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  1. 1. Department of Pathology, Faculty of Veterinary Medicine, Zagazig University, Egypt. Pathology of Bacterial Diseases BY Prof. Dr. Mohamed Hamed Mohamed +20124067373 2011
  2. 2. Mycoplasma and Bacterial Diseases Bacteria are a group of organisms which capable of inducing a diversity of diseases. Pathogenic and saprophytic bacteria are single-celled microorganisms that lack a nuclear membrane (prokaryotes), have both DNA and RNA and have few cell organelles. Bacteria are either extracellular or facultative intercellular. Pathognomonic Lesions: They are the most important lesions through which the disease can be identified. Septicemia: It is the circulation and multiplication of the m. o. and their toxins in the blood with production of lesions and clinical signs. Lesions of Septicemia: There are 3 major changes: 1-Retrogressive changes and necrosis. 2-Defensive reaction. 3-Local effect of the bacteria. 1-Retrogressive changes and necrosis: i-Cloudy swelling, hydropic and hyaline degenerations. ii-Focal necrosis in the parenchymatous organs. iii-Petechial hemorrhages and edema as a result of injured capillary endothelium.
  3. 3. 2-Defensive reaction: Hyperplasia of reticuloendothelial system is seen in the spleen, lymph nodes, liver and bone marrow. -The spleen is enlarged, congested and soft. -The L.ns are enlarged, hemorrhagic and edematous. -The defensive reaction of body results in fever, tachycardia and leukocytosis 3-Local effect of the bacteria: The bacteria usually produce acute inflammation and abscesses formation. The septicemic lesions are summarized in 7 points as following: 1-The subcutaneous blood vessels are congested. 2-L.ns and spleen are enlarged, swollen and edematous. 3-Degenerative changes and coagulative necrosis in parenchymatous organs. 4-Hydrothorax, hydroperitoneum and hydropericardium. 5-The skeletal muscles are congested and have hemorrhagic streaks. 6- Petechial and ecchymotic Hges around the coronary fat and on s. and m.m 7-Hemorrhages on the parenchymatous organs. Toxemia: It is the circulation of toxin in the blood stream with production of clinical signs and lesions.
  4. 4. Lesions of Toxemia: 1-The blood is dark red in color. 2-Sucutaneous and pulmonary edema. 3-Degenerative changes and coagulative necrosis in the parenchymatous organs (heart, liver and kidneys). 4-Severe congestion of the blood vessels and the mucous membrane is hyperemic. 5-Petechial and ecchymotic hemorrhages on the serous membrane. This lesion is resulted from the effect of the toxins on the intema of blood vessels. Pyemia: It is the circulation and multiplication of pyogenic microorganisms and their toxins in the blood with production of metastatic (embolic) abscesses. Bacteremia: It is the circulation of bacteria in the blood stream without multiplication or their production and without production of lesions or clinical signs. The bacteria may be localized and destroyed by the REC. Bacteremia may be caused by traumatic wounds may be the cause of isolated lesions. These bacteria are either: i-Brucella ii-TB iii-Para TB iv-Campylobacter Sapremia: It is the circulation of saprophytic microorganisms and their toxins (metabolites) in the blood with production of gangrene.
  5. 5. Infectious disease: It is a disease which caused by living m.o. such as bacteria, viruses, fungi and parasites. Contagious disease: It is an infectious disease transmitted by direct contact. Epizootic disease: It is an infectious disease of animals which appears in different locations at a same time. Enzootic disease: It is infectious or non infectious disease limited to a particular area e.g. Infectious disease Trypanosomiasis (due to presence of IMH). Non-Infectious Goiter (iodine-deficient area). Sporadic disease: It is the disease which involves a few members of the herd Zoonotic disease: It is an infectious disease which is transmissible between animals and human. Prevalence of disease: It is the percentage of infected cases with a disease, which is present all the time in different locations. Incidence of a diseased: It is the percentage of infected cases with a disease in only one location at a time. Infection: It is the invasion of living tissue by pathogenic microorganisms that causes diseases.
  6. 6. Diseases caused by Mycoplasmas Contagious Bovine Pleuropneumonia (CBPP) Causes: Mycoplasma mycoides var mycoides. Pathogenesis: The m.o. enters through the respiratory tract (droplet infection) and then through the bronchiolar wall and invade the peribronchial tissue, then go through the lymph vessels to the interlobular connective tissue and interalveolar septa where it induces an inflammatory edema with dilation and subsequent thrombosis of the lymph vessels and pulmonary artery branches. Large area of necrosis is resulted from the thrombosis of artery branches and surrounded with fibrous tissue (Sequestrum). Pathognomonic Lesions: In the early stage: 1-Usually one lung is affected and become i-Hepatized and firm in consistency. ii-Cut surface is marbled in appearance with red and grayish areas of parenchyma separated by thick yellowish interlobular septa. 2-Serofibrinous or fibrinous pneumonia. 3-The interlobular septa are thickened (due to collection of the fibrinous exudate) give the lungs the marbling appearance.
  7. 7. 4-Serofibrinous or fibrinous pleurisy and the pleura become thick with adhesion between the parietal and visceral pleura. 5-Large abscess may be seen. 6-Beaded appearance of interlobular septa is due to dilation and thromboses of lymph vessels In long standing cases: 1-Areas of necrosis within groups of lobules tend to become sequestrated from the adjacent tissue and surrounded by a dense layer of fibrous connective tissue. 2-Theses areas may be opened into the neighboring bronchi. 3-Round cells infiltration mainly lymphocytes and plasma cell are seen around blood vessels and bronchi. NB: 1-Bovine Mycoplasmal Arthritis: Mycoplasma bovis infection induces polyarthritis in young calf and seminal vasculitis in bull or vulvovaginitis in cow. 2-Contagious Caprine Pleuropneumonia in goats similar to CBPP 3-Infectious Bovine Keratoconjunctivitis chronic purulent keratitis, corneal opacity and pannus (vascularization of cornea).
  8. 8. Organ : Lung (buffalo). Disease : CBPP. Macro : Thickening of the interlobular septa (marbling).
  9. 9. Organ : Lung (buffalo). Disease : CBPP. Macro : Thickening of the interlobular septa (marbling appearance).
  10. 10. Organ : Lung (buffalo). Disease : CBPP. Macro : Thickening of the interlobular septa (marbling appearance).
  11. 11. Organ : Lung (buffalo). Disease : CBPP. Macro : Sequestration (necrotic area separated from lung tissue.
  12. 12. Organ : Eye (buffalo). Disease : CBPP. Macro : Keratoconjunctivitis.
  13. 13. Organ : Joints (goat). Disease : Mycoplasmal Arthritis. Macro : Polyarthritis.
  14. 14. Diseases caused by Rickettsiales Disease caused by Cowadria Heartwater disease Cause: Cowadria ruminantium (tick-borne rickettsiosis of ruminant). The tick (Amblyomma. maculatum) nymph considers the IMH of the disease. Pathognomonic Lesions: 1-Hydropericardium, pulmonary edema, hydrothorax, and ascites. 2-The edematous fluid is usually serous with few strands fibrin. 3-The spleen and L.ns (lymphopoietic tissues) are enlarged. 4-Microscopically, the tissues are edematous besides generalized perivascular leukocytic aggregation. The microorganisms are seen in cytoplasm at the pole of endothelial cells. NB: The organism is selectively parasitizes the endothelial cells of the jugular vein, vena cava, renal capillaries and cerebral gray matter. Diseases caused by Anaplasmataceae Anaplasmosis Anaplasma species are rickettsial organisms that may be transmitted by arthropods or blood contaminated needles. It is characterized by extravascular autoimmune anemia and hyperplasia of hemopoietic system.
  15. 15. Causes: Three species are of pathogenic importance. 1-Anaplasma marginale: affect cattle, sheep and goat and is very virulent. 2-Anaplasma centerale: affect cattle and cause milder disease. 3-Anaplasma ovis: affect only sheep and goat. Pathogenesis: 1-The M.O. reached the blood through biting by the IMH. The organisms invade erythrocytes without hemolysis or destruction of the RBCs. 2-The presence of anaplasma in erythrocytes induces type II hypersensitivity with formation of antibodies that facilitate phagocytosis of infected and sometimes the healthy RBCs by REC in the spleen (autoimmune anemia). NB: The hemoglobinuria does not occur. The young age is usually resistant to infection (up to one year). Pathognomonic Lesions: 1-Anemia such as pale mucous membrane and jaundice as yellow m.m. 2-The carcass is emaciated and the blood is thin and watery. 3-The liver is enlarged and yellowish in color associated with jaundice. 4-Centrolobular degeneration and necrosis are seen. 5-The gallbladder is distended with dark green bile. 6-The kidneys are enlarged and showed degenerative changes. 7-Hemosiderosis and extramedullary hematopoiesis in spleen and liver . 8-Petechial hemorrhage on serous and mucous membrane.
  16. 16. Organ Stain Disease Micro : Brain (endothelium of blood vessel). : H&E. : Cowdria ruminantum. : The organisms are seen in the endothelium.
  17. 17. Organ : Lung. Disease : Heart water disease (Cowdria ruminantum). Macro : Hydrothorax.
  18. 18. Organ : Lung. Disease : Heart water disease (Cowdria ruminantum). Macro : Severe interstitial edema.
  19. 19. Organ : Brain. Disease : Heart water disease (Cowdria ruminantum). Macro : Hemorrhage and edema in the brain.
  20. 20. Organ : Brain. Stain : H&E. Disease : Heart water disease (Cowdria ruminantum). Micro : Edema and perivascular cuffing.
  21. 21. Preparation : Blood smear. Stain : Giemsa. Disease : Anaplasmosis. Micro : Dark spots (dots) in the RBCs.
  22. 22. Preparation : Blood smear. Stain : Giemsa. Disease : Anaplasmosis. Micro : Dark spots (dots) in the RBCs.
  23. 23. Diseases by order Chlamydiales Psittacosis (Ornithosis, parrot fever) It is an infectious febrile pulmonary disease of human and various species of birds caused by Chlamydia psittaci. The disease is psittacine birds (parrot, parakeets) is called psittacosis, while in pigeons, fowl and turkey is called Ornithosis. Pathogenesis: Animals or birds infected through inhalation of infective stage (elementary body). The elementary body attaches to the epithelial cells of the lungs, air sac and pericardium. The elementary body forms the reticular body, which divided into smaller body to form again the elementary body which reinfects other cells. Pathognomonic Lesions: 1-The affected birds are emaciated. 2-The nares may be plugged by muconasal discharge. 3-Fibrinous pericarditis, perihepatitis and airsacculitis. 4-The liver is enlarged, mottled and showed petechiae and necrotic foci. 5-The spleen and kidneys are enlarged. 6-Microscopically: i-The M.O. are demonstrated in the cells. ii-Mononuclear cells infiltrate the various organs.
  24. 24. iii-Hyperplasia of reticuloendothelial cells and hemosiderosis in the spleen iv-Coagulative necrosis in the liver. v-Round basophilic bodies and necrosis in the renal tubular epithelium. vi-The lungs contain serous and fibrinous exudate besides round cells. Chlamydial abortion in cattle (Epizootic bovine abortion) It causes abortion in cattle (7th and 9th months of gestation). The dam is normal and the aborted fetus is weak and dies within few days. Pathognomonic Lesions (Fetus): Macroscopic picture: 1-Grayish foci in myocardium and kidneys. 2-The liver is swollen coarsely enlarged and friable. 3-subcutaneous edema, hydrothorax and hydroperitoneum. 4-The L.ns and spleen is enlarged. 5-Petechial hemorrhages the, conjunctiva, oral mucosa, larynx, trachea and conjunctiva. Microscopic picture: 1-Granulomas in the liver, kidneys, myocardium, skin and brain. 2-The granuloma consists of central necrosis, surrounded by epithelioid cells, giant cells and neutrophils.
  25. 25. 3-Hyperplasia of REC and vasculitis are seen. 4-The placenta was edematous, necrotic and showed fibrinopurulent exudate and leathery. NB: -Chlamydiae have also been recovered from semen, epididymis and seminal vesicles of bulls. -Chlamydia is a minute organism that multiplies only in vertebrate host cells. The Chlamydia is non motile, spherical and gram-negative organisms.
  26. 26. Stillbirth Calf is weak and show inability to stand. Disease : Chlamydial abortion.
  27. 27. Organ : Placenta. Stain : H&E. Disease : Chlamydial abortion . Micro : Edema, congestion, hemorrhages and necrosis of fetal membrane.
  28. 28. Organ : Placenta. Stain : H&E. Disease : Chlamydial abortion . Micro : A high magnification to show the organism.
  29. 29. Organ : Placenta impression. Stain : Giemsa’s stain. Disease : Chlamydial abortion . Micro : Dark red organism are seen in trophoblasts.
  30. 30. Diseased caused by bacteria I-Septicemic Diseases Leptospirosis Causes: Leptospira canicola Leptospira ictrohemorrhagica Leptospira pomona in dogs. in dogs and rats. in cattle and swine. NB: In man: it causes Weil’s disease (L. ictrohemorrhagica), Canicola fever (L. canicola) and swine herd disease (L. pomona). A-Canine Leptospirosis: Pathognomonic Lesions: I-Acute leptospirosis: (the affected dog die) Liver: Macroscopic Picture: 1-Theliver is enlarged and yellow in color. 2-Yellow m.m. due to icterus. 3-Peticheal hemorrhages on the pleura, pericardium and peritoneum. Microscopic Picture: 1-Retrogressive changes and coagulative necrosis in hepatic cells. 2-Dissociation of the hepatic cells (individualization).
  31. 31. 3-Toxic and hemolytic jaundice with dilation of the bile canaliculi with yellow bile pigments. 4-Hemosiderosis are seen in the kupffer cells. 5-Leptospira are demonstrated in the hepatic sinusoids and within liver cells by Levaditi’s stain (silver impregnation). Kidneys: Macroscopic Picture: 1-The kidneys are enlarged and pale in color. 2-Soft in consistency. 3-Bulged cut surface. 4-Petechial hemorrhage at corticomedullary junction. Microscopic Picture: 1-Degenerativ changes and necrosis in the lining epithelium. 2-Some tubules may contain regenerating epithelium with the formation of syncytial giant cells. 3-Acute interstitial lymphocytic nephritis. 4-Cellular casts are seen in the lumen of the renal tubules. 5-Leptospira are demonstrated by silver impregnation. Spleen and Lymph nodes: 1-They are enlarged and edematous. 2-Hemorrhages, depletion of the lymphocytes and hyperplasia of REC.
  32. 32. Gastrointestinal tract: 1-Hemorrhagic gastroenteritis (vomition). 2-Petechial hemorrhages on the intestinal mucosa. 3-Bloody diarrhea (emaciation). NB: Hemorrhages and edema may be seen in other organs as myocardium, adrenal glands, pancreas, gallbladder lung and pleura. II-Subacute and Chronic leptospirosis: The main lesions are seen in the kidneys. Macroscopic Picture: 1-The kidneys are enlarged (subacute) or small (chronic). 2-Grayish-white spots throughout the cortex (white spotted kidney) and the capsule is not easily detached. 3-Smooth or pitted surface with hemorrhage at the corticomedullary junction. Microscopic Picture: 1-Agggregations of lymphocytes (lymphocytic nephritis). 2-Extenssive coagulative necrosis (nephrosis). 3-Fibrosis and cystic dilation of some renal tubules in chronic. 4-Cellular and hyaline casts. NB: Dehydration, emaciation, icterus and uremia are clinically noticed.
  33. 33. B-Bovine leptospirosis I-Acute leptospirosis: The presence of the organism in the blood with its spiral movement induce: 1-Hemolytic anemia with hemoglobinuria and hyperplasia of bone marrow 2-Icterus and petechial hemorrhages on swollen liver. 3-Centrolobular necrosis and splenic hemosiderosis. 4-In kidney, there are swelling a disorganization of renal epithelium. II-Subacute leptospirosis: 1-Grayish white foci are scattered through the renal cortex. 2-Different degenerative changes in the renal tubular epithelium. 3-Lymphocytes and plasma cells infiltration around affected tubules. 4-Leptospira are demonstrated by silver impregnation. NB: It induces abortion after the septicemia.
  34. 34. Organ : Spleen. Disease : Leptospirosis. Macro : Splenomegaly with septicemic lesions.
  35. 35. Organ : Liver. Stain : H&E. Disease : Leptospirosis. Micro : Dissociation of hepatic cords.
  36. 36. Organ : Liver. Stain : H&E. Disease : Leptospirosis. Micro : Dissociation and individualization hepatic cells.
  37. 37. Organ : Kidney. Disease : Leptospirosis. Macro : Hemorrhages in the renal cortex.
  38. 38. Organ : Kidney. Disease : Leptospirosis. Macro : Hb nephrosis with dark black kidney.
  39. 39. Organ : Kidney. Stain : Levaditi’s stain . Disease : Leptospirosis. Micro : Wavy black organisms are seen among tubules.
  40. 40. Pasteurellosis Causes: Pasteurella species. P. hemolytica (Manheimia hemolytica) P. multocida Fowl cholera (P. multocida) H.S. (P. multocida) Shipping fever (Manheimia hemolytica) Sheep Pasteurellosis (P. hemolytica) Rabbits Snuffles (P. multocida) Several mammals and birds Tularemia (P. tularensis) Fowl Cattle I-Hemorrhagic septicemia: Pathognomonic Lesions: 1-Generalized petechial and ecchymotic hemorrhages on the s. and m.m. 2-Congestion in the internal organs and muscles with degenerative change 3-All lymph nodes are edematous and hemorrhagic. 4-The lungs are edematous and hemorrhagic {hepatized or consolidated). 5-Hydrothorax (serous or tinged with blood}. 6-Hemorrhagic enteritis. 7-S/C edema in the head, neck, throat, dewlap and pharynx. The edema in the throat and pharynx leads to narrowing of air and food passages with difficult breathing and swallowing (The animal finally dies of asphyxia).
  41. 41. II-Shipping Fever: Pathogenesis: Pasteurella are widely spread in nature and in normal animals. Under stress conditions such as bad weather, shipping, dipping or association with other viruses or mycoplasmal diseases, the Pasteurella species become pathogenic and invade the tissue, entering blood (septicemia) and spread through the body. Pasteurella cause their effect by combination of several mechanisms: 1-Release of endotoxins. 2- Release of the lipopolysaccharides. 3-Release of the outer membrane proteins. 4-Production of leukotoxin (important) that binds and kills bovine macrophages and neutrophils. During the infection, alveolar macrophages, neutrophils and mast cells release maximum amount of proinflammatory cytokines that attract more leukocytes which cause damage to bronchial and alveolar cells. Pathognomonic Lesions: Macroscopic Picture: 1-Hydrothorax (serous, serofibrinous exudate or tinged with blood. 2-Fibrinous pleuritis and petechial hemorrhages on its visceral layer.
  42. 42. 3-Fibrinous pneumonia, with hepatized areas in the apical and less diaphragmatic lobes. 4-Thickening the interlobular septa by yellow gelatinous edema and fibrin (marbling appearance). 5-Areas of necrosis surrounded with a gray zone and interlobular interstitial edema and congestion. Microscopic Picture: 1-The lungs showed fibrinous bronchopneumonia and necrotic areas. 2-Thrombosis that could be induced the necrosis. The necrotic areas contain a large number of bacteria and debris of inflammatory cells (release endotoxins and cytotoxin). 3-Large number of inflammatory cells with elongated nuclei (oat cells) NB: -Calves show fibrinopurulent meningitis and polyarthritis. -Cow shows severe fatal hemorrhagic mastitis. III-Pasteurellosis in sheep It is characterize by: 1-Septicemic lesions and hemorrhages. 2-The L.ns are swollen and edematous. 3-Necrotizing pharyngitis and bacterial emboli in the lungs are noticed. 4-Fibrinous bronchopneumonia without pleural effusion may be seen. 5-Hemorrhagic enteritis.
  43. 43. Calf-infected with Pasteurellosis show severe dyspnea.
  44. 44. Organ : Lung. Disease : Pasteurellosis. Macro : Acute fibrinonecrotic bronchopneumonia .
  45. 45. Organ : Lung. Disease : Pasteurellosis. Macro : Acute fibrinous pneumonia.
  46. 46. Organ : Lung. Disease : Pasteurellosis. Macro : Acute fibrinonecrotic pneumonia .
  47. 47. Organ : Lung. Stain : H&E. Disease : Pasteurellosis. Micro : Serofibrinous bronchopneumonia .
  48. 48. Organ : Lung. Stain : H&E. Disease : Pasteurellosis. Micro : Serofibrinous bronchopneumonia .
  49. 49. Organ : Lung. Stain : H&E. Disease : Pasteurellosis. Micro : Numerous neutrophils, macrophages, oat cells and lymphocytes in lung-tissue.
  50. 50. Anthrax Splenic Fever It is a rapidly fatal septicemic and Zoonotic disease of all worm blooded animals caused by a Bacillus anthracis and characterized by 1-Sudden death of animal. 2-Dark black and unclotted blood passes from natural orifices. 3-Cyanosis of m.m. 4-Acute splenitis (Severe enlarged spleen). Pathognomonic Lesions: 1-Rapid decomposition and putrefaction of carcasses. 2-Incomplete rigor mortis. 3-Dark black, unclotted blood passes from the natural orifices. 4-Cyanosis of all m.m. and rectal prolapse. 5-Acute splenitis characterized by -Severely enlarged (4-5 times) so it is called Splenic Fever. -Dark black in color. -Soft in consistency. -The capsule is tense 6-Hemorrhagic enteritis. 7-The L.ns are enlarged and hemorrhagic. 8-Congestion and edema in the lungs. 9-Hemorrhagic endocarditis. 10-Petechial hemorrhages on S. and m.m. 11-Degenerative changes in the parenchymatous organs.
  51. 51. Preparation Stain Disease Micro : Blood smear. : Gram’s stain. : Anthrax. : Bacillus anthracis are seen.
  52. 52. Organ : Spleen. Disease : Anthrax. Macro : Severe enlarged spleen with tense capsule .
  53. 53. Organ : Lymph nodes. Disease : Anthrax. Macro : Acute serohemorrhagic lymphadenitis.
  54. 54. Organ : GIT. Disease : Anthrax. Macro : Extensive hemorrhages admixed with feces.
  55. 55. Escherichia infection A variety of E. coli strains cause a number of forms of enteric colibacillosis 1-Enterotoxigenic E. coli (ETEC): They produce enterotoxins cause an ion imbalance leading to secretory diarrhea of small intestine in neonates i.e. edema disease (pigs). 2-Enteropathogenic E. coli (EPEC): They do not produce toxins and haven’t invasive factors but clump in groups to cause malabsorptive postweaning diarrhea (pigs and calves). 3-Enteroinvasive E. coli (EIEC): have invasive factors and cause tissue damage and inflammation. 4-Shiga-like toxin producing E. coli (STEC): produce toxin that crosses epithelial barrier causing systemic illness: diarrhea, HemorrhagicUremic-Syndrome (HUS) and edema disease. Colibacillosis Pathogenesis: The infection occurs through ingestion of contaminated food or water. Under certain condition (the animals not tack colostrum and bad weather with vit A deficiency), the E. coli acquired the virulence and enterotoxins factors and becomes pathogenic.
  56. 56. A-Enterotoxic Colibacillosis It occurs in animals up to 3 weeks of age. The disease is common in calves and lambs and piglets. Pathogenesis: 1-The postneonatal animals kill the most bacteria by lowering the gastric pH 2-The pathogenesis of diarrhea includes two steps: i-Intestinal colonization ii-Elaboration of enterotoxins The microorganisms come in contact and adhere with the microvilli and produce 2 types of potent enterotoxins. A-Heat labile toxin (LT): It activates adenyle cyclase leading to marked increase in cellular excretion resulting in diarrhea. B-Heat stable toxin (ST): It activates guanylate cyclase inducing fluid loss and diarrhea. Increase fluid excretion into the lumen leading to diarrhea Pathognomonic Lesions: 1-The affected animal is dehydrated (wrinkled skin and sunken eyeballs). 2-The small intestine is dilated and filed with yellow to white and watery to pasty fluid with some gas. 3-Villus atrophy.
  57. 57. B-Enterotoxemic Colibacillosis (edema disease) It is observed in mainly pigs (6-14 weeks) and calves due to proliferation of E. coli in the intestine with production of enterotoxin (verotoxin) in intestine, which spread hematogenously leading to vascular damage and noninflammatory edema in all parts of body especially gastric, colonic, palpebral, forehead and gallbladder. In brain, the arterial damage causes focal malacia in medulla, thalamus and basal ganglia. C-Enteroinvasive Colibacillosis The disease affects human, laboratory animals and rarely cattle and pigs. The enteric E coli penetrate and destroy the epithelial lining, invade the lamina propria and then to the mesenteric lymph nodes. The pathogenesis is depending on elaboration of toxin that inhibits protein synthesis and induces necrosis of enterocytes. -Ulcerative enteritis with blunting of villi, lengthening of crypt are seen D-Septicemic colibacillosis It is a disease of young calves, lambs and occasionally foals that not received sufficient colostrum to develop immunity (white scour). E. coli get entry through digestive and respiratory systems, -Polyserositis, arthritis, meningitis and pyelonephritis due to endotoxins produced by E coli are seen besides septicemic lesions.
  58. 58. Piglet-suffered Colibacillosis show septicemic lesions and hemorrhagic gastroenteritis.
  59. 59. Organ : Brain. Disease : Colibacillosis. Macro : Extensive hemorrhages on brain (septicemia).
  60. 60. Organ : Mesentery and intestine. Disease : Colibacillosis. Macro : Severe congestion and hemorrhages in mesentery and intestine (septicemia).
  61. 61. Organ : Colon. Disease : Colibacillosis. Macro : Ulcerative colitis (multiple ulcers in mucosa).
  62. 62. Organ : Colon. Stain : H&E. Disease : Colibacillosis. Micro : Inflamed and focally necrotic mucosa.
  63. 63. Necrobacillosis Causes: Fusobacterium necrophorum (Spheropherous necrophorum). Pathognomonic Lesions: In cattle: 1-Grayish white areas of coagulative necrosis in the liver and spleen. 2-Ulceration of the rumen. 3-Ulcerative and necrotizing stomatitis and enteritis. 4-Necrosis of the tail, teat, limbs and feet. Foot-rot or pododermatitis) In horse: 1-Severe necrotizing disease of feet (especially in dumpy areas). 2-Gangrenous dermatitis usually starts at the heel or in the deep structures of the frog and characterized by sharply demarcated necrosis. 3-It associated with Fistulus withers. In rabbits: 1-Yellowish-white necrotic mass in the lower lips, neck and thorax. 2-Bloody fluid in the pleural and pericardial cavities. 3-Pneumonia is seen. In calf (Calf diphtheria): 1-Diphtheritic membrane of Fibrinonecrotic exudate on the buccal mucosa, pharynx and larynx.
  64. 64. 2-Grayish-yellow dry cheesy-necrotic foci of coagulative necrosis on the borders of the tongue, inner surface of the cheek, gum, palate, pharynx and larynx. 3-Bronchopneumonia, purulent or necrotic pneumonia and pleurisy. 4-Acute catarrhal, ulcerative or necrotic enteritis. 5-The calf usually die from pneumonia and toxemia (4-5 days later). In sheep: 1-Digital infection (foot-rot). 2-Lip and leg ulceration. Digital Infections There are two groups of digital infections: 1-Contagious Foot Rot 2-Necrobacillosis of the Foot Causes: The contagious foot-rot is caused by Bacteroides nodosus that acts synergistically with Fusobacterium necrophorum. While, the necrobacillosis of the foot is usually caused by Fusobacterium necrophorum.
  65. 65. Pathogenesis: In contagious foot rot, initial colonization of Bacteroides nodosus and moistures or trauma is predisposing factors required for infection to occur. Bacteroides nodosus produces proteases and growth-enhancing factors that aid bacterial penetrations of the epidermis and bacterial growth especially Fusobacterium necrophorum that responsible for necrosis and inflammation. Pathognomonic Lesions: I-The contagious foot rot in sheep has 2 forms: i-Virulent Form ii-Benign Form i-Virulent Form: 1-The early lesions, red, moist and swollen skin with erosions are seen in the interdigital spaces or digits. 2-Later on, the inflammation spread to the epidermal matrix of the hoof leading to separation of the horn and prevention of new horn growth. 3-Lameness, chronic debility and weight loss are seen. ii-Benign Form: 1-The lesions are mild and confined to interdigital skin. 2-Separation of the horn may occur. 3-Hoof over growth may be seen.
  66. 66. II-Necrobacillosis of the foot (in sheep): 1-Acute necrotizing interdigital dermatitis and foot abscess. 2-Toe abscess and cellulitis may occur. NB: The Foot-Rot in cattle similar to the benign form in sheep.
  67. 67. Organ : Pharynx. Disease : Calf diphtheria (Necrobacillosis). Macro : Diphtheritic membrane of fibrinonecrotic exudate on the pharynx.
  68. 68. Organ : Tongue. Disease : Calf diphtheria (Necrobacillosis). Macro : Diphtheritic membrane of fibrinonecrotic exudate on the tongue.
  69. 69. Organ : Buccal cavity. Disease : Calf diphtheria. Macro : Fibrinonecrotic exudate on the tongue and epiglottis.
  70. 70. Organ : Tongue and lungs. Disease : Calf diphtheria (Necrobacillosis). Macro : Fibrinonecrotic exudate on the tongue and necrotic pneumonia.
  71. 71. Organ : Liver. Disease : Calf diphtheria (Necrobacillosis). Macro : Necrotic areas on the liver surface.
  72. 72. Organ : Rumen. Disease : Calf diphtheria (Necrobacillosis). Macro : Necrotic areas on the ruminal mucosa.
  73. 73. Salmonellosis Causes: Animals Cattle Sheep Equines Swine Poultry Rats Salmonella Species S. entertides, S. dublin S. abortus ovis S. abortus equi S. cholera suis S. gallinerum-pullorum S. typhimurium (reservoir) Pathogenesis: The route of infection by ingestion of contaminated food till reach the intestine lymphatics blood multiplication of m.o. with production of toxins Septicemia.
  74. 74. Pathognomonic Lesions: In Cattle: Acute (septicemic) Form: 1-Congestion of S/C blood vessels. 2-Hydrothorax, hydropericardium and hydroperitoneum. 3-Petechial hemorrhages on s. and m.m. 4-Degenerative changes in the parenchymatous organs. 5-Hemorrhagic streaks on the skeletal muscles. 6-The L.ns are enlarged, hemorrhagic and edematous. 7-Fibrinoid necrosis in the blood vessel and deposition of hyaline material in glomerular capillaries and minor vessels of dermis. Subacute and Chronic Forms: 1-Severe catarrhal to hemorrhagic gastroenteritis (stomach, intestine and colon). 2-Grayish necrotic foci (paratyphoid nodules) in the liver (coagulative necrosis surrounded by granulomatous reaction of macrophages and epithelioid cells). 3-The wall of gallbladder is thickened and inflamed. 4-Fibrinous sheath around enlarged spleen. 5-The mesenteric L.ns are enlarged, edematous and hemorrhagic. 6-Lesions of septicemia may be seen in the subacute form.
  75. 75. In Swine: 1-Septicemic lesions in acute stage. 2-Fibrinonecrotic or ulcerative (button-like) gastroenteritis (ileocecal). 3-Necrotic foci in the liver. 4-The mesenteric L.ns are enlarged, edematous and hemorrhagic. 5-Splenitis may occur. NB: In horse and sheep induce purulent orchitis in male and abortion in female with septicemic lesions in acute stages.
  76. 76. Organ : Colon. Disease : Chronic Salmonellosis. Macro : Ulcerative colitis (Button-like).
  77. 77. Listeriosis (Circling disease) Causes: Listeria monocytogens Pathognomonic Lesions: The Listeria has three forms: i-Septicemia Form. ii-Encephalitis (Nervous) Form. iii-Abortion Form. Septicemia Form: (mainly in newborn). 1-Focal necrosis in the liver, L.ns, spleen, lungs and GIT. 2-The necrotic areas are infiltrated with mononuclear cells and neutrophils (pyogranulomatous reaction). 3-Petechial hemorrhages on s. and m.m. 4-Gram positive rod-shape bacteria are seen in the lesions.
  78. 78. Encephalitis (Nervous) Form: 1-Small circumscribed collections of mononuclear cells with or without neutrophil infiltration are seen in the brain stem (pons, medulla oblongata and spinal cord). 2-Diffuse cellular infiltration (neutrophils) and microabscess are seen besides tissue necrosis and glial nodules. 3-Some nerve cells are destroyed in the gray matter. 4-Perivascular lymphocytic cuffing. 5-Intense meningeal infiltration of lymphoid cells (lymphocytic leptomeningitis). 6- Gram positive rod-shape bacteria are seen in the lesions. 7-Visceral lesions as in septicemia form. Abortion Form: see the diseases causing abortion.
  79. 79. Rabbit-Suffered Listeriosis show necrotic hepatitis and septicemia.
  80. 80. Organ : Medulla oblongata. Disease : Listeriosis. Macro : Medullary abscess is seen.
  81. 81. Organ : Brain. Stain : H&E. Disease : Listeriosis. Micro : Necrotic areas with intense aggregation of neutrophils.
  82. 82. Organ : Brain. Stain : H&E. Disease : Listeriosis. Micro : Necrotic areas with intense aggregation of neutrophils and congested blood capillaries.
  83. 83. Organ : Liver. Disease : Listeriosis. Macro : Grayish necrotic areas on the liver.
  84. 84. Organ : Liver. Stain : H&E. Disease : Listeriosis. Micro : Necrotic areas replaced by intense aggregation of neutrophils.
  85. 85. Organ : Liver. Stain : H&E. Disease : Listeriosis. Micro : Necrotic areas replaced by intense aggregation of neutrophils.
  86. 86. Swine Erysipelas Causes: Erysipelothrix rhusiopathiae Pathognomonic Lesions: It has 2 forms. I-Acute (septicemic) Form: 1-Petechial hemorrhages on serous membranes and epiglottis. 2-Degenerative changes in the parenchymatous organs. 3-Serous or hemorrhagic lymphadenitis. 4-Catarrhal gastritis with congested mucosa and mucus exudate. II-Chronic Form: 1-Vegetative endocarditis (in the left atrioventricular valve and sometimes pulmonary, aortic and tricuspid valves). These valves are gradually closed by cauliflower thrombotic mass. 2-Aortic and pulmonary valves show stenosis and lead to general passive hyperemia and edema. 3-Necrosis and sloughing of skin with thrombosed S/C blood vessels. 4-Arthritis with ankylosis (hardening of the joints). NB: Pathogenesis: The route of infection through intestinal tract penetrate the mucosa into the blood (facilitated by invasion of parasites) septicemia and then the organisms localized in particular organs as (capillary of the skin, the valves of the heart and joints) causing injury of the endothelium inducing hemorrhages, thrombosis and edema.
  87. 87. Organ : Skin. Disease : Swine Erysipelas (Diamond-skin disease). Macro : Grayish necrotic areas on the skin.
  88. 88. Organ : Endocardium (heart). Disease : Swine Erysipelas. Macro : Vegetative endocarditis.
  89. 89. Organ : Endocardium (heart). Disease : Swine Erysipelas. Macro : Vegetative endocarditis.
  90. 90. Organ : Joint. Disease : Swine Erysipelas. Macro : Arthritis with ankylosis.
  91. 91. Organ : Joint. Stain : H&E. Disease : Swine Erysipelas. Micro : Purulent arthritis.
  92. 92. II-Toxemic Diseases Diseases caused by clostridial infection The clostridium organisms can divide into two groups: The first group: They induced diseases through tissue invasion such as C. chauvoie, C. novyi, C. hemolytic which characterized by extensive tissue invasion and necrosis. The second group: They induce diseases without tissue invasion due to production of toxins such as C. botulinum (completely non invasive) and C. tetani (disease produce by circulating toxin produced by organism, which after entry to the body and remain locally. Species 1 2 3 4 5 6 C. chauvoie C. septicum C. hemolyticum C. novyi C. tetani C. perfringens Type A Type B Type C Type D Type E Disease Black leg disease Malignant edema &braxy Bovine bacillary hemoglobinuria Black disease tetanus Enterotoxemia in lamb Lamb dysentery Struck Pulpy kidney Enterotoxemia in calves, lamb, guinea pigs
  93. 93. Blackleg Disease Quarter ill or black quarter Cause: Clostridium chauvoie It produces four powerful exotoxins: 1-Alpha toxin: which is both necrotizing and hemolytic. 2-Beta toxin: which is DNase. 3-Gamma toxin: which is hyaluronidase. 4-Delta toxin: which is hemolysin. Pathogenesis: The infection occurs by ingestion, but in sheep wound infection may occur after castration, butting and shearing. The ingested spores multiply in intestine cross the intestine mucosa then to the circulation distributed to various organs and skeletal muscles. The spores remain dormant until the anaerobic environment occurs through necrosis of muscle by trauma. The microorganisms germinate, proliferate and start to produce toxins leading necrosis in the muscles and death occurs. The toxins damage the capillaries producing serohemorrhagic inflammation and gangrene. The proliferating organism can ferment carbohydrate (glucose) and produce gas.
  94. 94. Pathognomonic Lesions: 1-Emphysematous and edematous swelling in hind quarter and shoulder muscles. 2-The swellings are crepitated (gas gangrene) and microscopically, show coagulative necrosis. 3-The skin over the affected muscles is stiff and dark red or black in color. 3-The S/C tissue and inter and intramuscular connective tissue are infiltrated with yellowish gelatinous exudates. 4-The affected muscles are dirty brown and contain bloody fluid that has rancid-butter odor 5-Acute ulcerative endocarditis (left atrium). 6-The regional L.ns are Emphysematous and hemorrhagic. 7-The internal organs are congested and have hemorrhagic inflammation.
  95. 95. Organ : Shoulder muscles. Disease : Blackleg Disease. Macro : Emphysematous and edematous muscles.
  96. 96. Organ : Shoulder muscles. Disease : Blackleg Disease. Macro : Emphysematous and edematous muscles.
  97. 97. Organ : Heart. Disease : Blackleg Disease. Macro : Fibrinous pericarditis with hemorrhages.
  98. 98. Organ : Skeletal muscles. Stain : H&E. Disease : Blackleg Disease. Micro : Zenker’s necrosis with hemorrhages.
  99. 99. Organ : Lymph node. Stain : H&E. Disease : Blackleg Disease. Micro : focal replacement of the lymphoid tissue with round and oval spaces of variable sizes.
  100. 100. Malignant Edema Cause: Clostridium septicum. 1-By wound infection 2-By Ingestion Malignant Edema. Braxy Pathogenesis: The infection occurs through wound contamination (during shearing, butting or docking or parturition). The organisms gain to the heavy muscles after they reach the blood as blackleg disease. Pathognomonic Lesions: 1-Hot painful swelling at the site of infection. 2-These swellings become more edematous and hemorrhagic and contain more gas bubbles. 3-The swellings are pitted under pressure. 4-The lungs are congested and edematous. 5-The muscles are necrotic and dark red in color. 6-Some septicemic lesions in the parenchymatous organs.
  101. 101. Tetanus Lockjaw Cause: Clostridium tetani Pathogenesis: The infection occurs through wound infection. The bacteria grow in anaerobic environment and produce exotoxins, which spread allover, the body through lymph or blood and along nerve to CNS. The organism liberates 2 toxin component: i-Tetanolysin (hemolysin and fibrinolysin) ii-Tetanospasmin. Pathognomonic Lesions: No lesions are noticed but the animal die from asphyxia due to interference with respiratory and cardiac functions by tonic spasm. i-The blood is dark. ii-Rigor mortis occurs immediately after death. iii-Petechial hemorrhages on s. and m.m. iv-Fatty change in myocardium (tabby cat) may be detected.
  102. 102. Bovine Bacillary Hemoglobinuria Red water disease Cause: Clostridia hemolyticum (associated with liver flukes). Pathogenesis: The infection is through ingestion with wounds from the migration of liver fluke (initiate anaerobic condition). Under this condition, the clostridium starts to vegetate and produce exotoxins (necrotizing and hemolysin) and toxemia. Pathognomonic Lesions: 1-The liver is enlarged, mottled and friable and shows characteristic large areas of infarction (triangular area with hyperemic periphery). 2-The gallbladder is overdistended with bile. 3-The urinary bladder filled with red urine with mottled kidneys. 4-Presence of excessive amounts of clear or turbid, blood-stained fluid in the pleural, pericardial and peritoneal cavities. 5-Micro:i-Coagulative necrosis (infarctions). ii-Numerous thrombi in the blood vessels. -Moderate number of iii-neutrophils and Gram-positive bacilli are seen. iv-Hb-nephrosis.
  103. 103. Organ : Liver. Disease : Bovine bacillary Hb uria. Macro : Large areas of infarctions.
  104. 104. Organ : Liver. Disease : Bovine bacillary Hb uria. Macro : Large areas of infarctions associating with liver fluke.
  105. 105. Organ : Liver. Stain : Gram’s stain Disease : Bovine bacillary Hb uria. Micro : Long bacilli on necrotic liver tissue.
  106. 106. Black disease Infectious necrotic hepatitis Cause: Clostridia novyi type B (associated with liver flukes). Pathognomonic Lesions: 1-Dull grayish necrotic foci in the liver (coagulative necrosis). 2-The S/C veins are severely congested with dark red or black pelt. 3-Petechial hemorrhages on the epicardium and endocardium. 4-Hydropericardium is also seen.
  107. 107. Organ : Liver (sheep). Disease : Black disease . Macro : Large areas of necrosis associating with liver fluke.
  108. 108. Organ : Liver (sheep). Stain : H&E. Disease : Black disease . Micro : Coagulative necrosis.
  109. 109. Braxy Bradsot Cause: Clostridium septicum. Pathognomonic Lesions: 1-The abomasal wall is thickened, edematous and hemorrhagic (Hemorrhagic abomasitis and may be enteritis). 2-Similar lesions can be noticed in the first part of intestine. 3-Some septicemic lesions may be present as: -Hydrothorax, hydropericardium and hydroperitoneum. -Degenerative changes in the parenchymatous organs. -Petechial hemorrhages on s. and m.m.
  110. 110. Organ : Abomasum (sheep). Disease : Braxy. Macro : Hemorrhagic abomasitis
  111. 111. Organ : Abomasum (sheep). Disease : Braxy. Macro : Hemorrhagic abomasitis
  112. 112. Organ : Intestine (sheep). Disease : Braxy. Macro : Hemorrhagic enteritis
  113. 113. Diseases Caused by Clostridium perfringens Type Toxins Diseases Alpha Beta Epsilon Iota A + - - - Enterotoxemia in lamb B + + + - Lamb dysentery C + + - - Struck and enterotoxemia D + - + - Pulpy kidney E + - - + Enterotoxemia in calves, lamb, guinea pigs Enterotoxemia Yellow lamb disease Cuses: Clostridium perfringens types A and E Pathognomonic Lesions: 1-Intense icterus on serous and mucous membranes (yellowish). 2-Severe anemia (the carcass is paleness). 3-Hydropericardium. 4-The kidneys are dark red and enlarged. 5-The liver is friable.
  114. 114. Lamb dysentery Cause: Clostridia perfringens type B Pathognomonic Lesions: 1-Hemorrhagic enteritis and with ulcerated or necrotic mucosa. 2-Petechial and ecchymotic hemorrhages on the epicardium and endocardium. 3-Hydropericardium may be seen. Struck Cause: C. perfringens type C Pathognomonic Lesions: 1-Hemorrhagic enteritis with ulceration of the mucosa particularly of the duodenum and jejunum. 2-Pericarditis and Peritonitis with hydroperitoneum. 3-Petechial and ecchymotic hemorrhages are present on s. m. 4-Subendocardial and subepicardial hemorrhages are seen. Pulpy Kidney (over-eating disease) Cause: Clostridia perfringens type D . The bacteria produce protoxin which is converted to epsilon toxin by trypsin. Pathognomonic Lesions: 1-The dead lamb was in a good condition and with hydropericardium.
  115. 115. 2-The kidneys are soft, swollen and congested (rapidly autolyzed after death). 3-Petechial and ecchymotic hemorrhages are present in subepicardium and subendocardium, abdominal muscles and s. m. 4-Catarrhal gastroenteritis and the liver is dark and congested. 5-Focal malacia, edema and demyelination of the nerve fibers of basal ganglia, thalamus and cerebellum (white matter). Botulism It is a rapid fatal disease caused by the ingestion of the toxins of C. botulinum and characterized by motor paralysis {limberneck (torticollis) due to the released toxins prevent the release of acetylcholine at myoneural junction}. Pathognomonic Lesions: 1-There is no specific changes. 2-Subepicardium and subendocardium hemorrhages. 3-The intestinal mucosa is congested or hemorrhagic. 4-Perivascular hemorrhages in the brain and destruction of the Purkinje cells of cerebellum (the toxins do not affect on CNS).
  116. 116. Organ : Intestine (lamb). Disease : Lamb dysentery. Macro : Hemorrhagic enteritis.
  117. 117. Organ : Lymph nodes (mesentery). Disease : Lamb dysentery. Macro : Hemorrhagic and edematous lymph nodes.
  118. 118. Organ : Intestine (sheep). Disease : Struck. Macro : Hemorrhagic abomasitis
  119. 119. Organ : Kidney (lamb). Disease : Pulpy kidney. Macro : Autolytic, soft and swollen kidney.
  120. 120. Organ : Kidney (lamb). Disease : Pulpy kidney. Macro : Autolytic, soft and swollen kidney.
  121. 121. Organ : Kidney (lamb). Stain : H&E. Disease : Pulpy kidney. Micro : Retrogressive changes.
  122. 122. Pyemic Diseases Strangles Adenitis equorum Cause: Streptococcus equi Pathognomonic Lesions: 1-Catarrhal inflammation of upper respiratory tracts (rhinitis, pharyngitis) 2-The submaxillary, parotid and pharyngeal lymph nodes are enlarged and undergo abscess formation (suppurative inflammation 3-Mucopurulent nasal discharge may be seen. Complication of Strangles: 1-Septicemia and pyemia with metastatic abscesses in liver, lungs, kidneys, spleen and occasionally brain. 2-Extension of the inflammation from the upper to the lower respiratory tract (tracheitis, bronchitis, pneumonia, pleurisy and pericarditis). 3-Chronic valvular endocarditis. 4-Empyema in guttural pouch due to rupture of retropharyngeal L.ns. 5-Peritonitis due to rupture of mesenteric lymph nodes. 6-Purpura hemorrhagica (Petechial fever):
  123. 123. Purpura hemorrhagica (Petechial fever): It is complicated cases of strangles characterized by -Large areas of edema and hemorrhage in the subcutaneous tissue and mucous and serous membranes. The edema and hemorrhages are due to damaged endothelium and deficiency of blood platelets (thrombocytopenia) that are destructed by strep exotoxins. Joint-ill in Foals Navel-ill Septic Omphalophlebitis Causes: -Strept equi -Shigilla equi -E. coli -Coryne pyogenes -Brucella abortus equi. Pathognomonic Lesions: Prenatal-infected Lesions: (typical to the septicemic lesions). Postnatal-infected Lesions: mainly in the joint or umbilical cord. A-Lesions in the joint: especially in knee, hock and hip joints. 1-The affected joints are enlarged and contain excessive amount of synovial fluid (synovitis). 2-Serous arthritis (clear fluid) become turbid (fibrinous), tinged with blood or replaced by or discharging pus on the surface (purulent). 3-Focal necrosis of the cartilage and bones of the articular surface, inducing “osteomyelitis” inflammation of bone marrow.
  124. 124. B-Lesions in umbilicus: 1-The umbilical cord filled with pus (septic omphalophlebitis). 2-Hemothorax and hemoperitoneum. NB: With Brucella: (lesions mainly in the kidneys). 1-Suppurative arthritis and omphalophlebitis. 2-Embolic nephritis. With E. coli: (lesions mainly in the GIT). 1-Suppurative arthritis and omphalophlebitis. 2-Hemorrhagic gastroenteritis. 3-Cystitis (infection through urachus). Streptococcal mastitis There are three types of mastitis induced by different Strept serotypes. The first is contagious chronic mastitis induced by S. agalactiae. The second is acute self limiting mastitis caused by S. dysgalactiae. The last one is acute less severe mastitis with early complete recovery caused by S. uberis . Staphylococcus Infection It produces several exotoxins coagulase, fibrinolysins, hyaluronidase, hemolysins (alpha, beta, gamma and delta) and enterotoxin.
  125. 125. Pyoderma (Impetigo) It is subcorneal staphylococcal skin infection, characterized by vesicles and pustules (pyoderma), which is covered by yellow crusts. It is common in puppies, kittens and piglets. Botryomycosis Pathognomonic Lesions: Macroscopic Picture: -Single or multiple subcutaneous nodules -These nodules are ulcerated and exude a purulent exudate containing tiny, white or yellow granules, the so-called grains. Microscopic Picture: i- Pyogranulomatous dermatitis. ii-The predominant inflammatory cells are the epithelioid cells, macrophage and neutrophils besides giant cells, lymphocytes, and plasma cells. iii-Round or oval bodies in which a central core of bacterial colony is embedded in a homogeneous matrix (Splendore-Hoeppli material). iv- This material may coat the grains and take the form of a radiating corona of club-shaped bodies.
  126. 126. Corynebacterium (Actinomyces) Causes: Corynebacterium pyogenes, Corynebacterium renale, C. equi and C. pseudotuberculosis. C. pyogenes produces pyemia and embolic abscesses in different animals and organs (suppurative bronchopneumonia, hepatic abscesses, embolic nephritis, traumatic reticuloperitonitis and suppurative arthritis). While, the C. renale is associated with pyelonephritis in cattle. It may infect horse, sheep and dog. C. equi is an important cause of pneumonia in foals (2-6 months of age). Pathognomonic lesions: 1-Suppurative bronchopneumonia with multiple firm nodules in the lungs 2-The intestine show ulcerative enterocolitis in colon and cecum besides swollen and edematous mesenteric lymph nodes. 3-Microscopically, pyogranulomatous reactions (macrophages, giant cells, and less numerous neutrophils. Lymphocytes and plasma cells) are seen. C. Pseudotuberculosis or ovis: see the granulomatous diseases.
  127. 127. Foal suffered strangles show guttural pouch empyema.
  128. 128. Calf suffered Navel ill show inflamed navel (omphalophlebitis).
  129. 129. Organ : Liver and uricus. Disease : Chronic Omphalophlebitis. Macro : Embolic liver abscesses.
  130. 130. Organ : Peritoneum. Disease : Chronic Omphalophlebitis. Macro : Acute fibrinohemorrhagic exudate in the peritoneum.
  131. 131. Organ : Udder. Stain : H&E. Disease : Botryomycosis (chronic staph). Micro : Nidus of suppuration surrounded by fibrous tissue and granulomatous reaction.
  132. 132. Organ : Udder. Disease : Acute Staph (blue bag). Macro : Swollen, pedunculated and congested udder.
  133. 133. Organ : Udder. Disease : Acute Staph (blue bag). Macro : Swollen, pedunculated and congested udder.
  134. 134. Organ : Joint (pig). Disease : Chronic Staph infection. Macro : Joint-abscess.
  135. 135. Organ : Skin (pig). Stain : H&E. Disease : chronic staphylococcus (Greasy-pig disease). Micro : Pyoderma with extensive edema.
  136. 136. Diseases Causing Abortion Abortion: It is defined as the expulsion of a dead fetus or living conceptus at any period of gestation. Dead fetuses expelled at term are called stillbirths. Viable fetuses born before expected parturition are called premature birth. Causes: I-Non-Infectious Diseases: Non-infections causes of abortions are most difficult to determine and vary between animal species. It may include: 1-Toxic a-Plant eg. (Nitrate, ergot, Lupinus). b-Anthelmintics eg. (Benzimidazoles). c-Mycotoxins eg. Aflatoxins,.. 2-Hereditary eg. Protoporphyria. 3-Metabolic eg. Iodine or Vit. A deficiency and both selenium deficiency and selenium excess 4-Dystocia (any abnormalities during birth), which leads to Intra or PostPartum death. 5-In horses, twinning, premature placental separation, placentation insufficiency, umbilical abnormalities. II- Infectious Diseases:
  137. 137. There are three principal infectious manifestations in which abortions can be expected: a. Maternal systemic infection of the dam as with leptospirosis, salmonella septicemia or equine viral arteritis. b. Placental infections, as with brucellosis. c. Fetal infection as with herpesvirus. i-Bacterial-Induced Abortions Brucella, Campylobacter, Leptospira, Listeria, Salmonella, Chlamydia and others. ii-Viral Abortions Viruses may reach the fetus by one of three basic mechanisms: a-Direct infection by way of the vagina and cervix. b-Transplacental transmission from the mother to the fetus. c-Infection of the ovum (transovarian transmission). Examples: IBR, BVD, Blue tongue, RVF and Equine Viral Arteritis. iii-Protozoal Abortions: Trichomonas, Neospora, Toxoplasma, Sarcocystis. iv-Mycotic Abortions: Aspergillus spp., Absidia spp., Mucor spp., Rhizopus spp. and Mortierrella wolffii. Abortions occur late in pregnancy and the placenta is often retained. When passed, it has a thickened, dry appearance.
  138. 138. v-Mycoplasma, Ureaplasma and Rickettsia: Mycoplasma bovigenitalium, Coxiella burnetii (Q fever). vi- Unclassified Abortifactive Agent (Foothill Abortion): A tick-borne abortion disease of cattle. Brucellosis Bangle’s Disease (Animals) Undulating Fever (human) Causes: B. abortus (cattle) B. melitensis and B. ovis (sheep) B. suis (swine) Pathogenesis: The infections are through the digestive tract, conjunctiva, vagina and skin or from infected bull and AI. The organism reaches the digestive mucosa then to mesenteric Lns. engulfed by macrophages, where it multiplicates and migrates through LV. to thoracic duct then to the blood (bacteremia) without any clinical signs. In pregnant uteri: the organism attracted the uterus by the effect of Erythrinol substance (secreted from gravid uterus) then invaded the fetal membranes (placenta), uterine mucosa mammary gland and Lns of uterus and udder.
  139. 139. In non-pregnant uteri (calf or heifer): the infection via milk of infected dam reached to udder and its Lns. (supramammary) and stay till pregnancy. In Bull: after bacteremia the organism localized in testes, epididymis and seminal vesicles. Pathognomonic Lesions: In Pregnant Uterus and Placenta: 1-Focal necrotic placentitis (Acute or Chronic). 2-Retention of the placenta due to coagulative necrosis of fetal and maternal placentome associated with fibrosis. 3-The placenta is thick, yellowish brown in color, edematous, dull (opaque) and leathery in appearance. 4-Chronic inflammatory cells (macrophages, lymphocytes, plasma cells and neutrophils) are seen between the necrotic areas. 5-Endometritis and mastitis are seen. In Aborted Fetus: 1-Serosanguinous exudate in the subcutaneous and in the connective tissue between the muscles. 2-The umbilical cord are edematous. 3- The skin is covered with purulent exudate. 4-Serofibrinous inflammation of serous membrane of body cavities. 5-The newly borne fetus shows suppurative, hemorrhagic enteritis, or suppurative bronchopneumonia. 6-The spleen and L.ns are enlarged and may contain necrotic foci.
  140. 140. In Infected Male (Bull): 1-Suppurative orchitis and epididymitis are seen. 2-The seminal vesicles show hemorrhagic or necrotic foci. 3-Arthritis due to bacteremia may occur. In Sheep and Goat: As in cattle + Keratitis (cornea) focal chronic mastitis and bronchitis. In Horse: Suppurative inflammation in the bursa at crest and weathers (fistulus weathers) Campylobacteriosis (Vibriosis) Genital Form Abortion and infertility Intestinal Form Enteritis and diarrhea Causes: Campylobacter fetus Pathogenesis: In cow, through coitus (Venereal disease). In ewe, through ingestion of contaminated food. The organism reaches the capillaries between the maternal and fetal sides obstruction hypoxia and death of fetus expulsion outside (abortion). NB: The infection in cow lead to acquired resistance to reinfection (but in brucella, repeated abortions).
  141. 141. Pathognomonic Lesions: In Placenta: 1-The placenta is edematous, thickened and semi-opaque. 2-Petechiae (dark-red areas) with radiated dark streaks. 3-The cotyledons are yellowish and have yellow necrotic villi. 3-The placenta is not retained. In the Uterus: 1-Diffuse mucopurulent endometritis. The endometrium is covered with mucoid substance tinged with blood and infiltrated with neutrophils. In Fetus: 1-The fetus is usually died and autolyzed. 2-Reddish-brown fluid in the stomach of the fetus. 3-The whole body of the fetus is infiltrated with edematous fluid tinged with blood. 4-Focal necrosis in the liver, surrounded with hyperemic zone (Path). NB: Repeated breeders occur in cows due to early abortion which results from autolyzed fetus. Salmonellosis Causes: Salmonella abortus equi Salmonella abortus ovis Pathognomonic Lesions: (in equine) (in sheep) transmitted by coitus (venereal transmitted by ingestion.
  142. 142. Abortion Form: In Horse: 1-In placenta: -placenta is dark or hemorrhagic. -Thickened and edematous and necrotic foci. -Not retained. 2-In mare: -Severe Suppurative endometritis. -Cervicitis. -Septicemia. 3-In fetus: -Birth die or die after birth -Septicemia, pneumonia and gastroenteritis. 4-In stallion: Acute suppurative orchitis. In Sheep: 1-In placenta: -Placenta is thickened, edematous and necrotic (Retained placenta). -Bloody exudate (hematoma or hematocyst) between allantoins and chorion. 2-In ewe: -Severe Suppurative endometritis. -Septicemic lesions and gastroenteritis. -No Cervicitis.
  143. 143. 3-In fetus: -Birth die or die after birth -Septicemia, pneumonia and gastroenteritis. Listeriosis Cause: L. monocytogenes Abortion Form The dam shows septicemic lesions and endometritis. Abortion occurs in the last quarter of gestation (in cattle and sheep) without any clinical signs. 1-The abortion occurs due to intrauterine death of the fetus. So the aborted fetus is usually autolyzed with coagulative necrosis in the liver. 2-The placenta showed severe diffuse and necrotizing and suppurative inflammation of both cotyledons and intercotyledonary areas. Leptospirosis Cause: L. Pomona in cattle (dams show septicemic lesions). Placenta: 1-Avascular placenta 2-yellowbrown cotyledons 3-Placenta is slightly inflamed and edematous. Fetus: 1-Fetal death 2-Autolytic fetus. 3-Icterus may occur.
  144. 144. NB: (parasitic disease). Bovine Genital Trichomoniasis Causes: Tritrichomonas fetus Pathogenesis: The protozoan live in preputeal cavity (venereal) balanitis, seminal vesiculitis and epididymitis infected semen reach to vagina (Vaginitis) and uterus (endometritis). Pathognomonic Lesions: Placenta: 1-Destruction of placenta without inflammation. 2-Little edema. Fetus: 1-Emaciated or dead fetus, which coated with pus. 2- Fetal maceration and mummification In Cow or Bull: Pyometra, vaginitis and balanoposthitis.
  145. 145. Organ : Placenta. Disease : Brucellosis. Macro : Focal necrotic placentitis.
  146. 146. Organ : Placenta. Disease : Brucellosis. Macro : Chronic necrotic placentitis.
  147. 147. Organ : Joint. Disease : Brucellosis. Macro : Hygromas.
  148. 148. Organ : Joint. Disease : Brucellosis. Macro : Hygromas.
  149. 149. Organ : Joint. Stain : H&E. Disease : Brucellosis. Micro : Arthritis with round cells infiltrations.
  150. 150. Organ : Joint (horse). Disease : Brucellosis. Macro : Abscess in the withers.
  151. 151. Organ : Testes. Disease : Brucellosis. Macro : Chronic active periorchitis and epididymitis.
  152. 152. Organ : Testis. Stain : H&E. Disease : Brucellosis. Micro : Vasculitis with heavily neutrophils infiltrations.
  153. 153. Organ : Liver of aborted fetus. Stain : H&E. Disease : Brucellosis. Micro : Focal granuloma replaced the hepatic parenchyma.
  154. 154. Organ : Liver of aborted fetus. Stain : H&E. Disease : Brucellosis. Micro : Focal granuloma replaced the hepatic parenchyma.
  155. 155. Organ : Lung of aborted fetus. Stain : H&E. Disease : Brucellosis. Micro : Multifocal pneumonia.
  156. 156. Organ : Lung of aborted fetus. Stain : H&E. Disease : Brucellosis. Micro : Bronchopneumonia.
  157. 157. Organ : Liver of aborted lamb. Stain : H&E. Disease : Campylobacteriosis. Micro : Multinecrotic areas in the liver.
  158. 158. Organ : Placenta. Stain : Silver impregnation. Disease : Campylobacter. Micro : Several blackish-stained organisms.
  159. 159. Organ : Uterus (cow). Stain : H&E. Disease : Trichomoniasis. Micro : Pyometra.
  160. 160. Organ : Placenta (ewe). Disease : Toxoplasmosis. Macro : Multifocal cotyledonary necrosis .
  161. 161. Granulomatous Diseases These diseases are characterized by formation of granuloma. Granuloma: It is a chronic inflammatory reaction consisting of macrophages or macrophages, and giant cells. These diseases include: 1-Actinomycosis 2-Actinobacillosis 3-Tuberculosis 4-Glanders 5-Paratuberculosis 6Pseudotuberculosis 7-Nocardiosis 8-Parasitic diseases 9-Botryomycosis 10-Mycotic diseases 11-Leprosy Actinomycosis (Lumpy jaw) It is a chronic pyogranulomatous disease affecting hard tissue (mandible and maxilla) of cattle and man, and characterized by i-Abscess formation in the mandible and maxilla. ii-Rarefaction and necrosis of bone (honeycomb). Cause: Actinomyces bovis (Gram-positive long filamentous organism). NB: The infection through wound infection caused by sharp object localized or circulated through lymphatics to become generalized. Pathognomonic Lesions:
  162. 162. Macroscopic Picture: 1-Enlargement (large abscess) of the mandibular and maxillary bones (lumpy jaw). 2-The affected bone give honeycomb-appearance due to destructive rarefaction and regenerative process. 3-The abscess may rupture and thick creamy pus containing yellowish or sulfur granules which flow from one or several sinuses on the skin or in mouth. 4-Gritty texture (hard in consistency) due to calcification. Microscopic Picture: 1-The characteristic lesion consists of central irregular shaped mass of bacterial colonies (small). 2-These colonies surrounded by radiating eosinophilic clubs with rounded ends (Splendor-Hoeppli material). The clubs are usually thick and short. 3-These colonies are surrounded with 4 zones: i-Neutrophils forming adjacent zone. ii-Macrophages, giant cells and plasma cells zone. iii-Lymphocytes zone. iv-Vascular fibrous connective tissue capsule. 4-The colonies of Actinomyces may undergo calcification.
  163. 163. Bull-suffered Actinomycosis (Lumpy jaw) show large abscess in mandible bone
  164. 164. Bull-suffered Actinomycosis (Lumpy jaw) show chronic purulent osteomyelitis
  165. 165. Actinomycosis: Gram-positive long filamentous organism
  166. 166. Organ : Mandible. Stain : H&E. Disease : Actinomycosis. Micro : Central radiating colonies surrounded with pyogranulomatous reaction.
  167. 167. Organ : Mandible. Stain : H&E. Disease : Actinomycosis. Micro : Central radiating colonies surrounded with pyogranulomatous reaction.
  168. 168. Actinomycosis: radiating short and thick clubs Actinobacillosis (Woody Tongue) It is a chronic disease affecting soft tissue of cattle and sheep and characterized by pyogranuloma in the tongue and may be L.ns. The tongue is enlarged, immobile, hard in consistency and protruded from the mouth (woody tongue).
  169. 169. Cause: Actinobacillus lignieresi (Gram negative bacillus). Pathognomonic Lesions: similar to the Actinomycosis. 1-The affected tongue is enlarged, stiff and has multiple small abscesses. 2-The pus is thick, smooth and shiny and shows sulfur granules. 3-Abcesses are also seen in the lungs, liver, skin and forestomach. 4-The regional L.ns suffered from small, multiple abscesses and enlarged 5- The reaction around the colonies similar to Actinomycosis. Differentiation between Actinomycosis and Actinobacillosis Criteria Actinomycosis Actinobacillosis 1-Common name Lumpy Jaw Woody Tongue 2-The causes Actinomyces bovis Actinobacillus lignieresi 3-Gram stain Gram +Ve Gram -Ve 4-Affecting tissues Hard tissues (mandible and Soft tissues (tongue, Lns. maxilla) and others) 5-The colonies Small and eosinophilic 6-Radiating clubs Short and thick NB: Large and basophilic Long and thin Actinobacillus equuli induces septicemia (dead) or purulent arthritis and hemorrhages in the renal medulla (survived) foals.
  170. 170. Cow-suffered Actinobacillosis (Woody tongue) show chronic purulent glossitis.
  171. 171. Organ : Lymph nodes. Disease : Actinobacillosis. Macro : Multiple abscesses in the lymph nodes.
  172. 172. Organ Stain Disease Micro : Tongue. : H&E. : Actinobacillosis. : Thin and long radiating colonies with pyogranulomatous reaction.
  173. 173. Nocardiosis Bovine Farcy It is pyogranulomatous disease affecting the soft tissue of dog and cattle. Causes: Nocardia asteroides in man and dog. Nocardia farcinica in cattle. The organism is Gram positive and filamentous, and under some condition has acid-fast staining properties. Pathognomonic Lesions: In dogs: 1-The disease affects the lungs, pleura or skin (abscesses). 2-Under certain conditions, the disease become systemic and then localized in pleural and peritoneal cavities, brain or visceral organs. 3-Microscopically, central tangled indistinct colonies, surrounded by necrotic cellular debris, purulent exudate and granulation tissue. The colonies are not surrounded by radiating clubs. In cattle (Bovine Farcy): 1-The disease occurs as a chronic suppurative and granulomatous inflammation of the skin, lymphatics and draining L.ns. 2-The organism may circulate through the blood to the lung, liver, spleen and internal L.ns. 3-Nocardiosis may induce abortion, if it affects the fetus and placenta.
  174. 174. Buffalo-suffered Nocardiosis show bovine Farcy
  175. 175. Ovine Caseous Lymphadenitis Pseudotuberculosis It is a chronic infectious disease affecting adult sheep and characterized by enlargement of the L.ns (prescapular, mediastinal, bronchial, supramammary and prefemoral) and lymphadenitis with caseation and calcification. Cause: Corynebacterium pseudotuberculosis (C ovis). Pathogenesis: 1-The infection occurs through the wound and the m.o. localized in L.ns then engulfed with macrophages. The m.o. produces exotoxin (phospholipase D) and toxic lipids which kill these macrophages. 2-The lesions start first as small nidus of macrophages and epithelioid cells which die caseous necrosis developed. The central caseous mass is surrounded by epithelioid cells, lymphocytes and encircled by fibrous tissue. 3-As the lesions grow, the cells die and fibrous tissue remains visible. The results are spherical, onion-like concentrically laminated masses. Calcification occur. 4-Moreover, the m.o. may circulate in the blood and pyemia with embolic abscesses are developed in the lung, liver, kidney and spleen. Pathognomonic Lesions: Macroscopic Picture: 1-The affected L.ns are enlarged and swollen (mainly prescapular, mediastinal, bronchial, supramammary and prefemoral).
  176. 176. 2-Cut sections of the L.ns show “onion-like” lamination as fibrous connective tissue alternate with caseated friable mass. 3-Greenish or whitish-yellow pus surrounded by C.T. capsule. 4-Gritty sound may occur on cut section. 5-Multiple abscesses in the internal organs may be present. Microscopic Picture: 1-Central caseous necrosis and calcification surrounded by a thin layer of macrophages, epithelioid cells and lymphocytes. 2-Fibrous tissue capsule is formed the outer layer. NB: Acute focal areas of suppurative inflammation are seen in young lambs. The role of the lymphatics and lymph nodes in some diseases Diseases Causes Lesions Equine Pf. Mallei Lns are swollen. Burkholderia mallei Farcy Lvs are thickened, tortuous and discharge pus. Bovine Farcy Nocardia farcinica Suppurative and granulomatous inflammation of the skin, lymph vessels and Ln Ulcerative Coryne pseudo TB Only lymph vessels are affected (pus). lymphangitis Epizootic Cryptococcus or H. Lv and Ln are affected. lymphangitis farcinosa
  177. 177. Organ : Lymph nodes. Disease : Ovine caseous lymphadenitis. Macro : Onion-like lamination of caseous necrosis.
  178. 178. Organ : Liver. Disease : Ovine caseous lymphadenitis. Macro : Onion-like lamination of caseous necrosis.
  179. 179. Organ : Liver. Stain : H&E. Disease : Ovine caseous lymphadenitis. Micro : Focal replacement of the hepatic parenchyma with caseation and calcification .
  180. 180. John's disease Paratuberculosis Chronic Paratuberculous Enteritis It is a chronic infectious disease affecting cattle and sheep and characterized by chronic catarrhal enteritis, and lymphadenitis leading to profuse watery diarrhea. Cause: Mycobacterium paratuberculosis Pathogenesis: The infection occurs through ingestion of contaminated food and water with fecal mater. The m.o. penetrates intestinal mucosa (through M cells) to mesenteric L.ns then to the blood (bacteremia) or localized in the ileum to produce diffuse granulomatous reaction. The main affected parts are ileum, cecum, colon, ileocecal or cecocolic junctions. Pathognomonic Lesions: In Cattle: 1-The carcass is emaciated (thin). 2-The intestine (ileum, colon, and cecum) is thick, cord-like and the mucosa is corrugated similar to the convolutions of the brain (sulci and gyri) and ulcerated. 3-The mesenteric L.ns are swollen (granulomatous lymphadenitis).
  181. 181. 4-The crest of the folds are congested. 5-The intestine is covered from, the outside by grayish-white exudate 6-Micro, The mucosa and villi are thickened while the submucosa and lamina propria show diffuse leukocytic infiltrations (macrophages, epithelioid cells, giant cells, lymphocytes and few neutrophils (without nodular formation, caseation or calcification). Johne’s in Sheep: 1-The carcass is emaciated (thin). 2-The intestine (ileum, colon, and cecum) is thick and showed large granulomatous nodules. 3-The mesenteric Lns and Payer’s patches are swollen. 4-Micro, The nodules are consisted of central caseation with or without calcification and surrounded by macrophages, epithelioid cells, giant cells, lymphocyte and few neutrophils.
  182. 182. Cow- Johne’s Disease is severely emaciated (thin) and show watery diarrhea.
  183. 183. Organ : Iliocecal junction. Disease : Johne’s Disease. Macro : Irregular and thick mucosa similar to convolution of brain.
  184. 184. Organ : Iliocecal junction and lymph nodes. Disease : Johne’s Disease. Macro : Irregular mucosa and enlarged inflamed lymph nodes.
  185. 185. Organ : Intestine (Cow). Stain : H&E. Disease : Johne’s Disease. Micro : Diffuse granulomatous reaction.
  186. 186. Organ : Intestine (Cow). Stain : H&E. Disease : Johne’s Disease. Micro : Diffuse granulomatous reaction.
  187. 187. Organ : Lymph nodes (Cow). Stain : H&E. Disease : Johne’s Disease. Micro : Chronic granulomatous lymphadenitis.
  188. 188. Organ : Intestine (Cow). Stain : Ziehl nelson stain. Disease : Johne’s Disease. Micro : Acid Fast bacilli are seen.
  189. 189. Glanders It is a chronic contagious disease of solipeds (horse, donkey and mules). It affects the lower respiratory system and characterized by formation of vascular nodules in the septum nosi, lungs and skin (farcy). Cause: Pseudomonas mallei (Malleomyces mallei, Burkholderia mallei). Route of infections: 1-By ingestion of contaminated food. 2-By inhalation. 3-By direct contact (contagious) particularly through infected skin. NB: The male guinea pig are susceptible laboratory animal. When it injected IP, induces suppurative orchitis result s in 3 to 4 days (Strauss reaction). Pathogenesis: -The disease usually affects the old horse (3-7 years). -The m.o. (ingestion) reaches the stomach intestine L.ns Then to the blood where it localized in respiratory system and skin. Droplet infection is rare and localized in lungs and nose or passes to stomach through nasopharyngeal opening. Lv.
  190. 190. Pathognomonic Lesions: Three forms of glanders are seen: 1-Respiratory Form: i-In the early stage, the lungs feel as tough as if it contains shot-gun pellets ii-In the late stage, the lungs show nodules similar to TB ones. iii-The structure of this nodule is consisted of A-Young Nodules: Accumulation of neutrophils or pus surrounded with histiocytes and may be encircled with vascular connective tissue. B-Old Nodules: i-Central caseation without calcification ii-Surrounded by numerous neutrophils iii-Macrophages, epithelioid cells and giant cells iv-Vascular CT capsule. v-Purulent bronchopneumonia. iv-Sometime, the liver and spleen may be involved (show nodules).
  191. 191. 2-Nasal Form: The nodules in the septum nosi lead to ulceration and perforation of it due to invasion of secondary pyogenic bacteria. It heals by scar with formation of star-shaped. 3-Farcy or Cutaneous Form: affects lymph node and vessel of hind limbs. i-Swelling of the L.ns of hind limb. ii-The Lvs are thickened, cord-like, tortuous, ulcerated and contained or discharge pus (creamy). iii-Healing may occur slowly with scaring. Differences between Glanders and TB nodules Glanders nodules Presence of pus and neutrophils Vascular capsule Calcification not occur Pyogranulomatous reaction TB-nodules No pus and neutrophils Avascular capsule Calcification is present Granulomatous reaction only
  192. 192. Glanders: respiratory form (shot gun-pellets and nodules similar to TB)
  193. 193. Equine Farcy
  194. 194. Equine Farcy
  195. 195. Organ : Lung (Horse). Stain : H&E. Disease : Glanders. Micro : Focal replacement of the pulmonary tissue with purulent foci.
  196. 196. Tuberculosis It is a chronic granulomatous infectious disease affecting all species of animals and man, and characterized by formation of “avascular” tubercles nodules in different organs. Causes: Mycobacterium tuberculosis in human and primates. Mycobacterium bovis in all animals. Mycobacterium avium in birds NB: The cell wall is an important structure which plays an important role in pathogenesis of the disease. The cell wall contains mycolic acids, complex waxes and glycolipids (60% lipid). The Rout of Infection: 1-By Inhalation: It occurs in cattle (droplet infection) Lungs L.ns (primary complex) then invasion to the blood Bacteremia and dissemination of the bacteria to all organs (miliary TB). NB: Primary complex is the presence of the tuberculosis in the organ and its draining L.ns. 2-By Ingestion: It is common in horse, birds and young animals through drinking of infected milk. The primary lesions are seen in the digestive tract and liver. 3-Other Ways: e.g. wound or intrauterine infection.
  197. 197. Factors affecting development of the lesions: 1-The animal species, age and breed: guinea pigs are the susceptible host 2-Virulence and strain of the TB organisms. 3-The resistance and immunity of the animals. 4-Tissue involvement. Mechanism of tubercle formation: 1-When the bacilli inter the host’s tissue; they induce local reaction (edema, hyperemia and neutrophils). The neutrophils are rapidly disappear from the infected area due to their destruction and removed by macrophages. 2-The second cell arrived is macrophage which attract to the infected area in response to lipid content of the destructed bacillus-cell wall. The macrophages phagocytize neutrophils containing the organism or free bacilli. 3-The bacilli can proliferate inside normal macrophages. Only activated macrophages can kill bacilli. These macrophages could elicit both T helper CD4 and cytotoxic CD8 cell response. The main role of CD4 cell in tuberculosis is producing INF-γ which stimulates and activates macrophages. The CD8 cytotoxic cells may kill macrophages that unable to kill the bacilli. 4-Accumulation of mycobacterium stimulates an inflammatory response, which mature into a granulomatous lesion (macrophages, epithelioid and giant cells) and then encircled with fibrous tissue.
  198. 198. Post primary infection: can occurs in animal under stress, where the resistance of the body is lowered and activation of infection occurs from old encapsulated lesions resulting in formation of daughter tubercle or gets entry to general circulation and localized in various organs. Types of Tuberculous reactions: i-Proliferative Form: It is characterized by formation of nodules and fibrous tissue capsule (usually in the lungs of cattle. (Miliary, old and caseous nodules). ii-Productive Form: It is characterized by production of REC and there is no nodules formation as in Tuberculous mastitis. iii-Exudative Form: It is similar to suppuration and occurs in the pleura (dog) and pericardium (cattle). In this form, neutrophils and fibrin may be superimposed on the mononuclear cells. NB: The TB in cattle has 3 forms according to the tissue reaction: 1-Lungs Proliferative form. 2-Udder Productive form. 3-Pericardium Exudative form. Pathognomonic Lesions: Structures of TB nodules
  199. 199. Structures of TB nodules 1-Young TB Nodules 2-Old TB Nodules -Tuberculous bacilli in the center -Central caseation and calcification. (May undergo caseation). -Surrounded by neutrophils (up to 24 -Surrounded by macrophages, epithelioid and hrs), macrophages, epithelioid and giant giant cells besides lymphocytes. cells besides lymphocytes. -Reticular fibers may be seen. -Avascular fibrous connective tissue capsule. Tuberculosis in the lungs of cattle: 1-Miliary tuberculosis 2-Chronic nodular tuberculosis. 3-Tuberculous bronchopneumonia. Miliary Tuberculosis: (the spread through the blood). Macroscopic picture: 1-Like millet seed and its size. 2-Grayish-white and translucent in color. 3-Firm in consistency. 4-Difficult enucleated.
  200. 200. Microscopic picture: (similar to young nodules). 1-Central aggregation of tuberculous bacilli or caseation. 2-Surrounded by macrophages, epithelioid and Langhans giant cells besides lymphocytes. The neutrophils are seen at the first hours (up to 24 hrs) then completely absent later. 3-Few reticular fibers are seen at the periphery. Chronic Nodular Tuberculosis: (the spread through inhalation). Macroscopic picture: 1-Pea or bean-like nodules in size. 2-Grayish-white or yellow in color. 3-Hard in consistency. 4-Cut sections give gritty sound due to calcification. 5-Diffecult enucleated (can be differentiated from parasitic nodules which are easily enucleated). Microscopic picture: (similar to old nodules). 1-Central caseation and calcification. 2-Surrounded by macrophages, epithelioid and Langhans giant cells besides lymphocytes. 3-Avascular fibrous connective tissue capsule.
  201. 201. Tuberculous Bronchopneumonia: (the spread through inhalation) -It is associated with nodular formation in the bronchi (bronchitis) then extends to the alveoli (pneumonia). -The nodules in the bronchi are either: 1-Closed tuberculosis: it indicates that the bacilli remain in tubercle and don't contact the outer air (no infection to others). 2-Opened Tuberculosis: it indicates that the lesions reveal cavitations and the bacilli come out with secretion and excretion and cause infection to others (Vomica). Tuberculous pleurisy and peritonitis There are two forms or diseases: 1-Pearl Disease. 2-Grapes Disease. Pearl Disease: It is one type of tuberculosis of serous membranes (pleura and peritoneum) and characterized by the presence focal or diffuse areas or nodules of soft grayish velvety granulation tissue and granulomatous reactions. The tubercles may aggregate in clusters similar to pearls. Sometimes, the center of the nodules becomes caseated.
  202. 202. Grapes Disease: It is one type of tuberculosis of serous membranes due to extensive clusters or communication of pearls and takes the shape of grapes. These nodules are white in color and similar to the old TB nodules (central caseation with or without calcification and surrounded with granulomatous reaction and fibrous tissue capsule). Tuberculous Mastitis The Route of infections: 1-Through the teat canal from milkers. 2-Through the blood (miliary). 3-Wound infection (in the udder). There are three forms: 1-Miliary Tuberculous Mastitis. 2-Chronic Lobular or Productive Tuberculous Mastitis 3-Diffuse Caseous Tuberculous Mastitis. Miliary Tuberculous Mastitis: It is associated with generalized tuberculosis and similar to young nodules.
  203. 203. Chronic Lobular or Productive Tuberculous Mastitis: Macroscopic Picture: 1-The udder is enlarged. 2-Hard in consistency. 3-No nodular formation. 4-The udder is difficult to be cut. 5- The supramammary lymph nodes are not usually affected. Microscopic Picture: 1-The reaction is similar structure to young nodules; but diffusely infiltrated in inter- and intra-acinar tissue leading to atrophy and degeneration of milk acini. 2-The interlobular septa are not affected. 3-No nodular formation, no caseation and calcification. Diffuse Caseous Tuberculous Mastitis: It is similar in its structure to chronic productive type; but with diffuse caseation (no nodular formation). The supramammary lymph node is swollen and caseated. Microscopically, caseated areas are present surrounded with hemorrhagic granulation tissue.
  204. 204. NB: All organs (digestive tract, CNS, spleen, skin and others) are affected. In sheep and goat: The lesions are similar to those of cattle but calcification is not common. In equine: It is productive form (more cellular) with little connective tissue and softening of the center with rarely calcification. In dog: It is exudative form similar to liquefactive necrosis. In birds: It is characterized by extensive caseation without calcification besides deficient cellular elements and connective tissue framework.
  205. 205. Organ : Lung and pleura. Disease : Tuberculosis. Macro : Large white nodules in the lung and pleura.
  206. 206. Organ : Pleura. Disease : Tuberculosis. Macro : Large white nodules in the pleura.
  207. 207. Organ : Lung. Disease : Tuberculosis. Macro : On cut surface, white nodules in the lung are seen.
  208. 208. Organ : Lung (bronchus). Disease : Tuberculosis. Macro : Bronchopneumonia (Vomica).
  209. 209. Organ : Liver. Disease : Tuberculosis. Macro : Large white nodules are seen.
  210. 210. Organ : Liver. Disease : Tuberculosis. Macro : Large white nodules are seen.
  211. 211. Organ : Kidneys. Disease : Tuberculosis. Macro : Large white nodules are seen.
  212. 212. Organ : Lymph node. Disease : Tuberculosis. Macro : Large white nodules are seen.
  213. 213. Organ : Spleen. Disease : Tuberculosis. Macro : Large white nodules are seen.
  214. 214. Organ : Intestine. Disease : Tuberculosis. Macro : Small white nodules are seen.
  215. 215. Organ : Lung. Stain : H&E. Disease : Miliary Tuberculosis. Micro : Focal area of caseation necrosis with granulomatous reaction.
  216. 216. Organ : Lung. Stain : H&E. Disease : Miliary Tuberculosis. Micro : Focal area of caseation necrosis with granulomatous reaction.
  217. 217. Organ : Endometrium. Stain : H&E. Disease : Miliary Tuberculosis. Micro : Focal area of caseation necrosis with granulomatous reaction.
  218. 218. Organ : Lymph node. Stain : H&E. Disease : Miliary Tuberculosis. Micro : Focal area of caseation necrosis with granulomatous reaction.
  219. 219. Organ : Lymph node. Stain : H&E. Disease : Miliary Tuberculosis. Micro : Macrophages, epithelioid cells and Langhan’s giant cells besides the lymphocytes are seen.
  220. 220. Organ : Lymph node. Stain : Von Koss’s stain. Disease : Tuberculosis. Micro : Caseation and calcification which stained black.
  221. 221. The End of Bacterial diseases /.‫أ.د‬ ‫محمد حامد العرينى‬
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