This article was downloaded by: [Cornell University Library]On: 18 November 2014, At: 21:54Publisher: Taylor & FrancisInforma Ltd Registered in England and Wales Registered Number: 1072954 Registered office: Mortimer House,37-41 Mortimer Street, London W1T 3JH, UK

Avian PathologyPublication details, including instructions for authors and subscription information:http://www.tandfonline.com/loi/cavp20

Infectious Typhlitis in chickens caused by spirochetesF.G. Davelaar a , H.F. Smit b , K. Hovind‐Hougen c , R.M. Dwars d & P.C. vanderValk e

a Department of Poultry Diseases , State University of Utrecht , P.O. Box 43, Doom, 3940 AA,The Netherlandsb Department of Bacteriology , State University of Utrecht , The Netherlandsc State University Serum Laboratory , Copenhagen, Denmarkd Poultry Health Institute , Doorn, The Netherlandse Department of Herd Health and Ambulatory Clinic , State University of Utrecht , TheNetherlandsPublished online: 02 Jan 2008.

To cite this article: F.G. Davelaar , H.F. Smit , K. Hovind‐Hougen , R.M. Dwars & P.C. vanderValk (1986) Infectious Typhlitis inchickens caused by spirochetes, Avian Pathology, 15:2, 247-258, DOI: 10.1080/03079458608436285

To link to this article: http://dx.doi.org/10.1080/03079458608436285

PLEASE SCROLL DOWN FOR ARTICLE

Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in thepublications on our platform. However, Taylor & Francis, our agents, and our licensors make no representationsor warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Anyopinions and views expressed in this publication are the opinions and views of the authors, and are not theviews of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should beindependently verified with primary sources of information. Taylor and Francis shall not be liable for any losses,actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoevercaused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content.

This article may be used for research, teaching, and private study purposes. Any substantial or systematicreproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in anyform to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http://www.tandfonline.com/page/terms-and-conditions

Avian Pathology, 15: 247-258, 1986

INFECTIOUS TYPHLITIS IN CHICKENSCAUSED BY SPIROCHETES

F.G. DAVELAAR1, H.F. SMIT2, K. HOVIND-HOUGEN3,R.M. DWARS4 and P.C. van der VALK5

1 Department of Poultry Diseases, State University of Utrecht,P.O. Box 43, 3940 AA Doom, The Netherlands.

2 Department of Bacteriology, State University of Utrecht, The Netherlands.

3 State University Serum Laboratory, Copenhagen, Denmark.

"Poultry Health Institute, Doom, The Netherlands.

s Department of Herd Health and Ambulatory Clinic,State University of Utrecht, The Netherlands.

SUMMARY

A weakly haemolytic spirochete was detected with an unabsorbedfluorescent antiserum to Treponema hyodysenteriae in smears andcultures of scrapings of caecal mucosa of laying hens with diarrhoea.Two groups of experimental chickens were fed a pure culture of thisspirochete or homogenated intestinal contents of affected birds. Bothgroups showed clinical signs of disease such as increased water contentof faecal material and slight retardation of growth.

A non-specific typhlitis which histologically resembled milder formsof swine dysentery was seen in the birds from which spirochetes wereisolated. The isolate obtained differed in cultural, biochemical, anti-genic and morphological characteristics from T. hyodysenteriae.

The pathological significance of intestinal spirochetes and their possibleepidemiológica! relation to swine dysentery are discussed.

INTRODUCTION AND CLINICAL HISTORY

Diarrhoea occurred in chickens on a farm with approximately 12,000 laying hens.Furthermore 80 sows with their progeny and 250 fatteners were kept at the samefarm. There was a history of prolonged, intermittent diarrhoea among the chickensand also among the piglets and fatteners. Despite increased food intake, the hensshowed an early decrease in egg production. Piglets showed irregular growth andincreased mortality.

Received 15 March 1985Accepted 29 November 1985

Dow

nloa

ded

by [

Cor

nell

Uni

vers

ity L

ibra

ry]

at 2

1:54

18

Nov

embe

r 20

14

248 F.G. Davelaax et al.

Salmonellae could not be demonstrated in the faeces of pigs or in caeca and liverof chickens. Examination of sera from 12 chickens for antibodies against Myco-plasma gallisepticwn, Mycoplasma synoviae (serum plate agglutination test), avianinfluenza virus and infectious bronchitis virus (haemagglutination inhibition test)had negative results. Parasitological examinations revealed only moderate numbersof ascarids in the intestines of the chickens.

Because a common cause of the problems in both species was suspected, faecesfrom pigs and droppings from chickens were collected at several spots and pooledto be examined for the presence of spirochetes.

In smears of the droppings of chickens large numbers of spirochetes were present,which fluoresced by the fluorescent antibody test (FAT) with an unabsorbedantiserum to Treponema hyodysenteriae. Smears from initial faecal samples of thepigs were negative in a corresponding test. Examination of a larger number of pigfaecal samples revealed small numbers of fluorescing spirochetes in a few samples.

This paper presents information on the isolation, characterisation and pathogenicityof avian spirochetes.

MATERIALS AND METHODS

BacteriologyFluorescent antibody test. The direct FAT was performed as described by Hunterand Clark (1975). The conjugate used was prepared from unabsorbed antisera toa T. hyodysenteriae strain (Smit and Jongerius, 1983). The FAT was primarilyperformed on mucosa scrapings of the duodenum, the jejunum, the ileum and thecaecaum from two chicks from the farm mentioned above.

Isolation of spirochetes. Spirochetes were isolated from the same scrapings bycultivation on spectinomycin blood agar as described by Songer et al. (1976).Trypticase Soy Agar plates (BBL, to which was added 5% bovine blood and 400μgspectinomycin per ml) were incubated in an atmosphere of 80% hydrogen and 20%carbon dioxide in a GASPAK jar at 42°C.

Prior to further examinations isolates were purified by agar plug transfer (twotimes) (Baum and Joens, 1979).

Indole production. índole production was tested by a heavy inoculum of 5-day-oldsurface growth to prereduced Trypticase Soy Broth (Trypticase Soy Broth withoutDextrose, BBL, with added 0.05% cysteln HC1 and 0.004% resazurin) in stopperedtubes containing a stirring bar. Ten % newborn calf serum was added and anaerobicconditions were restored by leading equal parts of hydrogen and carbon dioxideover the suspension until the resazurin was decolourised. The tubes were incubatedon a magnetic stirrer for 48 hours at 42°C. índole production was checked byadding 1 ml of Kovac's reagent.

API ZYM system. The API ZYM system was used as described by Hunter and Wood(1979).

Growth inhibition test (GIT). This test was carried out by Dr Lemcke, Compton,UK (Lemcke and Burrows, 1979).

The growth inhibition has been tested with antisera against strains of T. hyodysen-teriae, seven serological types of weakly haemolytic porcine spirochetes and theTaylor P43/6/78 strain (Taylor et al., 1980).

Dow

nloa

ded

by [

Cor

nell

Uni

vers

ity L

ibra

ry]

at 2

1:54

18

Nov

embe

r 20

14

Infectious typhlitis 249

HistologyPortions of the caeca from which the spirochetes were isolated were frozen at-20°C and sectioned on a cryostat.

Sections were used for localisation of spirochetes by the direct FAT. Other portionswere fixed in 4.0% formalin for histological examination. Sections were stainedwith haematoxilin and eosin, or with a combination of the PAS-Warthin-stain andHarris-haematoxilin.

Electron MicroscopySpirochetes were cultivated on Trypticase Soy Agar plates and incubated at 42°Cfor 4 days in an atmosphere of 80% hydrogen and 20% carbon dioxide. Surfacegrowth was washed off the plates with 1 to 2 ml of a 0.03% sucrose solutioncontaining 0.01 M CaCl2 and 0.01 M MgCl2 (SMC) and the suspension was adjustedto a suitable density by addition of SMC. Specimen grids were prepared by themultiple drop technique (Hovind-Hougen and Birch-Andersen, 1971), and nega-tively stained with 1% ammonium molybdate, pH 7. Electron microscopy wascarried out with a Philips EM 200 electron microscope at primary magnificationsof 1,500, 3,000 and 11,000 x. Prints were obtained after photographic enlargementas described.

Transmission ExperimentPathogenicity studies were carried out with three groups of 10 SPF hens, agedapproximately 10 weeks. The groups were housed in separate isolators (Davelaarand Kouwenhoven, 1976).

Group A was given orally 2 ml of homogenised intestinal contents of diseasedbirds from the farm. A suspension of the isolated spirochete (strain Kl) com-prising the surface growth of 20 TSA plates was similarly given to group B. Birdsin group C served as controls.

The dry matter of faecal samples collected from each group was determined weeklyfor 9 weeks with the exception of week no. 7. Three to four chickens from eachgroup were killed at weeks 7, 8 and 9. Body weights were recorded and scrapingswere made from the caecal mucosa for examination with the FAT.

RESULTS

Bacteriological findingsWith the FAT, fluorescing spirochetes were found in the caeca, where they formeda tangled mass in the crypts and the adjacent lumen (Fig. 1). Spirochetes were notobserved on other intestinal mucosal surfaces. Clear evidence for invading spiro-chetes in the caecal mucosa was not found.

Growth of the isolate Kl was observed on Trypticase Soy agar with bovine bloodand spectinomycin commonly on the 2nd day of incubation and was primarilycharacterised by an extensive swarming zone. One the 2nd day a weak haemolysisdeveloped slowly within the inoculated area followed by local concentration ofthe surface growth in non-discrete colonies. Spirochetes were only isolated from thecaecal mucosa scrapings.

The organism was found to be more fastidious than T. hyodysenteriae and theoriginal Kl strain was lost after the transmission experiment with SPF chickens.Further observations were then made on strain Kla, reisolated from a group A

Dow

nloa

ded

by [

Cor

nell

Uni

vers

ity L

ibra

ry]

at 2

1:54

18

Nov

embe

r 20

14

250 F.G.Davelaai eíaZ.

chicken. Growth in the stirred liquid medium was minimal although the via-bility was well preserved as kudged by the active motility of the spirochetes after48 hours of incubation. Unlike T. hyodysenteriae these spirochetes did not produceÍndole under the growth conditions described.

The strain was not inhibited in the GIT by antisera against different strains ofT. hyodysenteriae. However, the isolate Kla was inhibited by antisera againststrain P43/6/78, which originally was isolated from intestinal spirochaetosis inpigs (Taylor et al, 1980).

Testing the strain Kla with the API ZYM system indicated the presence of thefollowing enzymes: alkaline phosphatase (API no. 2), C4 esterase (no. 3), C8esterase lipase (no. 4), alpha galactosidase (no. 13), beta galactosidase (no. 14),alpha glucosidase (no. 16) and beta glucosidase (no. 17).Electron microscopyThe cells were regularly waved and were 7 to 19 jum long. Wave-length was about4 /urn, and the maximum cell width 0.5 to 0,6 jum. The width decreased towardsthe ends of the cells where they were only 0.25 jum wide, but the cell ends assuch were blunt (Figs. 2 and 3). All cells were covered by a surface layer which onsome micrographs seemed to possess a regular substructure. Thirteen to 15 flagellae

. were inserted at each end of the cells, from which they wound around the cyto-plasmic bodies and overlapped in the mid region of the cell. Occasionally someflagellae were seen to extend all the way to the opposite end of the cell, thuscomplicating the determination of the exact number of flagellae at each end.The cells divide by dinary fission of their cytoplasmic membranes, and the newlyformed ends were truncated (Fig. 4). Quite frequently some spirochetes wereaccidentally damaged during preparation for electron microscopy showing theirflagellae freely distributed outside the periplasmic space. On these flagellae asheath surrounding the flagellar shaft could be observed. The sheath was frequentlyseen to be shorter than the core, so that approximately one-fourth to one-fifthof the distal part of the flagellum was unsheathed.

HistologyThe mucous membrane of the middle part of the caecum was studied. It con-sisted of normal columnar epithelial cells and goblet cells, and a lamina propriaalso of normal appearance. The number of goblet cells was slightly increased,compared with controls. The presence of several detached cells in the lumen indi-cated a desquamation of the epithelium in adjacent parts of the caecum. Further-more, spotwise lesions were found distributed in the epithelium by a close inspec-tion of PAS-Warthin-Harris haematoxylin-stained sections. Within these lesions,the epithelium showed a gap-like space or slit 10 to 40 jum wide, running in theapico-basal direction of the cells (Fig. 5). Large numbers of spirochetes were seenin these gaps. Adjacent epithelial cells showed no signs of degeneration. The under-lying connective tissue showed some cell lysis, some karyopyknosis and a slightinfiltration of mononuclear cells. The occurrence of degeneration and mononuclearinfiltration was confined to a region situated beneath the gap-like epithelial lesion.The size of such an infiltrated area could be up to 200 jum in diameter. Spirocheteswere observed in these areas and appeared to be associated with the pathologicalchanges described.

Transmission experimentIn group C (control group) the faecal dry matter content averaged 20 to 22%. In

Dow

nloa

ded

by [

Cor

nell

Uni

vers

ity L

ibra

ry]

at 2

1:54

18

Nov

embe

r 20

14

Infectious typhlitis 251

Fig. 1. Fluorescing spirochetes in the caeca forming a tangled mass in the cryptsand the adjacent lumen.

Dow

nloa

ded

by [

Cor

nell

Uni

vers

ity L

ibra

ry]

at 2

1:54

18

Nov

embe

r 20

14

F.G. Davelaai et al.

1 pm

0,5 pm

lpm

Dow

nloa

ded

by [

Cor

nell

Uni

vers

ity L

ibra

ry]

at 2

1:54

18

Nov

embe

r 20

14

Infectious typhlitis 253

Fig. 2. A cell strain Kla negatively stained with 1% ammonium molybdate.

Fig. 3. The tapering end of a cell of strain Kla. Seventeen flagella (F) are seen.Some of these may originate at the other end of the cell. Arrowheadsdenote some of the insertion points of the flagellae, and OE and CM outerenvelope and cytoplasmic membrane, respectively. Negatively stainedwith 1% ammonium molybdate.

Fig. 4. A dividing spirochete of strain Kla. The arrow indicates the point of division.Negatively stained with 1% ammonium molybdate.

Dow

nloa

ded

by [

Cor

nell

Uni

vers

ity L

ibra

ry]

at 2

1:54

18

Nov

embe

r 20

14

254 F.G. Davelaar et al.

Lu

Ü . * A a i s . ? « ^ « ^ > ^ ? î f j ^ j ^ •• - ; • ^ . • r ,

.̂ 5. Section through the wall of the caecum, showing epithelium and tunicapropria.Lu= lumen1 - Gap-like discontinuity in the epthelial surface. Dark appearance is

caused by large numbers of stained spirochetes (la).2 = Spirochetes, located within the epithelial layer.3 = Spirochetes, located in the tunica propria.PAS-Warthin-Harris haemotoxylin stain.

Dow

nloa

ded

by [

Cor

nell

Uni

vers

ity L

ibra

ry]

at 2

1:54

18

Nov

embe

r 20

14

Infectious typhlitis 255

group B the dry matter content dropped sharply to an average of 13% after the1st week. One week later the content had increased to about normal levels. Thebirds in group A produced normal faeces for 7 weeks. At 8 and 9 weeks the drymatter content decreased to an 18% level.

This drop in dry matter content at 8 and 9 weeks was paralleled by a massivefluorescence of tréponèmes in the caeca. In contrast the FAT was negative orshowed only a small number of fluorescing tréponèmes in group B at this time.The FAT was negative in group C all the time.

The mean body weight of chicks in groups B and C was about the same with aslight advantage for group C. The mean body weight.in group A decreased from1,447 g to 1,223 g in the period from 7 to 9 weeks after infection.

DISCUSSION

Spirochetes have been observed in the intestinal mucosa of a number of mammalianspecies. Their pathogenicity in some mammals, e.g. dog and man, is still a matterof discussion, but for most species the spirochetes are considered part of theindigenous enteric flora (Pindak et al., 1965; Davis et al., 1972; Leach étal., 1973;Takeuchi, 1974; Turek and Meyer, 1978; Nielsen et al., 1983). Pathogenic as wellas non-pathogenic spirochetes have been isolated from the intestines and faeces ofswine. The spirochetes thus obtained are morphologically rather similar and areserologically cross-reactive (Kinyon and Harris, 1979). Consequently, a possiblepathogenicity of a spirochete, isolated from the caeca of chickens, certainly de-serves careful consideration. In the present case the results of treatment of thenatural infection, the clinical signs observed in the experimental infection, and thehistopathological changes found in the caecal mucosa provide at least circumstantialevidence for the pathogenicity of the spirocheatal strain Kl.

The different reactions in the transmission experiment after oral infection withthe intestinal homogenate from diseased chickens and the pure spirochete culture,could be explained by a difference in the dosage of the infectious agent. In groupA, for example, a relatively low number of viable spirochetes needed approxi-mately 7 weeks of growth to cause a developing, clinically diagnostifiable typhlitis,whereas a larger number of spirochetes in group B produced diarrhoea by 1 week,but failed to give an equally serious typhlitis. The reason for this discrepancycould be the presence of other micro-organisms in the intestinal homogenatewhich may be responsible for a more permanent colonisation of the caeca in thechickens in group A.

The positive FAT demonstrates that the spirochetes isolated from chickens shareone or more antigenic determinant(s) with T. hyodysenteriae, the agent of swinedysentery. In the GIT the isolate Kl also shares antigens with the organisms ofstrain P43/6/78 which caused diarrhoea in experimentally infected pigs.

But morphologically the spirochetes of strain Kla differ from cells of strain B78,the type strain of T. hyodysenteriae (Kinyon and Harris, 1979 and Hovind-Hougen,in preparation) by being wider, 0.5 /urn versus 0.3 to 0.4 pm and by possessing alarger number of flagellae (13 to 15 versus 8 to 9). Cells of strain Kla also showa clear difference to those of strain P43/6/78 which were found to be 0.25 jumwide and to have only five flagellae inserted at each end (Taylor et al., 1980;Hovind-Hougen, in preparation).

Dow

nloa

ded

by [

Cor

nell

Uni

vers

ity L

ibra

ry]

at 2

1:54

18

Nov

embe

r 20

14

256 F .G. Davelaar et al.

In the API ZYM system the Kla strain revealed the presence of an alpha galacto-sidase, an enzyme which was absent in strains that are known to cause dysentery(Hunter and Wood, 1979). In addition, the inability to produce indole (Kinyonand Harris, 1979) gives further evidence that strain Kla differs from T. hyodysen-teriae.

It may still be an open question whether or not the spirochetes isolated as strainsKl and Kla are the causative pathogens of the diseased chickens and pigs studied.They certainly were the only pathogenic agents that could be demonstrated, butobviously more extensive studies are needed before other causative agents can becompletely ruled out.

AcknowledgementWe are indebted to Dr R.M. Lemcke, Compton, UK who kindly carried out theGrowth Inhibition Test and gave helpful suggestions for the preparation of themanuscript.

REFERENCESBaum, D.H. and Joens, LA. (1979). Serotypes of Beta-Hemolytic Tieponema hyodysenteriae.

Infection and Immunity, 25: 792-796.Davelaar, F.G. and Kouwenhoven, B. (1976). Changes in the Harderian gland of the chicken

following conjunctival and intranasal infections with infectious bronchitis in one-and 20-day-old chickens. Avian Pathology, 5: 39-50.

Davis. C.R., Mulcahy, D., Takeuchi, A. and Savage, D.C. (1972). Location and descriptionof spiral-shaped micro-organisms in the normal rat cecum. Infection and Immunity,6:184-192.

Hovind-Hougen, K. and Birch-Andersen, A. (1971). Electron microscopy of endoflagella andmicrotybules in Treponema Reiter. Acta Pathologica Microbiologica ScandinavicaSection B., 79: 37-50.

Hunter, D. and Clark, A. (1975). The direct fluorescent antibody test for the detection ofTreponema hyodysenteriae in pigs. Research in Veterinary Science, 19: 98-99.

Hunter, D. and Wood, T. (1979). An evaluation of the API ZYM system as a means of classi-fying spirochetes associated with swine dysentery. Veterinary Record, 104: 383-384.

Kinyon, J.M. and Harris, D.L. (1979). Treponema innocens.a new species of intestinal bacteria,and emended description of the type strain of Treponema hyodysenteriae Harris et al.Internationaljournal of Systematic Bacteriology, 29: 102-109.

Leach, W.D., Lee, A. and Stubbs, R.P. (1979). Localization of bacteria in the gastro intestinaltracts: a possible explanation of intestinal spirochaetosis. Infection and Immunity,7: 961-972.

Lemcke, RM. and Burrows. M.R. (1979). A disc growth inhibition test for differentiatingTreponema hyodysenteriae from other intestinal spirochaetes. Veterinary Record,104: 148-151.

Nielsen, R.H., Orholm, M., Pedersen, J.O., Hovind-Hougen, K., Teglbjaerg, P.S. and Thaysen,E.H. (1983). Colorectal spirochaetosis: Clinical significance of the infestation. Gastroen-terology, 85: 62-67.

Pindak, F.F., Clapper, W.E., Sherrod, J.H. (1965). Incidence and distribution of spirochaetesin the intestinal tract of dogs. American Journal of Veterinary Research, 26: 1391-1402.

Smit, H.F. and Jongerius, J.M. (1982). Swine dysentery: to isolate or to fluoresce? VeterinaryRecord, 11: 343.

Songer, J.G., Kinyon, J.M. and Harris, D.L. (1976). Selective medium for isolation of Tre-ponema hyodysenteriae. Journal of Clinical Microbiology, 4: 57-60.

Takeuchi, A., Jervis, H.R., Nakazawa, H. and Robinson, D.M. (1974). Spiral-shaped organismson the surface colonie epithelium of the monkey and man. American Journal of ClinicalNutrition, 27:1287-1296.

Taylor, D.J., Simmons, J.R. and Laird, H.M. (1980). Production of diarrhoea and dysenteryin pigs by feeding pure cultures of a spirochete differeing from Treponema hyodysen-teriae. Veterinary Record, 106: 326-331.

Dow

nloa

ded

by [

Cor

nell

Uni

vers

ity L

ibra

ry]

at 2

1:54

18

Nov

embe

r 20

14

Infectious typhlitis 257

Turek, J.J. and Meyer, R.C. (1978). Studies on a canine intestinal spirochete: scanning electronmicroscopy of canine colonie mucosa, nfection and Immunity, 20: 853-855.

RESUME !Typhlite infectieuse chez les poulets due à des spirochètes

Un spirochète hémolytique a été décelé à l'aide d'un sérum fluorescent non absorbéanti-Treponéma hyodysenteriae à partir de frottis et de cultures obtenues parraclage de la muqueuse caecale de pondeuses atteintes de diarrhée. Deux groupes depoulets d'expérience ont ingéré une culture pure de ce spirochète ou un contenuintestinal homogénéisé de poulets malades; ils ont montré tous les deux des symp-tômes cliniques de la maladie telle qu'une augmentation de la teneur en eau desfécès et un léger retard de croissance.

Une typhlite non spécifique, avec des lésions histologiques ressemblant à desformes atténuées de la dysenterie du porc, a été observée chez les oiseaux à partirdesquels les spirochètes ont été isolés. Ces derniers différaient sur le plan cultural,biochimique, antigénique et morphologique de T. hyodysenteriae.

La signification pathologique de la présence des spirochètes dans l'intestin et lesrelations épidémiologiques possibles avec la dysenterie du porc sont discutées.

ZUSAMMENFASSUNGEine durch Spirochaeten verursachte infektiöse

Typhlitis bei HühnernEine schwach haemolytische Spirochaete wurde in Ausstrichen und Kulturen ausAbschabsei der Blinddarmschleimhaut von Legehennen mit Durchfall mit einemnicht absorbierten Fluoreszenzantiserum gegen Treponema hyodysenteriae nach-gewiesen. An zwei Hühnerversuchsgruppen wurde eine Reinkultur dieser Spiro-chaete oder haemogenisierter Darminhalt erkrankter Tiere verfüttert. Beide Grup-pen zeigten klinische Symptome wie erhöhten Wassergehalt der Faeces und leichteWachstumsverzögerung.Bei den Tieren, aus denen Spirochaeten isoliert wurden, wurde eine nicht spezi-fische Typhlitis festgestellt, deren histologisches Bild den milden Formen derSchweinedysenterie gleicht. Die erhaltenen Isolate unterschieden sich kulturell,biochemisch, antigenisch und morphologisch von T. hyodysenteriae.

Die pathologische Bedeutung von Darmspirochaeten und ihre mögliche epidemio-logische Beziehung zur Schweinedysenterie werden diskutiert.

RESUMEN

Tiflitis infecciosa en pollos causada por espiroquetas

Se detectó una espiroqueta con un efecto hemoltico menor con en antisuerofluorescente no absorbido contra Treponema hyodysenteriae en frotis y en cultivosde raspados de la mucosa cecal de gallinas de postura con diarrea. Se alimentaronexperimentalmente a dos grupos de pollos con un cultivo puro de dicha espiro-queta o bien con contenido intestinal homogenizado de aves afectadas. Ambosgrupos mostraron signos clínicos de la enfermedad tales como aumento del con-tenido de agua de la materia fecal y un retraso ligero del crecimiento.

Una tiflitis no especifica que histológicamente era parecida a una forma benigna de

Dow

nloa

ded

by [

Cor

nell

Uni

vers

ity L

ibra

ry]

at 2

1:54

18

Nov

embe

r 20

14

258 F.G. Davelaai eí a/

disentería porcina fue observada en las aves a partir de las cuales se aislaron lasespiroquetas. El aislamiento hecho presentó características de cultivo bioquími-cas, antigénicas y morfológicas diferentes a las del T. hyodysenteriae. Se discutela importancia patológica de las espiroquetas intestinales y su posible relaciónepizootiológica con la disenteria de los cerdos.

Dow

nloa

ded

by [

Cor

nell

Uni

vers

ity L

ibra

ry]

at 2

1:54

18

Nov

embe

r 20

14