in Sinorhizobium meliloti.

To improve symbiotic nitrogen fixation on alfalfa plants, Sinorhizobium meliloti strains containing different average copy numbers of a symbiotic DNA region were constructed by specific DNA amplification (SDA). A DNA fragment containing a regulatory gene (nodD1), the common nodulation genes (nodABC), and an operon essential for nitrogen fixation (nifN) from the nod regulon region of the symbiotic plasmid pSyma of S. meliloti was cloned into a plasmid unable to replicate in this organism. The plasmid then was integrated into the homologous DNA region of S. meliloti strains 41 and 1021, which resulted in a duplication of the symbiotic region. Sinorhizobium derivatives carrying further amplification were selected by growing the bacteria in increased concentrations of an antibiotic marker present in the integrated vector. Derivatives of strain 41 containing averages of 3 and 6 copies and a derivative of strain 1021 containing an average of 2.5 copies of the symbiotic region were obtained. In addition, the same region was introduced into both strains as a multicopy plasmid, yielding derivatives with an average of seven copies per cell. Nodulation, nitrogenase activity, plant nitrogen content, and plant growth were analyzed in alfalfa plants inoculated with the different strains. The copy number of the symbiotic region was critical in determining the plant phenotype. In the case of the strains with a moderate increase in copy number, symbiotic properties were improved significantly. The inoculation of alfalfa with these strains resulted in an enhancement of plant growth.

Blotting, Southern↗

Molecular characterization of a major serotype M49 group A streptococcal DNase gene (sdaD).

Group A streptococci (GAS) express up to four types of secreted DNases. Although GAS infections are correlated with the production of anti-DNase B antibodies, the roles of DNases in the pathogenesis of GAS infections remain unclear. From a lambda library of serotype M49 strain CS101 GAS genome, a 2,147-bp fragment expressing DNase activity on an indicator agar was identified and sequenced. One 1,155-bp open reading frame (ORF) was identified in this fragment. This ORF was found to be 48% identical on the amino acid level to group C streptococcal DNase (Sdc). The regions of highest homology corresponded to amino acid residues that were also identified as part of the active site in staphylococcal nuclease. Transcription analysis revealed a specific 1.3-kb mRNA, which corresponded to the size predicted by the promoter and transcription termination signature sequences and indicated a monocistronic mode of transcription. Allelic replacement of the ORF rendered a M49 mutant devoid of extracellular DNase activity when cultured on indicator agar. Virulence parameters such as resistance to phagocytosis were not affected by the mutation. The sda gene was cloned and expressed in Escherichia coli as a thioredoxin fusion. By performing Ouchterlony immunodiffusion on the recombinant protein and by using protein preparations from culture supernatants of wild-type bacteria and the DNase mutant, the results of immunoreactivity with DNase type-specific polyclonal rabbit antisera classified the DNase as a type D enzyme. Fifty percent of patients with sera exhibiting high titers of antistreptolysin or anti-DNase B antibodies also had SdaD-reactive antibodies in comparison with <10% of serologically normal controls. While the value of recombinant SdaD for diagnostic purposes needs to be clarified, the isogenic DNase mutant pair of M49 should allow the significance of GAS DNase D as a bacterial virulence factor to be determined.

Amino Acid Sequence↗

Effects of oligopeptide permease in group a streptococcal infection.

The oligopeptide permease (Opp) of group A streptococci (GAS) is a membrane-associated protein and belongs to the ATP-binding cassette transporter family. It is encoded by a polycistronic operon containing oppA, oppB, oppC, oppD, and oppF. The biological function of these genes in GAS is poorly understood. In order to understand more about the effects of Opp on GAS virulence factors, an oppA isogenic mutant was constructed by using an integrative plasmid to disrupt the opp operon and confirmed by Southern blot hybridization. No transcript was detected in the oppA isogenic mutant by Northern blot analysis and reverse transcriptase PCR. The growth curve for the oppA isogenic mutant was similar to that for wild-type strain A-20. The oppA isogenic mutant not only decreased the transcription of speB, speX, and rofA but also increased the transcription of speF, sagA (streptolysin S-associated gene A), slo (streptolysin O), pel (pleotrophic effect locus), and dppA (dipeptide permease). No effects on the transcription of emm, sda, speJ, speG, rgg, and csrR were found. The phenotypes of the oppA mutant were restored by the oppA revertant and by the complementation strain. The oppA mutant caused less mortality and tissue damage than the wild-type strain when inoculated into BALB/c mice via an air pouch. Based on these data, we suggest that the opp operon plays an important role in the pathogenesis of GAS infection.

Animals↗

Chlamydial infection: an accurate model for opportunistic screening in general practice.

OBJECTIVES: To estimate the prevalence of Chlamydia trachomatis in women in general practice and to assess risk factors associated with infection. METHODS: The study was carried out in 2001-2 in different general practices in Antwerp, Belgium. Sexually active women, visiting their general practitioner for routine gynaecological care (mostly pill prescription or PAP smear), were offered opportunistic screening for chlamydia. 787 participants aged 15-40 delivered a self taken vaginal sample and filled in a questionnaire which included questions on demographic variables, urogenital symptoms, sexual history, and sexual behaviour. Samples were tested for presence of chlamydial DNA by means of a ligase chain reaction (LCR) assay, and positives were confirmed by two other amplification assays (PCR and SDA). RESULTS: Overall prevalence was 5.0% (95% CI: 3.5 to 6.5). Determinants of infection in logistic regression analysis were age 18-27 years, >1 partner in the past year, no use of contraceptives, frequent postcoital bleeding, having a symptomatic partner, painful micturition, and living in the inner city. The area under the ROC curve in the full model was 0.88. Selective screening based on a combination of the five first determinants detects 92.3% of infections in this sample; 37.5% of the population would need to be screened. CONCLUSION: Targeted screening for chlamydial infection is possible, even in a heterogeneous group of general practice attendants. Implementing this model would require considerable communication skills from healthcare providers.

Adolescent↗

Seizure suppression by shakB2, a gap junction mutation in Drosophila.

Gap junction proteins mediate electrical synaptic transmission. In Drosophila, flies carrying null mutations in the shakB locus, such as shakB2, have behavioral and electrophysiological defects in the giant fiber (GF) system neurocircuit consistent with a loss of transmission at electrical synapses. The shakB2 mutation also affects seizure susceptibility. Mutant flies are especially seizure-resistant and have a high threshold to evoked seizures. In addition, in some double mutant combinations with "epilepsy" mutations, shakB2 appears to act as a seizure-suppressor mutation: shakB2 restores seizure susceptibility to the wild-type range in the double mutant. In double mutant combinations, shakB2 completely suppresses seizures caused by slamdance (sda), knockdown (kdn), and jitterbug (jbug) mutations. Seizures caused by easily shocked (eas) and technical knockout (tko) mutations are partially suppressed by shakB2. Seizures caused by bang-sensitive (bas2) and bang-senseless (bss1, bss2 alleles) mutations are not suppressed by shakB2. These results show the use of Drosophila as a model system for studying the kinds of genetic interactions responsible for seizure susceptibility, bringing us closer to unraveling the complexity of seizure disorders in humans.

Animals↗

Genetic suppression of seizure susceptibility in Drosophila.

Despite the frequency of seizure disorders in the human population, the genetic and physiological basis for these defects has been difficult to resolve. Although many genetic defects that cause seizure susceptibility have been identified, the defects involve disparate biological processes, many of which are not neural specific. The large number and heterogeneous nature of the genes involved makes it difficult to understand the complex factors underlying the etiology of seizure disorders. Examining the effect known genetic mutations have on seizure susceptibility is one approach that may prove fruitful. This approach may be helpful both in understanding how different physiological processes affect seizure susceptibility and in identifying novel therapeutic treatments. In this study, we have taken advantage of Drosophila, a genetically tractable system, to identify factors that suppress seizure susceptibility. Of particular interest has been a group of Drosophila mutants, the bang-sensitive (BS) mutants, which are much more susceptible to seizures than wild type. The BS phenotypic class includes at least eight genes, including three examined in this study, bss, eas, and sda. Through the generation of double-mutant combinations with other well-characterized Drosophila mutants, the BS mutants are particularly useful for identifying genetic factors that suppress susceptibility to seizures. We have found that mutants affecting Na+ channels, mle(napts) and para, K+ channels, Sh, and electrical synapses, shak-B(2), can suppress seizures in the BS mutants. This is the first demonstration that these types of mutations can suppress the development of seizures in any organism. Reduced neuronal excitability may contribute to seizure suppression. The best suppressor, mle(napts), causes an increased stimulation threshold for the giant fiber (GF) consistent with a reduction in single neuron excitability that could underlie suppression of seizures. For some other double mutants with para and Sh(KS133), there are no GF threshold changes, but reduced excitability may also be indicated by a reduction in GF following frequency. These results demonstrate the utility of Drosophila as a model system for studying seizure susceptibility and identify physiological processes that modify seizure susceptibility.

Animals↗

Influence of a portable audio-biofeedback device on structural properties of postural sway.

BACKGROUND: Good balance depends on accurate and adequate information from the senses. One way to substitute missing sensory information for balance is with biofeedback technology. We previously reported that audio-biofeedback (ABF) has beneficial effects in subjects with profound vestibular loss, since it significantly reduces body sway in quiet standing tasks. METHODS: In this paper, we present the effects of a portable prototype of an ABF system on healthy subjects' upright stance postural stability, in conditions of limited and unreliable sensory information. Stabilogram diffusion analysis, combined with traditional center of pressure analysis and surface electromyography, were applied to the analysis of quiet standing tasks on a Temper foam surface with eyes closed. RESULTS: These analyses provided new evidence that ABF may be used to treat postural instability. In fact, the results of the stabilogram diffusion analysis suggest that ABF increased the amount of feedback control exerted by the brain for maintaining balance. The resulting increase in postural stability was not at the expense of leg muscular activity, which remained almost unchanged. CONCLUSION: Examination of the SDA and the EMG activity supported the hypothesis that ABF does not induce an increased stiffness (and hence more co-activation) in leg muscles, but rather helps the brain to actively change to a more feedback-based control activity over standing posture.

Journal Article↗

Effectiveness of provision of outdoor mobility services and devices in The Netherlands.

OBJECTIVE: To answer the following questions: What are the problems encountered by people with outdoor mobility disabilities? What solutions are being offered to them in The Netherlands? How effective are these solutions? How responsive is the IPPA instrument (Individually Prioritized Problem Assessment)? DESIGN: Analysing the results of a follow-up study using the IPPA instrument. SETTING: The Dutch Service for the Disabled Act (SDA, in Dutch: WVG) provision system. This act is responsible for the provision of mobility aids and home adaptations. SUBJECTS: Fifty-nine people with outdoor mobility disabilities. INTERVENTIONS: The provision of outdoor mobility service and devices. MAIN OUTCOME MEASURES: Effectiveness of provisions as measured using IPPA (i.e., the degree to which activities have become less difficult to perform), effect size of IPPA with this intervention. RESULTS: Problems identified by clients are very diverse and specific but can be classified fairly well on the basis of the International Classification of Functioning, Disability and Health (ICF); in the main, the solutions they are provided with are very similar and generic. Effectiveness is excellent at a group level, but insufficient for some at an individual level. The IPPA instrument is highly responsive in this setting. Most mobility problems respondents identified, although very individual and specific, were related to shopping, social visits or leisure activities. These specific sets of problems were solved using 'standard', generic solutions. CONCLUSIONS: The Dutch provision system should be more 'demand oriented' and less 'supply oriented'. IPPA turns out to be a useful, structured and individual-oriented method to evaluate service delivery.

Activities of Daily Living↗

Purified rat acid-labile subunit and recombinant human insulin-like growth factor (IGF)-binding protein-3 can form a 150-kilodalton binary complex in vitro in the absence of IGFs.

Insulin-like growth factors (IGFs) circulate in plasma mainly as part of a 150-kilodalton (kDa) complex with 40- to 45-kDa IGF-binding protein-3 (IGFBP-3) and an approximately 85-kDa acid-labile subunit (ALS) that does not bind IGFs directly. This complex sequesters IGFs in plasma, thereby providing a potential reservoir of the growth factors for tissues while constraining their potential hypoglycemic effects. Although it has been thought that IGFBP-3 must first bind IGF-I or IGF-II before it can complex with ALS to form the 150-kDa complex, we recently showed that unoccupied 150-kDa binary complexes of IGFBP-3 and ALS are abundant in adult rat serum. We now demonstrate that IGFBP-3 and rat (r)ALS can form 150-kDa complexes in the absence of IGFs. ALS was purified from rat serum by anion exchange chromatography and affinity chromatography on an IGF-I-Sepharose column to which human (h) IGFBP-3 had been noncovalently bound. The preparation contained less than 0.1 ng IGF-I/microgram(s) purified ALS. In the absence of IGF, radiolabeled (r)ALS and recombinant hIGFBP-3 formed complexes that could be immunoprecipitated by antiserum to hIGFBP-3; these complexes were identified by direct quantitation of the precipitated radioactivity or by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDA-PAGE). Inclusion of IGF-I in the incubation increased complex formation. Complex formation also was demonstrated by incubation of unlabeled rALS with hIGFBP-3, followed by affinity cross-linking. Complexes were fractionated by SDS-PAGE, blotted, and shown to contain unoccupied IGF-binding sites by their ability to bind radioiodinated IGF-II. In addition, when rALS was subjected to SDS-PAGE and blotted, radioiodinated recombinant hIGFBP-3 bound to the 85-kDa protein. In this experiment IGFBP-3 binding was slightly increased by coincubation with IGF-I. Thus, purified rALS can form a 150-kDa complex with hIGFBP-3 in the absence of IGF in vitro. The efficiency of complex formation was increased to variable extents by coincubation with IGF-I depending on the assay method.

Animals↗

[Pharmacological characteristics of perospirone hydrochloride, a novel antipsychotic agent].

It is now known that the blockade of 5-HT2 receptors can ameliorate the negative symptoms of schizophrenia and extrapyramidal side effects (EPS) associated with antipsychotic treatments. Perospirone hydrochloride (perospirone), which was identified as a novel serotonin-dopamine antagonist (SDA)-type antipsychotic agent in 1987 by Sumitomo Pharmaceuticals, possesses high affinities both for dopamine 5-HT2 and D2 receptors. Perospirone, like conventional antipsychotics, significantly inhibited various behaviors induced by dopaminergic hyperactivation. Perospirone also produced a significant improvement in animal models of the negative symptoms and mood disorders, where the conventional antipsychotics were unaffected. In addition, perospirone was weaker than the conventional antipsychotics (e.g., haloperidol) in inducing EPS signs (e.g., catalepsy and bradykinesia), suggesting that the drug has an atypical antipsychotic property. A recent double-blind study with schizophrenia patients demonstrated that perospirone was comparative with haloperidol in improving the positive symptoms, but was significantly superior to haloperidol against the negative symptoms. Furthermore, the extrapyramidal score in patients with perospirone treatment was lower that those with haloperidol treatment. These findings suggested that perospirone acts as an antagonist both for 5-HT2 and D2 receptors and has broader clinical efficacy and lower EPS liability than haloperidol in schizophrenia treatment.

Animals↗

Effect of the reporting-interval size on critical difference estimation: beyond "2.77".

BACKGROUND: The reporting interval is the bin size used to report numerical pathology results and must be determined for every analyte. The influence of the size of the reporting interval on the critical difference (CD) between two results from the same patient has not been addressed previously. METHODS: The effect of changing the reporting-interval size (RIS) on CDs was modeled by use of a spreadsheet application. The findings were applied to data on CDs with analytical precision values from our laboratory. RESULTS: As the RIS increases relative to the combined analytical and within-person biological variation, there is an approximately linear increase in the CD from the value determined by use of published techniques. The revised estimate is as follows: CD = 2(1/2) x z x (SDa(2) + SDi(2))(1/2) + 1.5 x RIS, where CD, SD, and RIS are all in the same units. This effect is seen for any probability associated with the critical difference and for both uni- and bidirectional changes. CONCLUSIONS: The choice of reporting interval should be made in the light of assay requirements. Where there is a clinical need for detection of small changes in analyte concentration, the reporting interval should be kept small relative to the combined variation attributable to assay precision and within-person biological variation.

Clinical Chemistry Tests↗

Drosophila couch potato mutants exhibit complex neurological abnormalities including epilepsy phenotypes.

RNA-binding proteins play critical roles in regulation of gene expression, and impairment can have severe phenotypic consequences on nervous system function. We report here the discovery of several complex neurological phenotypes associated with mutations of couch potato (cpo), which encodes a Drosophila RNA-binding protein. We show that mutation of cpo leads to bang-sensitive paralysis, seizure susceptibility, and synaptic transmission defects. A new cpo allele called cpo(EG1) was identified on the basis of a bang-sensitive paralytic mutant phenotype in a sensitized genetic background (sda/+). In heteroallelic combinations with other cpo alleles, cpo(EG1) shows an incompletely penetrant bang-sensitive phenotype with approximately 30% of flies becoming paralyzed. In response to electroconvulsive shock, heteroallelic combinations with cpo(EG1) exhibit seizure thresholds less than half that of wild-type flies. Finally, cpo flies display several neurocircuit abnormalities in the giant fiber (GF) system. The TTM muscles of cpo mutants exhibit long latency responses coupled with decreased following frequency. DLM muscles in cpo mutants show drastic reductions in following frequency despite exhibiting normal latency relationships. The labile sites appear to be the electrochemical GF-TTMn synapse and the chemical PSI-DLMn synapses. These complex neurological phenotypes of cpo mutants support an important role for cpo in regulating proper nervous system function, including seizure susceptibility.

Alleles↗

The mei-P26 gene encodes a RING finger B-box coiled-coil-NHL protein that regulates seizure susceptibility in Drosophilia.

Seizure-suppressor mutations provide unique insight into the genes and mechanisms involved in regulating nervous system excitability. Drosophila bang-sensitive (BS) mutants present a useful tool for identifying seizure suppressors since they are a well-characterized epilepsy model. Here we describe the isolation and characterization of a new Drosophila seizure-suppressor mutant that results from disruption of the meiotic gene mei-P26, which belongs to the RBCC-NHL family of proteins. The mei-P26 mutation reduces seizures in easily shocked (eas) and slamdance (sda) epileptic flies following mechanical stimulation and electroconvulsive shock. In addition, mutant mei-P26 flies exhibit seizure thresholds at least threefold greater than those of wild type. The mei-P26 phenotypes appear to result from missense mutation of a critical residue in the NHL protein-protein interaction domain of the protein. These results reveal a surprising role for mei-P26 outside of the germline as a regulator of seizure susceptibility, possibly by affecting synaptic development as a ubiquitin ligase.

Amino Acid Sequence↗

Pathological observations on natural cases of sialodacryoadenitis of rats.

Pathological observations were carried out on 100 male rats of Sprague-Dawley strain obtained from 5 outbreaks of sialodacryoadenitis (SDA). In accordance with clinical and macroscopic findings, principal microscopic changes were found in the salivary (submaxillary and parotid) and Harderian glands. Lesions observed in these different glands were essentially similar to each other, and characterized by degenerative changes in the epithelial cells of the ducts and acini associated with marked and extensive serous inflammation in the interstice. Furthermore, squamous metaplasia of the ductal epithelia was a common feature to these glands in the late stage of the disease. Some differences, however, were detected between the changes of the salivary glands and those of the Harderian glands. Firstly, the ductal epithelial cells were affected at first and the acinous epithelial cells were damaged only secondarily in the active inflammatory process in the salivary glands, while both ductal and acinous epithelial cells were involved equally in the primary lesion in the Harderian glands. Secondly, the increase in connective tissue elements in the reparatory process was extremely marked in the Harderian glands as compared with the salivary glands. Consequently, in the lesion of Harderian glands in the late stage, original construction was almost indiscernible, and the ducts and acini were only recognized as disseminated islets in actively proliferated connective tissue elements.

Animals↗

Ten years-long survey on pathogen status of mouse and rat breeding colonies.

Eleven pathogens including P. aeruginosa, Salmonella spp., E. coli O115a, c: K(B), P. pneumotropica, B. bronchiseptica, C. kutscheri, Tyzzer's organism, M. pulmonis, Sendai virus, MHV and Syphacia spp. were surveyed in 217 mouse and rat breeding colonies during 1972-1981. In conventional animals, P. pneumotropica and/or Syphacia spp. were detected in nearly 90% of 89 mouse and 64 rat colonies. Sendai virus, M. pulmonis, P. aeruginosa and MHV were positive in 51.7 to 23.6% of the colonies, and Tyzzer's organism, B. bronchiseptica and probably SDA virus were also detected in more than 10% of the rat colonies. Salmonella spp., E. coli O115a, c: K(B) and C. kutscheri were found in a few colonies. In SPF animals, P. aeruginosa was isolated from about one third of 33 mouse and 31 rat colonies, and P. aeruginosa was isolated from about one third of 33 mouse and 31 rat colonies, and P. pneumotropica was also positive in 3 rat colonies. Infection rates of P. pneumotropica, M. pulmonis, Sendai virus and Syphacia spp. were usually higher than 40% of animals sampled from colonies contaminated with them. Accidental contaminations of SPF colonies were usually caused by P. pneumotropica and Syphacia spp.

Animals↗