herbal coccidiostat on pathology of coccidiosis in broilers
A herbal coccidiostat on pathology of coccidiosis in broilers - Effect of Coxynil
Published: February 25, 2009
By: P. A. Pansare, P.S. Lonkar, Dept. of Pathology, Bombay Veterinary College, Parel, Mumbai, India (Courtesy of Growell India)
Anticoccidial efficacy of ‘Coxynil” a herbal feed additive was tested against Einieria tenella in broilers, vs. a vs. Salinomycin. Body weight of birds challenged with E. tenella in Coxynil treated groups was higher as compared to Coxynil untreated & Salinomycin treated groups.. Oocyst out put, lesion score, HI titres against New Castle disease virus and T Cells were significantly higher in Coxynil supplemented groups. Examination of ceaca of the birds, revealed that the Coxynil interfered with life cycle of coecidia. The typical second generation schizonts were absent in ceacal section of Coxynil treated groups. The results indicate that Coxynil is an effective herbal coccidiostat.
ABSTRACT
One hundred and sixty day old broiler chicks, procured from a recognized hatchery, were divided into eight groups, of 20 birds each as, CA- Normal feed, CB- Salinomycin @1 kg/ton of feed, CC-Coxynil @ 250 mg/kg of feed and CD- Coxynil @ 300 mg/kg of feed and respective infected groups as IA, IB, IC and ID. The birds were maintained on deep litter system and standard management practices were followed. Birds were weighed weekly and daily feed intake was recorded. This data was used to calculate the weekly FCR. Oocysts challenge with sporulated oocysts of E.tenella @20,000 oocysts/bird was carried out at the age of 21day. Birds were observed for clinical symptoms. Oocysts per gram (OPG) of droppings were calculated in infected groups on 4, 6, 8 and 10 day post infection (DPI). Three birds from each group were sacrificed on 3, 6 and 9 DPI. Gross changes in different organs, if any, and caecal lesion score was recorded. At the same time, tissue pieces from caeca, caecal tonsils, spleen and thymus were collected in 10% formaline for histopathological study; additionally pieces from caeca were collected in formal calcium to demonstrate T cells by ANAE method. Serum collected, at the time, was used for assessing the HI titer against NCDV.
Final body weights were significantly less in infected groups than the respective control groups. Weights were significantly higher in Coxynil groups than Salinomycin groups. Similar trend was observed for weekly weight gains. Total feed intake was less in infected groups than the respective control groups. Feed intake was higher in Coxynil groups than Salinomycin and control groups. After oocysts challenge, FCR in infected groups were higher than respective control groups. FCR in Coxynil groups was better than Salinomycin birds, while opposite was noted in infected groups.
Both the coccidiostats used in the study delayed the appearance of clinical symptoms as compared to infected control group (IA). Mortality was observed only in IA and IC. Average OPG was highest in IA followed by that in IC, ID and IB. Salinomycin was found to be better in reducing OPG as compared to Coxynil, and OPG, in Coxynil treated groups, was less than infected control (IA), over the period.
Haemorrhages, blood clots and distension of caeca, on 6 DPI and caecal core formation and thickening of caecal wall, on 9 DPI, were the prominent gross findings in IA. Salinomycin was found to be more effective than Coxynil in reducing the intensity of lesions. Caecal lesion score on 6 DPI was highest in the infected groups. Average score for the period did not differ significantly between the groups. Microscopically, catarrhal enteritis was evident in all the infected groups, on 3 DPI. Denuded epithelium, large number of schizonts and gametes, alongwith haemorrhages (in mucosa and submucosa), on 6 DPI and exfoliated epithelium alongwith oocysts in mucosa, on 9 DPI, were the prominent alterations in group IA. Salinomycin was found to be more effective than Coxynil, in reducing the changes.
ANAE cell counts, on 9 DPI, were significantly higher in infected groups than the respective control groups. Coxynil was found to be more beneficial over Salinomycin, as highest count, was observed in IC, amongst all the groups. Average HI titers, in the infected groups were low as compared to respective control groups and significantly lowest in IA, amongst all the groups. Coxynil groups revealed higher titers than Salinomycin treated birds.
MATERIALS AND METHODS
ABSTRACT
One hundred and sixty day old broiler chicks, procured from a recognized hatchery, were divided into eight groups, of 20 birds each as, CA- Normal feed, CB- Salinomycin @1 kg/ton of feed, CC-Coxynil @ 250 mg/kg of feed and CD- Coxynil @ 300 mg/kg of feed and respective infected groups as IA, IB, IC and ID. The birds were maintained on deep litter system and standard management practices were followed. Birds were weighed weekly and daily feed intake was recorded. This data was used to calculate the weekly FCR. Oocysts challenge with sporulated oocysts of E.tenella @20,000 oocysts/bird was carried out at the age of 21day. Birds were observed for clinical symptoms. Oocysts per gram (OPG) of droppings were calculated in infected groups on 4, 6, 8 and 10 day post infection (DPI). Three birds from each group were sacrificed on 3, 6 and 9 DPI. Gross changes in different organs, if any, and caecal lesion score was recorded. At the same time, tissue pieces from caeca, caecal tonsils, spleen and thymus were collected in 10% formaline for histopathological study; additionally pieces from caeca were collected in formal calcium to demonstrate T cells by ANAE method. Serum collected, at the time, was used for assessing the HI titer against NCDV.
Final body weights were significantly less in infected groups than the respective control groups. Weights were significantly higher in Coxynil groups than Salinomycin groups. Similar trend was observed for weekly weight gains. Total feed intake was less in infected groups than the respective control groups. Feed intake was higher in Coxynil groups than Salinomycin and control groups. After oocysts challenge, FCR in infected groups were higher than respective control groups. FCR in Coxynil groups was better than Salinomycin birds, while opposite was noted in infected groups.
Both the coccidiostats used in the study delayed the appearance of clinical symptoms as compared to infected control group (IA). Mortality was observed only in IA and IC. Average OPG was highest in IA followed by that in IC, ID and IB. Salinomycin was found to be better in reducing OPG as compared to Coxynil, and OPG, in Coxynil treated groups, was less than infected control (IA), over the period.
Haemorrhages, blood clots and distension of caeca, on 6 DPI and caecal core formation and thickening of caecal wall, on 9 DPI, were the prominent gross findings in IA. Salinomycin was found to be more effective than Coxynil in reducing the intensity of lesions. Caecal lesion score on 6 DPI was highest in the infected groups. Average score for the period did not differ significantly between the groups. Microscopically, catarrhal enteritis was evident in all the infected groups, on 3 DPI. Denuded epithelium, large number of schizonts and gametes, alongwith haemorrhages (in mucosa and submucosa), on 6 DPI and exfoliated epithelium alongwith oocysts in mucosa, on 9 DPI, were the prominent alterations in group IA. Salinomycin was found to be more effective than Coxynil, in reducing the changes.
ANAE cell counts, on 9 DPI, were significantly higher in infected groups than the respective control groups. Coxynil was found to be more beneficial over Salinomycin, as highest count, was observed in IC, amongst all the groups. Average HI titers, in the infected groups were low as compared to respective control groups and significantly lowest in IA, amongst all the groups. Coxynil groups revealed higher titers than Salinomycin treated birds.
MATERIALS AND METHODS
The present research work was conducted at the Department of Pathology, Bombay Veterinary College, Parel, Mumbai-12, India, to study the pathological and immunological changes following experimental coccidial infection and to evaluate the effects of Coxynil – a herbal coccidiostat on these changes and overall performance of broilers.
3.1 Experimental Chicks: One hundred and sixty, day old broiler chicks, obtained from a recognized hatchery, were maintained on deep litter system with optimum conditions of brooding and management.
3.2 Experimental Feed: Broiler starter and finisher feed, free of any coccidiostat was procured from recognized feed manufacturer.
3.2.1 Coccidiostats: Coxynil (Herbal coccidiostat) from M/S.‘GROWELL INDIA’, Pune, India was mixed in the feed as per the protocol. Salinomycin 6% (Coxistac premix) was purchased from market and mixed in the feed as per protocol.
3.3 Experimental Procedure:
The chicks were divided into eight different dietary treatment groups as below,
The chicks were divided into eight different dietary treatment groups as below,
|
Sr. No.
|
Treatment groups
|
Number of birds
|
Treatment of coccidiostat
|
Dose of coccidiostat
|
Oocyst challenge
|
|
1
|
CA
|
20
|
----------
|
-------
|
------
|
|
2
|
CB
|
20
|
Salinomycin- 6% w/w
|
1 kg/ton of feed
|
------
|
|
3
|
CC
|
20
|
Coxynil - Herbal coccidiostat
|
250 mg/kg of feed
|
------
|
|
4
|
CD
|
20
|
Coxynil - Herbal coccidiostat
|
300 mg/kg of feed
|
-------
|
|
5
|
IA
|
20
|
----------
|
----------
|
20,000
|
|
6
|
IB
|
20
|
Salinomycin-6% w/w
|
1 kg/ton of feed
|
20,000
|
|
7
|
IC
|
20
|
Coxynil - Herbal coccidiostat
|
250 mg/kg of feed
|
20,000
|
|
8
|
ID
|
20
|
Coxynil - Herbal coccidiostat
|
300 mg/kg of feed
|
20,000
|
3.4 Vaccination: Vaccination with Lasota F1 strains was carried out on 8th day of age by intraoccular route. Vaccination against IBD was done by intraoccular route on 11th day of age.
3.5 Isolation And Sporulation Of Eimeria tenella Oocysts For Infection: A field strain of E. tenella was isolated from the caeca collected from the local poultry slaughter house and the oocysts were identified on the basis of size, shape and location of lesions. Oocysts were separated by sedimentation method and were sporulated in 2.5% potassium dichromate solution at room temperature with intermittent bubbling. These sporulated oocyst of E. tenella were used for further experimental work (Chaudhari, 1993).
3.6 Oocyst Challenge: The oocysts challenge was carried out on 21st day by inoculating 20,000 sporulated oocysts per bird orally, as per the protocol.
3.7 Parameters Studied:
3.7.1 Body Weight And Feed Conversion Ratio: The birds were weighed at the end of every week and the daily feed consumption was recorded. Feed conversion ratio (FCR) was calculated as,
Average feed consumption per bird in the week (g)
FCR = ---------------------------------------------------------------------------------------------
Average weight gain per bird during the week (g)
3.7.2 Oocyst Production Per Gram Of Droppings: The numbers of oocysts per gram of droppings were estimated by Stoll’s method on 4, 6, 8 and 10th day post infection.
3.7.3 Pathology:Detailed post mortem of the birds died and sacrificed (3, 6 and 9 DPI) during the experiment was undertaken. Gross lesions in various organs, if any, were recorded. Tissue pieces from caeca, caecal tonsil, thymus and spleen were collected in 10% formaline for histopathological studies by Hematoxylin and Eosin staining method.
3.7.4 Lesion Scoring:Caeca were removed from the dead/sacrificed birds and lesion scored by 0 to + 4 scoring system as described by Johnson and Reid (1970). Wherein, 0 scores for no lesion and subsequent + 1 to + 4 scores allowed depending upon lesions noted in caeca from different groups.
3.7.5 Acid Alpha Naphthyl Acetate Esterase (ANAE) Staining : (Tissue section): Tissue pieces of caeca from the sacrificed birds were collected in formal calcium for demonstration of T cells. ANAE staining of tissue section: Identification of T cells in the tissue sections was carried out following combination of ANAE staining methods used by Yam et al. (1971) and Ranki et al. (1980) with slight modifications. from 20 oil immersion fields and for each group three different sections were taken.
3.7.6 HI Titer: Serum was collected at the time of sacrificing birds on 3, 6 and 9 day post infection. Serum was separated and stored at -200c for assessing the HI titer against NDV.
3.8 Preparation Of Soluble Oocyst Antigen Of E. tenella: A suspension of sporulated oocyst of E. tenella were thoroughly washed with normal saline and concentrated by sugar flotation method. Again, it was washed with normal saline. Then it was treated with 10% sodium hypochlorite solution at room temperature for 5 min. to remove any extraneous materials. The phosphate buffer saline was added to adjust the concentration of oocyst to 50,000 oocyst/ml. The suspension was then sonicated with Branson sonifier at 220 duty cycles. Three cycles of sonification of 20 min. each were used. The process was carried out on ice. After sonification, a drop of suspension was examined by light microscopy to confirm the disruption of the oocysts. Protein Estimation: Protein estimation of the antigen was carried out by the Lowery’ method. Antigen stored in refrigerator at - 200 C.
3.9 Statistical Analysis: Suitable statistical analysis was applied to the data obtained as suggested by Snedecor and Cochran (1994).
Observations and Results
The present study was carried out to understand the gross and microscopic changes and immunological status of birds having sub-clinical coccidiosis and to evaluate the effect of Coxynil – a herbal coccidiostat in broilers against it.
3.5 Isolation And Sporulation Of Eimeria tenella Oocysts For Infection: A field strain of E. tenella was isolated from the caeca collected from the local poultry slaughter house and the oocysts were identified on the basis of size, shape and location of lesions. Oocysts were separated by sedimentation method and were sporulated in 2.5% potassium dichromate solution at room temperature with intermittent bubbling. These sporulated oocyst of E. tenella were used for further experimental work (Chaudhari, 1993).
3.6 Oocyst Challenge: The oocysts challenge was carried out on 21st day by inoculating 20,000 sporulated oocysts per bird orally, as per the protocol.
3.7 Parameters Studied:
3.7.1 Body Weight And Feed Conversion Ratio: The birds were weighed at the end of every week and the daily feed consumption was recorded. Feed conversion ratio (FCR) was calculated as,
Average feed consumption per bird in the week (g)
FCR = ---------------------------------------------------------------------------------------------
Average weight gain per bird during the week (g)
3.7.2 Oocyst Production Per Gram Of Droppings: The numbers of oocysts per gram of droppings were estimated by Stoll’s method on 4, 6, 8 and 10th day post infection.
3.7.3 Pathology:Detailed post mortem of the birds died and sacrificed (3, 6 and 9 DPI) during the experiment was undertaken. Gross lesions in various organs, if any, were recorded. Tissue pieces from caeca, caecal tonsil, thymus and spleen were collected in 10% formaline for histopathological studies by Hematoxylin and Eosin staining method.
3.7.4 Lesion Scoring:Caeca were removed from the dead/sacrificed birds and lesion scored by 0 to + 4 scoring system as described by Johnson and Reid (1970). Wherein, 0 scores for no lesion and subsequent + 1 to + 4 scores allowed depending upon lesions noted in caeca from different groups.
3.7.5 Acid Alpha Naphthyl Acetate Esterase (ANAE) Staining : (Tissue section): Tissue pieces of caeca from the sacrificed birds were collected in formal calcium for demonstration of T cells. ANAE staining of tissue section: Identification of T cells in the tissue sections was carried out following combination of ANAE staining methods used by Yam et al. (1971) and Ranki et al. (1980) with slight modifications. from 20 oil immersion fields and for each group three different sections were taken.
3.7.6 HI Titer: Serum was collected at the time of sacrificing birds on 3, 6 and 9 day post infection. Serum was separated and stored at -200c for assessing the HI titer against NDV.
3.8 Preparation Of Soluble Oocyst Antigen Of E. tenella: A suspension of sporulated oocyst of E. tenella were thoroughly washed with normal saline and concentrated by sugar flotation method. Again, it was washed with normal saline. Then it was treated with 10% sodium hypochlorite solution at room temperature for 5 min. to remove any extraneous materials. The phosphate buffer saline was added to adjust the concentration of oocyst to 50,000 oocyst/ml. The suspension was then sonicated with Branson sonifier at 220 duty cycles. Three cycles of sonification of 20 min. each were used. The process was carried out on ice. After sonification, a drop of suspension was examined by light microscopy to confirm the disruption of the oocysts. Protein Estimation: Protein estimation of the antigen was carried out by the Lowery’ method. Antigen stored in refrigerator at - 200 C.
3.9 Statistical Analysis: Suitable statistical analysis was applied to the data obtained as suggested by Snedecor and Cochran (1994).
Observations and Results
The present study was carried out to understand the gross and microscopic changes and immunological status of birds having sub-clinical coccidiosis and to evaluate the effect of Coxynil – a herbal coccidiostat in broilers against it.
4.1 Average Weekly Body Weights: (gm) - Average weekly body weights, in grams, for different groups are presented in Table No.1
Table No. 1: Average weekly body weights (gm)
a) Before oocysts challenge.
Table No. 1: Average weekly body weights (gm)
a) Before oocysts challenge.
|
Gr./ week
|
CA
|
CB
|
CC
|
CD
|
IA
|
IB
|
IC
|
ID
|
|
I
|
137.3
|
130.8
|
138.1
|
138.8
|
136.6
|
133.4
|
138.1
|
137.6
|
|
II
|
304
|
287.2
|
308.1
|
322.5
|
298.9
|
281
|
312.3
|
316.4
|
|
III
|
513.95
|
472.2
|
524.1
|
551.5
|
503.4
|
461
|
526.7
|
550.6
|
| Average |
318.42bc
|
296.73ab
|
323.43c
|
337.6c
|
312.97abc
|
291.8a
|
325.7c
|
334.87c
|
* Significant at 5% level.
b) After oocysts challenge.
|
Gr./ week
|
CA
|
CB
|
CC
|
CD
|
IA
|
IB
|
IC
|
ID
|
|
IV
|
790.3
|
727.5
|
797.85
|
826
|
564.98
|
529.9
|
632.8
|
668.6
|
|
V
|
1030.3
|
965.8
|
1084.9
|
1136
|
724.99
|
730.8
|
848.4
|
887
|
|
VI
|
1345.6
|
1256.4
|
1413.1
|
1484.8
|
954.99
|
989.2
|
1144.7
|
1203.4
|
| Average |
1055.4d
|
983.23c
|
1098.6de
|
1148.9e
|
748.32a
|
749.97a
|
875.3b
|
919.67bc
|
Mean with at least one common superscript do not differ significantly. ** Significant at 1% level.
Control group - CA : Control, CB : Salimomycin, CC : Coxynil @ 250gm/T, CD : Coxynil @ 300 gm/Ton
Infected group - IA : Control, IB : Salimomycin, IC : Coxynil @ 250gm/T, ID : Coxynil @ 300 gm/Ton
Control group - CA : Control, CB : Salimomycin, CC : Coxynil @ 250gm/T, CD : Coxynil @ 300 gm/Ton
Infected group - IA : Control, IB : Salimomycin, IC : Coxynil @ 250gm/T, ID : Coxynil @ 300 gm/Ton
4.2 Average Weekly Weight Gains: (gm)
Average weekly gains in body weights, in grams, for all the groups are presented in Table No.2.
Table No. 2: Average weekly weight gains (gm).
a) Before oocysts challenge.
|
Gr./ week
|
CA
|
CB
|
CC
|
CD
|
IA
|
IB
|
IC
|
ID
|
| I |
92.2
|
85.8
|
91.9
|
92.7
|
90.3
|
87.6
|
91.3
|
92.3
|
|
II
|
166.7
|
156.4
|
170
|
183.7
|
162.3
|
148
|
174.2
|
178.8
|
|
III
|
209.95
|
185
|
216
|
229
|
204.5
|
180
|
214.4
|
234.2
|
| Average |
156.28bcd
|
142.4ab
|
159.3cd
|
168.47d
|
152.37abc
|
138.53a
|
159.97cd
|
168.43d
|
|
Total
|
468.85
|
427.2
|
477.9
|
505.4
|
457.1
|
415.6
|
479.9
|
505.3
|
b) After oocysts challenge.
|
Gr./ week
|
CA
|
CB
|
CC
|
CD
|
IA
|
IB
|
IC
|
ID
|
|
IV
|
276.35
|
255.3
|
273.75
|
274.5
|
61.58
|
68.5
|
106.1
|
118
|
|
V
|
240
|
238.3
|
287.04
|
310
|
160.01
|
200.9
|
215.6
|
218.4
|
|
VI
|
315.3
|
290.6
|
328.2
|
348.8
|
230
|
258.4
|
296.3
|
316.4
|
| Average |
277.22de
|
261.4cde
|
296.33e
|
311.1e
|
150.53a
|
175.93ab
|
206abc
|
217.6abcd
|
|
Total
|
831.65
|
784.2
|
888.99
|
933.3
|
451.59
|
527.8
|
618
|
652.8
|
Mean with at least one common superscript do not differ significantly.
** Significant at 1% level
** Significant at 1% level
4.3 Average Weekly Feed Intake: (gm)
Average weekly feed intake, in grams, for all the groups are presented in Table No.3.
Table No. 3: Average weekly feed intake (gm).
a) Before oocysts challenge.
Group/week |
CA
|
CB
|
CC
|
CD
|
IA
|
IB
|
IC
|
ID
|
|
I
|
139.22
|
131.27
|
137.85
|
138.12
|
137.25
|
132.27
|
139.68
|
138.45
|
|
II
|
311.72
|
300.28
|
302.6
|
330.66
|
287.27
|
303.4
|
313.56
|
325.41
|
|
III
|
466.08
|
423.65
|
434.16
|
471.74
|
470.35
|
421.2
|
435.23
|
480.11
|
|
Average
|
305.67
|
285.07
|
291.54
|
313.51
|
298.29
|
285.62
|
296.16
|
314.66
|
|
Total
|
917.02
|
855.2
|
874.61
|
940.52
|
894.87
|
856.87
|
888.47
|
943.97
|
NS- Non Significant
b) After oocysts challenge.
|
Group/week
|
CA
|
CB
|
CC
|
CD
|
IA
|
IB
|
IC
|
ID
|
| IV |
630.07
|
589.74
|
626.88
|
625.86
|
193.97
|
239.75
|
385.14
|
403.56
|
|
V
|
619.2
|
679.92
|
711.85
|
725.4
|
475.22
|
548.45
|
605.83
|
604.96
|
|
VI
|
819.78
|
726.5
|
823.78
|
854.56
|
650.9
|
671.84
|
802.97
|
838.46
|
| Average |
689.68cd
|
665.39cd
|
720.84cd
|
735.27d
|
440.03a
|
486.68ab
|
597.98bc
|
615.66cd
|
|
Total
|
2069.1
|
1996.2
|
2162.5
|
2205.8
|
1320.1
|
1460
|
1793.9
|
1847
|
Mean with at least one common superscript do not differ significantly.
** Significant at 1% level.
Control group - CA : Control, CB : Salimomycin, CC : Coxynil @ 250gm/T, CD : Coxynil @ 300 gm/Ton
Infected group - IA : Control, IB : Salimomycin, IC : Coxynil @ 250gm/T, ID : Coxynil @ 300 gm/Ton
** Significant at 1% level.
Control group - CA : Control, CB : Salimomycin, CC : Coxynil @ 250gm/T, CD : Coxynil @ 300 gm/Ton
Infected group - IA : Control, IB : Salimomycin, IC : Coxynil @ 250gm/T, ID : Coxynil @ 300 gm/Ton
4.4 Feed Conversion Ratio: (FCR)
Weekly feed conversion ratio, before and after oocysts challenge, for all the groups are presented in Table No.4.
Table No. 4: Weekly FCR.
a) Before oocysts challenge.
| Group/week |
CA
|
CB
|
CC
|
CD
|
IA
|
IB
|
IC | ID |
|
I
|
1.51
|
1.53
|
1.5
|
1.49
|
1.52
|
1.51
|
1.53
|
1.5
|
|
II
|
1.87
|
1.92
|
1.78
|
1.8
|
1.77
|
2.05
|
1.8
|
1.82
|
|
III
|
2.22
|
2.29
|
2.01
|
2.06
|
2.3
|
2.34
|
2.03
|
2.05
|
|
Average
|
1.86
|
1.91
|
1.76
|
1.78
|
1.86
|
1.96
|
1.78
|
1.79
|
Mean with at least one common superscript do not differ significantly.
* Significant at 5% level.
Control group - CA : Control, CB : Salimomycin, CC : Coxynil @ 250gm/T, CD : Coxynil @ 300 gm/Ton
Infected group - IA : Control, IB : Salimomycin, IC : Coxynil @ 250gm/T, ID : Coxynil @ 300 gm/Ton
* Significant at 5% level.
Control group - CA : Control, CB : Salimomycin, CC : Coxynil @ 250gm/T, CD : Coxynil @ 300 gm/Ton
Infected group - IA : Control, IB : Salimomycin, IC : Coxynil @ 250gm/T, ID : Coxynil @ 300 gm/Ton
4.5 Clinical Symptoms:
The clinical symptoms observed and mortality during experimental period are presented in Table No. 5
Table No. 5: Clinical symptoms.
|
Sr. No.
|
Description
|
IA
|
IB
|
IC
|
ID
|
|
|
|
DPI
|
|||
|
1
|
Appearance of dullness
|
3
|
4
|
4
|
4
|
|
2
|
Appearance of loose droppings
|
3
|
4
|
4
|
4
|
|
3
|
Appearance of blood in droppings
|
4
|
5
|
5
|
5
|
Mortality pattern in different groups:
|
DPI
|
IA
|
IB
|
IC
|
ID
|
|
4
|
-
|
-
|
-
|
-
|
|
5
|
3
|
-
|
1
|
-
|
|
6
|
-
|
-
|
-
|
-
|
|
Total
|
3
|
0
|
1
|
0
|
Dullness and loose droppings, with slight mucus, were the first symptoms observed 3 days post infection (DPI) in infected group (IA). In Salinomycin treated (IB) and Coxynil groups (IC and ID), similar symptoms, were observed on 4 DPI. Appearance of blood in dropping was noted on 4 DPI in group IA and on 5 DPI in groups IB, IC and ID. The mortality was 15% in group IA and 5% in IC. Control groups CA, CB, CC and CD did not reveal any clinical symptoms or mortality. Clinical symptoms were first noticed in IA followed by those in treated groups. The symptoms observed in Salinomycin and Coxynil groups and those at two different dose levels were almost similar. Mortality was high in infected group (IA) as compared to treatment groups. Besides, birds in all the infected groups appeared lethargic and huddled together.
4.6 Oocyst Per Gram (OPG): (104)
The numbers of oocysts per gram of droppings were estimated by Stoll’s method on 4, 6, 8 and 10 days post infection and are depicted in Table No. 6.
Table No. 6: Average OPG count (104)
|
Gr./ DPI
|
IA |
IB
|
IC
|
ID
|
|
4
|
0
|
0
|
0
|
0
|
|
6
|
6.76
|
4.85
|
7.88
|
6.33
|
|
8
|
28.98
|
20.4
|
27.11
|
24.76
|
|
10
|
6.02
|
3.03
|
5.27
|
4.23
|
|
Average
|
10.44
|
7.07
|
10.07
|
8.83
|
No coccidial oocysts could be observed in any of the control groups (CA, CB, CC and CD) during the period of experiment.
The average OPG count in infected group, IA, was highest followed by that in Coxynil groups IC and ID and it was lowest in Salinomycin treated group (IB). The differences in OPG count amongst infected groups were non-significant.
4.7 Gross Lesions:
The birds which died and those sacrificed on 3, 6 and 9 DPI during the experiment were autopsied to note the gross abnormalities.
|
Gr./ DPI
|
IA
|
IB
|
IC
|
ID
|
|
3
|
0
|
0
|
0
|
0
|
|
6
|
+ 3.66
|
+ 2.33
|
+ 4
|
+ 3.66
|
|
9
|
+ 2.66
|
+ 1.66
|
+ 2
|
+ 2.33
|
|
Average
|
+ 2.11
|
+ 1.33
|
+ 2.0
|
+ 1.99
|
NS- Non Significant
4.7.1 Dead Birds:
Three birds from group IA and one from Coxynil group (IC), died during the experiment. These birds revealed pale subcutaneous tissue and musculature. The gross lesions were found to be confined to caeca. Caecal pouches were distended with blood, blood clots and reddish brown contents. Extensive haemorrhages were observed in the caeca. Other organs did not reveal any gross abnormality.
4.7.2 Sacrificed Birds:
Three birds from each group were sacrificed on 3, 6 and 9 DPI. Control groups (CA, CB, CC and CD) did not reveal any gross abnormality during the experimental period. Except watery to stringy caecal contents, no prominent lesions could be noticed on 3 DPI in any of the infected groups (IA, IB, IC and ID). On 6 DPI, group IA revealed scattered petechiae, visible from serosal surface, distended caecae, which contained clotted and unclotted blood mixed with fibrin shreds. Caecal wall was thickened and congested with extensive haemorrhages. On comparison, lesions of petechial haemorrhages and distention of caeca appeared more pronounced in IC and ID than in IB. On 9 DPI, in group IA, caecal mucosa revealed few foci of petechiae and formation of caecal core, which appeared as detached from mucosa. It was dry and hard. Caecal wall was slightly thickened and edematous. Similar lesions were observed in rest of the infected groups, except absence of caecal core in groups IB and IC. Haemorrhagic foci were comparatively more in group IC. Thymus and Spleen did not reveal any gross abnormality in any of the groups.
4.8 Caecal Lesion Score:
Caecal lesions were scored from the three birds sacrificed on 3, 6 and 9 DPI and the results are presented in Table No. 7. Control groups (CA, CB, CC and CD) did not reveal any lesions during observation period.
Table No. 7: Average caecal lesion score.
|
Gr./ DPI
|
IA
|
IB
|
IC
|
ID
|
|
3
|
0
|
0
|
0
|
0
|
|
6
|
+ 3.66
|
+ 2.33
|
+ 4
|
+ 3.66
|
|
9
|
+ 2.66
|
+ 1.66
|
+ 2
|
+ 2.33
|
|
Average
|
+ 2.11
|
+ 1.33
|
+ 2.0
|
+ 1.99
|
NS- Non Significant
No lesions were observed on 3 DPI in any of the treatment groups.
Amongst all the infected groups, Salinomycin treated group (IB), revealed lowest caecal lesion score followed by that in Coxynil groups (IC and ID) while infected group (IA) revealed highest lesion score.
Amongst all the infected groups, Salinomycin treated group (IB), revealed lowest caecal lesion score followed by that in Coxynil groups (IC and ID) while infected group (IA) revealed highest lesion score.
4.9 Microscopic Findings:
4.9.1 Dead Birds:
The birds died from groups IA and IC, revealed denuded caecal epithelium, increased thickness of the mucosa with developing schizonts and edematous changes in caecal wall. Thickened muscularis externa and narrowed submucosal space, as if compressed, were also observed. Large numbers of schizonts were observed in mucosal epithelium up to the muscularis and at some places muscularis mucosae revealed necrotic changes. Patchy areas of haemorrhages were observed in mucosa and submucosa. Infiltration of heterophils and mononuclear cells in all the three layers was observed.
4.9.2 Sacrificed Birds:
On 3 DPI, group IA revealed proliferation of caecal epithelium and exudate consisted of desquamated cells mixed with mucus. Vacuolation in glandular epithelium, suggestive of increased goblet cell activity and reduced submucosal space were also observed. Large numbers of merozoites were observed in the crypts and in caecal glands. Infiltration of lymphocytes and heterophils in the mucosa and around the glands was observed. Similar changes, with reduced intensity, were observed in Salinomycin (IB) and Coxynil groups (IC and ID).
On 6 DPI, group IA revealed wide spread damage to the caecal epithelium, which was necrotic and at most of the places it was totally exfoliated. Hyperemia of the mucosa and patchy areas of haemorrhages were observed in different depths of the thickness of the wall. Large numbers of second generation schizonts, micro and macro gametocytes were observed in mucosa and submucosa replacing the normal structures Microgametocytes were oval with multiple nuclei and of variable size. The macrogametocytes were oval with peripheral plastic granules in the cytoplasm. The nucleus of epithelial cells appeared displaced against cell wall due to gametocytes. Inflammatory cells, predominantly macrophages, lymphocytes and heterophils, along with few plasma cells, were found infiltrating mucosa, submucosa and in between muscle fibers of the intestinal wall.
Caecal lumen contained large number of erythrocytes along with exfoliated epithelium.
Salinomycin treated group (IB) revealed distorted epithelium, increased thickness of caecal mucosa, compressed submucosa, but the second generation schizonts and gametocytes were less in numbers. The patchy areas of haemorrhages in mucosa and submucosa were with low intensity than in IA.
Coxynil groups (IC and ID) revealed similar changes, but damage to the epithelium, intensity of the haemorrhages (in mucosa and submucosa), gametocytes and infiltration of inflammatory cells were more in IC than in ID. The lesions in these groups were with more intensity than IB.
On 9 DPI, group IA revealed desquamated superficial caecal mucosa. At some of the places it was totally exfoliated exposing mucosa and muscularis mucosae. In epithelial cells and many of the internal glands, gametogenous stages and oocysts were present. Musuclaris externa revealed increased thickness, thereby pushing the submucosa upwards. Infiltration of lymphocytes and heterophils was seen in the mucosa, submucosa and to some extent in between muscle layers of the caecal wall.
Similar changes were observed in Salinomycin treated group (IB), but the intensity of lesions was less and the regeneration of epithelial lining was evident. Thymus revealed mild depopulation of cells in cortex and medulla and degenerative changes in Hassall’s corpuscles.
In Coxynil groups (IC and ID) the severity of lesions was less than that of infected group (IA). The gametogenous stages and oocysts appeared in large numbers than in IB. At some places regeneration of the epithelium was noticed. No appreciable lesions were observed in thymus and spleen. In both the groups (IC and ID) the lesions were nearly similar and were comparable with IB.
4.10 T Cell Counts: (ANAE)
The ANAE activity, in lymphocytes, was characterized by the presence of small reddish brown dots or globules, either single or multiple in the cytoplasm. The monocytes revealed similar, brownish, but diffused reaction. ANAE negative lymphocytes did not reveal any reaction and had pale green cytoplasm. ANAE positive cells were counted from 20 oil immersion fields and for each group three different sections were taken. The mean cell count per 20 oil immersion fields are given in Table No. 8.
Table No. 8: Average ANAE cell count.
|
Gr./DPI
|
CA
|
CB
|
CC
|
CD
|
IA
|
IB
|
IC
|
ID
|
|
3
|
63.33
|
66.66
|
84.33
|
76
|
68
|
68.66
|
83.33
|
78.66
|
|
6
|
72.33
|
74.66
|
86.33
|
78.33
|
74.33
|
72.66
|
84.66
|
80.33
|
|
9
|
68.66
|
72.33
|
82.66
|
70.66
|
108
|
118
|
129.66
|
110
|
|
AVERAGE
|
68.10
|
72.21
|
84.44
|
74.99
|
83.44
|
86.44
|
99.21
|
89.66
|
NS- Non Significant
Average ANAE cell counts of infected groups were higher than the respective control groups. Infected birds revealed significantly higher counts on 9 DPI. Within control groups highest count was noted in group CC. Amongst all the groups, lowest count was recorded in group CA and highest in group IC.
4.11 HI Titer: (log 2)
HI titer was calculated for each group from serum samples collected from the sacrificed birds. The titers were expressed in log2 values and are presented in Table No. 9.
Table No. 9: Average HI titer (log 2).
|
Gr./DPI
|
CA
|
CB
|
CC
|
CD
|
IA
|
IB
|
IC
|
ID
|
|
3
|
5.25
|
5.0
|
5.25
|
5.25
|
5.0
|
5.25
|
5.25
|
5.0
|
|
6
|
6.0
|
6.25
|
6.0
|
6.0
|
5.25
|
5.75
|
5.75
|
5.5
|
|
9
|
6.5
|
6.5
|
6.75
|
6.75
|
6.0
|
6.0
|
6.25
|
6.5
|
|
AVERAGE
|
5.91b
|
5.91b
|
6.0b
|
6.0b
|
5.41a
|
5.66ab
|
5.75ab
|
5.66ab
|
* Significant at 5% level.
The average titers of infected groups were lower than that of the respective control groups. Within control groups, higher titers were observed in Coxynil groups (CC and CD), but the differences were non-significant. Amongst infected groups, highest titer was observed in group IC. Significantly low titer, compared to control groups, was noted in IA. Titers in Coxynil groups, at two different dose levels did not show significant difference.
4.12 Oocysts Antigen: The protein percentage of oocysts antigen was 0.8 gm%.
4.12 Oocysts Antigen: The protein percentage of oocysts antigen was 0.8 gm%.
SUMMARY AND CONCLUSIONS
Present study was conducted on 160 day old broilers chicks randomly divided into eight groups of 20 birds each, maintained on deep litter system for 42 days. Two different coccidiostats were used in the study and oocysts challenge was carried out by oral inoculation, on 21 day of age with 20,000 sporulated oocysts of E. tenella per bird. Three birds from each group were sacrificed on 3, 6 and 9 DPI and lesion score, gross and microscopic changes were studied.
Birds given oocysts and without treatment (Gr. IA) exhibited dullness, loose droppings on 3 DPI and blood in droppings appeared on 4 DPI. Both the coccidiostat used in the study delayed the appearance of clinical symptoms in treated groups as compared to IA. Mortality was observed in IA and IC and both the drugs were effective in reducing the mortality.
Body weights were significantly less in infected groups than their respective controls. Salinomycin group (IB) revealed higher body weight than IA and highest weights were observed in Coxynil birds. After oocysts challenge, weight gains were significantly less in infected groups than the respective control groups. Highest gains in weights were observed in CD and ID, amongst control and infected groups, respectively. After oocysts challenge, feed intake was significantly less in infected groups than the respective control groups, except for Coxynil birds, where the differences were non-significant. FCR for infected groups, were significantly higher than the respective control groups, after oocysts challenge. Amongst control groups, FCR was lowest in CD and amongst infected groups in IB and ID.
OPG count was high on 8 DPI in infected groups and it decreased later in the treated groups as compared to IA, where it was highest. Amongst treatment groups, Salinomycin was found to be more effective than Coxynil in reducing OPG.
Gross changes in sacrificed birds were confined to caecae. Haemorrhages, blood clots and distention were observed on 6 DPI; caecal core formation and thickening of caecal wall was seen on 9 DPI, in infected group (IA). Salinomycin was found to be more effective than Coxynil in reducing the intensity of lesions, over the period.
Lesion score on 6 DPI was highest in all the treatment groups. Average score, for the period, did not differ significantly between the groups. Highest score was noted in IA and lowest in IB. Coxynil was found to be more effective on late developmental stages of coccidia rather than early stages.
Microscopically, on 3 DPI, catarrhal enteritis was evident in all the infected groups. On 6 DPI, denuded epithelium, large number of second generation schizonts and gametes, alongwith haemorrhages (in mucosa and submucosa) and on 9 DPI, exfoliated epithelium, gametogenous stages and oocysts in mucosa, were the prominent findings, in IA. Salinomycin was found to be more effective than Coxynil in reducing the severity of lesions and later on, microscopic alterations were comparable within treated groups.
ANAE cell counts, on 9 DPI, were significantly higher in infected groups than the respective control groups. Coxynil was found to be more beneficial over Salinomycin, as highest count, was observed in IC, amongst all the groups.
Average HI titers, in all the infected groups were low as compared to respective control groups and significantly lowest titer was observed in IA, amongst all the groups. Coxynil groups revealed higher titers than Salinomycin treated birds.
Thus from the present study it could be concluded that:
1. Poor performance, as indicated by clinical symptoms, body weights, feed intake, FCR, OPG count, lesion score, ANAE cell count and HI titer, in coccidial infection indicated the adverse effects of disease, in absence of preventive medication.
2. Salinomycin was found to arrest early and late developmental stages of coccidia, while Coxynil was effective against late developmental stages. They both were effective in alleviating the adverse effects of coccidiosis.
3. Coxynil had beneficial effects on weight gain, feed intake, feed conversion ratio and reduced the severity of lesions. It was effective as a feed additive and coccidiostat.
2. Salinomycin was found to arrest early and late developmental stages of coccidia, while Coxynil was effective against late developmental stages. They both were effective in alleviating the adverse effects of coccidiosis.
3. Coxynil had beneficial effects on weight gain, feed intake, feed conversion ratio and reduced the severity of lesions. It was effective as a feed additive and coccidiostat.
BIBLIOGRAPHY
Adams, C., Vahi, H. A. and Veldman, A. (1995). Effects of coccidiosis on nutrient utilization of broiler chickens. Poultry Adviser. 28 (9): 53-57.
Allen, P.C., Lydon, J. and Danforth, H.D. (1997). Effects of components of Artemisia annua on coccidia infections in chickens. Poultry Sci., 76 (8): 1156-1163.
Augustine, P.C. and Danforth, H.D. (1986). A study of the dynamics of the invasion of immunized birds by Eimeria sporozoites. J. of Parasitol., 73: 494-502.
Bajawa, R.S. and Gill, B.S. (1979). Poultry coccidiosis and its control., Punjab Agriculture Uni., Ludhina.
Bakos, K. (1934) (Huhnerkokzidiose-studien). Diss. Budapest. (Cited by Pellardy, 1965).
Basith, A.S. and Srinivasan, K. (2000). Proceedings of the International Conference held on small holder livestock production systems in developing countries.24-27th Nov. 2000., Thrissur, Kerala.
Befus, A.D., Johnston, N., Leslie, G.A. and Bienestock, J. (1980). Gut associated lymphoid tissue in the chicken. J. Immunol.,125: 2626-2632.
Ben Dawes. (1968). Advances in Parasitology. Vol. 6 pp: 313-323. Academic Press, London.
Bessay, M., Le, V. Y., Kerboeuf, D., Yvore, P. and Quere, P. (1996). Changes in intestinal intra-epithelial and systemic T cell sub populations after an Eimeria infections in chickens: comparative study between E. acervulina and E. tenella. Vet. Res., 27: 503.
Bhandarkar, A.G. (2001). Role of Coxynil in pathology of coccidiosis in poultry. Personal communication. Nagpur Veterinary College, Nagpur, Maharashtra.
Bhatia, B.B. and Pandey, B.P. (1968). A hitherto unknown aspects of histopathology in outbreaks of Eimeria necatrix infection. Indian J. Microbiol., 8: 129-134.
Bhople, S. T. (1991). ‘Studies on the effect of mixed subclinical parasitic infections on immune response and pathogenecity in poultry’. M.V.Sc., Thesis submitted to Konkan Krishi Vidyapeeth, Dapoli, Maharashtra.
Brackett, S. and Bliznick, A. (1952). The reproductive potential of five species of coccidia of the chicken as demonstrated by oocyst production. J. of Parasitol., 38: 133-139.
Bumstead, A. and Millard, B.J. (1987). Genetics of resistance to coccidiosis: response of inbred lines to infection to E. tenella and E. maxima. British Poultry Sci., 28: 705-716.
Burns, W.C. and Challey, J.R. (1959). Resistance of birds to challenge with E. tenella. Exp. Parasitol., 8: 515.
Cacho-E-del., Gallego, M., Banuelos, M., Lopez, B.F., Gutierrez, J.F., Quilez, J., Zapatu, A., Sanchez-Acedo-C. and Castella, J. (1998). Local immune response to E. tenella. Research-and-Reviews in Parasitol., 58 (2): 109-115.
Calnek, B.W., with Barnes, H.J., Beard, C.W., Reid, W.M. and Yoder, H.W. (1997). Poultry Diseases. 9th Edn. Iowa state University Press.
Cerna, Z. (1969). Antibodies in chicks infected by E. tenella and E. acervulina detected by an indirect fluorescent reaction. Vet. Bull., 40: 63.
Chapman, H.D. (1999). The development of immunity to Eimeria species in broilers given anticoccidial drugs. Avian Pathol., 28 (2): 155-162.
Charyulu, N.S. (1962). ‘Species differentiation of the commonly occurring coccidia in domestic fowls of Bombay region with particular reference to their relative pathogenecity’. M.V.Sc., Thesis submitted to University of Bombay, Maharashtra.
Chaudhari, P.R. (1993). ‘Experimental studies on Biology, Pathogenecity and Immunogenecity of attenuated strains of Eimeria tenella (Ralliet and Lucet, 1891) Fantham, 1909, together with a note on incidence of coccidiosis’. M.V.Sc., Thesis submitted to Konkan Krishi Vidyapeeth, Dapoli, Maharashtra.
Chol, S.H., Kim, K.S. and Kim, Y.H. (1984). Epidemiological survey of coccidiosis in broiler chickens. Research report of the office of Rural Development (Livestock Veterinary) 26 (2): 44-52 (Vet. Bull., 55:4285)
Churchil, R. R. and Naryankutty, K. (2002). Indian poultry industry- current status and future prospectus. Poultry Times of India. 3:16-20.
Clausen, J.K. (1970). Polymorphonuclear leukocytes in the specific antigen-induced inhibition of the in-vitro migration of human peripheral leukocytes. Acta. Med. Scand., 188: 59-64.
Conway, D. P., McKenzie, M. F. and Dayton, A.P. (1990). Relationship of coccidial lesion score and weight gain in infection of E. tenella, E. acervulina, E. maxima in broilers. Avian Pathol., 19 (3): 489-496.
Cook, G.C. (1988). Small intestinal coccidiosis: an emergent clinical problem. J. Infect., 16: 213-219.
Crane, M.S.J., Gnozzio, M.J. and Murray, P.K. (1986). Eimeria tenella (Eucoccidiorida): A qualitative assay for sporozoite infectivity in vivo. J. Protozool., 33 (1): 94-98.
Davies, S.P.M., Joyner, Z.P. and Kendall, S.B. (1963). Coccidiosis. Ist Edn:109. Oliver and Boyd Ltd., Edinburgh, London.
Davis, P.J., Parry, S.H. and Parter, P. (1978). The role of secretary IgA in anticoccidial immunity in chickens. Immunol., 34 (5): 879-888.
Dhande, P.L. (1996). ‘Organogenesis of Bursa of fabricius, Thymus and Spleen (lymphoid organs) in relation to immunity in broilers’. Ph.D., Thesis submitted to Konkan Krishi Vidyapeeth, Dapoli, Maharashtra.
Dunkley, M.J.W. (1968). Laboratory trials with Buquinolate a broad spectrum coccidiostat for poultry. Vet. Record. 83: 30-34.
Gardiner, J.L. (1955). The severity of caecal coccidiosis infection in chicken, as related to the age of the host and the number of oocyst ingested. Poultry Sci., 34: 415-420.
Ghadge, S.B. (2000). ‘Studies on anticoccidial efficacy of Holarrhena Antidysentrica (Kuda) in Broiler chicks.’ M.V.Sc., Thesis submitted to Marathwada Agril.Uni., Parbhani, Maharashtra.
Giambrone, J.J., Klesius, P.H. and Edgar, S.A. (1980). Avian coccidiosis: Evidence for a cell-mediated immune response. Poultry Sci., 59: 38-43.
Gill, B.S. (1954). Specification and viability of poultry coccidia in 120 fecal samples preserved in 2.5% potassium dichromate solution. Indian J. Vet. Sci. & A.H. 24: 245-247.
Gill, B.S. (1960). Incidence of E. necatrix (Johnson, 1930) infection in Indian poultry. Indian Vet. J. 31: 304-309.
Gill, B. S. and Bajwa, R.S. (1979). Drug resistance in field isolates of chicken coccidia from Punjab State. Indian J. Parasitol., 3: 131-134.
Greif, G. (2000). Immunity to coccidiosis after treatment with tolrazuril. Parasitology-Res., 86 (10): 787-790.
Handa, S.S. (1996). Medicinal plants- Priorities in Indian medicines, disease studies and implications. In ‘supplement to cultivation and utilization of medicinal plants’; Editors: Handa, S.S. and Kaul, M.K. pp: 35-51, C S I R, Jammu-Tawi.
Harms, R.H., Ruiz-N. and Buresh, R.E. (1989). Influence of Monensin and Salinomycin on the performance of broiler chicks. Poultry Sci., 68 (1): 86-88.
Haugh, R.J. and Lee, Y. C. (1975). Immunization against caecal coccidiosis of chicken with the use of anticoccidial agents. J. Chin. Soci. Vet. Sci., 1 (2): 104-110.
Hegazy, A.M., Nada, M.S. and Gawady, H.E.L. (1986). E. tenella infection in chickens and immune response to N.D vaccine. Vet. Bull., 56 (11): 7826.
Hein, H. (1968). The pathogenic effects of E. acervulina in young chicks. Exp. Parasitol., 22: 1-11.
Herrick, C.A., Holmes, C.E. and Degiusti, D.L. (1942). The experimental use of organic sulphur compounds for the prevention of caecal coccidiosis in chickens. Am. J. Vet. Res., 3: 117-127.
Herrick, C.A., Ott, G.L. and Holmes, C.E. (1936). Age as a factor in the development of resistance of the chickens to the effect of E. tenella. J. Parasitol., 22: 264-275.
Higgins, D.A. (1981). Markers for T and B lymphocytes and their application to animals. (Cited by Kumthekar, 2001)
Hofstad, M.S. with Calnek, B.W., Helmboldt, C.F., Reid, W.M. and Yoder Jr., H.W. (1978). Diseases of Poultry. 7th Edn. Iowa state Uni. Press, Ames.
Hortan-Smith, C. (1949). Some factors influencing the origin and course of epidemics of coccidiosis in poultry. Ann. N.Y. Acad. Sci., 52: 449-457. (Cited by Pellardy, 1965)
Horton-Smith, C. and Long, P.L. (1963). Cited by Ben Dawes. (1968).
Jagdish Babu, K.S., Seshadri, S.J. and Mohiyuddin Syed. (1976). Studies on the pathology of field cases of coccidiosis in poultry. Indian Vet. J. 53: 47-54.
Jaipurkar, S.G., Deshpande, P.D., Narladkar, B.W. and Rajurkar, S.R. (2002). Evaluation of Herbal anticoccidials against experimentally induced caecal coccidiosis in broiler chicks. Indian Vet. J. 79 (2): 891-895.
Jankiewicz, H.A. and Scofield, R.H. (1934). The administration of heated oocyst of E. tenella as a means of establishing resistance and immunity to caecal coccidiosis. J. Am.Vet. Med. Assoc., 84: 507-526.
Johnson, J. and Reid, W.M. (1970). Anticoccidial drugs, lesion scoring technique in battery and floor pen experiments in chickens. Exp. Parasitol., 28: 30.
Jones, T. C., Hunt, R.D. and King, N.W. (1996). Veterinary Pathology. 6th Edn. Williams and Wilkins. A Waverly company.
Jordan, F.T.W. and Pattison, M. (1998). Poultry Diseases. 4th Edn. W.B. Saunders Company Ltd., London.
Joyner, L.P. and Norton, C.C. (1976). Immunity arising from continuous low level infection with Eimeria maxima and Eimeria acervulina. Parasitol., 72 (1):115-125.
Karlsson, T. and Reid, W. M. (1978). Development of immunity to coccidiosis in chickens administered anticoccidials in feed. Avian Dis., 22 (3): 487-495.
Kaspers, B., Lillehoj, H.S., Jenkins, M.C. and Pharr, G.T. (1994). Chicken interferon-mediated induction of major histocompatibility complex class II antigens on peripheral blood monocytes. Vet. Immunol. Immunopathol., 44: 71-84.
Kirtikar, K.R. and Basu, B.D. (1935). Indian medicinal plants. Vol.11:1569-1573. IBD, Dehradun.
Klesius, P.H., Kramer, T., Burger, D. and Malley, M. (1975). Passive transfer of coccidian oocyst antigen and diphtheria toxoid hypersensitivity in calves across speeres barriers. Transplant Proc., 7: 449-452. (Cited by Giambrone et al., 1980)
Klesius, P.H., Qualis, D.F., Elston, A.L. and Fadenberg, H.H. (1978). Effects of bovine transfer factor (TFd) in mouse coccidiosis. Clin. Immunol. Pathol., 10: 214-221.
Knowles, D.M., Hoffman, T., Ferranin, M. and Kunkel, H.G. (1978). The demonstration of alpha naphthyl acetate esterase activity in human lymphocytes: usefulness as a T cell marker. Cell Immunol., 35: 112-123.
Knowles, D.M. and Holck, S. (1978). Tissue localization of T lymphocytes by the histochemical demonstration of acid alpha naphthyl acetate esterase. Lab. Invest., 39: 70-76.
Kulenkampff, J., Janossy, G. and Greaves, M.F. (1977). Acid esterase in human lymphoid cells and leukemic blast: A marker for T lymphocytes. British J. Hematol., 36: 231-240.
Kumthekar, S. M. (2001). ‘Immunopathology of occular squamous cell carcinoma in Bovines.’ M.V.Sc., Thesis submitted to Konkan Krishi Vidyapeeth, Dapoli, Maharashtra.
Kurkure, N.V., Walse, S.H., Sharma, D.C., Richaria, M., Ganorkar, A.G., Bhandarkar, A.G. and Kalorey, D.R. (2001). Effect of Royal Jelly on coccidiosis in Poultry: Biochemical and Immunopathological study. J. Immunol. Immunopathol., 3: 70-73.
Kvale, D., Krajci, P. and Brandizaeg, P. (1992). Expression and regulation of adhesion molecules ICAM-1 (CD 54) and LFA-3 (CD 58) in human intestinal epithelial lines. Scand. J. Immunol., 35: 669-676.
Levine, N.D. (1985). Veterinary Protozoology. Ist Edn. pp: 187-188. Iowa State Uni. Press, Ames.
Liburd, E.M., Armstrong, W.D. and Mahrt, J.L. (1973). Immunity to the protozoan parasite Eimeria miescbulzi in inbred CD-rats. Cell Immunol., 7: 442-452. (Cited by Giambrone et al., 1980)
Lillehoj, H.S. (1994). Analysis of E. acervulina induced changes in the intestinal lymphocyte subpopulation in two chicken strains showing different levels of susceptibility to coccidiosis. Research in Veterinary Sci., 56 (1): 1-7.
Lillehoj, H.S. (1998). Role of T lymphocytes and cytokines in coccidiosis. Int. J. for Parasitol., 28 (7):1015-1018.
Lillehoj, H.S., Bacon, M.D., Lamont, S.J. and Jeffers, T.K. (1989). Genetic control of immunity to E. tenella. Parasitol., 104: 407-417.
Lillehoj, H.S. and Ruff, M.D. (1987). Comparison of disease susceptibility and subclass-specific antibody response in SC and FP chickens experimentally inoculated with E. tenella, E. acervulina or E. maxima. Avian Dis., 31:112-119.
Lin, Y. and Feng, Z.G. (1993). Pathomorphological studies of the chickens experimentally infected with E. tenella. Acta.Veterinaria et Zootechnica Sinica (1993). Poultry Abstract. 21 (10): 3130.
Long, P. L. (1968). Breed resistance to Eimeria. British Poultry Sci., 9: 72-78.
Long, P. L. (1984). Gordon memorial lecture- Coccidiosis control: past, present and future. British Poultry Sci., 25: 3-18.
Long, P.L., Johnson, J., McKenzie, M.E., Perry, E., Carne, M.S. and Murray, P.K. (1986). Immunization of young broiler chickens with low level infection of E. tenella, E. acervulina or E. maxima. Avian Pathol., 5 (2): 271-278.
Long, P.L. and Rose, M.E. (1965). Active and passive immunization of chickens against intravenously induced infections of E. tenella. Exp. Parasitol., 16:1-7.
Majarao, O. M. (1980). The epidemiology and economic importance of poultry coccidiosis. Revue d’ Elevage et de Medecine Veterinaire des pays Tropicaux., 33 (4): 377-379. (Vet. Bull., 52:190)
Martin, A., Lillehoj, H.S., Kaspers, B. and Bacon, L.D. (1993). Antigen specific T cell proliferation following coccidia infection. Poultry Sci., 72: 2084-2094.
Mayhew, R.L. (1934). Studies on coccidiosis (vi) effect on early attack on egg production. Poultry Sci., 13: 148.
Mc Dougald, L.R. and Reid, W.M. (1994). Coccidiosis. In: B.W. Calnek (Ed.), Diseases of Poultry.
Mir, S.A. and Ahmed, S.N. (1995). Anticoccidials update- applied aspects. Poultry Adviser. 28 (5): 49-60.
Mueller, J., Brundel, R.G., Buerki, H., Keller, H. V., Hees, M.W. and Coittier, H. (1975). Non specific acid esterase activity: a criterion for differentiation of T and B lymphocytes in mouse lymphnodes. Euro. J. Immunol., 5: 270-274.
Mukherjee, J., Guha, C. and Mitra, S.K. (1994). Therapeutic efficacy of Supercox, Duocoxin and Zycox against experimental caecal coccidiosis in broiler chicks. Indian Vet. J. 71: 870.
Mureau, G. (1980). The avian coccidiosis problem seen by a diagnostic laboratory. Chaiers de Medecine Vetrinaire. 49:15-23. (Vet. Bull., 51: 4150)
Odend’hal, S. and Player E.C. (1979). Histochemical localization of T cells in tissue sections. Avian Dis., 24 (4): 886-895.
Panda, D.N., Mishra, A., Misra, S.C. and Rao, A.G. (1997). Studies on efficacy of Supercox against experimental Eimeria tenella infection in broiler chicks. J. of Vet. Parasitol., 11 (1):91-93.
Patel, H.R. (1980). ‘A study on Broiler Mortality’. M.V.Sc., Thesis submitted to Konkan Krishi Vidyapeeth, Dapoli, Maharashtra.
Patil, D. M. (1996). ‘Evaluation of biological behaviour of isolated strain of Eimeria tenella from Mumbai region’. M.V.Sc., Thesis submitted to Konkan Krishi Vidyapeeth, Dapoli, Maharashtra.
Pellardy, L.P. (1965). Coccidia and Coccidiosis. Publishing House of the Hungarian Academy of Sciences.
Pohl, R. (1965). Species of coccidia from fowls. Dt. tierarzti wschri., 72: 230-232. (Cited by Chaudhari, 1993)
Potter, L. M., Blake, J.P., Blair, M.E., Bliss, B.A. and Denbow, D.M. (1986). Salinomycin toxicity in Turkeys. Poultry Sci., 65: 1955-1959.
Powell, P.C. (1987). Immune mechanism in infections of poultry. Vet. Immuno. and Immunopathol., 15: 105-114.
Prabaharan, S. and George, Y.J. (1999). Effect of Aflatoxin and Eimeria tenella infection on mortality and lesion score in broiler chicken. Indian Vet. J. 76: 693-695.
Prabaharan, S., George, T.V. and Balasubramaniam. (1999). Influence of dietary Aflatoxin and Coccidiosis on growth rate in broiler chicken. Indian Vet. J. 76: 827-828.
Pruthi, A.K., Gupta, R.K.P. and Sadana, J.R. (1987). Acid alpha naphthyl acetate esterase reacting lymphocytes in the peripheral blood of chickens challenged with Marek’s disease after vaccination with three different vaccines. Research in veterinary Sci., 43: 92-96.
Quin-Ze Rong., Kong, F. Y. and Arakawa, A. (2000). Effects of Eimeria tenella infection on the population of some caecal facultative anaerobic flora. Acta-Parasitologica-et-Medica-Entomologica-Sincia. 7 (2): 76-79.
Rahman, S.A., Adel Fatema. and Jagannath, M.S. (1989). Role of Levamisole in the induction of cell mediated immunity in experimental caecal coccidiosis of chickens. Indian Vet. J. 66 (8): 706-710.
Rahman, S.A. and Anantraman, M. (1970). The species of coccidia in fowls and pigeon. Mysore J. of Agr. Sci., 4: 157-162.
Ranki, A., Reitamo, S., Konttinen, Y.T. and Harry, P. (1980). Histochemical identification of human T lymphocytes from paraffin section. J. Histo Chem. And Cytochem., 28: 704-707.
Ray, H.N. (1945). A new coccidium Wenyonella gallinae in chickens. Current Sci., 14: 275.
Richardson, U.F. and Kendall, S.B. (1963).Veterinary Protozoology. 3rd Edn. pp: 103-104. Oliver and Boyd, Edinburgh, London.
Ripsom, C.A. and Herrick, C.A. (1945). Effect of various sulpha compounds on the protozoan parasite E. tenella. J. Parasitol., 31: 98-108.
Rose, M. E. (1971). Immunity to coccidia- protective effect of transferred serum to E. maxima infection. Parasitol., 62: 11-25.
Rose, M.E. and Hesketh, P. (1976). Immunity to coccidiosis: stages of the life cycle of Eimeria maxima which induce, and are affected by, the response of the host. Parasitol., 73: 25-37.
Rose, M.E. and Hesketh, P. (1984). Infection with E. tenella: modulation of lymphocyte blastogenesis by specific antigen and evidence for immunodepression. J. Protozool., 31: 549-553.
Rose, M.E., Lawn, A.M. and Millard, B.J. (1984). The effect of immunity on the early events in the life cycle of Eimeria tenella in the caecal mucosa of the chickens. Parasitol., 88: 199-210.
Ryley, J.F. (1980). Recent development in coccidian biology, where do we go from here? Parasitol., 80 (1): 189-209.
Sastry, G.A. (1983). Veterinary Pathology. 6th Edn., CBS Publication and Distributor., New Delhi.
Shalaby, M.A., Sanousi-EL, A.A., Yehia, M.M. and Reda, I. M. (1994). The effect of Salinomycin on the immune response of chicks. Poultry Abst., 20 (4): 989.
Sherkov, S.N., Rabie, E.L., Kokasb, L. and Bakri, M. (1976). A survey of Eimeria species and coccidiosis in chicken in Jordan. Vet. Bull., 49:763.
Shukla, S.K., Joshi, H.C. and Kumar, M. (1990). Clinico-pathological changes in experimental coccidiosis of broiler chicks. J. of Vet. Parasitol., 4 (1): 65-67.
Smith, C.K., Galloway, R.B. and White, S.L. (1981). Effect of ionophores on survival, penetration and development of E. tenella sporozoites in vitro. J. of Parasitol., 67: 511-516.
Smith, C.K. and Strout, R.G. (1979). Accumulation and retention of anticoccidial ionophores by extra cellular sporozoites. Exp. Parasitol., 48: 325-330.
Snedecor G. W. and Cochran W. C. (1994). Statistical Methods. 8th Edn. Iowa State University Press. USA.
Subramanian, R., Kumaravelu, N. and Arunachalam, K. (1995). Subclinical coccidiosis in broilers. Poultry Adviser. 28 (4): 31-34.
Swales, W.E. (1944). Chemotherapy of caecal coccidiosis (Eimeria tenella) of chickens. Canad. J. Res., 22: 131-140. (Cited by Chaudhari, 1993).
Tankhiwale, M. (1987). ‘Studies on epidemiology of coccidiosis of broilers in Bombay region with special reference to E. necatrix (Johnson, 1930).’ M.V.Sc., Thesis submitted to Konkan Krishi Vidyapeeth, Dapoli, Maharashtra.
Trees, A.J., Crozier, S.J., McKellar, S.B. and Wachira, T.M. (1985). Class specific circulating antibodies in infections with Eimeria tenella. Vet. Parasitol., 18: 349-357.
Trout, J.M. and Lillehoj, H.S. (1996). T lymphocyte role during E. acervulina and E. tenella infections. Vet. Immunol. Immunopathol., 53: 163-172.
Tyzzer, E. E. (1929). Coccidiosis in gallinaceous birds. Am. J. Hyg., 10: 269-383.
Udayakumar, M., Padmavathi, P. and Ramesh, A.J. (1995). Effect of Aflatoxin B1 and E. tenella infection on mortality and growth in broiler chicks. Indian Vet. J. 72 (11): 1141-1144.
Vervelde, L., Vermeulen, A.N. and Jeurissen, S.H.M. (1998). E. tenella sporozoites rarely enter leukocytes in the caecal epithelium of the chicken. (Gallus domesticus) Exp. Parasitol., 81: 29-38.
Voeten, A.C., Braunius, W.S., Orthel, F.W., Rijen, M.A. and Van, J. (1988). Influence of coccidiosis on growth rate and feed conversion in broilers after experimental infection with E. acervulina and E. maxima. Vet. Quarterly.10: 256-264.
Wakelin, D. and Rose, M.E. (1990). Immunity to coccidiosis. In coccidiosis of man and domestic animals. CRC press.
Williams, R.B. (1973). Effects of different infection rates on the oocyst production of Eimeria acervulina or Eimeria tenella in the chickens. Parasitol., 67: 279-288.
Witlock, D.R., Ruff, M.D. and Chute, M.B. (1981). Physiological basis of Eimeria tenella-induced mortality in individual chicken. The J. of Parasitol., 67 (1): 65-69.
Wyatt, D.R., Ruff, M.D. and Page, R.K. (1975). Interaction of Aflatoxin with Eimeria tenella infection and Monensin in young broiler chickens. Avian Dis.,19 (4): 730-740.
Yang, K., Bearman, R.N., Pargalis, G.A., Zelman, R.J. and Rappapore, H. (1982). Acid phosphates and alpha naphthyl acetate esterase in neoplastic and non-neoplastic lymphocytes.J. Clin. Pathol., 78: 141-149.
Yam, L.T., Li, C.Y. and Croshy, W.H. (1971). Cytochemical identification of monocytes and granulocytes. Am. J. Clin. Pathol., 55: 283.
Yun, C.H., Lillehoj, H.S. and Choi, K.D. (2000b). Eimeria tenella infection induces local gamma interferon production and intestinal lymphocyte subpopulation changes. Infection-and-Immunity. 68 (3): 1282-1288.
Yun, C.H., Lillehoj, H.S. and Lillehoj, E.P. (2000a). Intestinal immune response to coccidiosis. Developmental and comparative Immunol., 24: 303-324.
Allen, P.C., Lydon, J. and Danforth, H.D. (1997). Effects of components of Artemisia annua on coccidia infections in chickens. Poultry Sci., 76 (8): 1156-1163.
Augustine, P.C. and Danforth, H.D. (1986). A study of the dynamics of the invasion of immunized birds by Eimeria sporozoites. J. of Parasitol., 73: 494-502.
Bajawa, R.S. and Gill, B.S. (1979). Poultry coccidiosis and its control., Punjab Agriculture Uni., Ludhina.
Bakos, K. (1934) (Huhnerkokzidiose-studien). Diss. Budapest. (Cited by Pellardy, 1965).
Basith, A.S. and Srinivasan, K. (2000). Proceedings of the International Conference held on small holder livestock production systems in developing countries.24-27th Nov. 2000., Thrissur, Kerala.
Befus, A.D., Johnston, N., Leslie, G.A. and Bienestock, J. (1980). Gut associated lymphoid tissue in the chicken. J. Immunol.,125: 2626-2632.
Ben Dawes. (1968). Advances in Parasitology. Vol. 6 pp: 313-323. Academic Press, London.
Bessay, M., Le, V. Y., Kerboeuf, D., Yvore, P. and Quere, P. (1996). Changes in intestinal intra-epithelial and systemic T cell sub populations after an Eimeria infections in chickens: comparative study between E. acervulina and E. tenella. Vet. Res., 27: 503.
Bhandarkar, A.G. (2001). Role of Coxynil in pathology of coccidiosis in poultry. Personal communication. Nagpur Veterinary College, Nagpur, Maharashtra.
Bhatia, B.B. and Pandey, B.P. (1968). A hitherto unknown aspects of histopathology in outbreaks of Eimeria necatrix infection. Indian J. Microbiol., 8: 129-134.
Bhople, S. T. (1991). ‘Studies on the effect of mixed subclinical parasitic infections on immune response and pathogenecity in poultry’. M.V.Sc., Thesis submitted to Konkan Krishi Vidyapeeth, Dapoli, Maharashtra.
Brackett, S. and Bliznick, A. (1952). The reproductive potential of five species of coccidia of the chicken as demonstrated by oocyst production. J. of Parasitol., 38: 133-139.
Bumstead, A. and Millard, B.J. (1987). Genetics of resistance to coccidiosis: response of inbred lines to infection to E. tenella and E. maxima. British Poultry Sci., 28: 705-716.
Burns, W.C. and Challey, J.R. (1959). Resistance of birds to challenge with E. tenella. Exp. Parasitol., 8: 515.
Cacho-E-del., Gallego, M., Banuelos, M., Lopez, B.F., Gutierrez, J.F., Quilez, J., Zapatu, A., Sanchez-Acedo-C. and Castella, J. (1998). Local immune response to E. tenella. Research-and-Reviews in Parasitol., 58 (2): 109-115.
Calnek, B.W., with Barnes, H.J., Beard, C.W., Reid, W.M. and Yoder, H.W. (1997). Poultry Diseases. 9th Edn. Iowa state University Press.
Cerna, Z. (1969). Antibodies in chicks infected by E. tenella and E. acervulina detected by an indirect fluorescent reaction. Vet. Bull., 40: 63.
Chapman, H.D. (1999). The development of immunity to Eimeria species in broilers given anticoccidial drugs. Avian Pathol., 28 (2): 155-162.
Charyulu, N.S. (1962). ‘Species differentiation of the commonly occurring coccidia in domestic fowls of Bombay region with particular reference to their relative pathogenecity’. M.V.Sc., Thesis submitted to University of Bombay, Maharashtra.
Chaudhari, P.R. (1993). ‘Experimental studies on Biology, Pathogenecity and Immunogenecity of attenuated strains of Eimeria tenella (Ralliet and Lucet, 1891) Fantham, 1909, together with a note on incidence of coccidiosis’. M.V.Sc., Thesis submitted to Konkan Krishi Vidyapeeth, Dapoli, Maharashtra.
Chol, S.H., Kim, K.S. and Kim, Y.H. (1984). Epidemiological survey of coccidiosis in broiler chickens. Research report of the office of Rural Development (Livestock Veterinary) 26 (2): 44-52 (Vet. Bull., 55:4285)
Churchil, R. R. and Naryankutty, K. (2002). Indian poultry industry- current status and future prospectus. Poultry Times of India. 3:16-20.
Clausen, J.K. (1970). Polymorphonuclear leukocytes in the specific antigen-induced inhibition of the in-vitro migration of human peripheral leukocytes. Acta. Med. Scand., 188: 59-64.
Conway, D. P., McKenzie, M. F. and Dayton, A.P. (1990). Relationship of coccidial lesion score and weight gain in infection of E. tenella, E. acervulina, E. maxima in broilers. Avian Pathol., 19 (3): 489-496.
Cook, G.C. (1988). Small intestinal coccidiosis: an emergent clinical problem. J. Infect., 16: 213-219.
Crane, M.S.J., Gnozzio, M.J. and Murray, P.K. (1986). Eimeria tenella (Eucoccidiorida): A qualitative assay for sporozoite infectivity in vivo. J. Protozool., 33 (1): 94-98.
Davies, S.P.M., Joyner, Z.P. and Kendall, S.B. (1963). Coccidiosis. Ist Edn:109. Oliver and Boyd Ltd., Edinburgh, London.
Davis, P.J., Parry, S.H. and Parter, P. (1978). The role of secretary IgA in anticoccidial immunity in chickens. Immunol., 34 (5): 879-888.
Dhande, P.L. (1996). ‘Organogenesis of Bursa of fabricius, Thymus and Spleen (lymphoid organs) in relation to immunity in broilers’. Ph.D., Thesis submitted to Konkan Krishi Vidyapeeth, Dapoli, Maharashtra.
Dunkley, M.J.W. (1968). Laboratory trials with Buquinolate a broad spectrum coccidiostat for poultry. Vet. Record. 83: 30-34.
Gardiner, J.L. (1955). The severity of caecal coccidiosis infection in chicken, as related to the age of the host and the number of oocyst ingested. Poultry Sci., 34: 415-420.
Ghadge, S.B. (2000). ‘Studies on anticoccidial efficacy of Holarrhena Antidysentrica (Kuda) in Broiler chicks.’ M.V.Sc., Thesis submitted to Marathwada Agril.Uni., Parbhani, Maharashtra.
Giambrone, J.J., Klesius, P.H. and Edgar, S.A. (1980). Avian coccidiosis: Evidence for a cell-mediated immune response. Poultry Sci., 59: 38-43.
Gill, B.S. (1954). Specification and viability of poultry coccidia in 120 fecal samples preserved in 2.5% potassium dichromate solution. Indian J. Vet. Sci. & A.H. 24: 245-247.
Gill, B.S. (1960). Incidence of E. necatrix (Johnson, 1930) infection in Indian poultry. Indian Vet. J. 31: 304-309.
Gill, B. S. and Bajwa, R.S. (1979). Drug resistance in field isolates of chicken coccidia from Punjab State. Indian J. Parasitol., 3: 131-134.
Greif, G. (2000). Immunity to coccidiosis after treatment with tolrazuril. Parasitology-Res., 86 (10): 787-790.
Handa, S.S. (1996). Medicinal plants- Priorities in Indian medicines, disease studies and implications. In ‘supplement to cultivation and utilization of medicinal plants’; Editors: Handa, S.S. and Kaul, M.K. pp: 35-51, C S I R, Jammu-Tawi.
Harms, R.H., Ruiz-N. and Buresh, R.E. (1989). Influence of Monensin and Salinomycin on the performance of broiler chicks. Poultry Sci., 68 (1): 86-88.
Haugh, R.J. and Lee, Y. C. (1975). Immunization against caecal coccidiosis of chicken with the use of anticoccidial agents. J. Chin. Soci. Vet. Sci., 1 (2): 104-110.
Hegazy, A.M., Nada, M.S. and Gawady, H.E.L. (1986). E. tenella infection in chickens and immune response to N.D vaccine. Vet. Bull., 56 (11): 7826.
Hein, H. (1968). The pathogenic effects of E. acervulina in young chicks. Exp. Parasitol., 22: 1-11.
Herrick, C.A., Holmes, C.E. and Degiusti, D.L. (1942). The experimental use of organic sulphur compounds for the prevention of caecal coccidiosis in chickens. Am. J. Vet. Res., 3: 117-127.
Herrick, C.A., Ott, G.L. and Holmes, C.E. (1936). Age as a factor in the development of resistance of the chickens to the effect of E. tenella. J. Parasitol., 22: 264-275.
Higgins, D.A. (1981). Markers for T and B lymphocytes and their application to animals. (Cited by Kumthekar, 2001)
Hofstad, M.S. with Calnek, B.W., Helmboldt, C.F., Reid, W.M. and Yoder Jr., H.W. (1978). Diseases of Poultry. 7th Edn. Iowa state Uni. Press, Ames.
Hortan-Smith, C. (1949). Some factors influencing the origin and course of epidemics of coccidiosis in poultry. Ann. N.Y. Acad. Sci., 52: 449-457. (Cited by Pellardy, 1965)
Horton-Smith, C. and Long, P.L. (1963). Cited by Ben Dawes. (1968).
Jagdish Babu, K.S., Seshadri, S.J. and Mohiyuddin Syed. (1976). Studies on the pathology of field cases of coccidiosis in poultry. Indian Vet. J. 53: 47-54.
Jaipurkar, S.G., Deshpande, P.D., Narladkar, B.W. and Rajurkar, S.R. (2002). Evaluation of Herbal anticoccidials against experimentally induced caecal coccidiosis in broiler chicks. Indian Vet. J. 79 (2): 891-895.
Jankiewicz, H.A. and Scofield, R.H. (1934). The administration of heated oocyst of E. tenella as a means of establishing resistance and immunity to caecal coccidiosis. J. Am.Vet. Med. Assoc., 84: 507-526.
Johnson, J. and Reid, W.M. (1970). Anticoccidial drugs, lesion scoring technique in battery and floor pen experiments in chickens. Exp. Parasitol., 28: 30.
Jones, T. C., Hunt, R.D. and King, N.W. (1996). Veterinary Pathology. 6th Edn. Williams and Wilkins. A Waverly company.
Jordan, F.T.W. and Pattison, M. (1998). Poultry Diseases. 4th Edn. W.B. Saunders Company Ltd., London.
Joyner, L.P. and Norton, C.C. (1976). Immunity arising from continuous low level infection with Eimeria maxima and Eimeria acervulina. Parasitol., 72 (1):115-125.
Karlsson, T. and Reid, W. M. (1978). Development of immunity to coccidiosis in chickens administered anticoccidials in feed. Avian Dis., 22 (3): 487-495.
Kaspers, B., Lillehoj, H.S., Jenkins, M.C. and Pharr, G.T. (1994). Chicken interferon-mediated induction of major histocompatibility complex class II antigens on peripheral blood monocytes. Vet. Immunol. Immunopathol., 44: 71-84.
Kirtikar, K.R. and Basu, B.D. (1935). Indian medicinal plants. Vol.11:1569-1573. IBD, Dehradun.
Klesius, P.H., Kramer, T., Burger, D. and Malley, M. (1975). Passive transfer of coccidian oocyst antigen and diphtheria toxoid hypersensitivity in calves across speeres barriers. Transplant Proc., 7: 449-452. (Cited by Giambrone et al., 1980)
Klesius, P.H., Qualis, D.F., Elston, A.L. and Fadenberg, H.H. (1978). Effects of bovine transfer factor (TFd) in mouse coccidiosis. Clin. Immunol. Pathol., 10: 214-221.
Knowles, D.M., Hoffman, T., Ferranin, M. and Kunkel, H.G. (1978). The demonstration of alpha naphthyl acetate esterase activity in human lymphocytes: usefulness as a T cell marker. Cell Immunol., 35: 112-123.
Knowles, D.M. and Holck, S. (1978). Tissue localization of T lymphocytes by the histochemical demonstration of acid alpha naphthyl acetate esterase. Lab. Invest., 39: 70-76.
Kulenkampff, J., Janossy, G. and Greaves, M.F. (1977). Acid esterase in human lymphoid cells and leukemic blast: A marker for T lymphocytes. British J. Hematol., 36: 231-240.
Kumthekar, S. M. (2001). ‘Immunopathology of occular squamous cell carcinoma in Bovines.’ M.V.Sc., Thesis submitted to Konkan Krishi Vidyapeeth, Dapoli, Maharashtra.
Kurkure, N.V., Walse, S.H., Sharma, D.C., Richaria, M., Ganorkar, A.G., Bhandarkar, A.G. and Kalorey, D.R. (2001). Effect of Royal Jelly on coccidiosis in Poultry: Biochemical and Immunopathological study. J. Immunol. Immunopathol., 3: 70-73.
Kvale, D., Krajci, P. and Brandizaeg, P. (1992). Expression and regulation of adhesion molecules ICAM-1 (CD 54) and LFA-3 (CD 58) in human intestinal epithelial lines. Scand. J. Immunol., 35: 669-676.
Levine, N.D. (1985). Veterinary Protozoology. Ist Edn. pp: 187-188. Iowa State Uni. Press, Ames.
Liburd, E.M., Armstrong, W.D. and Mahrt, J.L. (1973). Immunity to the protozoan parasite Eimeria miescbulzi in inbred CD-rats. Cell Immunol., 7: 442-452. (Cited by Giambrone et al., 1980)
Lillehoj, H.S. (1994). Analysis of E. acervulina induced changes in the intestinal lymphocyte subpopulation in two chicken strains showing different levels of susceptibility to coccidiosis. Research in Veterinary Sci., 56 (1): 1-7.
Lillehoj, H.S. (1998). Role of T lymphocytes and cytokines in coccidiosis. Int. J. for Parasitol., 28 (7):1015-1018.
Lillehoj, H.S., Bacon, M.D., Lamont, S.J. and Jeffers, T.K. (1989). Genetic control of immunity to E. tenella. Parasitol., 104: 407-417.
Lillehoj, H.S. and Ruff, M.D. (1987). Comparison of disease susceptibility and subclass-specific antibody response in SC and FP chickens experimentally inoculated with E. tenella, E. acervulina or E. maxima. Avian Dis., 31:112-119.
Lin, Y. and Feng, Z.G. (1993). Pathomorphological studies of the chickens experimentally infected with E. tenella. Acta.Veterinaria et Zootechnica Sinica (1993). Poultry Abstract. 21 (10): 3130.
Long, P. L. (1968). Breed resistance to Eimeria. British Poultry Sci., 9: 72-78.
Long, P. L. (1984). Gordon memorial lecture- Coccidiosis control: past, present and future. British Poultry Sci., 25: 3-18.
Long, P.L., Johnson, J., McKenzie, M.E., Perry, E., Carne, M.S. and Murray, P.K. (1986). Immunization of young broiler chickens with low level infection of E. tenella, E. acervulina or E. maxima. Avian Pathol., 5 (2): 271-278.
Long, P.L. and Rose, M.E. (1965). Active and passive immunization of chickens against intravenously induced infections of E. tenella. Exp. Parasitol., 16:1-7.
Majarao, O. M. (1980). The epidemiology and economic importance of poultry coccidiosis. Revue d’ Elevage et de Medecine Veterinaire des pays Tropicaux., 33 (4): 377-379. (Vet. Bull., 52:190)
Martin, A., Lillehoj, H.S., Kaspers, B. and Bacon, L.D. (1993). Antigen specific T cell proliferation following coccidia infection. Poultry Sci., 72: 2084-2094.
Mayhew, R.L. (1934). Studies on coccidiosis (vi) effect on early attack on egg production. Poultry Sci., 13: 148.
Mc Dougald, L.R. and Reid, W.M. (1994). Coccidiosis. In: B.W. Calnek (Ed.), Diseases of Poultry.
Mir, S.A. and Ahmed, S.N. (1995). Anticoccidials update- applied aspects. Poultry Adviser. 28 (5): 49-60.
Mueller, J., Brundel, R.G., Buerki, H., Keller, H. V., Hees, M.W. and Coittier, H. (1975). Non specific acid esterase activity: a criterion for differentiation of T and B lymphocytes in mouse lymphnodes. Euro. J. Immunol., 5: 270-274.
Mukherjee, J., Guha, C. and Mitra, S.K. (1994). Therapeutic efficacy of Supercox, Duocoxin and Zycox against experimental caecal coccidiosis in broiler chicks. Indian Vet. J. 71: 870.
Mureau, G. (1980). The avian coccidiosis problem seen by a diagnostic laboratory. Chaiers de Medecine Vetrinaire. 49:15-23. (Vet. Bull., 51: 4150)
Odend’hal, S. and Player E.C. (1979). Histochemical localization of T cells in tissue sections. Avian Dis., 24 (4): 886-895.
Panda, D.N., Mishra, A., Misra, S.C. and Rao, A.G. (1997). Studies on efficacy of Supercox against experimental Eimeria tenella infection in broiler chicks. J. of Vet. Parasitol., 11 (1):91-93.
Patel, H.R. (1980). ‘A study on Broiler Mortality’. M.V.Sc., Thesis submitted to Konkan Krishi Vidyapeeth, Dapoli, Maharashtra.
Patil, D. M. (1996). ‘Evaluation of biological behaviour of isolated strain of Eimeria tenella from Mumbai region’. M.V.Sc., Thesis submitted to Konkan Krishi Vidyapeeth, Dapoli, Maharashtra.
Pellardy, L.P. (1965). Coccidia and Coccidiosis. Publishing House of the Hungarian Academy of Sciences.
Pohl, R. (1965). Species of coccidia from fowls. Dt. tierarzti wschri., 72: 230-232. (Cited by Chaudhari, 1993)
Potter, L. M., Blake, J.P., Blair, M.E., Bliss, B.A. and Denbow, D.M. (1986). Salinomycin toxicity in Turkeys. Poultry Sci., 65: 1955-1959.
Powell, P.C. (1987). Immune mechanism in infections of poultry. Vet. Immuno. and Immunopathol., 15: 105-114.
Prabaharan, S. and George, Y.J. (1999). Effect of Aflatoxin and Eimeria tenella infection on mortality and lesion score in broiler chicken. Indian Vet. J. 76: 693-695.
Prabaharan, S., George, T.V. and Balasubramaniam. (1999). Influence of dietary Aflatoxin and Coccidiosis on growth rate in broiler chicken. Indian Vet. J. 76: 827-828.
Pruthi, A.K., Gupta, R.K.P. and Sadana, J.R. (1987). Acid alpha naphthyl acetate esterase reacting lymphocytes in the peripheral blood of chickens challenged with Marek’s disease after vaccination with three different vaccines. Research in veterinary Sci., 43: 92-96.
Quin-Ze Rong., Kong, F. Y. and Arakawa, A. (2000). Effects of Eimeria tenella infection on the population of some caecal facultative anaerobic flora. Acta-Parasitologica-et-Medica-Entomologica-Sincia. 7 (2): 76-79.
Rahman, S.A., Adel Fatema. and Jagannath, M.S. (1989). Role of Levamisole in the induction of cell mediated immunity in experimental caecal coccidiosis of chickens. Indian Vet. J. 66 (8): 706-710.
Rahman, S.A. and Anantraman, M. (1970). The species of coccidia in fowls and pigeon. Mysore J. of Agr. Sci., 4: 157-162.
Ranki, A., Reitamo, S., Konttinen, Y.T. and Harry, P. (1980). Histochemical identification of human T lymphocytes from paraffin section. J. Histo Chem. And Cytochem., 28: 704-707.
Ray, H.N. (1945). A new coccidium Wenyonella gallinae in chickens. Current Sci., 14: 275.
Richardson, U.F. and Kendall, S.B. (1963).Veterinary Protozoology. 3rd Edn. pp: 103-104. Oliver and Boyd, Edinburgh, London.
Ripsom, C.A. and Herrick, C.A. (1945). Effect of various sulpha compounds on the protozoan parasite E. tenella. J. Parasitol., 31: 98-108.
Rose, M. E. (1971). Immunity to coccidia- protective effect of transferred serum to E. maxima infection. Parasitol., 62: 11-25.
Rose, M.E. and Hesketh, P. (1976). Immunity to coccidiosis: stages of the life cycle of Eimeria maxima which induce, and are affected by, the response of the host. Parasitol., 73: 25-37.
Rose, M.E. and Hesketh, P. (1984). Infection with E. tenella: modulation of lymphocyte blastogenesis by specific antigen and evidence for immunodepression. J. Protozool., 31: 549-553.
Rose, M.E., Lawn, A.M. and Millard, B.J. (1984). The effect of immunity on the early events in the life cycle of Eimeria tenella in the caecal mucosa of the chickens. Parasitol., 88: 199-210.
Ryley, J.F. (1980). Recent development in coccidian biology, where do we go from here? Parasitol., 80 (1): 189-209.
Sastry, G.A. (1983). Veterinary Pathology. 6th Edn., CBS Publication and Distributor., New Delhi.
Shalaby, M.A., Sanousi-EL, A.A., Yehia, M.M. and Reda, I. M. (1994). The effect of Salinomycin on the immune response of chicks. Poultry Abst., 20 (4): 989.
Sherkov, S.N., Rabie, E.L., Kokasb, L. and Bakri, M. (1976). A survey of Eimeria species and coccidiosis in chicken in Jordan. Vet. Bull., 49:763.
Shukla, S.K., Joshi, H.C. and Kumar, M. (1990). Clinico-pathological changes in experimental coccidiosis of broiler chicks. J. of Vet. Parasitol., 4 (1): 65-67.
Smith, C.K., Galloway, R.B. and White, S.L. (1981). Effect of ionophores on survival, penetration and development of E. tenella sporozoites in vitro. J. of Parasitol., 67: 511-516.
Smith, C.K. and Strout, R.G. (1979). Accumulation and retention of anticoccidial ionophores by extra cellular sporozoites. Exp. Parasitol., 48: 325-330.
Snedecor G. W. and Cochran W. C. (1994). Statistical Methods. 8th Edn. Iowa State University Press. USA.
Subramanian, R., Kumaravelu, N. and Arunachalam, K. (1995). Subclinical coccidiosis in broilers. Poultry Adviser. 28 (4): 31-34.
Swales, W.E. (1944). Chemotherapy of caecal coccidiosis (Eimeria tenella) of chickens. Canad. J. Res., 22: 131-140. (Cited by Chaudhari, 1993).
Tankhiwale, M. (1987). ‘Studies on epidemiology of coccidiosis of broilers in Bombay region with special reference to E. necatrix (Johnson, 1930).’ M.V.Sc., Thesis submitted to Konkan Krishi Vidyapeeth, Dapoli, Maharashtra.
Trees, A.J., Crozier, S.J., McKellar, S.B. and Wachira, T.M. (1985). Class specific circulating antibodies in infections with Eimeria tenella. Vet. Parasitol., 18: 349-357.
Trout, J.M. and Lillehoj, H.S. (1996). T lymphocyte role during E. acervulina and E. tenella infections. Vet. Immunol. Immunopathol., 53: 163-172.
Tyzzer, E. E. (1929). Coccidiosis in gallinaceous birds. Am. J. Hyg., 10: 269-383.
Udayakumar, M., Padmavathi, P. and Ramesh, A.J. (1995). Effect of Aflatoxin B1 and E. tenella infection on mortality and growth in broiler chicks. Indian Vet. J. 72 (11): 1141-1144.
Vervelde, L., Vermeulen, A.N. and Jeurissen, S.H.M. (1998). E. tenella sporozoites rarely enter leukocytes in the caecal epithelium of the chicken. (Gallus domesticus) Exp. Parasitol., 81: 29-38.
Voeten, A.C., Braunius, W.S., Orthel, F.W., Rijen, M.A. and Van, J. (1988). Influence of coccidiosis on growth rate and feed conversion in broilers after experimental infection with E. acervulina and E. maxima. Vet. Quarterly.10: 256-264.
Wakelin, D. and Rose, M.E. (1990). Immunity to coccidiosis. In coccidiosis of man and domestic animals. CRC press.
Williams, R.B. (1973). Effects of different infection rates on the oocyst production of Eimeria acervulina or Eimeria tenella in the chickens. Parasitol., 67: 279-288.
Witlock, D.R., Ruff, M.D. and Chute, M.B. (1981). Physiological basis of Eimeria tenella-induced mortality in individual chicken. The J. of Parasitol., 67 (1): 65-69.
Wyatt, D.R., Ruff, M.D. and Page, R.K. (1975). Interaction of Aflatoxin with Eimeria tenella infection and Monensin in young broiler chickens. Avian Dis.,19 (4): 730-740.
Yang, K., Bearman, R.N., Pargalis, G.A., Zelman, R.J. and Rappapore, H. (1982). Acid phosphates and alpha naphthyl acetate esterase in neoplastic and non-neoplastic lymphocytes.J. Clin. Pathol., 78: 141-149.
Yam, L.T., Li, C.Y. and Croshy, W.H. (1971). Cytochemical identification of monocytes and granulocytes. Am. J. Clin. Pathol., 55: 283.
Yun, C.H., Lillehoj, H.S. and Choi, K.D. (2000b). Eimeria tenella infection induces local gamma interferon production and intestinal lymphocyte subpopulation changes. Infection-and-Immunity. 68 (3): 1282-1288.
Yun, C.H., Lillehoj, H.S. and Lillehoj, E.P. (2000a). Intestinal immune response to coccidiosis. Developmental and comparative Immunol., 24: 303-324.
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Prinzvet Livestock Consult
13 de marzo de 2009
I wish to congratulate you for job well done. Is this herbal drug effective on other species of coccidiosis since the birds were exposed to E. tenella only? What is the cost benefit of using the herbal drug in relation to other drugs? Is there any drug residue in the meat?
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28 de marzo de 2009
It's a beneficial Web for related professions. Knowledge must gather as addition from here.
I'm personally interested to know how to increase feed taste that feeding hehavior in 25-30% for broiler. Plz can you Help?
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26 de febrero de 2009
Je vous felicite pour votre chef doeuvre // Je souhaite essayer ce traitement. Restant en contact // Merci.
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26 de febrero de 2009
There is no confidence of efficiency of this product. Probably somebody can that overpersuade me?
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Guybro Chemical
26 de febrero de 2009
In past also several trials have been conducted against Herbal Coccidiostats, but results were not so encouraging. This is a good break through and may add a feather on legacy of Herbal Category.
Comments from actual end user would be more heartening.
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Alpharma
26 de febrero de 2009
Can you highlight where from Salinomycin 6% sourced?
The birds were challenged only with E. tenella?
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25 de febrero de 2009
Very nice, and it is much useful not only to nutritionists, but also technicians like me.
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