P.M Poultry Diseases 4th year series By Mohamed Mahmoud Salem gab AllahAssistant lecturer of pathology Faculty of Veterinary Medicine, Benha University, Moshtohor, Tukh; 13736 , Qalyuobia, EGYPT
MYCOTIC AND MYCOTOXICOSIS
 Clinical Description  In T-2 toxicosis, caused by ingestion of Fusarium spp. of fungi, early signs of the condition may include refusal to eat as well as ulceration, crusting, and necrotic lesions in the oral mucosa caused by direct contact with the fungal toxin. In this photo, there is
ulceration of the proximal esophagus.
Clinical Description This image shows erosions in the proximal esophagus caused by exposure to T-2 toxin, a mycotoxin.
 Clinical Description  Fusarium toxicity may also produce a variety of digestive abnormalities. The gizzard (ventriculus) may be thickened and have a roughened lining. Additionally, the proventriculus and gizzard may also have ulcers, as
seen in the 2 organs in the middle and right of this photo. The gizzard on the left is normal and is shown for comparison.
 Clinical Description  On post-mortem examination, Fusarium toxins may be associated with acute and chronic digestive disease. Here, the gizzard (ventriculus) has been opened, revealing a
deep
ulcer that has extended into the underlying mucosa.
 Clinical Description  This image shows
erosions and a roughened lining of the gizzard. These findings are typical in aflatoxicosis.
 Clinical Description  In mycotoxicosis, the ingestion of fungal toxins in feed may be associated with liver abnormalities on postmortem examination. In
aflatoxicosis, the liver may be enlarged, pale, and friable, as shown here. In more chronic cases, the liver may become small, firm, and nodular and the gallbladder may become distended. Additionally, hemorrhages may also be observed.
 Clinical Description  On post-mortem examination, aflatoxicosis may produce lesions in the liver. In acute
cases, the liver may be enlarged, pale, and friable (shown here). In chronic cases, the liver may be small, firm, nodular and the gallbladder may be distended . Additionally, hemorrhages may be present on the liver.
ORGAN : LESIONS : SUSP.DIS. :
Head of chicken Ulceration of beak commeasure Fusario toxins
ORGAN : LESIONS : SUSP.DIS. :
Mouth cavity Ulceration with caseated material Fusario-toxicosis
ORGAN : LESIONS : SUSP.DIS. :
Chicken Hemorrhagic patch on thigh muscle mycotoxins
ORGAN : LESIONS : SUSP.DIS. :
Liver Heamorrhages Mycotoxins
ORGAN : LESIONS : SUSP.DIS. :
Head of chick Panophthalmitis Asperaglosis
ORGAN : LESIONS : SUSP.DIS. :
Lung Nodular formation Asperaglosis
ORGAN : LESIONS : SUSP.DIS. :
Pelvic cavity Caseaous air saculitis Asperaglosis
ORGAN : LESIONS : SUSP.DIS. :
Chest cavity Caseaous Plug in tracheal biforcation Asperaglosis
ORGAN : Brain LESIONS : Nodular formation SUSP.DIS. : Asperaglosis
ORGAN : LESIONS : SUSP.DIS. :
Opened crop Necrosis with Turkish towel apperance Candidiasis
MALNUTRETIONAL PROBLEMS
ORGAN : LESIONS : SUSP.DIS. :
Head of chicken Conjunctivitis Vitamin A def.
Vitamin A 428. In most cases, it is seen in young birds at the age of 1 - 8 weeks. Chickens from the progeny of parents with low vitamin A concentrations, have very low stores and soon after hatching, manifest a deficiency. In recently hatched chickens with vitamin A deficiency, swelling and adhesion of eyelids with a sticky exudate could be observed.
Vitamin A 429. In layer hens, dystrophic changes in the epithelia of the conjunctiva and the cornea occur, and later inflammations following secondary infection, affecting also the adjacent sinuses.
ORGAN : LESIONS : SUSP.DIS. :
Opened Esophagus Pustule like nodule Vitamin A def.
ORGAN : Chest cavity LESIONS : Rosary beaded appearance of osteo-chondrial Junction SUSP.DIS. : Vitamin D, Ca, Ph. def. or imbalance
ORGAN : LESIONS : SUSP.DIS. :
Head of chicken Rubbery beak Vitamin D, Ca, Ph. def. or imbalance
Vit E
 Clinical Description  The clinical signs of vitamin E deficiency typically develop in chicks between 15 and 30 days old. Nervous signs may include ataxia, opisthotonus, torticollis, myoclonus, paresis, and
eventually prostration, as seen here. These nervous signs are caused by
encephalomalaci a of the cerebellum and cerebrum.
 Clinical Description  This chick is exhibiting
opisthotonus, a backward flexion of the head and neck. This nervous sign, associated with vitamin E deficiency, is caused by encephalomalacia.
 Clinical Description  In the exudative
diathesis form of vitamin E deficiency, capillary walls become abnormally permeable and leak fluid and red blood cells. This fluid typically accumulates along the ventrum of the bird. Here, the thorax and abdomen have
subcutaneous edema and hemorrhage. The greenish-blue discoloration is caused by hemoglobin breakdown from the leaking red blood cells.
Clinical Description Similar edema and discoloration of the neck region, as seen here, can also occur.
Clinical Description Swelling and discoloration of the unfeathered skin of the head of this chick.
 Clinical Description  Edema and discoloration of the legs and feet caused by exudative diathesis, a manifestation of vitamin E deficiency.
 Clinical Description  This chick is exhibiting a characteristic leg posture associated with exudative diathesis. The
accumulation of subcutaneous edema along the ventrum may cause birds to stand with their legs spread apart. Affected birds may also have difficulty walking. Edema and skin discoloration is also evident.
 Clinical Description  Discoloration of the skin proximal to the hock joint, associated with exudative diathesis.
 Clinical Description  In the muscular dystrophy form of vitamin E deficiency, skeletal, smooth, and cardiac muscles can all develop lesions resulting in clinical signs. Here a young duck is unable to stand and its legs are spread laterally. These signs are the result of muscular dystrophy of the leg muscles.
 Clinical Description  If vitamin E deficiency is identified and treated in its early stages, some birds do respond to treatment. In the encephalomalacia form of the disease however, birds do not always respond to therapy. This adult chicken continues to
exhibit torticollis, a neurologic sign consisting of an abnormal twisting of the head and neck.
 Clinical Description  In the exudative diathesis form of vitamin E deficiency, post-mortem examination will reveal subcutaneous edema over the ventral areas of the body. This edema will produce a wet
glistening appearance to the surface of the underlying muscles, as seen here.
 Clinical Description  Subcutaneous edema tends to accumulate in ventrally dependent areas, such as the subcutaneous tissue located under the mandible, as shown here.
 Clinical Description  In exudative diathesis, fluid and red blood cells leak from blood vessels. In this photo,
edema and hemorrhages can be seen in the crop and over the ventral keel region.
Clinical Description
Large accumulations of subcutaneous edema can have a thick gelatinous appearance, as shown here.
 Clinical Description  In the muscular dystrophy form of vitamin E deficiency, skeletal muscles can undergo muscle fiber degeneration, resulting
in pale areas and white streaking, as observed on this pectoral muscle.
 Clinical Description  In vitamin E deficiency, all skeletal muscles are susceptible to
muscular dystrophy. Here, the wing muscles have extensive pale white areas.
Clinical Description Pale white areas in the leg muscles associated with muscular dystrophy.
Morphologic Diagnosis Pectoral muscles: Severe
locally extensive degeneration and necrosis Clinical Description White lesions in the pectoral muscles associated with muscular dystrophy. Pathologic Description The cranial aspects of both pectoral muscles (on the left of the picture) are markedly pale and contain a small foci of hemorrhage.
 Clinical Description  Pale white lesions in the pectoral muscles associated with muscular dystrophy, caused by vitamin E deficiency.
Morphologic Diagnosis Pectoral muscles: Severe multifocal to coalescing necrosis and degeneration Clinical Description
Extensive pale white areas on the pectoral muscles. Pathologic Description The pectoral muscles contain numerous variably thick, sometimes coalescing, welldemarcated pale white linear streaks.
Morphologic Diagnosis Heart: Severe multifocal to
coalescing necrosis and degeneration Clinical Description Muscular dystrophy lesions can also occur in the cardiac muscles. Here, the epicardial surface has numerous pale white areas. Pathologic Description The muscle of the heart is mottled by numerous poorlydemarcated coalescing pale white area
Morphologic Diagnosis Ventricular muscle: Moderate
multifocal degeneration and necrosis Clinical Description White lesions in the muscles of the gizzard associated with muscular dystrophy. Pathologic Description The muscles on the wall of the ventriculus contain numerous, variably-sized, welldemarcated, sometimes coalescing pale foci.
Morphologic Diagnosis Ventricular muscle: Severe locally extensive necrosis and degeneration Clinical Description White lesions in the muscles of the gizzard (ventriculus) associated with muscular dystrophy. Pathologic Description This picture shows the proventriculus and ventriculus of two birds. The organs on the left are normal. The ventricular wall on the right contains extensive areas where the muscle is pale white, slightly granular, and swollen.
Morphologic Diagnosis Proventricular and ventricular muscles: Severe diffuse necrosis and degeneration Clinical Description Extensive white lesions in the muscles of the gizzard associated with muscular dystrophy. Pathologic Description The proventriculus and ventriculus have been opened to reveal full thickness views of the muscular walls, lumina, and mucosae. The muscular walls of both organs are diffusely and markedly pale. The most normal section of muscle in this picture is located in the top left hand corner of the ventriculus, adjacent to its junction with the proventriculus. This dark red color is normal.
 Clinical Description  In vitamin E deficiency, one to two days after the onset of clinical signs, necrotic lesions may be found in the brain. These necrotic lesions may appear as green or yellow opaque lesions, as seen here.
Morphologic Diagnosis Cerebellum: Severe edema and mild hemorrhage Clinical Description On post-mortem examination, gross lesions may be observed on the brains of birds with encephalomalacia. The most common lesions are usually found on the cerebellum. The cerebellum of the affected bird on the left shows swelling, blunting of the ridges, and small petechial hemorrhages on its surface. The normal brain on the right is shown for comparison. Pathologic Description This picture shows the brains of two birds. The brain on the right is normal. The cerebellum of the bird on the left is markedly swollen, the normal ridges are obscured, and the surface of the tissue is covered by multiple variably-sized petechiae.
 Clinical Description  In this image, marked hemorrhagic lesions can be seen on the surface of the upper cerebellum. A normal brain is shown on the bottom for comparison.
 Clinical Description  In this image, marked hemorrhagic lesions are seen on the surface of the cerebellum of a chicken affected by vitamin E deficiency.
ORGAN : LESIONS :
SUSP.DIS. :
Brain Grayish white Necrotic focci with Liqification and softening of the brain tissues Vitamin E def.
ORGAN : Breast muscle LESIONS : Grayish white striation (Muscular dystrophy) SUSP.DIS. : Vitamin E def.
ORGAN : LESIONS : SUSP.DIS. :
Gizzard Muscle Grayish white patches Vitamin E def.
ORGAN : LESIONS : SUSP.DIS. :
Chick Star Gazing posture Vitamin B1 def.
ORGAN : LESIONS : SUSP.DIS. :
Chick Curled toe paralysis Vitamin B2 def.
432, 433. The hypovitaminosis
B2 (riboflavin deficiency) is characterized with impaired oxidation processes and dystrophic changes in the peripheral nerves. The typical clinical sign are curled toes due to paralysis. In the beginning, the toes are slightly flexed and chickens tend to stand on their hocks. In moderate cases, a marked leg weakness and toe flexion in a different extent are observed.
432, 433. The hypovitaminosis
B2 (riboflavin deficiency) is characterized with impaired oxidation processes and dystrophic changes in the peripheral nerves. The typical clinical sign are curled toes due to paralysis. In the beginning, the toes are slightly flexed and chickens tend to stand on their hocks. In moderate cases, a marked leg weakness and toe flexion in a different extent are observed.
ORGAN : LESIONS : SUSP.DIS. :
Small intestine Round worms Ascaridiasis
ORGAN : LESIONS : SUSP.DIS. :
Small intestine Long segmented worms Cestodiasis
ORGAN : LESIONS : SUSP.DIS. :
Small intestine Cestodiasis Cestodiasis
ORGAN : Trachea LESIONS : Y-shape worms SUSP.DIS. : Gape worm (Syngamus tracheae)
Organ : SUSP.DIS. :
Hair worm Capillariasis
Microscopical field showing yellow bi-operculated eggs SUSP.DIS. : Capillariasis
Microscopical field showing yellow bi-operculated eggs SUSP.DIS. : Capillariasis
Microscopical field showing round caecal worm SUSP.DIS. : Hetrakis infestion
ORGAN : LESIONS : SUSP.DIS. :
Chickens Depression & ruffling feather Coccidiosis Heamorrhagic dropping
ORGAN LESIONS
: :
SUSP.DIS. :
Caecum Hemorrhagic typhlitis Ceacal coccidiosis (Eimeria Tenella)
ORGAN : Caecum LESIONS : Hemorrhagic typhlitis SUSP.DIS. : Ceacal coccidiosis (E. Tenella)
Microscopical field showing Eimeria oocyst SUSP.DIS. : Coccidiosis
ORGAN : LESIONS : SUSP.DIS. :
Small intestine Distention and mottled hemorrhage Eimeria Necatrix
ORGAN : LESIONS : SUSP.DIS. :
Small intestine Orange brown content Eimeria Maxima
ORGAN : LESIONS : SUSP.DIS. :
Small intestine of turkey Distended with pale fluid content E. Meleagrimitis
ORGAN : LESIONS : SUSP.DIS. :
Liver and Caecum Distended Caeca with cores and button shape like ulcer in liver Histomonasis
ORGAN : LESIONS : SUSP.DIS. :
Leg of bird Raised scales Scally leg mite
ORGAN : Feathers of birds LESIONS : Heavy infestation with lice eggs SUSP.DIS. : Lice infestation
Red Mite
Buccal cavity showing heavy infestation of red mite