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TURKEY INTESTINAL
COCCIDIOSIS
Etiology- Eimeria meleagridis, E. meleagrimitis,
E.adenoeide
Economic importance/Distribution
 Occurs world-wide
 Major cause of mortality and suboptimal growth
and feed conversion efficiency
 The cost of anticoccidial feed additives and
treatment is estimated to exceed $40 million
annually in all poultry producing areas of the world.
Mode of Transmission
The sporulated oocyst is the infective stage of
the life-cycle. Infected, recovered chickens shed
oocysts representing a problem in multi-age
operations. Oocysts can be transmitted
mechanically on the clothing and footwear of
personnel, contaminated equipment, or in some
cases, by wind spreading poultry-house dust and
litter over short distances.
TURKEY INTESTINAL
COCCIDIOSIS
Clinical Signs
Severity of the disease depends on the
number of oocysts ingested. Little pathogenicity is
attributed to E.meleagridis, whereas E.
Meleagrimitis and E. Adenoeides may be quite
harmful. Generally the disease is most often seen
in young birds.
 Infected birds stop eating
 Huddle together
 Pass fluid droppings which may be
brown or blood tinged.
TURKEY INTESTINAL
COCCIDIOSIS
Lesions
 E. Meleagrimitis- lesions appear about 4 days after
infection
 jejunum becomes thickened and contains colorless
fluid and mucus, small amounts of blood, and other
cellular material.
 On the 5th or 6th day the duodenum becomes
involved, the blood vessels are engorged, and a
necrotic core may develop. The small intestine
becomes congested and has petechial
haemorrhages throughout.
TURKEY INTESTINAL
COCCIDIOSIS
Lesions
TURKEY INTESTINAL
COCCIDIOSIS
Lesions
 In E. Adenoeides a severe enteritis with petechiae
may occur about the 4th day postinfection. Feces
may be fluid and blood-tinged, and contain mucous
casts; occasionally caseous plugs are found in the
ceca.
 Other species such as E. gallopavonis parasitizes a
similar region but primarily infects the rectum, with
limited involvement of the caecum.
TURKEY INTESTINAL
COCCIDIOSIS
Diagnosis
 Clinical signs
 Response to treatment
 Postmortem exam
Differential Diagnosis
 Salmonella
 Blackhead (caecum)
 Necrotic enteritis (Clostridium perfringes)
 Hemorrhagic enteritis
TURKEY INTESTINAL
COCCIDIOSIS
Treatment (if possible)
 Sulphonamides
 Amprolium.
Control/Prevention
 Good management and sanitation
 Coccidiostatic medication in feed or water
 Young birds should be raised apart from older birds.
 If deep litter is used, it should be mixed well, and kept
dry.
 Feeders and waterers should be thoroughly cleaned
weekly and kept on wire platforms to prevent fecal
contamination.
TURKEY INTESTINAL
COCCIDIOSIS
Etiology
 Eimeria necatrix
 E. acervulina
 E. maxima
 E. mitts
 E. praecox
 E. hagani
 E. mivati
 E. brunette
E. Necatrix is usually
located in the anterior or
midportion of the gut.
E.brunetti is found in the
lower small intestine,
rectum, cecum, or cloaca.
E. acervulina, E. mivati, E.
hagani, E. mitis, and E.
praecox are all found in the
upper half of the small
intestine.
Eimeria maxima, oocyst Eimeria brunetti, oocysts
Economic importance/Distribution
 Worldwide
 Even low levels of infection causes ill thrift and loss of
production.
Mode of Transmission
 Ingestion of contaminated food or water.
Clinical Signs
 Decreased feed intake
 Increased water consumption
 weight loss
 fall in egg production
Lesions (Gross/Histopathology)
 Catarrhal enteritis
 Thickened intestinal wall
 The intestinal lumen maybe filled with clotted or
unclotted blood
 Petechial haemorrhages
 Intestinal epithelium may slough and be replaced by
connective tissue that interferes with intestinal
absorption.
 Circumcumscribed white spots may be seen
through the mucosa
 On microscopic examination, these are seen to
contain developing coccidial forms
Gross lesions of E necatrix with frank hemorrhaging into the midgu
Gross lesions of E acervulina with white longitudinal plaques in
the duodenal loop of a broiler chicken.
Gross lesions of E brunetti in small intestine of a broiler chic
Diagnosis
 Demonstration of coccidial forms from characteristic
lesions in specific locations in the intestine.
Differential Diagnosis
 Blackhead (caecum)
 Salmonella (caecum)
 Necrotic enteritis (Clostridium perfringens) (small
intestine/ileum)
 Capillarisis (small intestine)
 Salt poisoning (small intestine)
 Mycotoxicoses (small intestine)
 Cannibalism (blood in feces)
Treatment (if possible)
 Sulfonamide
 Amprolium
 Pyrimidine
Control/Prevention
 Similar to the procedures suggested for E.
Tenella
 Vaccination
 Continuous use of anticoccidials in feed and
water.
 sulfonamides, nitrofurazones, nicarbazin,
pyrimidine derivatives, and others.
Synonyms/Abbreviations- Intestinal coccidiosis
Etiology
 Eimeria tenella
Economic importance/Distribution
 Worldwide
 Even low levels of infection causes ill thrift and loss
of production.
Mode of Transmission
 Ingestion of sporulated oocysts with food or water
Clinical Signs
 Frequently seen in younger birds of 4-6 weeks
old.
 Frequently an acute disease with diarrhea and
massive cecal hemorrhage.
 Blood is seen in the droppings 4 days after the
initial infection.
 The birds become listless, eat little, and are notably
thirsty.
 If the bird remains alive until the 8th or 9th day
Lesions (Gross/Histopathology)
 Extensive epithelial sloughing of the ceca
 Cecum filled with partially clotted blood that
ultimately consolidate s to form cecal cores.
 The wall of the cecum becomes markedly
thickened and enlarged
Gross lesions of E tenella with frank hemorrhaging into cecal
pouches in a broiler chicken.
Diagnosis
 Demontration of oocysts from feces or mucosal
scrapings at necropsy .
 Clinical signs
Differential Diagnosis
 Blackhead (caecum)
 Salmonella (caecum)
 Cannibalism (blood in feces)
Treatment (if possible)
 Sulfonamide
 Amprolium
Control/Prevention
 Good management and sanitation
 Coccidiostatic medication in feed or water
 Young birds should be raised apart from older
birds
 Feeders and waterers should be thoroughly
cleaned weekly and kept on wire platforms
 Coccidiosis vaccine
Synonyms/Abbreviations- Infectious catarrhal
enteritis
Etiology- Hexamita meleagridis
Economic importance/Distribution
 Problem in every commercial turkey-producing
area
 Major problem in localized areas during a particular
year
Mode of Transmission
 Ingestion of freshly contaminated food or water.
Clinical Signs
 Adult birds are frequently asymptomatic carriers
 Disease of turkey poults less than 10 weeks
old.
 Nervous
 Stilted gait
 Ruffled feathers
 Lose weight rapidly, become weak and listless, and
die.
Lesions (Gross/Histopathology)
 Severe catarrhal inflammation of the intestine
 Intestinal contents are thin and watery; a white
foamy diarrhea is often present
Diagnosis
 Demonstration of the organism in fresh scrapings
from the mucosa of the small intestine, particularly
the duodenum and jejunum.
 Clinical signs
Differential Diagnosis
Treatment (if possible)
 No effective treatment
Control/Prevention
 Good management
 Strict sanitation
 Poults should be separated from adults
 Feeders and waterers should be on wire
platforms to prevent contamination.
Synonyms/Abbreviations-
 Blackhead
 Infectious enterohepatitis
Etiology- Histomonas meleagridis
Mode of Transmission
 Ingestion of infected egg of H. gallinarum.
 Ingestion of large numbers of infective trophozoites in
very fresh droppings.
Clinical Signs
 Turkeys of any age may be affected
 Most often seen in birds 3-12 weeks old
 The first signs of disease are weakness
and drowsiness; birds stand with heads
lowered, droopy wings, and closed eyes. They
do not eat and lose weight, and the droppings
may be sulfur-colored .
Lesions (Gross/Histopathology)
 Concave liver lesions are pathognomic
 saucer-shaped, depressed, yellow-green areas of
necrosis and degeneration.
 Cecal lesions are first seen as pin point ulcers that
enlarge and appear as yellow patches on the serosal
surface.
 The lumen of the cecum may contain a hard caseous
core to which the cecal epithelium adheres .
Diagnosis
 Gross post-mortem lesions
 Stained sections from the periphery of liver lesions
 Identification of living organisms in wet preparations
from caecal lesions
Differential Diagnosis
 Pseudoblackhead
Treatment (if possible)
 No drugs are currently approved for use as
treatments
Control/Prevention
 Good management.
 The cardinal rule is to keep chickens completely
separate from turkeys.
 Turkeys should be placed in clean runs that have
not been used for at least 10 months and preferably
for 2 years.
 Turkeys must not be placed on ground that
has been fertilized with chicken or turkey
manure.
 Continuous feeding of a ration containing
enheptin or hepzide has proved satisfactory in
prevention of the disease.
 Feeders and waterers should be kept off the
ground and on wire platforms .
Synonyms/Abbreviations- Intestinal roundworm
Etiology
 Ascaridia galli
 A. columbae
 A. dissimilis
Economic importance/Distribution
 heavy economic losses in form of retarded growth,
reduce weight gain, decreased egg production,
diarrhea, morbidity and high mortality rate
Mode of Transmission
 Ingestion of egg containing infective 2nd-stage larva
Clinical Signs
 Birds are unthrifty
 Weak
 Emaciated
 Egg production drops
 Diarrhea may be accompanied by anemia
 Intestinal obstruction in very heavy infections
Lesions (Gross/Histopathology)
 Ascarids may migrate up the oviduct (via the
cloaca) to become enshelled later within the egg.
 A dissimilis (turkey roundworm) may also migrate
out of the intestine, through the portal system, and
into the liver, causing hepatic granulomas.
Diagnosis
 Demonstration of eggs in feces or worms in the
intestine on necropsy.
Ascaridia egg Ascaridia galli
Ascaridia galli
Treatment (if possible)
 Piperazine citrate
 Tetramisole
Control/Prevention
 Good management
 Young birds should be separated from old
 Yards and pens should be rotated and well
drained
 Deep litter in pens must be kept dry.
 Droppings should be removed frequently.
Etiology- C. obsignata
Mode of Transmission
 Ingestion of capillaria egg
Clinical Signs
 Birds lose weight steadily
 May become severely emaciated
 Frequently die
Lesions (Gross/Histopathology)
 Severe catarrhal enteritis
 Scattered hemorrhages
Diagnosis
 Demonstration of worms on necropsy
 Identification of eggs in feces
Treatment (if possible)
 Haloxon
 Tetramisole
Control/Prevention
 Removal and destruction of contaminated beddings
Synonyms/Abbreviations- Cecal worm
Etiology- Heterakis gallinarum
Mode of Transmission
 Ingestion of an infective Heterakis egg or an
earthworm
Clinical Signs
 In domestic fowl the adult worm is not generally
considered a pathogen.
 Effects of the worm are slight
Lesions (Gross/Histopathology)
 Only in heavy infections may there be
thickening of the cecal mucosa.
 In some species of wild birds, a nodular typhlitis
may occur
Diagnosis
 Demonstration of eggs from feces
 Identification of adult worms on necropsy
Differential Diagnosis
 Ascaridiasis
Treatment (if possible)
 Phenothiazine
 Tetramisole
Control/Prevention
 If birds are penned, routine removal of feces and
litter is important.
 In game farms, rotation of lots and pens should be
practiced.
Synonyms/Abbreviations- Minute tapeworm
Etiology
 Davainea proglottina
Mode of Transmission
 Ingestion of slugs (Limax, Arion, or Agriolimax)
containing the cysticercoids.
Clinical Signs
 Marked emaciation
 General debility
 Loss of weight.
Lesions (Gross/Histopathology)
 Intestinal mucosa appears thickened and may be
hemorrhagic because hold-fast organs are heavily
armed
Diagnosis
 Demonstration of the cestodes on necropsy by
examining mucosal scrapings or by opening the
duodenum under water and observing the activity of
the papillaelike, minute tapeworms.
Treatment (if possible)
 Di-n-butyl tin dilaurate
 Albendazole
 Febantel
 Fenbendazole
 Mebendazole
 Oxfendazole
Control/Prevention
 Soil may be treated with metaldehyde to destroy
slugs.
 Pens and range should be well drained.
 A sandy soil is preferable.
Synonyms/Abbreviations- Thread tapeworm
Etiology
 Hymenolepis spp.
Mode of Transmission
 Ingestion of the infective cysticercoids in suitable
intermediate host.
Clinical Signs
 Growth retardation
Diagnosis
 Necropsy. If the fresh intestine is opened in a small
amount of warm water, the worms may be seen
actively moving in the water above the mucosal
surface.
 Intestinal scrapings should be examined under the
binocular dissecting microscope.
Treatment (if possible)
 Butynorate
Control/Prevention
 Proper disposal of droppings.
 Houses should be cleaned regularly and the
manure spread thinly on arable land where sunlight
and desiccation will soon destroy the parasitic
forms.
 Numbers of intermediate hosts maybe reduced by
using insecticides, molluscicides, and other
appropriate control measures.
Synonyms/Abbreviations- Broad-headed tapeworm
Etiology
 Raillietina cesticellus
 R. Tetragona
 R. Echinobothridia
Mode of Transmission
 Ingestion of the intermediate host containing the cysticercoid
Clinical Signs
 Emaciation
 Stunted growth
 In laying birds, egg production may be decreased or may stop
altogether.
Lesions (Gross/Histopathology)
 Conspicuous intestinal nodules in chicken, with
characteristic hyperplastic enteritis associated with the
formation of granuloma.
 Intestinal nodules often result in degeneration and
necrosis of intestina villi, accompanied by anaemia
Diagnosis
 Presence of large numbers of segments or eggs in
the feces
 Demonstration of worms on necropsy
Treatment (if possible)
 Di-n-butyltindilaurate (Butynorate ) or Yomesan in
the food
Control/Prevention
 Control of intermediate hosts with insecticides
 Removal and disposal of droppings
Etiology- Echinostoma revolutum
Mode of Transmission
 Ingestion of an infected 2nd
intermediate host
Clinical Signs
 In light infections these flukes cause little injury.
 If large numbers are present, it is claimed they
may cause severe enteritis, hemorrhagic
diarrhea, and progressive emaciation.
Lesions (Gross/Histopathology)
 Mild hyperaemia
 Severe catarrhal enteritis.
Diagnosis
 Identification of eggs in the feces or adult worms in
the intestine on necropsy examination.
Treatment (if possible)
 Albendazole
 Praxiquanntel
Control/Prevention
 Avoid wet marsh areas
 Snail control should be considered
REFERENCE:
 Alcorn M.J. et al., 2008. Poultry Diseases. 7th Edition. W.B. Saunders
Publishing Inc, New York, USA. Pp. 445-449
 Griffiths H.J. 1978. A Handbook of Veterinary Parasitology. University of
Minnesota Press, United States of America
 Puttalakshmamma G.C., et al. 2008. Prevalence of Gastrointestinal
parasites of Poultry in and around Banglore. Available at
http://www.veterinaryworld.org/2008/July/Prevalence%20of%20Gastroin
testinal%20parasites%20of%20Poultry%20in%20and%20a.pdf
[Accessed last 29th January 2015]
 THE MERCK MANUAL, PET HEALTH EDITION (2011). Overview of
Coccidiosis in Poultry. Available from
http://www.merckmanuals.com/vet/poultry/coccidiosis/overview_of_cocc
idiosis_in_poultry.html [Accessed 29th January 2015]
 http://www.nadis.org.uk/bulletins/diseases-of-farmyard-poultry/part-3-
control-of-coccidiosis.aspx

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Intestinal Parasites of Poultry

  • 1.
  • 2.
  • 3. TURKEY INTESTINAL COCCIDIOSIS Etiology- Eimeria meleagridis, E. meleagrimitis, E.adenoeide Economic importance/Distribution  Occurs world-wide  Major cause of mortality and suboptimal growth and feed conversion efficiency  The cost of anticoccidial feed additives and treatment is estimated to exceed $40 million annually in all poultry producing areas of the world.
  • 4. Mode of Transmission The sporulated oocyst is the infective stage of the life-cycle. Infected, recovered chickens shed oocysts representing a problem in multi-age operations. Oocysts can be transmitted mechanically on the clothing and footwear of personnel, contaminated equipment, or in some cases, by wind spreading poultry-house dust and litter over short distances. TURKEY INTESTINAL COCCIDIOSIS
  • 5. Clinical Signs Severity of the disease depends on the number of oocysts ingested. Little pathogenicity is attributed to E.meleagridis, whereas E. Meleagrimitis and E. Adenoeides may be quite harmful. Generally the disease is most often seen in young birds.  Infected birds stop eating  Huddle together  Pass fluid droppings which may be brown or blood tinged. TURKEY INTESTINAL COCCIDIOSIS
  • 6. Lesions  E. Meleagrimitis- lesions appear about 4 days after infection  jejunum becomes thickened and contains colorless fluid and mucus, small amounts of blood, and other cellular material.  On the 5th or 6th day the duodenum becomes involved, the blood vessels are engorged, and a necrotic core may develop. The small intestine becomes congested and has petechial haemorrhages throughout. TURKEY INTESTINAL COCCIDIOSIS
  • 8. Lesions  In E. Adenoeides a severe enteritis with petechiae may occur about the 4th day postinfection. Feces may be fluid and blood-tinged, and contain mucous casts; occasionally caseous plugs are found in the ceca.  Other species such as E. gallopavonis parasitizes a similar region but primarily infects the rectum, with limited involvement of the caecum. TURKEY INTESTINAL COCCIDIOSIS
  • 9. Diagnosis  Clinical signs  Response to treatment  Postmortem exam Differential Diagnosis  Salmonella  Blackhead (caecum)  Necrotic enteritis (Clostridium perfringes)  Hemorrhagic enteritis TURKEY INTESTINAL COCCIDIOSIS
  • 10. Treatment (if possible)  Sulphonamides  Amprolium. Control/Prevention  Good management and sanitation  Coccidiostatic medication in feed or water  Young birds should be raised apart from older birds.  If deep litter is used, it should be mixed well, and kept dry.  Feeders and waterers should be thoroughly cleaned weekly and kept on wire platforms to prevent fecal contamination. TURKEY INTESTINAL COCCIDIOSIS
  • 11. Etiology  Eimeria necatrix  E. acervulina  E. maxima  E. mitts  E. praecox  E. hagani  E. mivati  E. brunette E. Necatrix is usually located in the anterior or midportion of the gut. E.brunetti is found in the lower small intestine, rectum, cecum, or cloaca. E. acervulina, E. mivati, E. hagani, E. mitis, and E. praecox are all found in the upper half of the small intestine.
  • 12. Eimeria maxima, oocyst Eimeria brunetti, oocysts
  • 13. Economic importance/Distribution  Worldwide  Even low levels of infection causes ill thrift and loss of production. Mode of Transmission  Ingestion of contaminated food or water. Clinical Signs  Decreased feed intake  Increased water consumption  weight loss  fall in egg production
  • 14. Lesions (Gross/Histopathology)  Catarrhal enteritis  Thickened intestinal wall  The intestinal lumen maybe filled with clotted or unclotted blood  Petechial haemorrhages  Intestinal epithelium may slough and be replaced by connective tissue that interferes with intestinal absorption.  Circumcumscribed white spots may be seen through the mucosa  On microscopic examination, these are seen to contain developing coccidial forms
  • 15. Gross lesions of E necatrix with frank hemorrhaging into the midgu
  • 16. Gross lesions of E acervulina with white longitudinal plaques in the duodenal loop of a broiler chicken.
  • 17. Gross lesions of E brunetti in small intestine of a broiler chic
  • 18. Diagnosis  Demonstration of coccidial forms from characteristic lesions in specific locations in the intestine. Differential Diagnosis  Blackhead (caecum)  Salmonella (caecum)  Necrotic enteritis (Clostridium perfringens) (small intestine/ileum)  Capillarisis (small intestine)  Salt poisoning (small intestine)  Mycotoxicoses (small intestine)  Cannibalism (blood in feces)
  • 19. Treatment (if possible)  Sulfonamide  Amprolium  Pyrimidine Control/Prevention  Similar to the procedures suggested for E. Tenella  Vaccination  Continuous use of anticoccidials in feed and water.  sulfonamides, nitrofurazones, nicarbazin, pyrimidine derivatives, and others.
  • 20. Synonyms/Abbreviations- Intestinal coccidiosis Etiology  Eimeria tenella Economic importance/Distribution  Worldwide  Even low levels of infection causes ill thrift and loss of production.
  • 21. Mode of Transmission  Ingestion of sporulated oocysts with food or water Clinical Signs  Frequently seen in younger birds of 4-6 weeks old.  Frequently an acute disease with diarrhea and massive cecal hemorrhage.  Blood is seen in the droppings 4 days after the initial infection.  The birds become listless, eat little, and are notably thirsty.  If the bird remains alive until the 8th or 9th day
  • 22. Lesions (Gross/Histopathology)  Extensive epithelial sloughing of the ceca  Cecum filled with partially clotted blood that ultimately consolidate s to form cecal cores.  The wall of the cecum becomes markedly thickened and enlarged
  • 23. Gross lesions of E tenella with frank hemorrhaging into cecal pouches in a broiler chicken.
  • 24. Diagnosis  Demontration of oocysts from feces or mucosal scrapings at necropsy .  Clinical signs Differential Diagnosis  Blackhead (caecum)  Salmonella (caecum)  Cannibalism (blood in feces)
  • 25. Treatment (if possible)  Sulfonamide  Amprolium Control/Prevention  Good management and sanitation  Coccidiostatic medication in feed or water  Young birds should be raised apart from older birds  Feeders and waterers should be thoroughly cleaned weekly and kept on wire platforms  Coccidiosis vaccine
  • 26. Synonyms/Abbreviations- Infectious catarrhal enteritis Etiology- Hexamita meleagridis Economic importance/Distribution  Problem in every commercial turkey-producing area  Major problem in localized areas during a particular year
  • 27. Mode of Transmission  Ingestion of freshly contaminated food or water. Clinical Signs  Adult birds are frequently asymptomatic carriers  Disease of turkey poults less than 10 weeks old.  Nervous  Stilted gait  Ruffled feathers  Lose weight rapidly, become weak and listless, and die.
  • 28. Lesions (Gross/Histopathology)  Severe catarrhal inflammation of the intestine  Intestinal contents are thin and watery; a white foamy diarrhea is often present
  • 29. Diagnosis  Demonstration of the organism in fresh scrapings from the mucosa of the small intestine, particularly the duodenum and jejunum.  Clinical signs
  • 30. Differential Diagnosis Treatment (if possible)  No effective treatment Control/Prevention  Good management  Strict sanitation  Poults should be separated from adults  Feeders and waterers should be on wire platforms to prevent contamination.
  • 31. Synonyms/Abbreviations-  Blackhead  Infectious enterohepatitis Etiology- Histomonas meleagridis
  • 32. Mode of Transmission  Ingestion of infected egg of H. gallinarum.  Ingestion of large numbers of infective trophozoites in very fresh droppings. Clinical Signs  Turkeys of any age may be affected  Most often seen in birds 3-12 weeks old  The first signs of disease are weakness and drowsiness; birds stand with heads lowered, droopy wings, and closed eyes. They do not eat and lose weight, and the droppings may be sulfur-colored .
  • 33. Lesions (Gross/Histopathology)  Concave liver lesions are pathognomic  saucer-shaped, depressed, yellow-green areas of necrosis and degeneration.  Cecal lesions are first seen as pin point ulcers that enlarge and appear as yellow patches on the serosal surface.  The lumen of the cecum may contain a hard caseous core to which the cecal epithelium adheres .
  • 34.
  • 35. Diagnosis  Gross post-mortem lesions  Stained sections from the periphery of liver lesions  Identification of living organisms in wet preparations from caecal lesions Differential Diagnosis  Pseudoblackhead Treatment (if possible)  No drugs are currently approved for use as treatments
  • 36. Control/Prevention  Good management.  The cardinal rule is to keep chickens completely separate from turkeys.  Turkeys should be placed in clean runs that have not been used for at least 10 months and preferably for 2 years.  Turkeys must not be placed on ground that has been fertilized with chicken or turkey manure.  Continuous feeding of a ration containing enheptin or hepzide has proved satisfactory in prevention of the disease.  Feeders and waterers should be kept off the ground and on wire platforms .
  • 37.
  • 38. Synonyms/Abbreviations- Intestinal roundworm Etiology  Ascaridia galli  A. columbae  A. dissimilis Economic importance/Distribution  heavy economic losses in form of retarded growth, reduce weight gain, decreased egg production, diarrhea, morbidity and high mortality rate
  • 39. Mode of Transmission  Ingestion of egg containing infective 2nd-stage larva Clinical Signs  Birds are unthrifty  Weak  Emaciated  Egg production drops  Diarrhea may be accompanied by anemia  Intestinal obstruction in very heavy infections
  • 40. Lesions (Gross/Histopathology)  Ascarids may migrate up the oviduct (via the cloaca) to become enshelled later within the egg.  A dissimilis (turkey roundworm) may also migrate out of the intestine, through the portal system, and into the liver, causing hepatic granulomas. Diagnosis  Demonstration of eggs in feces or worms in the intestine on necropsy.
  • 43. Treatment (if possible)  Piperazine citrate  Tetramisole Control/Prevention  Good management  Young birds should be separated from old  Yards and pens should be rotated and well drained  Deep litter in pens must be kept dry.  Droppings should be removed frequently.
  • 44. Etiology- C. obsignata Mode of Transmission  Ingestion of capillaria egg
  • 45. Clinical Signs  Birds lose weight steadily  May become severely emaciated  Frequently die Lesions (Gross/Histopathology)  Severe catarrhal enteritis  Scattered hemorrhages
  • 46. Diagnosis  Demonstration of worms on necropsy  Identification of eggs in feces
  • 47. Treatment (if possible)  Haloxon  Tetramisole Control/Prevention  Removal and destruction of contaminated beddings
  • 48. Synonyms/Abbreviations- Cecal worm Etiology- Heterakis gallinarum Mode of Transmission  Ingestion of an infective Heterakis egg or an earthworm
  • 49. Clinical Signs  In domestic fowl the adult worm is not generally considered a pathogen.  Effects of the worm are slight Lesions (Gross/Histopathology)  Only in heavy infections may there be thickening of the cecal mucosa.  In some species of wild birds, a nodular typhlitis may occur
  • 50. Diagnosis  Demonstration of eggs from feces  Identification of adult worms on necropsy Differential Diagnosis  Ascaridiasis
  • 51. Treatment (if possible)  Phenothiazine  Tetramisole Control/Prevention  If birds are penned, routine removal of feces and litter is important.  In game farms, rotation of lots and pens should be practiced.
  • 52.
  • 53.
  • 54. Synonyms/Abbreviations- Minute tapeworm Etiology  Davainea proglottina Mode of Transmission  Ingestion of slugs (Limax, Arion, or Agriolimax) containing the cysticercoids.
  • 55. Clinical Signs  Marked emaciation  General debility  Loss of weight. Lesions (Gross/Histopathology)  Intestinal mucosa appears thickened and may be hemorrhagic because hold-fast organs are heavily armed Diagnosis  Demonstration of the cestodes on necropsy by examining mucosal scrapings or by opening the duodenum under water and observing the activity of the papillaelike, minute tapeworms.
  • 56. Treatment (if possible)  Di-n-butyl tin dilaurate  Albendazole  Febantel  Fenbendazole  Mebendazole  Oxfendazole Control/Prevention  Soil may be treated with metaldehyde to destroy slugs.  Pens and range should be well drained.  A sandy soil is preferable.
  • 57. Synonyms/Abbreviations- Thread tapeworm Etiology  Hymenolepis spp. Mode of Transmission  Ingestion of the infective cysticercoids in suitable intermediate host.
  • 58.
  • 59. Clinical Signs  Growth retardation Diagnosis  Necropsy. If the fresh intestine is opened in a small amount of warm water, the worms may be seen actively moving in the water above the mucosal surface.  Intestinal scrapings should be examined under the binocular dissecting microscope.
  • 60. Treatment (if possible)  Butynorate Control/Prevention  Proper disposal of droppings.  Houses should be cleaned regularly and the manure spread thinly on arable land where sunlight and desiccation will soon destroy the parasitic forms.  Numbers of intermediate hosts maybe reduced by using insecticides, molluscicides, and other appropriate control measures.
  • 61. Synonyms/Abbreviations- Broad-headed tapeworm Etiology  Raillietina cesticellus  R. Tetragona  R. Echinobothridia
  • 62. Mode of Transmission  Ingestion of the intermediate host containing the cysticercoid Clinical Signs  Emaciation  Stunted growth  In laying birds, egg production may be decreased or may stop altogether. Lesions (Gross/Histopathology)  Conspicuous intestinal nodules in chicken, with characteristic hyperplastic enteritis associated with the formation of granuloma.  Intestinal nodules often result in degeneration and necrosis of intestina villi, accompanied by anaemia
  • 63. Diagnosis  Presence of large numbers of segments or eggs in the feces  Demonstration of worms on necropsy Treatment (if possible)  Di-n-butyltindilaurate (Butynorate ) or Yomesan in the food Control/Prevention  Control of intermediate hosts with insecticides  Removal and disposal of droppings
  • 64.
  • 65. Etiology- Echinostoma revolutum Mode of Transmission  Ingestion of an infected 2nd intermediate host Clinical Signs  In light infections these flukes cause little injury.  If large numbers are present, it is claimed they may cause severe enteritis, hemorrhagic diarrhea, and progressive emaciation.
  • 66. Lesions (Gross/Histopathology)  Mild hyperaemia  Severe catarrhal enteritis. Diagnosis  Identification of eggs in the feces or adult worms in the intestine on necropsy examination.
  • 67. Treatment (if possible)  Albendazole  Praxiquanntel Control/Prevention  Avoid wet marsh areas  Snail control should be considered
  • 68. REFERENCE:  Alcorn M.J. et al., 2008. Poultry Diseases. 7th Edition. W.B. Saunders Publishing Inc, New York, USA. Pp. 445-449  Griffiths H.J. 1978. A Handbook of Veterinary Parasitology. University of Minnesota Press, United States of America  Puttalakshmamma G.C., et al. 2008. Prevalence of Gastrointestinal parasites of Poultry in and around Banglore. Available at http://www.veterinaryworld.org/2008/July/Prevalence%20of%20Gastroin testinal%20parasites%20of%20Poultry%20in%20and%20a.pdf [Accessed last 29th January 2015]  THE MERCK MANUAL, PET HEALTH EDITION (2011). Overview of Coccidiosis in Poultry. Available from http://www.merckmanuals.com/vet/poultry/coccidiosis/overview_of_cocc idiosis_in_poultry.html [Accessed 29th January 2015]  http://www.nadis.org.uk/bulletins/diseases-of-farmyard-poultry/part-3- control-of-coccidiosis.aspx