Selected Cases of Alimentary System Diseases PDF
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Dr. Adnan Fayyad
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This document discusses various alimentary system diseases and conditions in animals, including congenital anomalies, stomatitis, oral neoplasia, enterotoxemias, and liver diseases. It covers common conditions like salmonellosis, hepatic lipidosis, and congestive hepatopathy. The document explains clinical signs, gross findings, and microscopic features of different diseases highlighting potential causes and consequences for the animals affected.
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Selected Cases of Alimentary system Diseases Dr. Adnan Fayyad DIGESTIVE PATHOLOGY Systemic changes Broken Mouth Cleft palate Hereditary – Charolais, Hereford cattle – Hampshire pigs – Boxer dogs – Siamese...
Selected Cases of Alimentary system Diseases Dr. Adnan Fayyad DIGESTIVE PATHOLOGY Systemic changes Broken Mouth Cleft palate Hereditary – Charolais, Hereford cattle – Hampshire pigs – Boxer dogs – Siamese, Abyssinian cats Teratogenic toxins – Veratrum californicum – lambs – Crotalaria, poison hemlock, - pigs – Griseofulvin – cats and horses Cleft palate CONGENITAL ANOMALIES Jaws – Agnathia Absence of jaws – Brachygnathia Shortened jaw – Prognathia Elongated jaws Brachygnathia inferior (aka mandibular brachygnathism) Prognathia inferior (aka mandibular prognathism) Stomatitides Lips? Pharynx? Tongue? Gums? Tonsils? Palate? Cheilitis On the bottom is ORF contagious ecthyma PPR foot-and-mouth disease FMD Malignant Catarrhal Fever FMD contagious ecthyma Johne’s disease BVD Salmonella Wooden tongue Lumpy jaw Oral papillomas Oral neoplasia What are the cell types that can become neoplastic? Oral Neoplasia SCC – dogs and cats, but differing locations Melanoma – dogs Fibrosarcoma Osteosarcoma Squamous Cell Carcinoma Melanoma Fibrosarcoma Kidney Salmonellosis ◼ Salmonella, a rod-shaped gram-negative bacterium ◼ Enterobacteriaceae ◼ Clinical disease is characterized by two major syndromes: - a systemic septicemia (also termed as typhoid) - an enteritis ◼ Pathogenesis: ◼ Following ingestion, bacteria attach to and quickly invade M cells in the Peyer’s patches, epithelial cells of the distal small intestine, cecum, upper colon, and tonsillar epithelium ◼ Bacteria are phagocytized by macrophages of the lamina propria or Peyer’s patches and transported to mesenteric lymph nodes ◼ Bacteria are able to survive and replicate in macrophages; resulting bacteremia can disseminate organism to other sites including liver and gall bladder, lung, joints, meninges, or placenta and fetus ◼ Adherence of organisms causes microvillar degeneration allowing bacteria to invade through the brush border and intercellular junctional complexes ◼ Diarrhea is due to: malabsorption due to reduced mucosal surface area from apoptosis and necrosis of enterocytes and inflammatory exudation, and electrolyte secretion ◼ Typical Gross Findings: ◼ Enlargement, congestion, and random necrosis of the liver, spleen, lymphoid tissues and intestines (Peyer’s patches) leading to lymphoid depletion ◼ Massive splenomegaly ◼ Focal suppurative lesions in lymphoid tissues of intestinal tract ◼ Purulent metritis in pregnant animals ◼ Typical Light Microscopic Findings: ◼ Multifocal granulomatous and necrotizing hepatitis, splenitis, and lymphadenitis ◼ Paratyphoid nodules vary from foci containing few necrotic hepatocytes surrounded by low numbers of mononuclear cells and neutrophils to foci of pure necrosis to foci of mostly macrophages Invasion of the ileum of a calf by Salmonella typhimurium Equine cecum ulcers Equine Large Colon - multi-focal ulceration Enterotoxemias ◼ Enterotoxemia caused by Clostridium perfringens type A ◼ normal intestinal microflora ◼ Gram positive, sporulating, anaerobic bacillus that has a worldwide distribution and causes disease in neonatal lambs, calves, foals, and piglets (often suckling piglets during the first week of life) and in adult sheep, cattle, goats and humans C. perfringens enterotoxin (CPE) is associated with food- borne illness and is most commonly linked to type A; it is activated by proteolysis and alters plasma membrane ◼Type B enterotoxemia - in lambs …….. lamb dysentery ◼ type C enterotoxemia - in mature sheep ……. "struck", - in calves, lambs and piglets ……… hemorrhagic enterotoxemia ◼ type D enterotoxemia in sheep and goats is pulpy-kidney disease or overeating disease. ◼ Typical Gross Findings: ◼ Acute hemorrhagic necrotizing enteritis, particularly of the jejunum and ileum with mucosal ulceration surrounded by zone of hyperemia, and free intraluminal blood ◼ Etiology: Clostridium perfringens type D epsilon toxin Disease: Clostridial enterotoxemia ◼ Blood injected intestine typical of Type C enterotoxemia in a young lamb. ◼ Clostridium perfringens Type C enterotoxemia typically presents as what appear to be blood-filled small intestines. Intestinal walls are dark red to black... ◼ Typical Light Microscopic Findings: ◼ Acute necrohemorrhagic enteritis with large numbers of bacilli limited to necrotic tissue ◼ Mucosal or submucosal thrombosis ◼ Mucosal/submucosal hemorrhage ◼ +/-Fibrinonecrotic pseudomembranes ◼ +/- Fibrinoid necrotizing vasculitis in submucosa ◼ Gross lesions include fluid cecal contents with serosal hemorrhages and edema on the cecum, and occasionally the ileum and proximal colon (A). Microscopically, there is necrotic erosive or ulcerative typhlitis with swollen or vacuolated enterocytes, pseudomembrane formation, heterophilic infiltration, as well as submucosal edema and hemorrhage (B). Large Gram-positive bacilli are present on the mucosal surface. Liver Diseases Hepatic lipidosis ◼ Hepatic lipidosis is the abnormal accumulation of triglycerides within hepatocytes ◼ affects : ponies (Shetland ponies are predisposed), donkeys, miniature horses, cattle, cats sheep * pregnant, obese or lactating animals are affected ◼ Typical Clinical Findings: ◼ Depression, anorexia, weakness, colic, pasty feces, icterus ◼ Hepatic rupture is a frequent cause of death ◼ Typical Gross Findings: ◼ Enlarged greasy yellow liver, bulges on cut surface, floats in formalin – Enlargement of liver may cause rupture of the liver capsule ◼ Lipidosis may also involve the heart, skeletal muscle, kidney, adrenal cortex ◼ Typical Gross Findings: ◼ Enlarged greasy yellow liver, bulges on cut surface, floats in formalin – Enlargement of liver may cause rupture of the liver capsule ◼ Lipidosis may also involve the heart, skeletal muscle, kidney, adrenal cortex ◼ Hemorrhage and infarction if DIC is present Fatty liver Normal liver ◼ Typical Light Microscopic Findings: ◼ Swollen hepatocytes that contain variably sized discrete lipid vacuoles, which often displace the nucleus to the periphery Diffusely the hepatocytes are markedly enlarged by a discrete clear cytoplasmic vacuole (lipid) that flattens and displaces the nucleus to the periphery Congestive Hepatopathy nutmeg liver ◼ Is liver dysfunction due to venous congestion, usually due to: dysfunction of the heart - right heart failure - Congestive heart failure ◼ Typical Gross findings "speckled" like a grated nutmeg kernel; the dark spots represent the dilated and congested hepatic venules and small hepatic veins. The paler areas are unaffected surrounding liver tissue Liver necrosis ◼ Periportal necrosis is a rare lesion caused by complex interaction between specific types of hepatotoxins and the hepatic microsomal apparatus. ◼ A toxin that comes in through the blood and reaches the peripheral cells of the lobule first most often causes this form of necrosis ◼ Ex: Both Carbon Tetrachloride and Blue- Green Algae cause periportal necrosis of the liver. ◼ Animals drinking from this pond would ingest some of the cyanobacteria (blue-green algae) and perhaps get liver failure.The toxic principle in these blooms is microcystin ◼ Carbon Tetrachloride (CCl4) isn't really used anymore. It used to be widely used in dry cleaning, household cleaners, and fire extinguishers. Because of its health hazards and the fact that it contributes to greenhouse gases, it is now tightly regulated. Periportal Necrosis ◼ centrilobular necrosis means necrosis around the central vein (called zone 3) ◼ Causes of Centrilobular Necrosis In Liver: 1= Acetaminophen toxicity 2= Chronic passive congestion as in Cardiac failure (pt:Right sided) ◼ in cases of anemia, centrilobular area is the area that will the most hypoxic and therefore undergo the most significant necrosis. ◼ This is because the has blood that is the least well oxygenated ◼ massive necrosis liver, pig. ◼ Acute centrilobular necrosis is the principal lesion of this disorder. Midzonal necrosis ◼ Cocklebur plant is an example of a plant that causes mid-zonal necrosis. ◼ Other forms of hepatic necrosis are paracentral (a wedge-shaped band of necrosis extending from the centrilobular to the portal area) and midzonal necrosis (affects hepatocytes halfway between the centrilobular area and the periportal area). FIBROSIS. ◼ If regeneration is NOT successful, the primary concern is another general reaction of the liver to injury - FIBROSIS. ◼ Fibrosis a frequent end result of hepatic damage. ◼ The liver in this histologic picture has wide bands of fibrous connective tissue separating small islands of hepatic tissue. ◼ notice how the liver looks lobated like a kidney. This is due to scaring or fibrosis from a chronic disease. ◼ Any hepatic insult severe enough to cause hepatocellular necrosis with subsequent regeneration will result in some local fibrogenesis. After recovery from mild insults, this immature collagen is removed by enzymatic degradation. ◼ The balance is tipped in favor of progressive fibrosis when the insult continues to act or when the initial damage is so severe that the scar that results is extensive enough to damage the parenchyma by progressive sclerosis. ◼ What is the "end result" of extensive fibrosis and regeneration? ◼ Cirrhosis ◼ CIRRHOSIS is defined as nodular regeneration combined with fibrosis. This is an undesirable sequelae because it is an "END STAGE" LIVER. Repair and return to normal function will not occur. ◼ The word "cirrhosis" comes from the greek word "kirrhos" that means orange colored and that is the way many cirrhotic livers appear grossly. ◼ To have cirrhosis, there must be three features: ◼ necrosis of hepatocytes ◼ hyperplasia of nodules, and ◼ fibrosis ◼ dog had severe hepatic cirrhosis or "end- stage" liver disease. hepatitis ◼ Viral hepatitis ◼ Infectious Canine Hepatitis ◼ Infectious Canine Hepatitis is one of the puppyhood diseases for which routinely vaccinate pets and vaccination of dogs for this disease has drastically reduced its prevalence in the United States. ◼ The main post mortem lesion is hepatic necrosis and hemorrhage, and dogs will occasionally be icteric. ◼ Intranuclear inclusion bodies in the hepatocytes is diagnostic for Infectious Canine Hepatitis. ◼ The enlarged, swollen liver, icteric mucous membranes, and swollen, reddened tonsils are all suggestive of this disease.In the microscopic section, basophilic inclusion bodies are present in many hepatocytes clinching the diagnosis. ◼ Viral hepatitis ◼ Rift Valley Fever ◼ The Rift Valley virus ◼ The disease affects both people and animal and causes abortion and neonatal death in ruminants. ◼ The disease causes extensive hepatic necrosis often with hemorrhage. ◼ Rift Valley Fever (ruminant) ◼ Section reveals that the liver is pale, swollen and contains multiple foci of hemorrhage. ◼ Sheep, liver. Liver is pale and swollen and contains many areas of severe congestion. ◼ Hemorrhagic fever viruses such as dengue virus, yellow fever virus, and Rift Valley virus. Bacterial Hepatitis ◼ Campylobacter fetus and Campylobacter jejuni can both cause abortion in sheep. ◼ The circumscribed round target-like foci (spots) are classical lesions. ◼ these spots are areas of necrosis due toCAMPYLOBACTER sp. ◼ Fetal animals that are aborted often have hepatic lesions Tuberculosis ◼ there is a GRANULOMATOUS REACTION with MULTINUCLEATED GIANT CELLS Parasitic Hepatitis ◼ his is a very common problem in ruminants in some geographical regions. The most common cause are the flukes Fasciola hepatica and Fascioloides magna. ◼ FASCIOLOIDES MAGNA causes focal hepatitis. This is not a normal parasite of cattle and thus lesions are more severe than in wildlife. ◼ FASCIOLA HEPATICA causes necrosis and secondary fibrosis of the biliary tree in cattle. Mycotoxins ◼ …..Aflatoxins ◼ Corn can be contaminated with Aspergillus flavus, a mold that produces AFLATOXIN as a metabolite. ◼ Aflatoxins ingested by animals may be further metabolized by the hepatic mixed function oxidation system with resultant hepatic toxicity. ◼ Other toxic effects include carcinogenesis, teratogenesis, mitotic inhibition and immunosuppression. ◼ Dogs can also get aflatoxicosis. If they get into garbage, they could ingest old mouldy food. Other ◼ Leptospirosis is a serious disease that usually affects the kidneys or liver. ◼ It also may cause abortion, stillbirths, and life- threatening whole body infections (septicemia). ◼ Leptospirosis is found in many species of animals, including dogs, cats (rarely), and people. ◼ It is considered a zoonotic disease (a disease that can be spread from animals to humans). ◼ Liver of a dog that died of leptospirosis. Multifocal hepatic necrosis is associated with a mottled appearance of this organ ◼ Liver Hematoxylin and Eosin | 256x Diffusely throughout the section, there is loss of hepatic plate architecture. Heptaocytes are individualized, rounded up, and exhibit single cell necrosis macrophages and hepatocytes contain abundant red globular pigment (copper). Image Collection (Noah's Arkive) Dr. Adnan Fayyad Bovine, Adult, Cranial half marked congestion of the esophagus Horse, 1 month old Foal, Stomach, Duodenum, Chronic locally extensive gastroduodenal ulceration Dog, Spirocerca lupi parasites - Two isolated parasites from the distal tumor of the esophagus Dog, Distal esophagus and thoracic aorta, C HRO N I C GRAN ULOMATOU S S P I R O C E R C A LUPI B R O O D P O U C H AND AORTIC SCARRING Dog, PARASITIC GRANULATION TISSUE AND NEOPLASIA C A U S E D BY S P I R O C E R C A LUPI Dog, Esophagus, PARASITIC (SPIROCERCA LUPI) INDUCED S A R C O M A. Steer, Esophagus, adventitia, Parasitic maggot in adventitia, HYPODERMA LINEATION Cat, Chronic Severe Esophageal Dilatation, Dysautonomia Piglet, Tongue, Chronic active cellulitis due to a penetrating wire foreign body through the esophagus Puppy, Esophagus, Normal melanosis Dog, Fibrosarcoma secondary to the esophogeal worm, S P I R O C E R C A LUPI Dog, Lung and esophagus, Megaesophagus with secondary inhalation pneumonia. Sheep, Esophagus, muscle, Sarcocystosis Alpaca, Megaesophagus, LEAD TOXICITY IS POSSIBLE ABOMASUM LYMPHOSARCOMA, BOV ABOMASUM ABOMASAL U L C E R , BOV ABOMASUM U L C E R S LYMPHOSARCOMA, BOV ABOMASUM PERFORATING U L C E R , BOV ABOMASUM PERFORATING U L C E R , BOV Dog, Locally extensive rugal hyperplasia or hypertrophy Dog, Multifocal smooth muscle tumors Dog, Locally extensive rugal hyperplasia or hypertrophy Dog, Locally extensive gastric mucosal mineralization, Uremic gastritis Dog, U R E M I C MINERALIZATION O F THE G S T R I C MUCOSA Horse, Gastric Wall Rupture Dog, cute hemorrhagic locally extensive gastritis with mineralization, Uremic Gastritis Horse, adult, Normally filled stomach Dog, Gastric inversion and torsion Horse, Acute gastric rupture, PROBABLE LOWER BOWEL OBSTRUCTION This case did have a volvulus of the lower intestine. Dog, Gastric torsion Foal, 10 day old, Ulceration and perforation, NSAIDS RELATED U L C E R S Dog, stomach, mucosa, Leiomyoma Cat, Thread foreign body Piglets, tongue, esophagus, stomach, Candidiasis Lamb, Chronic surface trauma of tongue and esophagus, STOMACH TUBING TRAUMA Dog, Gastric eversion (intussusception) into the esophagus Dog, Gastrinoma with hepatic metastases ABOMASUM O S TE RTAG O SIS , BOV ABOMASUM CLOSTRIDIAL ABOMASITIS, BOV ABDOMEN MESOTHELIOMA, BOV RUMEN LACTIC ACIDOSIS GRAIN OVERLOAD, BOV ABOMASUM F O C A L NECROTIZING MYCOTIC ABOMASITIS, BOV ABOMASUM-CONTENT HAE MO NCHUS, OVI OMASUM MYCOTIC OMASITIS, BOV ABOMASUM VERMINOUS ABOMASITIS OSTERTAGIA, BOV RUMEN MYC O TIC ULCERATIVE RUMENITIS, BOV RUMEN CHRONIC RUMENITIS S C A R S , BOV RUMEN CONTENTS PHYTOBEZOARS, BOV RETICULUM ACUTE RETICULITIS, BOV RETICULUM ACUTE RETICULITIS, BOVI ABOMASUM MYCOTIC ULCERATIVE ABOMASITIS, BOV Image Collection (Noah's Arkive) Dr. Adnan Fayyad BOV, LUNG INTERSTITIAL PNEUMONIA EMPHYSEMA BOV, TRACHEA TRACHEITIS IBR BOV, NASAL SEPTATE RHINITIS IBR BOV, LUNG FETAL ATELECTASIS BOV, LUNG ATELECTASIS BOV, LUNG ATELECTASIS OVI, NASAL CAVITY ADENOCARCINOMA BOV, SINUS CHRONIC PURULENT SINUSITIS BOV, NARES FIBRINONECROTIC RHINITIS IBR BOV, TRACHEA FIBRINONECROTIC TRACHEITIS IBR BOV, LUNG MELANOSIS BOV, SINUS-FRONTAL MUCINOUS POLYPS MAXILLARY SINUS BOV, NASAL CAVITY CARCINOMA BOV, NASAL CAVITY CARCINOMA OVI, NASAL CAVITY ADENOCARCINOMA BOV, LARYNX NECROTIC LARYNGITIS FUSOBACTERIUM BOV, LARYNX FIBRINOUS LARYNGITIS BOV, LUNG(SECTION) ALVEOLAR EDEMA EMPHYSEMA BOV, LARYNX NECROTIC LARYNGITIS FUSOBACTERIUM Bov, LUNG FETAL ATELECTASIS BOV, LUNG NORMAL PLEURA Image Collection (Noah's Arkive) Dr. Adnan Fayyad Bov, Lung Verminous Bronchitis Dictyocaulus OVI, HEAD NASAL BOTS SINUS NASAL OVI, HEAD NASAL BOTS SINUS NASAL Bov, Lung Verminous Bronchitis Dictyocaulus Ovi, Lung Diffuse Interstitial Pneumonia Ovine Progressive Pneumonia BOV, LUNG PNEUMONIA HEMOPHILUS somnus OVI, THORAX BRONCHOPNEUMONIA PASTEURELLA LUNG BOV, LUNG DICTYOCAULUS viviparous BRONCHIOLE OVI, LUNG PASTEURELLOSIS CAP, LUNG PLEURITIS PNEUMONIA PASTEURELLA hemolyticum CAP, LUNG FIBRINOUS PLEURITIS PNEUMONIA CAP, LUNG BRONCHOPNEUMONIA DICTYOCAULUS FILARIA BOV, LUNG FIBRINOUS PNEUMONIA BOV, LUNG MULTIPLE ABSCESSATION CORYNEBACTERIUM equi CAP, LUNG LUNGWORMS MUELLERIUS sp OVI, LUNG FIBRINOUS PLEURITIS OVI, LUNG PNEUMONIA PASTEURELLOSIS OVI, LUNG OVINE PROGRESSIVE PNEUMONIA OVI, LUNG OVINE PROGRESSIVE PNEUMONIA OVI, LUNG MAEDI BOV, LUNG TUBERCULOSIS BOV, LUNG FIBRINOUS PLEUROPNEUMONIA PASTEURELLA BOV, LUNG CHRONIC BRONCHOPNEUMONIA BOV, LUNG BRONCHOPNEUMONIA BRONCHIECTASIS CHR OVI, LUNG BRONCHOPNEUMONIA PASTEURELLA OVI, LUNG PNEUMONIA CHRONIC ABSCESSING - SPLENIC AB C. pyogenes SPLEEN BOV, LUNG-FETUS FIBRINOUS PLEURITIS FETAL ATELECTASIS BUFFALO- BRUCELLOSIS BOV, LUNG FIBRINOPURULENT BRONCHOPNEUMONIA BOV, LUNG-FETUS FIBRINOUS PLEURITIS BRUCELLOSIS BOV, THORAX FIBRINOUS PLEURITIS HARDWARE DISEASE CAP, LUNG(HISTO) MUELLERIUS capillaris BOV, LUNG FIBRINOUS PLEURITIS PNEUMONIA BOV, LUNG(SECT) FIBRINOPURULENT PNEUMONIA BOV, LUNG CALF ENZOOTIC PNEUMONIA BOV, LUNG ABSCESSES BOV, LUNG BOVINE TUBERCULOSIS BOV, LUNG(HISTO) VERMINOUS PNEUMONIA OVI, LUNG(HISTO) PULMONARY ADENOMATOSIS BOV, LUNG DICTYOCAULUS OVI, LUNG MUELLERIUS OVI, LUNG(HISTO) MAEDI BOV, LUNG PULMONARY THROMBOEMBOLISM BOV, LUNG DICTYOCAULUS viviparous BOV, LUNG VERMINOUS BRONCHITIS PNEUMONIA OVI, LUNG ABSCESSING PNEUMONIA CASEOUS BOV, LUNG EMBOLIC PNEUMONIA BOV, LUNG(HISTO) TB GRANULOMA BOV, THORAX FIBRINOUS PLEURITIS AND PERITONITIS E. coli BOV, LUNG ATELECTASIS BOV, THORACIC WALL MESOTHELIOMA LUNG(HISTO) INTERSTITIAL OVI, LUNG HYDATIDOSIS OVI, LUNG HYDATIDOSIS OPENED VESICLE Cap, Lung Granulomatous Pneumonia Lymphadenitis Tuberculosis Lymph Node BOV, THORAX PLEURAL EFFUSION CONTAG. PLEUROPNEUMONIA CAP, LUNG BRONCHOPNEUMONIA PASTEURELLA multocida BOV, LUNG EMBOLIC PNEUMONIA OVI, DICTYOCAULUS FILARIA