Isolation of Yersinia Enterocolitica from a Dog with Chronic Enteritis

During recent years, Yersinia enterocolitica has been isolated from humans and various animal species in connection with intestinal disorders, such as acute ileitis and appendicitis. Cases of septicaemia, polyarthritis and erythema nodosum have also been described (Mollaret & Destombes 1964, Nilehn 1969, Winblad 1969, Lassen 1972, Langford 1972). Y. enterocolitica has been isolated most frequently from chinchillas and hares, but sporadic isolations from deer, cow, horse, rabbit, goat and dog have been reported (Langford, Krogstad et al. 1972). In Norway, an outbreak of the disease in a goat herd is the only described case of yersiniosis among animal species (Krogstad et al.). A case of chronic enteritis in a dog from which Y. enterocolitica was isolated is presented in the following.     

Use of Bromodeoxyuridine For Cell Kinetic Studies In Intact Animals

Abstract. A method is described for the use of BUdR for tracing cell proliferation patterns in the intestinal mucosa of intact mice.
The method has several distinct advantages over existing methods.
Bromodeoxyuridine (BUdR) is a well-established alternative to tritiated thymidine ([³H]TdR) as a tracer for studying DNA replication. However, its use in cytological as opposed to biochemical studies has been largely confined to examination of metaphase spreads, particularly analysis of sister chromatid exchange (Block, 1982). For this, BUdR incorporation into DNA has been demonstrated using the fluorescent dye Hoechst 33258, together with fluorescence microscopy (Latt, 1973), or Giemsa staining (Perry & Wolf, 1974). Recently, introduction of a monoclonal antibody which recognizes BUdR in single-stranded DNA (Gratzner, 1982) has enabled BUdR to be used for studying cell cycle kinetics in a manner exactly analogous to the use of [³H]TdR. This has been reported for whole cells in suspension and in monolayer (Dolbeare et al. , 1983; Dean et al. , 1984; Raza et al. , 1984). BUdR included in tissue culture medium is taken up and incorporated into newly synthesized DNA via the same pyrimidine salvage pathway as [³H]TdR (thymidine kinase). A concentration of as little as 10 μm—well below cytotoxic levels (Cerni, 1984)—is sufficient to give readily detectable labelling by immunocytochemistry with a pulse of less than 15 min. the validity of BUdR labelling for cell kinetic studies has been well established in comparisons with other methods by Dolbeare et al. (1983), Dean et al. (1984), and Raza et al. (1984).
We describe here the use of BUdR together with an immunocytochemical detection system applied to sections of wax-embedded tissues, which provides a convenient method of cell cycle analysis in intact animals.     

Enteroendocrine cells and 5-HT availability are altered in mucosa of guinea pigs with TNBS ileitis

Enteroendocrine cells act as sensory transducers, releasing 5-HT and numerous peptides that are involved in regulating motility, secretion, and gut sensation. The action of mucosal 5-HT is terminated by a 5-HT reuptake transporter (SERT). In this study, we examined the hypothesis that ileitis leads to changes in enteroendocrine cell populations and mucosal 5-HT availability. Ileitis was induced in guinea pigs by intraluminal injection of 2,4,6-trinitrobenzenesulfonic acid and experiments were conducted 3, 7, and 14 days after treatment. The number of somatostatin, neurotensin, and 5-HT-immunoreactive cells increased at 3 and 7 days of ileitis, respectively, whereas no significant changes in the numbers of cholecystokinin, glucagon-like peptide-2, glucose-dependent insulinotropic peptide, and peptide YY-immunoreactive cells were observed. Chemical stimulation of the inflamed mucosa with sodium deoxycholic acid significantly increased 5-HT release compared with basal release. Mechanical stimulation of the mucosa potentiated the effect of the chemical stimuli at day 7. Epithelial SERT immunoreactivity was significantly reduced during the time course of inflammation. Thus changes in enteroendocrine cell populations and 5-HT availability could contribute to the altered motility and secretion associated with intestinal inflammation by disrupting mucosal signaling to enteric nerves involved in peristaltic and secretory reflexes.     

Induction of Swine Dysentery with a Pure Culture of Treponema Hyodysenteriae in Vitamin E and Selenium Deficient Pigs

Several successful attempts have been made to induce swine dysentery in pigs using pure cultures of Treponema hyodysen-teriae (Taylor & Alexander 1971, Harris et al. 1972, Akkermans & Pomper 1973, Hughes et al. 1975). In these studies, either conventional or specific-pathogen-free pigs were used. In the present study, 2 approximately 8 weeks old conventional pigs (Nos. 1 and 2) were purchased and fed the same basic ration as used by Teige et al. (1977). In addition, 10 % cod liver oil was incorporated in the diet at each feeding. After a feeding period of 25 days rectal swabs were applied and examined for the presence of spirochaetes. The pigs were then fed a 3 days old primary and pure culture of T. hyodysenteriae on TSA-S400 medium (Songer et al. 1976). The culture originated from the colon of a pig with swine dysentery (Pig No. 4, Teige et al. 1977). Each pig received the agar contents of 5 petri dishes which were mixed with the food.     

Focal Symmetrical Poliomyelomalacia in a Calf

Focal symmetrical poliomyelomalacia (FSP) is a neurological disorder mainly described in pigs in connection with experimental or spontaneous cases of selenium toxicosis (Harrison etal. 1983, Wendtetal. 1992, Wilson etal. 1983 & 1989). However, a few cases of FSP have been reported in other domestic animals including sheep, goat, and cattle (Innes & Plow-right 1955, Cordy et al. 1984, Bonniwell & Barlow 1985, Palmer et al. 1986). Common for reports on FSP in other species than pigs is an unsolved aetiology. In cattle only 1 report on FSP has been published previously describing 2 cases (Palmer et al. 1986). The present report describes a further case of FSP in cattle. A 4-month- old Red Danish × American Brown Swiss calf (♀) suddenly became lame on both fore limbs and unwilling to rise. The calf had a swelling around the coronary band and a temperature of 40°C. The calf was treated with antibiotics by a veterinary surgeon. The condition got severe during the next 24 h, and the calf became unable to stand on the fore limbs while the function of the rear limbs was normal. As the condition progressively got worse during the next week, the calf was euthanized by intravenous injection of pentobarbitone sodium and submitted for necropsy.     

Spontaneous terminal ileitis resembling Crohn disease in captive tamarins

Five tamarins (four Saguinus mystax and one S. labiatus) died with wasting syndrome characterized by chronic diarrhea at the Center for Reproduction and Conservation of Non-Human Primates in Iquitos, Peru. At necropsy, the terminal ileum of all affected tamarins was found to be markedly thickened. Histologically, the terminal ileal mucosa was completely ulcerated, and effaced by debris and mononuclear inflammatory cells. The submucosa and serosa were thickened by fibroplasia, mononuclear cell infiltrates and variable edema. No infectious agent was observed. The lesions were similar to those described previously for Crohn disease. This is to our knowledge the first report of terminal ileitis resembling Crohn disease in non-human primates.     

Feline Pansteatitis: A Report of Five Cases

Pansteatitis (yellow fat disease, panniculitis, steatitis) is an inflammatory disease of adipose tissue throughout the body (Holzworth 1987). It was first experimentally induced by Mason & Dam in 1946 in cats fed a diet deficient in vita-min E and high in cod liver oil (Mason & Dam 1946). It has since been reported as a clinical condition by several authors (Cordy & Stil-linger 1953, Watson et al 1973, Gaskell et al 1975, Summers et al 1982, Hagiwara et al 1986). Pansteatitis occurs naturally in cats, mink, and pigs as a result of vitamin E deficiency. Vitamin E (α-tocopherol) is a biological antioxidant found in vegetable oils (Holzworth 1987). It serves as a protector of the fats in the diet and in the body. Pansteatitis is caused by a mismatch between intake of unsaturated fatty acids and antioxidants, i.e. vitamin E. The ensu-ing peroxidation of the body fat causes a for-eign body reaction with severe inflammation and cell death. The foremost clinical sign is hy-peraesthesia or severe pain on palpation/han-dling, especially over the back and of the abdo-men. The final diagnosis rests with the histo-logical findings of the above-mentioned lesions in conjunction with acid-fast ceroid pigment (i.e. end-product of lipid peroxidation) in fat cells, in macrophages, in Langhans-type giant cells, and extracellularly (Holzworth 1987).     

The Indirect Fluorescent Antibody Test (IFAT) for the Detection of Nosema Cuniculi Antibodies in the Blue Fox (Alopex Lagopus)

During recent years nosematosis has been a major problem in the breeding of blue fox in the Scandinavian countries, causing heavy losses among growing pups (Nordstoga 1972, Nordstoga et al. 1974). The lack of reliable methods for diagnosing the infection in live foxes has so far made epizootiologic studies of the disease very difficult. However, reports on the IFAT in rabbits with nosematosis (Cox et al. 1972, Chalupsky et al. 1971, 1973, 1974), encouraged the search for a method of detecting Nosema antibodies in fox sera.     

Bacteriophage P22 virion protein which performs an essential early function. I. Analysis of 16-ts mutants.

The product of gene 16 of phage P22, P16, is a head protein. P16 does not play an essential role in phage assembly since particles formed without this protein appear normal by electron microscopy examination (Botstein et al., 1973). P16 is essential when the particle infects a cell in the following cycle of infection (Botstein et al., 1973; King et al., 1973). We have characterized a mutant of P22 carrying a temperature-sensitive allele of gene 16. This mutant has previously been referred to as P22 25-ts (Levine et al., 1970, 1972) and P22 X-ts (Bezdek and Soska, 1970, 1973). P22 16-ts behaves as an early mutant at the nonpermissive temperature. Temperature shift experiments show that P16 of the infecting virion acts within the first 10 min at 25 C and that gene 16 product is required late in the latent period for incorporation into infectious phage. Induction does not require P16 for the production of particles. Particles produced either in a P22 16-ts thermal shift-up infection or after induction of 16-ts lysogens at 41 C are missing P16 and are, therefore, defective. P16 in P22 16-ts virions formed at the permissive temperature appears to be heat labile; it is inactivated after infection at 41 C. A simple assay for defective particles based on a complementation test is described.     

Further studies on the E blood group system in pigs

The blood group system E in pigs is similar to the B system in cattle, one of the most complicated of the hitherto known blood group systems.
Studies of Andresen (1957), Saison (1958), Andresen & Wroblewski (1959), Andresen et al. (1959), Andresen (1962, 1965), Rasmusen (1965), Hojný et al. (1966), Dinklage et al. (1966), Dinklage & Major (1968), Hradecký & Hojný (1972), Hojný & Hradeck (1972, 1973) lead to the determination of the various E alleles.
This report presents information of a new blood group factor E_p in pigs.     

Hematological and Biochemical Analyses of Blood and Serum in Pigs with Regional Ileitis with Special Reference to the Pathogenesis

Biochemical and hematological analyses of blood and serum were performed in pigs with regional ileitis and in wasting pigs with a negative necropsy. In sera from pigs with regional ileitis the levels of total protein, albumin, transferrin, alkaline phosphatase and zinc were significantly decreased compared with normal pigs of the same age. The number of white blood cells, and the concentration of Cortisol and α1-antitrypsin were significantly increased. In wasting pigs with early signs of regional ileitis or with a negative necropsy the same blood changes were observed but to a less degree. It was concluded that a wasting syndrome after weaning may precede regional ileitis. Concerning the etiology of regional ileitis the significance of malabsorption and wasting syndrome in combination with invasion of intestinal intercellular microorganisms is discussed.     

IGF-I and procollagen alpha1(I) are coexpressed in a subset of mesenchymal cells in active Crohn's disease

This study tested the hypothesis that insulin-like growth factor I (IGF-I) expression is increased at sites of fibrosis in diseased intestine of patients with Crohn's disease (CD). IGF-I mRNA was quantified by RNase protection assay in uninvolved and involved intestine of 13 CD patients (10 ileum, 3 colon) and 7 ulcerative colitis (UC) patients (colon). In situ hybridization histochemistry compared the localization of IGF-I and procollagen alpha1(I) mRNAs. Masson's trichrome staining and immunohistochemistry for IGF-I precursor, alpha-smooth muscle actin (A), vimentin (V), desmin (D), and c-kit were used to examine the mesenchymal cell subtypes that express IGF-I and collagen in uninvolved and involved ileum and colon of CD patients and "normal" ileum and colon from noninflammatory controls. IGF-I mRNA was elevated in involved ileum and colon of patients with CD but not in involved colon of patients with UC. IGF-I and procollagen alpha1(I) mRNA showed overlapping distribution within fibrotic submucosa and muscularis propria of involved CD ileum and colon. In involved CD intestine, increased IGF-I precursor expression localized to mesenchymal cells in regions of tissue disorganization and fibrosis in muscularis mucosa, submucosa, and muscularis propria. In these regions, there were increased numbers of V(+) cells relative to normal or uninvolved intestine. Increased IGF-I expression was localized to cells with a phenotype typical of fibroblasts (V(+)/A(-)/D(-)), myofibroblasts (V(+)/A(+)/D(+)), and, to a lesser extent, cells with normal enteric smooth muscle phenotype (V(-)/A(+)/D(+)). We conclude that increased IGF-I expression in multiple mesenchymal cell subtypes and increased numbers of cells with fibroblast/myofibroblast phenotype are involved in fibrosis associated with CD.     

Chorio-Retinitis in Porcine Toxoplasmosis

Porcine toxoplasmosis generally occurs as a latent disease in adolescent and adult pigs, but now and then also manifests itself as a fatal congenital disease in piglets. It is known to occur in USA (Farrel et al. 1952), Germany (Becker 1954), Denmark (Momberg-Jørgensen 1956), Mexico (Varela et al. 1956), Japan (Sato et al. 1958), England (Harding et al. 1961) and Sweden (Hansen et al. to be published).     

An attempt at comparison of the morphology of normal and RSV--transformed cells in a scanning microscope

The electronic scanning microscope (SEM) was first used to analyze biological material in 1965 (Hollenberg M. et al. The Journal of Histochem. and Cytochem. 21, 109-130, 1973). It has since been possible to collect specific data on cell morphology and the changes in cell surface and structure caused by external factors, such as oncogenic viruses.     

Regional Ileitis in Pigs

Twenty-seven weaned pigs with a wasting appearance were investigated. From a morphological point of view the pigs were divided into three groups. In the group of pigs with macro-scopical signs of regional ileitis, affected tissue showed substantial epithelial proliferation, and electron microscopic studies revealed the presence of microorganisms within the cytoplasm of the epithelial cells. There was a loss of, or only faint, enzymatic activity of alkaline phosphatase in the mucosal epithelium. In another group of five pigs there was no, or only slight, light microscopical signs of regional ileitis but presence of intracellular microorganisms. The enzymatic activity of the ileal epithelium was low. Low enzymatic activity of the ileal epithelium was observed in a third group of wasting pigs, which had no histological or electron microscopical signs of regional ileitis.     

Infection with Streptococcus Suis Serotypes 1 and 2 in the Same Diseased Pig

Streptococcus suis is an important pig pathogen which is associated with respiratory problems, meningitis and less fre-quently with a variety of other conditions(Hommez et al. 1986). S. suis type 1 causes disease mainly in 1–2 week old pigs while serotype 2 is found commoaily in 2–22 week old pigs, S. suis type 2 is a zoonosis. It can cause meningitis and septicaemia in man (Christensen & Kronvall 1985). Several other serotypes of S. suis have also been identified on the basis of the capsular poly-saccharide (Perch et al. 1983, Hommez et al. 1986). We present a case where we isolated S. suis types 1 and 2 from the brain and lungs respectively of the same diseased suckling piglet. This i/s the first reported case of S. suis types 1 and 2 in Finland.     

The transition zone in Hirschsprung's bowel contains abnormal hybrid ganglia with characteristics of extrinsic nerves

The aganglionic bowel in short-segment Hirschsprung's disease is characterized both by the absence of enteric ganglia and the presence of extrinsic thickened nerve bundles (TNBs). The relationship between the TNBs and the loss of enteric ganglia is unknown. Previous studies have described decreasing numbers of ganglia with increasing density of TNBs within the transition zone (TZ) between ganglionic and aganglionic gut, and there is some evidence of spatial contact between them in this region. To determine the cellular interactions involved, we have analysed the expression of perineurial markers of TNBs and enteric ganglionic markers for both neural cells and their ensheathing telocytes across four cranio-caudal segments consisting of most proximal ganglionic to most distal aganglionic from pull-through resected colon. We show that in the TZ, enteric ganglia are abnormal, being surrounded by perineurium cells characteristic of TNBs. Furthermore, short processes of ganglionic neurons extend caudally towards the aganglionic region, where telocytes in the TNB are located between the perineurium and nerve fibres into which they project telopodes. Thus, enteric ganglia within the TZ have abnormal structural characteristics, the cellular relationships of which are shared by the TNBs. These findings will help towards elucidation of the cellular mechanisms involved in the aetiology of Hirschsprung's disease.