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Differences in resistance to Salmonella enterica serovar Gallinarum infection among indigenous local chicken ecotypes in Tanzania a
P.L.M. Msoffe , U.M. Minga
b c
a
b
, M.M.A. Mtambo , P.S. Gwakisa & J.E. Olsen
d
a
Department of Veterinary Medicine and Public Health , P.O. Box 3021, Morogoro, Tanzania b
Department of Veterinary Microbiology and Parasitology , P. O. Box 3019, Morogoro, Tanzania c
The Open University of Tanzania , P. O. Box 23409, Dar es salaam, Tanzania
d
Department of Veterinary Pathobiology , The Royal Veterinary and Agricultural University , Stigb⊘jlen 4 , 1870, Frederiksberg, C., Denmark Published online: 18 Jan 2007.
To cite this article: P.L.M. Msoffe , U.M. Minga , M.M.A. Mtambo , P.S. Gwakisa & J.E. Olsen (2006) Differences in resistance to Salmonella enterica serovar Gallinarum infection among indigenous local chicken ecotypes in Tanzania, Avian Pathology, 35:4, 270-276, DOI: 10.1080/03079450600817024 To link to this article: http://dx.doi.org/10.1080/03079450600817024
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Avian Pathology (August 2006) 35(4), 270 276
Differences in resistance to Salmonella enterica serovar Gallinarum infection among indigenous local chicken ecotypes in Tanzania P.L.M. Msoffe1*, U.M. Minga2,3, M.M.A. Mtambo1, P.S. Gwakisa2 and J.E. Olsen4 Department of Veterinary Medicine and Public Health, P.O. Box 3021, Morogoro, Tanzania, 2Department of Veterinary Microbiology and Parasitology, P. O. Box 3019, Morogoro, Tanzania, 3The Open University of Tanzania, P. O. Box 23409, Dar es salaam, Tanzania, and 4Department of Veterinary Pathobiology, The Royal Veterinary and Agricultural University, Stigbøjlen 4, 1870 Frederiksberg, C., Denmark
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1
A study was conducted to evaluate the disease resistance potential in 105 chickens of six indigenous local chicken ecotypes in Tanzania by orally challenging 1-week-old chicks with 2.5108 colony-forming units of virulent S. Gallinarum. For 14 days post infection, clinical signs, necropsy findings, antibody titres, packed cell volume, leukocyte population count, and viable bacterial cell counts in the liver and spleen were recorded. Clinical signs were recorded daily but other parameters were recorded on the day of infection, then on days 3, 6, 10 and 14 after infection. Clinical signs of fowl typhoid were evident in chickens from day 3 post infection and disappeared by day 9 post infection. Pathological lesions on sacrificed birds included enlargement of the liver and spleen with foci of necrosis on the liver, spleen and myocardium. The mean viable bacterial cell counts in the liver and spleen varied between ecotypes, although the differences were not statistically significant. There were significant differences in the leukocyte population in the peripheral blood, with one ecotype (Morogoro-medium) showing a consistent and significantly higher heterophil count compared with other ecotypes. It was concluded that there is a selectable resistance potential to S. Gallinarum among the local chicken ecotypes in Tanzania that may be attributable to non-specific host immune responses. Further studies are suggested. /
Introduction The free-range local chicken production in Tanzania is faced with several challenges, including high morbidity with high losses due to diseases and predation (Kitalyi, 1998). However, the local chickens survive all these constraints with virtually no or minimal input from the owners (Crawford, 1984). It is therefore suggested that the local chickens may have natural resistance to diseases found in their localities (Kulube, 1990; Chrysostome et al ., 1995). However, research findings addressing this hypothesis are limited. Other investigations contradict this assumption; for example, Nigerian local chickens were found to be more susceptible to Gumboro disease than exotic chickens (Okoye & AbaAdulugba, 1998). It is therefore useful to study carefully the phenomenon of natural disease resistance in indigenous chicken populations in order to avoid erroneous generalizations. Fowl typhoid caused by Salmonella enterica serovar Gallinarum is a significant problem in poultry, especially in the developing world, prompting efforts to identify genetic markers for resistance to this disease (Alvarez et al ., 2003). We have previously described different local chicken ecotypes that show phenotypic and genetic variations in Tanzania (Msoffe et al ., 2001, 2004,
2005). In terms of phenotypic parameters, the local chicken ecotypes have been found to differ in adult body weight, egg weight, growth rate, shank length and immune responses to sheep red blood cells (Msoffe et al ., 2001, 2004). In one study, the disease resistance potential of the local chicken ecotypes were tested with one ecotype named Kuchi , showing promising results on resistance against S. Gallinarum (Msoffe et al ., 2002). It was only unfortunate that this ecotype was not available for this experiment for reasons beyond the author’s control. Recently, a study on characterization of the local chicken ecotypes based on microsatellite DNA polymorphisms revealed genetic variations between them (Msoffe et al ., 2005). The results from this study showed the tendency of chickens from the same ecotype to cluster together in a phylogenetic tree. With these results in mind, one is more confident in using ecotypes to represent a lesser-sophisticated form of world’s renowned breeds, albeit as out-bred populations. This study utilized a direct method of testing the disease resistance potential in chicks. Birds were challenged with S. Gallinarum, and the cellular dynamics in response to the infection as a potential measure of disease resistance was tested. Based on the results we
*To whom correspondence should be addressed. Tel: /255 23 260 4542. Fax /255 23 260 4647. E-mail:
[email protected] Received 7 October 2005 ISSN 0307-9457 (print)/ISSN 1465-3338 (online)/06/40270-07 # 2006 Houghton Trust Ltd DOI: 10.1080/03079450600817024
Disease resistance in local chicken ecotypes 271
propose that selectable variation exists among indigenous population of chicken, and that this can be used with regard to future breeding of disease resistant variants.
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Materials and Methods Experimental chickens. One-week-old chicks from six indigenous local chicken ecotypes (in local language Unguja , Tanga , Morogoro-medium , Mbeya , N’zenzegere, and Pemba ) and an exotic hybrid commercial layer chicken were used in the experiment. All chicks were hatched onstation with eggs coming from a parental local chicken ecotype population, which were earlier purchased from selected villages in Tanzania. The ecotypes have previously been described with respect to production parameters and genetic relatedness (Msoffe et al ., 2004, 2005). The eggs for the commercial layer chicken were purchased from a local breeding farm. The chicks were wing tagged and given prophylactic doses of Mebendazole antihelmintic (Kukuzole† ; Interchem Pharma, Moshi, Tanzania) and Amprolium anticoccidial (Amprolium 200† ; Diocare Vet Ltd, AV Lab. Syva, South Africa) in accordance with the manufacturer’s recommendations. A group of 15 chicks were maintained away from the inoculated birds and served as negative controls.
Experimental design. Fifteen chicks from each ecotype/breed were inoculated orally into the crop with 100 ml overnight culture containing 2.5/108 colony-forming units/ml virulent S. Gallinarum RD8 (Mdegela et al ., 2000) grown in lauryl L broth incubated at 378C. Negative control birds were given 100 ml sterile lauryl L broth that was incubated overnight. The chicks were observed twice daily for clinical signs and mortalities. On the day of infection (day 1), approximately 200 ml whole blood was taken directly into capillary tubes coated with heparin by brachial venipuncture from three randomly selected chicks from each groups. On days 3, 6, 10 and 14, two blood samples were collected from each bird for packed cell volume (PCV) (stabilized by heparin) determination and for serology.
Clinical signs and pathological features determination. The presentation of clinical signs was a modification of the system used by Christensen et al. (1996), with (/) indicating no clinical signs; (/) and (//) referring to drowsiness, occasional closure of the eyes and drowsiness, closure of the eyes and reluctance to move, respectively. On the same days, three randomly selected chicks from each ecotype were sacrificed for pathological investigations. The liver and spleen of the sacrificed chicks were aseptically removed for determination of viable bacterial cell counts by the methods described by Mdegela et al . (2002). Each colony was given a value equivalent to 2 log10 considering the two-fold serial dilution used in preparation of the inoculum. All plates that did not give any viable bacterial count was given a value of less than 2 log10. All chicks that were sacrificed were subjected to a thorough post-mortem examination as described by Fowler (1996).
Determination of PCV and antibody titres to S. Gallinarum . The PCV was determined by centrifugation of the stabilized blood in a microhaematocrit centrifuge (Hawksley and Sons Ltd, Lancing, UK) then read on a haematocrit reader. The serum rapid plate agglutination test and serum agglutination tests were conducted on all sera in order to detect anti-S. Gallinarum antibodies in accordance with Office International d’Epizooties guidelines (Office International d’Epizooties, 1996).
Enumeration of selected leukocytes. Some of the stabilized blood was used to make thin microscopic blood films for leukocyte enumeration. The thin blood films made were air-dried and fixed on absolute methanol for 30 sec and stained by Wright’s staining method (Drijver & Boon, 1986). The films were observed under light microscopy (/1000 magnification) and the cells (heterophils, lymphocytes and monocytes) were enumerated according to their morphology (100 cells were counted on each slide). The cells were counted, and the results are expressed as the percentage distribution (Pd).
Statistical analysis. Data collected from the experiment were analysed using the Statistix for Windows† version 7 statistical package (Analytical Software, USA). Descriptive statistics was conducted and the means, standard error and range were determined. All data were normally distributed and were hence analysed using a parametric oneway analysis of variance. Comparison of means was carried out using the least significant difference procedure at a P B/ 0.05 level of significance.
Results Clinical signs, mortality pathological lesions and bacterial counts. Table 1 presents the clinical signs for the local chicken ecotypes infected with S. Gallinarum. Clinical signs for fowl typhoid were evident in chickens from day 3 after inoculation, and included drowsiness and occasional closure of the eyes. From days 5 to 7, the clinical signs were more severe with marked decrease in feed intake and reluctance to move. Clinical signs separated the chicks into most affected (N’zenzegere ecotype) and least affected (Morogoro-medium ecotype) based on the scoring system used. No clinical signs were observed beyond 9 days after infection. The uninfected control group did not show any clinical signs of the disease. Only four of the infected chicks were severely affected and were humanely sacrificed on days 8 and 9 after infection (Table 1). Necropsy of these four chicks and those sacrificed on day 6 onwards revealed enlargement of the liver and spleen, and small whitish foci of necrosis on the two organs and on the myocardium. These pathological features appeared in chickens of all ecotypes. Chicks sacrificed on day 3 after infection did not show notable pathology in internal organs. The mean viable bacterial cell counts (log10) in the liver and spleen varied between ecotypes. The lowest overall viable counts were obtained on day 14 while the highest mean values were recorded on day 10 from both the liver and spleen. The counts from the spleen were consistently lower compared with those from the liver. The highest mean live bacterial counts in the liver on day 3 were shown in the Morogoro-medium ecotype (2.0 / 105) and the lowest counts were shown in the Unguja ecotype (1.58/103). The commercial layer hybrid and N’zenzegere ecotype did not show any viable counts on day 3 after infection. With the exception of the Mbeya and Pemba ecotypes, the peak viable count was attained on day 10 after infection (Table 2). It was observed also that the highest viable counts from the liver on day 10 after infection were in the commercial layer strain (5.01 /106). Viable counts from the spleen presented a less obvious trend, with only Tanga ecotype showing values above 2 log10 on each of the 4-day time points. The highest count obtained from the spleen was 3.16/ 104 (day 10 Unguja ecotype). The Mbeya and N’zenzegere ecotypes did not show any viable counts in the spleen over the entire period of the experiment (Table 2). Antibody, PCV and cellular dynamics. No specific antibodies were present in birds at the onset of the experiments, nor at any time point following challenge. PCV values for all the infected local chickens as well as the non-infected controls were within the normal range (/30%). No further analysis was therefore performed on this parameter. Figure 1 shows the change in heterophilic population over the 14-day experimental period for each local chicken ecotype, including the overall (all ecotypes
272 P.L.M. Msoffe Table 1.
Clinical signs for the local chicken ecotypes infected with S. Gallinarum Ecotypes (n/15 for each)
Days after infection 3 4 5 6 7 8 9 10 14
Commercial layer strain
Unguja
Tanga
Morogoro-medium
Mbeya
N’zenzegere
Pemba
/ (5)a /(2)//(2) // (3) // (3) // (2) // (2)b
/ (3) / (3) // (1) // (2)
/ (5) / (5) /(2)//(1) // (2)
/ (5) / (3)
/(5) /(2)//(3) // (4) // (3) // (1) // (1)b
/ (8) /(2)//(4) //(5) // (4) // (2) // (2)b // (1)b
/ (3) / (2) //(1)
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a
Number of chickens showing the specified clinical signs. Number of chicks that died each represented by an asterisk.
b
combined) trend. The N’zenzegere ecotype showed the lowest mean Pd for heterophils at all times except on day 10. The Morogoro-medium ecotype showed a higher mean Pd on days 1, 3 and 6, followed by a sharp decrease on day 10 and a plateau on day 14. Comparing the means, significant differences were detected between the ecotypes (P B/0.05). The N’zenzegere ecotype had a consistently and significantly lower mean Pd throughout the experiment; the highest significant mean Pd changed from day to day (Figure 1). The mean Pd for monocytes is presented in Figure 2. There was a sharp decrease of mean Pd for all ecotypes from day 1 to 3, followed by a small increase on day 6 (Morogoro-medium , Tanga , Unguja , Pemba , commercial layer chicken, and Mbeya ecotypes) then a decrease at day 14. Only the N’zenzegere ecotype showed a continuous decrease and the Tanga ecotype showed an increasing trend on day 14. The day 1 mean Pd for N’zenzegere was the highest and significantly different from all other ecotypes. It was also seen that on day 6 the Morogoro-medium and Unguja ecotypes had means that were significantly different from the other ecotypes (P B/0.05). On day 14, the mean Pd for Tanga ecotype was the highest and was significantly different from the other ecotypes, whose means were similar (P B/0.05).
The mean Pd for lymphocytes is presented in Figure 3. The Mbeya and Morogoro-medium ecotypes showed only a slight change on days 3 and 6 after infection *a feature that was not seen in the other ecotypes. Another peculiar feature was that shown by the Tanga ecotype, where the mean values increased until day 10 after infection and then decreased on day 14 after infection. Generally most ecotypes presented two peaks that coincided with their highest means. These peaks were seen on day 3 after infection (all ecotypes except for Mbeya , Morogoro-medium and Tanga ) and on either day 10 after infection (commercial layer strain and Unguja ecotype) or day 14 after infection (N’zenzegere and Pemba ecotypes). However, other ecotypes showed only one peak on either day 10 after infection (Mbeya and Tanga ecotypes) or day 14 after infection (Morogoromedium ecotype). Peaks were mostly followed by a nadir. Comparison of means showed that some means were significantly different from each other. However, no one ecotype had a consistently lower or higher mean that was significantly different from others.
Discussion The present study shows induction of both chronic and subacute forms of experimental fowl typhoid in local
Table 2. Mean log10 liver and spleen bacterial cell count from local chicken ecotypes infected with S. Gallinarum Ecotype
Tissue
3 days p.i.
6 days p.i.
10 days p.i.
14 days p.i.
Commercial layer strain
Liver Spleen Liver Spleen Liver Spleen Liver Spleen Liver Spleen Liver Spleen Liver Spleen
B/2 2 3.29/0.4 B/2 4.99/0.6 2.69/1 5.39/0.6 B/2 3.99/2.3 B/2 B/2 B/2 3.99/0.5 2
3.39/0.5 B/2 49/1.8 B/2 4.19/0.6 3.3 3.49/0.4 B/2 4.39/0.4 B/2 2.2 B/2 4.89/0.2 2.59/1.3
6.7 3.2 4 4.5 4.99/2.8 4.4 4.7 49/0.6 B/2 B/2 4.29/0.9 B/2 3.59/0.2 B/2
3.59/0.3 B/2 3.39/0.4 2 4.19/1.3 2.8 4.4 2.6 2.9 B/2 3.2 B/2 59/1 B/2
Unguja Tanga Morogoro-Medium Mbeya N’zenzegere Pemba
Data presented as mean9/standard error. p.i., post infection.
Disease resistance in local chicken ecotypes 273 100 90
70 60
Unguja Overall
50
Tanga 40
Pemba Morogoro
30
Mbeya N'zenzegere
20 10 0 0
3
6
10
14
Days after infection Figure 1. Mean Pd for heterophils in local chicken ecotypes infected with S. Gallinarum (mean9/standard error).
chicken ecotypes of Tanzania as demonstrated by the clinical and pathological features. These findings support previous observations that showed induction of experimental fowl typhoid in chickens (Christensen et al ., 1996; Alvarez et al ., 2003). Clinical signs were most severe and lasted the longest among the commercial layer chicken, Mbeya and N’zenzegere ecotypes. Other studies have shown that the severity of clinical and pathological features in experimental fowl typhoid is related with the strain of S. Gallinarum used (Christensen et al ., 1996). In this study, only one strain, RD8 (Mdegela et al ., 2000), was used, thereby suggesting that the differences observed between the chicken
ecotypes was based on their genetic differences. Earlier work by Bumstead and Barrow (1993) reported genetic variation in susceptibility to some S. enterica serovars in in-bred White Leghorn lines due to what they suggested to be a general mechanism of resistance applied to various serotypes of Salmonella . Since there is evidence that local chickens used in this study do represent different genetic groups (Msoffe et al ., 2001, 2004, 2005), it is reasonable to assume that the differences observed reflect different genetic background. This suggested to us that the ecotypes differed in natural disease resistance, which prompted us to investigate whether the differences in immune-cell dynamics
70
60
Mean percent distribution
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Mean percent distribution
80
50 Unguja Overall Tanga Pemba Morogoro Mbeya N'zenzegere Commercial
40
30
20
10
0 0
3
6
10
14
Days after infection Figure 2.
Mean Pd for monocytes in local chicken ecotypes infected with S. Gallinarum (Mean9/standard error).
274 P.L.M. Msoffe 90 80
Unguja Mean percent distribution
70
Commercial Tanga
60
Pemba 50
Morogoro
40
Mbeya N'zenzegere
30
Overall
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20 10 0 0
3
6
10
14
Days after infection Figure 3.
Mean Pd for lymphocytes in local chicken ecotypes infected with S. Gallinarum (Mean9/standard error).
following challenge with S. Gallinarum can explain some of the mechanisms involved in the resistance. The overall mean counts for the liver and spleen peaked on day 10 after infection and were lowest on day 14 after infection, indicating that the infection was being cleared. These findings are in agreement with a study by Mdegela et al. (2002), who reported peak viable bacterial cell counts from the liver and spleen of the local chicken on day 9 after infection. In that study, a similar trend where bacteria were being cleared after the peak counts was observed. Other studies (Christensen et al ., 1996; Waihenya et al ., 2002) have shown peak counts to occur on day 7 and 6, respectively, contrasting the current results. However, the clearance of the bacteria from the two organs followed a trend similar to that obtained in the current experiment. The differences between the current observations and those made by Christensen et al. (1996) may be due to the genetic difference between the strains of bacteria used as well as the chickens used in the study. The most probable reason for the discrepancies on the peak bacterial counts between the current experiment and that of Waihenya et al. (2002) would be the fact that the current results were influenced by the presence of different ecotypes. The mean viable counts from different ecotypes showed different peaking times, but most ecotypes peaked on day 10 after infection. Two ecotypes (Morogoro-medium and Tanga ) showed peak viable counts from the liver on day 3 after infection. On the other hand, the Mbeya ecotype peaked on day 6 after infection and the Pemba ecotype on day 14 after infection. It was seen, therefore, that between ecotypes some were in agreement with the previous studies (Christensen et al ., 1996; Mdegela et al ., 2002; Waihenya et al ., 2002). The results may hence suggest the existence of different host response mechanisms between the different local chicken ecotypes studied. Other studies using a ceacal colonization model to study resistance of outbred strains of egg-type chickens suggested a genetic basis for the differences that were
observed (Berthelot et al ., 1998). It would be interesting to study the caecal carrier states of the different ecotypes since it has direct bearing on the possibility of contamination of both environment and eggs (vertical transmission), and hence the persistence of the disease. However, there was no correlation between the viable bacterial cell counts and the clinical signs in the current experiment. This is in contrast to the observation by Christensen et al. (1996), who reported that the peak viable bacterial cell counts coincided with severe anaemia and other clinical signs. But, as seen in the current experiment, there was no anaemia and the clinical signs were not seen beyond 9 days after infection. The results from the current experiment were challenging because, although the bacteria were detected from the liver and spleen as early as day 3 after infection and persisted up to 14 days, the clinical signs or the pathological picture did not reflect this fact. The overall mean pre-challenge Pd for heterophils, lymphocytes and monocytes in the local chickens showed deviations from the established mean values (Jain, 1986). Whereas the mean Pd values for heterophils and monocytes were well above the standard values, lymphocytes values were below the standard. The deviations may be partly due the genetic differences between the birds from which the standard values were derived and the local chickens in this experiment. The trend for the leukocyte population dynamics observed following challenge for both heterophils and lymphocytes, however, was consistent with reports by Allan & Duffus (1971), albeit with higher values in the current experiment, suggesting that the cellular response to S. Gallinarum infection might be conserved in chicken. The results from the heterophils, lymphocytes and monocytes dynamics revealed significant difference between ecotypes, both in terms of starting and peak values (P B/0.05). A sharp decline in the Pd for monocytes from day 1 to day 3 after infection may have been attributed to the cytotoxic effects of Salmonella that
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Disease resistance in local chicken ecotypes 275
leads to apoptosis on these leukocytes (Monack et al ., 1996). The fall of Pd for monocytes coincided with the increase in Pd for both heterophils and lymphocytes to other cells known to influence resistance to Salmonella infections (Stabler et al ., 1994; Kogut et al ., 1994Kogut et al ., 1998; Harmon, 1998). It was noted that the Pd for heterophils fell 10 days after infection, corresponding in the majority of the ecotypes with the peak viable counts in the internal organs. Lam and Munn (2002) earlier reported on the cytolytic effects of S. Typhimurium on heterophils. It may therefore follow that during this time, when the number of bacteria was increasing in the internal organs, the number of heterophils was decreasing. Nevertheless, there was clearance of the bacteria as indicated by the low numbers of viable counts on day 14 after infection. This can be explained by the dynamics of the lymphocytes at this time. At 10 days after infection the Pd for lymphocytes was peaking in most ecotypes, indicating that they were involved in clearing the bacteria in the absence or in conjunction with the heterophils. It has long been proposed that the clearance of Salmonella from the tissues is dependent on the cellmediated immune responses (Lee et al ., 1983). Since there were no detectable antibodies, it appears that it was mostly the T lymphocytes that were involved. These results support some earlier observations that CD8 T lymphocytes contribute to the host defence against Salmonella (Lo et al ., 1999). Based on the evidence given, it can therefore be summed that, during the early days of infection, the bacteria will be combated by the monocytes (macrophages); as the bacteria overcome these leukocytes, other cells (heterophils/lymphocytes) take over*with heterophils first and finally lymphocytes. It can therefore be safely assumed that an individual chicken or ecotype that cannot attain this trend will be susceptible to the infection and will become worse for the disease. Based on the results we suggest that the observed differences between indigenous chicken ecotypes are genetic and could be utilized in selective breeding both within and between ecotypes. This suggestion is also supported by earlier studies where indigenous naked neck and normally feathered chickens in Mexico were reported to show higher survival rates compared with a commercial line (Alvarez et al ., 2003). It would be interesting to establish the link between high disease resistance potential in indigenous chicken ecotypes with productivity parameters such as body weight, egg weight, growth rate and shank length. Further studies on non-specific immune responses such as those mediated through the major histocompatibility complex (B-complex), mannan binding lectins and response to sheep red blood cells may provide better insights into the natural disease resistance potential of the indigenous local chicken ecotypes.
Acknowledgements Mr Maulid Mdaki and M.O. Mwangalimi are thanked for technical assistance. Dr Amandus Muhairwa is thanked for critically reading the manuscript. This study was supported by DANIDA under the ENRECA project ‘‘Improvement of Health and Productivity of Rural Chickens in Africa’’. The authors are grateful for the support.
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Avian Pathology (August 2006) 35(4), 1 2
Non-English Abstracts
Differences in resistance to Salmonella enterica serovar Gallinarum infection among indigenous local chicken ecotypes in Tanzania P.L.M. Msoffe1*, U.M. Minga2,3, M.M.A. Mtambo1, P.S. Gwakisa2 and J.E. Olsen4
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1
Department of Veterinary Medicine and Public Health, P.O. Box 3021, Morogoro, Tanzania, and 2Department of Veterinary Microbiology and Parasitology, P. O. Box 3019, Morogoro, Tanzania, and 3The Open University of Tanzania, P. O. Box 23409, Dar es salaam, Tanzania, and 4Department of Veterinary Pathobiology, The Royal Veterinary and Agricultural University, Stigbøjlen 4, 1870 Frederiksberg, C., Denmark
Re´sistances diffe´rentes a` l’infection par S. Gallinarum des souches indige`nes de poulets en Tanzanie Une e´tude a e´te´ conduite pour e´valuer les possibilite´s de re´sistance chez 105 poulets appartenant a` six souches indige`nes de poulets en Tanzanie suite a` une e´preuve orale administre´e a` des poussins d’une semaine avec 2,5 108 CFU d’une souche virulente de S. Gallinarum. Durant 14 jours apre`s infection, ont e´te´ enregistre´s les symptoˆmes, les le´sions a` l’autopsie, les titres des anticorps, l’he´matocrite, le nombre des leucocytes, et le nombre des cellules bacte´riennes viables dans le foie et la rate. Les symptoˆmes ont e´te´ enregistre´s quotidiennement, mais les autres parame`tres ont e´te´ enregistre´s le jour de l’infection puis 3, 6, 10, et 14 jours apre`s l’infection. Des symptoˆmes de typhoı¨de aviaire ont e´te´ observe´s chez les poulets a` partir de 3e`me jour apre`s l’infection et ont disparu le 9e`me jour apre`s l’infection. Les le´sions pathologiques note´es chez les sujets sacrifie´s incluaient une hypertrophie du foie et de la rate avec des foyers de ne´crose sur le foie, la rate et le myocarde. La moyenne du nombre des cellules bacte´riennes viables dans le foie et la rate a varie´ en fonction des souches, bien que les diffe´rences ne soient pas statistiquement significatives. Des diffe´rences significatives ont e´te´ enregistre´es en ce qui concerne les leucocytes du sang pe´riphe´rique pour une des souches indige`nes (Morogoro-medium) qui a pre´sente´ un nombre d’he´te´rophiles significativement supe´rieur compare´e aux autres souches. En conclusion il existe un potentiel de re´sistance a` S. Gallinarum parmi les souches indige`nes de poulets en Tanzanie, qui peut eˆtre attribue´ a` des re´ponses immunitaires non spe´cifiques de l’hoˆte, et qui pourrait eˆtre se´lectionne´. Des e´tudes comple´mentaires sont sugge´re´es. /
Resistenzunterschiede gegen die S. Gallinarum-Infektion bei einheimischen regional vorkommenden Hu¨hnero¨kotypen in Tansania Es wurde eine Untersuchung durchgefu¨hrt, um das Krankheitsresistenzpotential gegenu¨ber S. Gallinarum bei einheimischen Hu¨hnerrassen in Tansania festzustellen. Dazu wurden 105 Hu¨hnerku¨ken von sechs verschiedenen einheimischen, regional vorkommenden Hu¨hnero¨kotypen im Alter von 1 Woche oral mit 2,5 108 KBE eines virulenten S. Gallinarum-Stamms infiziert. Innerhalb von 14 Tage nach der Infektion wurden klinische Symptome, pathologisch-anatomische Vera¨nderungen, Antiko¨rpertiter, Ha¨matokritwerte, Leukozytenanzahl sowie die Anzahl lebensfa¨higer Bakterien in Leber und Milz ermittelt. Die klinischen Symptome wurden ta¨glich protokolliert, die anderen Parameter wurden jedoch am Tag der Infektion und dann am Tag 3, 6, 10 und 14 nach der Infektion u¨berpru¨ft. Ab dem 3. Tag nach der Infektion traten die ersten klinischen Symptome des Hu¨hnertyphus auf, die bis zum 9. Tag nach der Infektion wieder verschwanden. Pathologische Vera¨nderungen bei den geto¨teten Tieren umfassten Milz- und Leberschwellung sowie Nekroseherde in Leber, Milz und Myokard. Die mittlere Anzahl lebensfa¨higer Bakterien in der ¨ kotypen; die Unterschiede waren jedoch statistisch nicht Leber und der Milz variierte zwischen den O signifikant. In der Leukozytenpopulation im peripheren Blut gab es signifikante Unterschiede, wobei ein ¨ kotyp (Morogoro-medium) im Vergleich zu den anderen O ¨ kotypen eine besta¨ndig signifikant ho¨here O Heterophilenanzahl aufwies. Daraus wurde geschlossen, dass es ein selektierbares Resistenzpotential gegen S. Gallinarum, das den unspezifischen Immunantworten des Wirttiers zugeordnet werden kann, bei den einheimischen Hu¨hnero¨kotypen in Tansania gibt. Dazu werden weitere Untersuchungen empfohlen. /
*To whom correspondence should be addressed. Tel: /255 23 260 4542. Fax /255 23 260 4647. E-mail:
[email protected] Received 7 October 2005 ISSN 0307-9457 (print)/ISSN 1465-3338 (online)//40001-02 # 2006 Houghton Trust Ltd DOI: 10.1080/03079450600817024
2 P.L.M. Msoffe
Diferencias en la resistencia frente a la infeccio´n por S. Gallinarum entre ecotipos de pollos locales indı´genas en Tanzania Se llevo´ a cabo un estudio para valorar la capacidad de resistencia a la enfermedad de 105 pollos pertenecientes a seis ecotipos locales indı´genas de Tanzania mediante la infeccio´n oral de pollos de una semana de vida con 2.5 108 CFU de S. Gallinarum virulenta. Durante los 14 dı´as post infeccio´n se valoraron los signos clı´nicos, hallazgos en la necropsia, tı´tulos de anticuerpos, volumen celular aglomerado, recuento de la poblacio´n leucocitaria, y recuentos de bacterias viables en hı´gado y bazo. Los signos clı´nicos se valoraron diariamente, mientras que otros para´metros se valoraron el dı´a de la infeccio´n, y despue´s a los 3, 6, 10 y 14 dı´as post infeccio´n. Se evidenciaron signos clı´nicos caracterı´sticos de tifus aviar en los pollos desde el tercer dı´a post infeccio´n hasta los 9 dı´as post infeccio´n. Las lesiones patolo´gicas observadas en las aves sacrificadas incluyeron aumento del taman˜o del hı´gado y bazo, asociado a focos de necrosis en el hı´gado, bazo y miocardio. La media de los recuentos de bacterias viables en hı´gado y bazo vario´ entre ecotipos aunque estas diferencias no fueron estadı´sticamente significativas. Hubo diferencias significativas en la poblacio´n leucocitaria en sangre perife´rica en uno de los ecotipos (Morogoro-medium), que mostro´ un mayor recuento de hetero´filos reiteradamente en comparacio´n con otros ecotipos. Se concluyo´ que existe un potencial de resistencia frente a S. Gallinarum seleccionable entre los ecotipos de pollo locales en Tanzania que podrı´a atribuirse a respuestas inmunes no especı´ficas del hue´sped. Se sugiere la necesidad de ma´s estudios.
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