becterial disease patho.pdf

Bacterial Diseases  Tuberculosis Bovine tuberculosis, caused by Mycobacterium bovis, is a chronic disease characterized by caseating granulomas in lung, lymph nodes, and other organs. Control programs have minimized the occurrence of bovine tuberculosis in many developed co...

Bacterial Diseases  Tuberculosis Bovine tuberculosis, caused by Mycobacterium bovis, is a chronic disease characterized by caseating granulomas in lung, lymph nodes, and other organs. Control programs have minimized the occurrence of bovine tuberculosis in many developed countries.  Etiology Mycobacteria spp.- M. tuberculosis, M. bovis, M. avium and others Nonmotile, nonspore-forming pleomorphic coccobacilli. Gram-positive but almost unstainable by the simpler bacterial stains because of their high content of lipids. They are routinely stained with carbol-fuchsin, and then resist decoloration by inorganic acids. This property of acid-fastness of the stained bacilli depends on the amount and spatial arrangement of mycolic acids and their esters in the bacterial wall.  Etiology Cell membrane and peptidoglycan layers found in other bacteria, the mycobacterial cell wall contains a large hydrophobic layer of mycolic acids, which bestows hydrophobicity on the cell wall, conferring environmental and antimicrobial resistance. Following facters in the cell wall are associated with increased virulence – Increased glycolipid content of mycobacterial cell walls, – acid-fastness, and – the amount of trehalose dimycolate (cord factor).  Etiology Survive after phagocytosis by macrophages- glycolipids (mycosides) form a barrier against lysosomal digestion Intracellular survival is also facilitated by preventing fusion of phagosomes and lysosomes.  Etiology Both tuberculoproteins and the adjuvant lipids are present in infection, - result is the development of both humoral and cell-mediated immune responses. Humoral antibodies can be demonstrated by – serologic techniques, – but do not participate in the development of lesions or in the production of immunity. Cell-mediated responses are responsible for both aspects of the disease.  Transmission Inhalation of droplet nuclei or dust particles containing M. bovis - the most common route. Oral infection requires a greater dose of bacilli than airborne infection to cause disease. Transplacental transmission is a sequel of endometrial tuberculosis, and leads to fetal lesions in hepatic and portal lymph nodes. Less common routes of infection include percutaneous inoculation and genital transmission.  Transmission Success of tuberculosis eradication schemes is complicated by wildlife reservoirs, which maintain infection and transmit disease to cattle Immunosuppressed individuals (AIDS), are at particular risk. Ingestion of milk from cows with mammary tuberculosis - major route of infection in humans by aerosol or by contamination of cutaneous wound, when close contact with infected cattle.  Pathogenesis Contact with infected animals, discharges, morbid tissues Organisms through sputum at coughing- droplet infection Fomites- instruments, utensils and beddings Localizes and produce typical tubercle in lymph node Mostly pharyngeal and mesenteric lymph nodes Inhaled organism enter in the bronchial tree Macrophages, epithelioid cells, giant cells, Lymphocytes Fibrous connective tissues formed around tubercle  Pathogenesis Important concepts in the pathogenesis of tuberculosis include the ability of mycobacteria to survive within macrophages, and the role of cellular immune responses in inciting granulomatous inflammation and enhancing the ability of macrophages to kill bacilli. Initial innate immune response develops at this site of primary infection, as macrophages secrete cytokines—TNF-α and C-C chemokines—that recruit additional macrophages and lymphocytes to the site.  Pathogenesis Stimulated Macrophages secretes- interleukin (IL-12), which skews the immune response- to favor secretion of interferon-γ (IFN-γ) and IL-2 by CD4+ T-helper-1 lymphocytes. These IFN-γ–producing T-helper lymphocytes signal the development of cell-mediated immunity, First detected at 14-28 days after infection by positive tuberculin skin test reactions. The cytokines TNF-α and IFN-γ act synergistically to promote formation of the tuberculoid granuloma, a dynamic structure that prevents spread of infection to other sites in the lung, as well as animal-to-animal transmission, and represents a localized target for the immune response.  Clinical Signs Low grade fever Progressive wasting/ weakness loss of production Coughing Diarrhea Bovine, lung. Lung parenchyma is almost entirely replaced by variably-sized, coalescing, raised pale nodules. Pig, tracheobronchial lymph nodes. The center of the sectioned node is replaced by caseous, mineralized debris. Lung & lymph node. The lung contains multiple coalescing foci of caseous necrosis surrounded by thin pale fibrous tissue capsules (tubercles). Most of the lymph node is replaced by caseonecrotic debris with a laminated appearance reminiscent of caseous lymphadenitis. Bovine, uterus. The endometrium contains numerous raised tubercles Pig, liver. Pale, slightly raised granulomas are disseminated throughout all liver lobes. Tuberculosis lymph node with caseous granules Lung, Granulomatous Nodules Ulcerative tuberculosis-cattle Calcified caseous tuberculosis-cattle Ulcerative tuberculosis-cattle Granulomatous inflammation, Tuberculosis (Lung) Tuberculosis: submucosal intestinal granulomatous nodules Granulomatous meningoencephalitis in bovine tuberculosis. Affected areas are malacic and filled with partially liquefied caseous material (arrows). Granulomatous lymphadenitis in a cow : Mycobacterium bovis can cause severe granulomatous inflammation or caseous necrosis. Tuberculosis in a cow. A. Diffuse caseous necrosis of pulmonary lymph node caused by Mycobacterium bovis. B. M. bovis causing miliary granulomatous inflammation of retropharyngeal lymph node. Tuberculosis in a cow. Multifocal caseous necrosis of lymph node caused by Mycobacterium bovis.  Cutaneous infections caused by M. tuberculosis and M. bovis (the “bovine bacillus”) are rare but can occur in cattle, dogs, cats, and possibly horses. M. tuberculosis causes tuberculosis in humans. M. bovis, which infects many animals, historically spread to humans when they began drinking milk following cattle domestication. These facultative or obligate intracellular parasites grow best in tissue with high oxygen concentrations, such as lungs. Pulmonary and alimentary infections are more common in cattle, horses, and dogs, but skin infections can develop alone or in combination with disseminated infection. Most cases of tuberculosis in cats are cutaneous, with alimentary and respiratory forms less  Microscopic lesions Histologic features of the tubercle (1) a central coagulum of caseous necrosis, consisting of eosinophilic homogeneous material with scant nuclear debris and a variable degree of mineralization (2) a mantle of macrophages and Langhans-type multinucleate giant cells (3) a capsule containing lymphocytes, clusters of neutrophils in some cases, and a rim of collagenous connective tissue in chronic lesions (4) rare to numerous acid-fast bacteria within macrophages and giant cells of the mantle zone or extracellularly in the caseous core  MATERIALS TO BE COLLECTED FOR DIAGNOSIS Teased impression smear from the inner surface of the tuberculous lesions and the smears are fixed by heat Swabs of pus from lesions Pieces of affected organs in 10% formal saline along with lymph nodes Tuberculous mastitis: Milk from affected quarter in sterile containers.  Diagnosis Symptoms and lesions Tuberculin testing of animals Immunodiagnostic tests- ELISA Demonstration of acid fast bacilli Paratuberculosis/ Johne’s disease  Introduction It is a chronic, contagious granulomatous enteritis characterized by persistent diarrhea, progressive weight loss, debilitation, thickening of the intestine (corrugations), and eventually death. Synonyms: Johne’s disease  Etiology Mycobacterium paratuberculosis, also known as Mycobacterium avium subsp paratuberculosis Excreted – in large numbers in feces of infected animals and – in lower numbers in their colostrum and milk. It is resistant to environmental factors and can survive – on pasture for >1 yr; – survival in water is longer than in soil.  Host Most common in domestic ruminants, Spontaneous disease also occurs rarely in a number of free-ranging and captive nondomestic ruminants, camelids and rabbits, equids, swine, and captive primates. Wild mammals including lagomorphs, rodents, and carnivores, and several species of wild birds  Transmission Transmitted predominantly by the fecal-oral route, either directly by ingestion in feces or indirectly via contaminated milk, colostrum, or water. Present in semen or urine, and may cross the placenta, particularly during advanced disease.  Pathogenesis Faeces primary source of infection Ingestion of contaminated feed and water Localizes in intestinal mucosa, lymph nodes Residence within macrophages Multiplies, resistant to intracellular digestion Distributed in body from ileum, large intestine Decreased absorptive surface, chronic diarrhoea and malabsorption  Clinical signs Chronic diarrhoea Progressive wasting/ weakness, loss of production Hide bound condition Johne’s disease showing diarrhoea  Gross lesions Emaciation, cachexia Thickening of the intestinal wall Presence of ‘rugae’ Corrugations cannot be removed even after stretching of intestinal wall Lymphnodes (Mesenteric) enlarged Johne’s disease-normal and abnormal ileum (right) with prominent rugae Serosal edema and lymphangitis in a goat with Johne’s disease. Ileal subserosal granulomatous lymphangitis with prominent giant cells in a cow with Johne’s disease. Johne’s disease -Enlargement of mescentric lympn node Thickened mucosal folds that can also be seen from the serosal surface in the jejunum of a cow with Johne’s disease. Granulomatous enteritis in paratuberculosis sheep JD-Corrugation of intestine Corrugation of intestine- JD JD - Thickened ileum (top) and normal ileum (bottom)  Microscopic lesions Infiltration of macrophages, epithelioid cells and lymphocytes Presence of acid fast bacilli in epithelioid cells Absence of caseative necrosis, calcification in cattle Present in sheep and goat Nests of epithelioid cells in mesenteric lymph nodes Jejunum. Thickening of the mucosa caused by an accumulation of small lymphocytes, large epitheloid cells and multinucleated langhans-type giantcells (arrow). Granulomatous inflammation, predominantly in the villi. Paratuberculosis (Mycobacterium avium subspecies paratuberculosis). Cow. HE. Large number of acid fast bacteria in the cytoplasm of macrophages and giant cells of a cow with Johne’s disease. (Modified Ziehl Neelsen stain.) Chronic granulomatous lymphadenitis Mesenteric lymphnode. Infiltration of groups of epithelioidcells (large macrophages, pale-staining cytoplasm) in paracortex (left). Insert: manyred stained bacilli in epithelioid cells. Paratuberculosis (Mycobacterium avium subspecies paratuberculosis). Goat. HE, insert: Ziehl-Neelsen stain for acidfastness of mycobacteria.  MATERIALS TO BE COLLECTED FOR DIAGNOSIS Bowel washings in a sterile bottle Smears of mucosa pinched from rectum Affected piece of intestine and mesenteric lymph glands in 10% formalin.  Diagnosis Symptoms and lesions Demonstration of acid fast bacteria in rectal pinch Johnin testing of animals Immunodiagnostic tests- ELISA Demonstration of organisms in tissue  Anthrax Anthrax is an acute septicemic disease of animals caused by Bacillus sp. and characterized by sudden death, absence of rigor mortis, tary colour blood from natural openings and widespread haemorrhage. India, anthrax is mostly seasonal, occurring usually in rainy season.  Etiology Bacillus anthracis large, gram-positive, spore-forming organism when exposed to air or oxygen, form spores of most remarkable durability. Spores are known to remain viable in soil for at least 15 years, and probably much longer, because they have been noted to retain their vitality and virulence for 50 years in the laboratory. Number of organisms and the resistance of spores, which is of paramount importance in the epidemiology of the disease.  Host Highly pathogenic for most herbivorous animals and humans, whereas carnivorous birds and reptiles are resistant. Domestic animals are susceptible to B. anthracis in the decreasing order of goats, sheep, cattle, horses, pigs, and dogs. Farmed mink are highly susceptible. In ruminants, the disease is usually brief and septicemic; in horses, pigs, and dogs, it is frequently localized to the throat or intestine and may be fatal before invasion of the blood occurs. When the disease is septicemic, as it  Transmission Cattle and sheep – – by ingestion of contaminated food and water, – entry through mucous membranes by local trauma. – Cutaneous infection is rare – inhalation of spore-laden dust Dogs and pigs - infection as a result of eating an infected animal. Ingestion is an important mode of infection in horses and dogs It is also thought that infection can be transmitted to horses by blood-sucking insects. Pigs has been traced to the ingestion of bone meal that was not sufficiently sterilized. Humans have occurred after eating inadequately cooked meat from a goat dead of anthrax.  Pathogenesis Upon ingestion of the spores, infection may occur – through the intact mucous membrane, – through defects in the epithelium around erupting teeth, – through scratches from tough, fibrous food materials. Spores then germinate, and after localized multiplication, spread by means of lymphatics to lymph nodes and further to the bloodstream, Leading to massive septicaemia. B. anthracis - both a capsule and an exotoxin. Antitoxic immunity is protective, but develops slowly.  Pathogenesis Toxin production continues for a long time,- encapsulated, and phagocytic cells are unable to eliminate its source- resistant to phagocytosis, as well as to neutralizing antibodies. The severity of the disease is due to the production – lethal exotoxin -oedema and tissue damage. Death results from shock and acute renal failure, and terminal anoxia mediated by the central nervous system.  Pathogenesis Exotoxin has three components: – 1. Oedema factor (EF)/ Factor I – 2. Protective antigen (PA)/ Factor II and – 3. Lethal factor (LF)/ Factor III Oedema factor is - adenylate cyclase, which causes an increase in cellular cAMP levels- causing electrolyte and fluid loss.  Pathogenesis Protective antigen – has anti-phagocytic activity. Lethal factor – Stimulates macrophages to produce oxidizing radicals and – cytokines, such as interleukin-l, beta and tumour necrosis factor-alpha – which induce systemic shock and death.  Clinical signs Cattle and sheep - peracute or the acute form. – High fever (105-107°F)- febrile disease – Haemorrhage from natural orifices – Dyspnoea – Tary colour blood – Sudden mortality up to 90% Pigs and dogs – – Infection is usually localized to the pharynx, – with enlargement of the cervical lymph nodes, or – appears as an acute haemorrhagic gastroenteritis. Horses – Pharyngeal, or enteric disease.  Gross lesions PM examination of animals suspected for anthrax should not be conducted Blood smear examined for anthrax bacilli Discharge of blood from vagina, anus and mouth Tary colour of blood Enlargement of spleen Widespread haemorrhage on serous surfaces of visceral organs Subcutaneous oedema Failure of the blood to clot, absence of rigor mortis, and the presence of splenomegaly are the most important necropsy findings. Anthrax: enlarged dark spleen in cow Anthrax: enlarged dark spleen Bovine, lymph node. The node is hyperemic and contains multiple dark foci of hemorrhage.  Microscopic lesions Anthrax bacilli and spores in blood smear Spleen shows haemorrhage and accumulation of blood in red pulp Haemorrhage in lymphnodes, liver, lungs & kidneys Degenerative and necrosis in kidneys and liver Because of the tremendous number of anthrax bacilli observed in the blood of animals dying of the disease (109 bacteria/ml), it was assumed that death was due to blockage of the capillaries, popularly known as the "log- jam" theory.  Anthrax, in a cow. A. The red pulp is expanded by sludged red cells admixed with numerous leukocytes and bacilli in chains. Cytologic smears of sections of spleen stained with M’Faydean stain reveal very large numbers of bacilli. Bacillus anthracis is a large, blunt- to square-ended bacterial rod that forms short chains. Bacillus anthracis, methylene blue stain of tissue smear, high power. Note the intense red stain of the large capsule of this organism and the large number of bacteria. Demonstration of the capsule distinguishes this from post-mortem contamination  Zoonotic Importance Humans usually acquire anthrax from contact with infected animals, or animal products (hides, wool, shaving brushes made from infected pig bristies). The disease manifests as a localized, persistent cutaneous pustule, described as "malignant pustule" or "malignant carbuncle"; or as a systemic, often fatal pulmonary disease, known as "woolsorter's disease". Human, skin. Lesions are raised and have necrotic centers  Diagnosis Symptoms and lesions Demonstration of bacteria in blood smear Immunodiagnostic tests– ELISA, AGPT (Ascoli test) Ascoli test: B. anthrac is antigens can be demonstrated in extracts of contaminated products by a precipitation test using high-titred antiserum. Animal inoculation test causes death of mouse within 24 hrs  MATERIALS TO BE COLLECTED FOR DIAGNOSIS Blood smears from the ear or tail vein Smears of oedematous fluid from the swelling in throat/abdomen (pigs, horses). Swab of blood / exudate from throat swelling. Muzzle dried in shade for biological test- Putrefied case; piece of ear or muzzle in boric acid. Bacillus anthracis, ground glass colonies Bacillus anthracis, medusa head morphology.  Clostridia Infection 82  Diseases caused by Pathogenic Clostridia 83  Clostridium perfringens types (strains), toxins, and diseases 84  BLACK QUARTER Black Quarter is an acute disease of cattle and sheep caused by Clostridium chauvei and characterized by lameness, hot painful swelling in thigh muscles producing crepitating sound on pressure & accumulation of serosanguinous fluid in affected area.  Etiology Clostridium chauvei Gram positive, anaerobe, spore forming bacteria  Pathogenesis Ingestion of contaminated soil Wound infection Multiply in the intestines Bacteraemia– deposited in skeletal muscles Dormant stage until anaerobic environment Proliferation and release of toxins Necrosis and gas gangrene of muscles 87  Characteristic symptoms High fever (104-107°F) Swelling in thigh muscles Crepitating sound on pressure 88  Macroscopic features Serosanguinous fluid in thigh muscles Crepitating sound on pressure The affected area looks like greenish or bluish Oedema of subcutaneous tissue Affected muscles have porous appearance due to presence of gas Black colour of muscles is due to iron sulfide (FeS) Fibrino haemorrhagic pericarditis, pleurisy and ulcerative endocarditis 89 Blackleg (C. chauvoei): massive left gluteal swelling in calf Swelling in thigh muscles Blackleg: dark, necrotic, gluteal musculature (left), and normal Blackleg (gangrenous myositis) Pelvic muscle, cut surface. The muscle is darkred in color, dry, friable, and porous due to the presence of gas bubbles. The fascia is edematous. Clostridium chauvoei infection. Cow. extensive necrosis of the leg musculature with a blackish-red discoloration with a "bubbly" appearance Blackleg, muscle of a cow. Note the characteristic black color and the dry appearance of the necrotic muscle, with tiny gas bubbles just visible in the tissue  Microscopic features Degeneration and coagulative necrosis of muscles Streaks of haemorrhage between fibers Presence of ‘Rod’ shaped bacteria, oedema and infiltration of leucocytes 96 damage to muscle cells including extensive vacuole formation; a Gram stain is positive for a rod-like organism (right, arrows). Serum values for creatine kinase (CK) and aspartate aminotransferase (AST) enzymes are twice normal. Blackleg (myositis) Hind quarter muscle with hemorrhage. necrosis, edema and gas. Clostridium chauvoei infection. Cow. HE.  Diagnosis Symptoms and lesions Demonstration of Gram positive bacteria in exudate Isolation of bacteria Immunodiagnostic tests for demonstration of antigen /antibody- ELISA Demonstration of organism in muscle tissue section using special stains 99  Enterotoxaemia/pulpy kidney disease/ overeating disease Acute disease of sheep, goat and camel caused by Clostridium perfringens and characterized by endocardial haemorrhage, gastroenteritis and pulpy kidneys. Etiology Clostridium perfringens type D-sheep Clostridium perfringens type A-camel 100  Enterotoxaemia/pulpy kidney disease/ overeating disease Important disease of sheep and goats with a worldwide distribution. It occurs occasionally in cattle. The rarely observed subacute and chronic forms of the disease in sheep have been called focal symmetrical encephalomalacia (FSE), because for many years they were thought to be a different disease, but FSE is only one of pathologic manifestations of the subacute and chronic forms of type D enterotoxemia. 101  Clostridium perfringens types (strains), toxins, and diseases 102  Pathogenesis Normal inhabitant of gut Anaerobic condition due to over feeding Organism proliferates and produce toxins Toxins are readily absorbed to cause disease in animals Epsilon toxin is the third most potent Clostridial toxin (after botulinum and tetanus toxins) Epsilon toxin, is first produced as a nontoxic compound, which is converted to a potent toxin by proteolytic enzymes such as trypsin. It causes increased vascular permeability and tissue necrosis. 103  Pathogenesis Activated epsilon toxin apparently facilitates its own absorption through the intestinal mucosa and it is then transported to several target organs, including the brain, lungs, and kidneys. Alpha toxin is a phospholipase C – causes tissue destruction (necrosis) and – haemolysis. In this way it facilitates bacterial growth and invasion. This toxin is important in gas gangrene. 104  Clinical signs Over filled stomach Sudden mortality Opisthotonus (an arched position of the body) progresses into coma. In a few cases, convulsions, coma, and death is more quick. Sometimes, animals show a desire to push the forehead against a solid wall, such animals being referred to as "blind staggers". Sometimes these acute symptoms are preceded by anorexia and diarrhoea. There is usually hyperglycaemia and glycosuria. 105  Macroscopic features Epsilon- injurious effect on vascular endothelium leads to haemorrhage, oedema, and damage to parenchymal organs and the brain. There are petechial and ecchymotic haemorrhages beneath the epicardial and endocardial surfaces, the serous surfaces of the intestines, in abdominal muscles, in the diaphragm, and in the thymus. Hydropericardium is usually present. Other findings include distension of the rumen, reticulum, a bomasum, and lower intestine by ingesta and gas. The intestinal mucosa is usually hyperaemic. The gallbladder is often distended. kidneys are soft and friable, giving rise to the name" pulpy kidney disease". Usually, this is the result of postmortem autolysis, which occurs rapidly. 106  Macroscopic features Neurological signs are explained by lesions in the central nervous system,which are the most specific and diagnostic for the disease. These consist of bilaterally symmetrical focal malacia (softening) of the basal ganglia. Damaged endothelial cells develop pyknotic nuclei, and the vessels become surrounded by a zone of 0edema. 107  Pulpy Kidney, Enterotoxaemia 108  Classical enterotoxaemia : pulpy kidney 109  Hydropericardium with presence of fibrin strands in a sheep with Clostridium perfringens type D enterotoxemia 110  Colitis in a goat with Clostridium perfringens type D enterotoxemia. A. Mucosal hemorrhage and ulceration. 111 Focal symmetrical encephalomalacia in a sheep. Hemorrhage and softening in internal capsules and cerebellar white matter in a sheep with Clostridium perfringens type D enterotoxemia. (Courtesy University of California-Davis Anatomic Pathology.)  Microscopic features Cloudy swelling and necrosis of tubular epithelium in kidneys Congestion in liver, spleen and intestines Endocardial haemorrhage Oedema in lungs 113  Diagnosis History of over feeding Symptoms and lesions Demonstration of toxin Isolation and identification of causative organism 114  Braxy/ Bradsot Braxy, or bradsot, is an acute abomasitis of sheep and, less commonly, calves, caused by Clostridium septicum and characterized by oedema, necrosis and haemorrhage in abomasum. Etiology Clostridium septicum 115  Host The disease affects mainly young sheep, and usually occurs during the winter months. Spread- – Ingestion – Soil borne infection 116  Pathogenesis The pathogenesis is not understood, but it is presumed that a primary abomasitis, caused by the ingestion of grass or other feed, Permits invasion by C. septicum resulting in a fatal toxaemia. Soil borne infection Occurs in enterotoxaemia vaccinated sheep Ingestion of spores Spores localized in stomach Germinate under anaerobic conditions Abomasitis 117  Clinical signs Over filled stomach Sudden mortality History of enterotoxaemia vaccination 118  Macroscopic features Oedema of abomasal folds Congestion and haemorrhage in abomasum Necrosis of abomasal mucosa Congestion and necrosis in intestines 119  Microscopic features Congestion and haemorrhage of abomasal mucosa Presence of ‘Rod’ shaped organism in mucosal epithelium of abomasum Necrosis and presence of ulcers in abomasal mucosa 120  Diagnosis History of over feeding and enterotoxaemia vaccination Symptoms and lesions Demonstration of toxin Isolation and identification of bacteria 121  Black disease/ Infectious necrotic hepatitis Black disease is an infectious disease of sheep, cattle and buffaloes caused by Clostridium novyi and characterized by necrotic hepatitis, hydropericardium and black discolouration of skin. An acute fatal infection of sheep, and rarely cattle 122  Etiology Clostridium novyi Gram positive, rod, anaerobes Predisposed by Fasciola hepatica and Fasciola gigantica infection C. novyi is widely distributed in soil in the form of three strains of A, B, and C, Common inhabitant of the intestinal tract of sheep. 123  Etiology The strains are differentiated on the basis of toxin production. Type A produces alpha toxin, a necrotizing and lethal toxin. Type B produces both alpha toxin and beta toxin, a necrotizing, haemolytic, and lethal toxin. Type C is nontoxigenic and non-pathogenic. C. haemolyticum, which produces beta toxin, is considered to be a toxigenic variant of C. novyi. The type B strain, which is almost similar to C. haemolyticum, is the strain which causes black disease. 124  Hosts Well-nourished adult sheep in the 2-4 year age group are particularly susceptible, lambs being rarely affected. 125  Pathogenesis Following ingestion, C. novyi pass through the intestinal wall and lodge in the liver, where they remain as a latent infection. Organism normally present in intestine Favourable for growth of clostridial organism Metacercariae of liver fluke provides anaerobic environment It reaches in liver through metacercariae Produces alpha and beta toxin Hepatic necrosis 126  Clinical signs Fever (105-107°F) Sudden death 127  Macroscopic features Focal or diffused necrosis in liver along the track of liver fluke migration Petechiae on endocardium, epicardium with hydropericardium Black discolouration of subcutaneous / skin Subcutaneous venous congestion causes a dark discoloration of the skin (pelt)- which is the reason for the name "black disease 128  Microscopic features Necrosis in liver, infiltration of neutrophils Congestion, haemorrhage Presence of gram positive rods in necrotic lesions 129  Diagnosis Symptoms and lesions Isolation and identification of organism and its toxin Demonstration of organisms in tissue sections/ smear using special stains 130  Botulism Botulism is a fatal disease of animals caused by toxins of Clostridium botulinum and characterized by paralysis and sudden death. Clostridium botulinum is responsible for an extremely serious food intoxication, botulism. Etiology Clostridium botulinum Neurotoxin C1 and C2 Predisposing factor- phosphorus deficiency leading to pica. 131  Spread a common inhabitant of the alimentary tract of herbivores. The source of infection for animals is almost always carrion (i.e., dead and putrefying flesh), which includes domestic and wild animals, and birds. Ingestion of contaminated materials Bone chewing Bone meal Food of animal origin 132  Pathogenesis As stated, botulism almost always results from the ingestion of preformed toxin in a food source. C. botulinum makes numerous extremely potent neurotoxins, which are released when the organisms die and autolyse. Botulinum toxins act at the peripheral nerve endings, where they get bound and cause nerve blockage. These toxins cause death as a result of respiratory paralysis. 133  Pathogenesis However, there are two other pathogenetic mechanisms which have been called "toxicoinfectious". The first is "wound botulism“ The second mechanism in which the toxin is not ingested results from colonization of the gastrointestinal tract with C. botulinum, with subsequent production of toxin and absorption by the host. 134  Clinical Signs Paralysis Sudden death Botulism usually occurs in cattle with phosphorus deficiency who chew bones and remaining bits of decaying meat. This bone-chewing form of botulism is known as  "lamsiekte" in South Africa, "bulbar paralysis" in Australia, and "loin disease“ in the Unites States. 135  Clinical Signs Wound botulism resulting from type B toxin occurs in humans and foals, and is known as "shaker foal syndrome". Botulism is seen in most species of birds, except, vultures, which are resistant. 136  PM lesions Macroscopic features No characteristics gross lesion Microscopic features No characteristic gross lesion 137  Diagnosis History Symptoms Very difficult to establish diagnosis 138  Tetanus Tetanus is a bacterial disease of animals caused by the toxins of clostridia and characterized by prolonged spasmodic contractions of muscles, stiffness and immobilization. It is also known as lock jaw. Horses are most susceptible and cattle the least. Etiology Clostridium tetani Gram positive, anaerobe, rod shaped, produces toxins 139  Spread The portal of entry is usually through puncture wounds, – such as nail-pricks, or those produced by castration, docking or shearing, or those received during parturition. 140  Pathogenesis Sequel to a wound Growth of anaerobic Clostridium tetani Releases neurotoxins The toxin known as tetanospasmin, reaches the interspinal site by entering the bloodstream, attacking the peripheral nerve endings, and travelling along nerves to the central nervous system. The secretion of inhibitory neuro-transmitters, which normally control muscle spasms, is blocked by tetanospasmin. As a result of this blockage, tetanic spasm of voluntary muscles, and ultimately, nerve block and paralysis occur. 141  Pathogenesis "tetanolysin (a haemolysin), and "non-spasmogenic toxin". The former may help C. tetani to establish itself in wounds, and the latter may interfere with motor nerve function. It is tetanospasmin, however, which is responsible for the clinical picture of tetanus. Death occurs from asphyxiation due to fixation of the muscles of respiration. 142  Clinical signs Convulsions Immobilization Stiffness of muscles Lock jaw 143  PM lesions No specific gross or microscopic lesions are produced; and have no been described. Macroscopic features Presence of wound or history of wound. Stiffness of muscles Microscopic features Gram positive organism in wound Necrosis in muscles and gray matter of brain 144  Diagnosis Symptoms and lesions Presence of wound and bacteria 145  Bovine Bacillary Haemoglobinuria Also known as "red water disease" and "infectious icterohaemoglobinuria”. An acute, highly fatal toxaemia of cattle and sheep characterized clinically by a high fever, haemoglobinuria and jaundice, and by the presence of necrotic infarcts in the liver. 146  Etiology Clostridium haemolyticum (C. haemolyticus bovis or C. novyi type D ), – which is very similar, and identical in some respects, to C. novyi type B. Spread Like certain other clostridia (C. chauvoei, C. novyi), infection occurs following ingestion of the organisms in the soil. 147  Pathogenesis Following ingestion, organisms multiply in the intestinal tract, and finally enter into the systemic circulation. C. haemolyticum then localizes in the liver, and remains latent until an appropriate anaerobic environment allows its multiplication at this site. The migration of liver flukes is believed to be most effective method of causing the hepatic damage. This results in activation of the clostridia. 148  Pathogenesis Exotoxins then contribute to further liver damage, with the production of a characteristic "infarct", haemolysis, and death. The main toxin is beta toxin (identical to that of C. novyi), a phospholipase C which hydrolyzes lecithin and sphingomyelin and haemolyzes red blood cells. 149  Clinical signs sudden onset of haemoglobinuria, fever, anaemia, leukocytosis, collapse, and death within a day or two. The mortality rate is high. 150  PM lesions Macroscopic features large area of necrosis in the liver, resembling an infarct. It is always a solitary (single) lesion, in contrast to black disease, where multiple areas of hepatic necrosis can occur. Microscopic features Gram positive organism in wound Necrosis in muscles and gray matter of brain 151  PM lesions Microscopic features Necrotic tissue contains the Gram-positive bacilli Surrounded by a polymorphonuclear infiltrate. The kidneys are mottled as a result of haemoglobinuria Urine in the bladder is deep red. 152  Diagnosis Diagnosis is based on the pathological findings of hepatic infarct and haemoglobinuria, Isolation of C. haemolyticum. Differential diagnosis from many other bovine diseases which are accompanied by haemoglobinuria. Babesiosis Post parturient haemoglobinuria 153 Bacterial Diseases  Haemorrhagic septicaemia/ septicaemic pasteurellosis / barbone/ Stockyards disease Haemorrhagic septicaemia is a highly contagious bacterial disease of animals characterized by oedematous swelling in neck region, dyspnoea, pneumonia and wide spread haemorrhage in visceral organs. Progressive atrophic rhinitis in swine Hemorrhagic septicaemia in cattle and buffalo A severe and frequently fatal septicemic pasteurellosis of cattle  Introduction  Pasteurella multocida  Important killer bacteria of animals and birds  Heavy morbidity and mortality  Pasteurella multocida – primary causative agents of  Hemorrhagic septicemia (Ungulates )  Atrophic rhinitis (Pig)  Fowl cholera (Poultry)  Snuffles (Rabbit)  Pasteurella multocida – major contributor to  Bovine Respiratory Disease Complex (BRDC)  Enzootic pneumonia of swine  Enzootic pneumonia of calves  Pneumonia in sheep  Pasteurella multocida Etiology  Commensal organism  Normal microbiota of the oral, nasopharyngeal, and upper respiratory tract  An opportunistic pathogen or  Primary pathogen  Nonmotile  Gram – negative  coccobacillary - to rod - shaped organisms  0.3 – 1.0 μ m in width and 1.0 – 2.0 μ m in length  SerotypeEtiology of P. multocida  On basis of capsular antigens  Developed by Carter (1952)  Passive hemagglutination test  Five serogroups :- A, B, D, E, and F  On basis of lipopolysaccharide (LPS)  Developed by Heddleston et al. (1972)  Gel diffusion immunoprecipitation test  Sixteen serotypes:- 1 to 16  The serotype of Pm prevalent in India  B:2, A:1, A:1,3, A:3, A:4, A:3,4,12, F:3, D:1,D:3, F:1, F:4 and F:4,12 (Hemandri and Hiremath, 2011)  Haemorrhagic septicaemia of cattle is caused by P. multocida serotype 1 (or biotype B), and occasionally serotype 4 (D) and serotype E.  Transmission Spread occurs by the ingestion of contaminated foodstuffs The saliva of affected animals contains large numbers of organisms during the early stages of the disease. The disease occurs mainly during the rainy season.  Pathogenesis Ingestion of contaminated feed and water Saliva contains large number of organisms Organism is normal inhabitant in the terminal bronchioles and alveoli Cannot invade the lungs because of pulmonary defense Depend on – Bacterial products – Host products and/or – Host responses  Pathogenesis Stress, malnutrition, transportation, climatic changes Organism become virulent and destroys macrophages Death occurs due to hypoxia and toxaemia Organisms on entry into the system reaches blood, proliferate and spread throughout the body due to its septicaemic nature and produces petechial and ecchymotic haemorrhjages on serous and mucous menbranes in different organs. Hence it is called as - “ HAEMORRHAGIC SEPTICAEMIA ”  Clinical Signs The overall mortality in buffaloes is nearly three times more than in cattle. Acute septicaemia acute onset of fever (106°-107° F), profuse salivation, submucosal petechiation, severe depression, and death within 24 hours. Localization may occur in subcutaneous tissue resulting in the development of warm, painful swellings about the throat, dewlap, brisket or perineum.  Clinical Signs Severe dyspnoea occurs if the respiration is obstructed. In the later stages of an outbreak, some affected animals develop signs of pulmonary or alimentary involvement. Pasteurellae can be isolated from the saliva or bloodstream. The disease in pigs is similar to that in cattle.  PM lesion- Gross Widespread petechiae and ecchymoses on mucous and serous membranes are the main pathological findings Oedema of the lungs and lymph nodes. Oedema of the subcutaneous tissue with gelatinous fluid In a few animals there are lesions of early pneumonia and haemorrhagic gastroenteritis. Bovine, heart. There are numerous often coalescing petechiae on the epicardium. Bovine, submandibular region. There is severe subcutaneous/fascial edema and multifocal hemorrhage. The parotid gland exhibits interlobular edema.  Buffalo Calf …. Pathology Lung; buffalo calf, 2 days post infection (dpi). Congestion and consolidation of the cranial lobes. Praveena et al., 2014  Buffalo Calf …. Pathology Lung; buffalo calf, 6 days post infection (dpi). Consolidation, with sheets of fibrin on lung surface. Praveena et al., 2014  Buffalo Calf …. Pathology Dorsal surface of lungs at 1 dpi with P. multocida A:3 pneumonia. Clearly demarcated areas of deep red consolidation are present (black arrows) in the right cranial and middle lung lobes in this animal and many of the interlobular septa in the affected areas are oedematous (blue arrow). Dagleish et al., 2010  Buffalo Calf …. Pathology Dorsal surface of lungs at 7 dpi with P. multocida A:3 pneumonia. Multiple coalescing areas of pus are present in the subpleura in the affected consolidated left anterior lung lobe (black arrow) and to a lesser extent in the right anterior lung lobe also (blue arrow). Dagleish et al., 2010  Rabbit ….. Pathology Severe fibrinopurulent pleuropneumonia with extensive fibrinous adhesions on parietal pleura and lung surfaces, Serohaemorrhagic exudate in thorax also could be observed Jaglic et al., 2008  Rabbit ….. Pathology Pulmonary hyperemia and haemorrhagic pneumonia Jaglic et al., 2008  Rabbit ….. Pathology Patel et al., 2015  Rabbit ….. Pathology Patel et al., 2015  PM lesion- Microscopic The pneumonia is a classical fibrinous bronco pneumonia, mainly affecting the cranio-ventral portions of the lungs. Interlobular septa are thickened, the pleura is covered with fibrin, and alveoli are filled with neutrophils and mononuclear inflammatory cells. Numerous bacteria are present as are areas of necrosis.  Rabbit ….. Pathology Lung Patel et al., 2015  Rabbit ….. Pathology Lung Patel et al., 2015  Mouse….. Pathology Lung from a mouse with acute bronchopneumonia with infiltration of neutrophils into the alveoli and bronchioles Pors et al., 2011  Diagnosis Symptoms and lesions Demonstration of bipolar bacteria in blood smears Isolation of bacteria Immunodiagnostic tests– ELISA 26  Pneumonic Pasteurellosis of Cattle Also known as "shipping fever pneumonia" or simply as "shipping fever“. Etiology Pasteurella haemolytica - biotype A (serotype 1). There are two biotypes of P. haemolytica: biotype A (serotype 1) biotype T Pneumonic pasteurellosis of cattle, sheep and goats is associated with biotype A (serotype 1), biotype T is associated with systemic pasteurellosis in sheep and goats.  Spread Inhalation of infected droplets coughed up or exhaled by infected animals which may be clinical cases, or recovered carriers in which the infection persists in the upper respiratory tract.  Pathogenesis By Inhalation or part of the normal flora of the upper respiratory tract get down into the terminal bronchioles and alveoli Loss of effective lung clearance mechanism due to- – combination of viral infection of the respiratory tract – devitalizing influences from transportation, – temporary starvation, – weaning, – rapid fluctuations in ambient (surrounding) temperature, and – mixing of cattle from different origins  Pathogenesis collectively promote an increase in the total no. and virulence of pasteurella in the nasopharynx, alveoli - effectively cleared. Under normal conditions, clear pasteurella from alveoli by phagocytic mechanisms. Bovine pulmonary macrophages release 'superoxide anion' (free radical) when exposed to P. haemolytica. The response depends on the presence of opsonizing antibody and the quantity of organisms presented to the phagocyte.  Pathogenesis The pathogenesis of pneumonic pasteurellosis is complex and still not clearlyunderstood. Four virulence factors of P. haemolytica: fimbriae, a polysaccharide capsule, endotoxin (lipopolysaccharide), and leukotoxin. Capsule -inhibits complement-mediated serum killing as well as phagocytosis and intracellular killing of the organism  Pathogenesis The endotoxin can alter bovine leukocyte functions, and is directly toxic to bovine endothelium. It also raises circulating 5-hydroxytryptamine (serotonin), cAMP, and cGMP. Leukotoxin is produced by all known serotypes, and highly toxic to bovine neutrophils and macrophages when destroyed by the leukotoxin, - release of proteolytic enzymes, oxidant products, and basic proteins which degrade cellular membranes, increasing capillary permeability. Fluid accumulation in the interstitium of the alveolar wall, alveolar wall necrosis, and pulmonary oedema. Death occurs a s a result of hypoxia and toxemia.  Clinical signs High fever (105-107°F) Oedema in throat and brisket region Dyspnoea Ghar-ghar sound on respiration Pasteurellosis (“shipping fever”) severe respiratory distress in calf (Hereford cross) 34  PM lesion- Gross Widespread petechiae and ecchymoses on mucous and serous membranes are the main pathological findings Oedema of the lungs and lymph nodes. Oedema of the subcutaneous tissue with gelatinous fluid In a few animals there are lesions of early pneumonia and haemorrhagic gastroenteritis.  PM lesion- Microscopic The pneumonia is a classical fibrinous or lobar pneumonia, mainly affecting the cranio-ventral portions of the lungs. Interlobular septa are thickened, the pleura is covered with fibrin, and alveoli are filled with neutrophils and mononuclear inflammatory cells. Numerous bacteria are present as are areas of necrosis.  Diagnosis Symptoms and lesions Demonstration of bipolar bacteria in blood smears Isolation of bacteria Immunodiagnostic tests– ELISA 37 ACTINOBACILLOSIS / wooden tongue Actinobacillosis is a disease of cattle caused by Actinobacillus sp. and characterized by granulomatous lesions in tongue, lymph nodes. This is also known as wooden tongue. Etiology Actinobacillus legniresei 38  ACTINOBACILLOSIS Pathogenesis Organism is normally present in the oral cavity Traumatic injury of oral mucosa Reaches to regional lymph nodes and nasal mucosa Affinity with soft tissues of head and neck Acute inflammation with necrosis, suppuration and granuloma 39  ACTINOBACILLOSIS Characteristic symptoms Anorexia, pain in tongue due to hardening Sporadic occurrence Drooling of saliva 40  ACTINOBACILLOSIS Macroscopic features Enlargement of tongue due to granuloma formation Nodular lesions may also appear in rumen, skin, lungs and liver Flooding of pus from lesions present in tongue 41 Actinobacillosis - Thickened dorsum of tongue Actinobacillosis on mandible Actinobacillosis - Tongue Protrusion in Cow Actinobacillosis-cattle Actinobacillosis : Cattle Tongue, cross section. Diffuse sclerosing actinobacillosis (also called 'wooden tongue'). The tongue is enlarged, white, and firm as a result of a severe proliferation of connective tissue which replaces the muscular tissue. Actinobacillus Iignieresii. Cow. Actinobacillosis- Cattle Chronic pyogranulomatous lymphadenitis Mandibular lymph node, cut surface. A fibrous capsule around soft, gray-yellow, bulging granulomatous tissue containing multiple small abscesses. Actinobacillosis (Actinobacillus Iignieresil)  ACTINOBACILLOSIS Microscopic features Presence of colony of organism Palisade of Indian club like surrounded by neutrophils, mononuclear cells and lymphocytes Such lesions are surrounded by fibrous tissue Muscle tissue of tongue is replaced by fibrous tissue 52  ACTINOBACILLOSIS Microscopic features The colonies are much smaller, radiating clubs longer and more slender, and the purulent exudate is more abundant than in actinomycosis. Gram's staining of smears or sections reveals Gram-negative, rod-shaped organisms in the centre of the colonies. However, they are difficult to detect because of the acidophilic staining of the background. 53 Miliary abscess in pyogranulomatous lymphadenitis 'Sulfurgranule' (blue stained colony of bacteria) with a red regular peripheral rim of eosinophilic clubs surrounded by viable and necrotic macrophages and neutrophils (pus). Actinobacillosis (Actinobacillus Iignieresil). Cow. HE.  MATERIALS TO BE COLLECTED FOR DIAGNOSIS Smears of pus from deeper portion of the lesions - heat fixed; Pus in sterile tubes, small pieces of affected tissue in 10% formalin.  ACTINOBACILLOSIS Diagnosis Symptoms and lesions Isolation of bacteria Demonstration of organisms/colony in tissue sections (Demonstration of rosettes and the absence of Gram-positive organisms) DD- actinomycosis, nocardiosis, and staphylococcal infections ("botryomycosis"). 56  ACTINOMYCOSIS Actinomycosis is a disease of cattle, buffaloes and camels caused by Actinomyces sp. and characterized by suppurative osteomyelitis of mandible and Miliary nodules in lungs. This is also known as lumpy jaw. Etiology Actinomyces bovis 57  ACTINOMYCOSIS Pathogenesis Causative organism is a normal inhabitant of bovine buccal cavity Infection occurs through wounds in buccal mucosa After entry it causes rarefaction of bone Osteomyelitis Chronic suppurative and granulomatous reaction 58  ACTINOMYCOSIS Characteristic symptoms Anorexia due to pain in jaw Abscess in mandible and swelling of jaw Discharging of pus from lesion 59  ACTINOMYCOSIS Macroscopic features Lumpy jaw Swelling of jaw at mandible Miliary nodules in lungs and mammary gland Discharging of pus from jaw 60  ACTINOMYCOSIS Microscopic features Suppurative osteomyelitis of mandible Central liquifactive necrosed area with colonies of the organism surrounded by mononuclear and lymphocytic cells Colonies are known as sulphur granules Bigger in size than actinobacillosis Gram positive stain 61 Actinomycosis Actinomycosis with several granulomata on maxillary region of cow (Guernsey) Actinomycosis with large granulomatous mass on jaw of cow  MATERIALS TO BE COLLECTED FOR DIAGNOSIS  Smears of pus from deeper portion of the lesions - heat fixed; Pus in sterile tubes , small pieces of affected tissue in 10% formalin.  ACTINOMYCOSIS Diagnosis Symptoms and lesions Isolation of bacteria Demonstration of organisms/colony in tissue sections using special stains 66  BOTRIOMYCOSIS (STAPHYLOCOCCOSIS) Botriomycosis is an infectious disease of animals caused by staphylococci and characterized by suppurative granulomatous lesions in udder, jaw, shoulder or sternal region. Etiology Staphylococcus aureus 67  BOTRIOMYCOSIS (STAPHYLOCOCCOSIS) Pathogenesis Contact of infected animals Organism possesses number of virulent factors – Surface proteins for adherence – Enzyme for protein degradation – Toxins for host cell damage 68  BOTRIOMYCOSIS (STAPHYLOCOCCOSIS) Pathogenesis Toxin contains coagulase, fibrinolysins, hyaluronidase, hemolysins and endotoxins Lipases destroy the skin surface and help in abscessation 69  BOTRIOMYCOSIS (STAPHYLOCOCCOSIS) Characteristic symptoms Hardening of udder Papillary projections from jaw Yellow pus discharge from lesion 70  BOTRIOMYCOSIS (STAPHYLOCOCCOSIS) Macroscopic features Hard and nodular enlargement of udder Hard over growth in lower jaw or at shoulder or sternal region Yellow pus discharges from lesions Enlargement of lymph nodes 71  BOTRIOMYCOSIS (STAPHYLOCOCCOSIS) Microscopic features Infiltration of neutrophils, macrophages and lymphocytes surround the necrotic lesion which contain colony of organism Gram positive cocci are seen 72  BOTRIOMYCOSIS (STAPHYLOCOCCOSIS) Diagnosis Symptoms and lesions Isolation of bacteria Demonstration of organisms in tissue sections using special stains 73  Exudative Epidermitis (Greasy Pig Disease) in Pigs Caused by Staphylococcus hyicus that produce exfoliative toxin. Skin trauma is considered the most common triggering factor allowing the bacteria to establish in the dermis. Initially, the pigs have yellowish - brown crusts on the face and the ears. When the disease becomes more severe, the skin feels greasy and becomes covered with a dark - brown coating in which dirt easily is entrapped. 74  NECROBACILLOSIS Necrobacillosis is an infectious disease of animals caused by Spherophorus necrophorus and characterized by necrosis of liver, foot rot, diphtheria and enteritis. Etiology Spherophorus necrophorus 75  NECROBACILLOSIS Pathogenesis Common inhabitant of the oral cavity Toxins including exo- and endotoxins Cause of necrosis, oedema, laryngitis and dyspnoea Formation of diphtheritic membrane over oral mucosa Abscess formation in foot in sheep 76  NECROBACILLOSIS Characteristic symptoms Nasal discharge Coughing Sneezing Diarrhoea Lameness 77  NECROBACILLOSIS Macroscopic features Presence of diphtheritic membrane on tongue and pharynx in calves On removal of diphtheritic membrane, ulcer is left Necrotic areas in trachea Suppurative pneumonia Necrotic lesions in esophagus, rumen, abomasum, liver, spleen and heart Necrotic lesions and gangrenous foot 78  NECROBACILLOSIS Microscopic features Necrosis and infiltration of neutrophils in liver Necrosis and bronchopneumonia in lungs Necrosis of epithelium, ulcer and infiltration of neutrophils in tongue Congestion in lungs and liver 79  NECROBACILLOSIS Diagnosis Symptoms and lesions Isolation of bacteria Immunodiagnostic tests – ELISA Demonstration of organisms in tissue sections using special stains 80  NOCARDIOSIS Nocardiosis is a bacterial disease of animals caused by gram-positive bacteria and characterized by pneumonia, mastitis, lymphangitis and lymphadenitis. This is also known as Bovine Farcy. Etiology Nocardia asteroids Gram-positive, acid fast, aerobic, filamentus 81  NOCARDIOSIS Pathogenesis Organism enter via soil contamination of wounds Local subcutaneous oedema Spreads to lymph nodes Lesions may break skin to form abscess and sinuses Pyogranuloma formation 82  NOCARDIOSIS Characteristic symptoms Purulent nasal discharge Discharge from lymphatics and lymph nodes Bovine Farcy Mastitis and abortion 83  NOCARDIOSIS Macroscopic features Granulomatous lesions in lungs Mastitis- hardness of udder Lymphatics discharging pus Enlargement of lymph nodes, spleen and liver with abscess 84  NOCARDIOSIS Microscopic features Granulomatous lesion in lungs- in central area acid-fast organism surrounded by neutrophils, macrophages, lymphocytes and giant cells Tangled colonies of organism in necrotic debris. Purulent exudate 85  NOCARDIOSIS Diagnosis Symptoms and lesions Isolation and identification of bacteria Demonstration of organisms in tissue sections using special stains 86  CORYNEBACTERIM INFECTION (ACTINOMYCES PYOGENES) It is a common and important organism in pyogenic processes in cattle, pigs, sheep and goats 87 Cornybacterium Disease C. diphtheriae Diphtheria in Humans C. renale Pyelonephritis, ureterits, cystitis in cows; haemarrhagic cystitis and pyelonephritis in cows C. pilosum Cystitis and pyelonephritis in cows C. pseudo tuberculosis Caseous lymphadenitis in sheep and goats ulcerative C. ovis lymphangitis and pectoral abscesses in horses C. bovis Pyelonephritis and cystitis in pigs C. suis Pyelonephritis and cystitis in pigs C. Pyogenes Suppurative infection in cattle, sheep, ,goats and pigs; (Actinomyces summer mastitis in cattle pyogenes) C. ulcerans Wound infections and abscess C. equi Pneumonia in horses (Rhodoccous equi) 88  PSEUDOTUBERCULOSIS Pseudotuberculosis is a chronic disease of sheep, goat and camel caused by Corynebacterium pseudotuberculosis and characterized by pyogranulomatous lesions in lymph nodes. This is also known as caseous lymphadenitis. Etiology Corynebacterium pseudotuberculosis or C. ovis Gram-positive, diphtheroid bacillus 89  PSEUDOTUBERCULOSIS Pathogenesis Infection enters through abraded skin/ oral mucous membrane , through inhalation Reaches in local lymph nodes Intracellular and survive within macrophages C.pseudotuberculosis produces an exotoxin (a phospholipase D) and possesses toxic surface lipid, which allows the organism to survive within macrophages. Absecess and caseation in lymph nodes, lungs, liver, kidney, brain, skin and spinal cord. 90  PSEUDOTUBERCULOSIS Characteristic symptoms Enlargement of superficial lymph nodes Discharge of thick green pus from lymph nodes Nodular lesions on skin (camels) Paraplegia/paralysis of hind legs 91  PSEUDOTUBERCULOSIS Macroscopic features Enlargement of lymph nodes Nodules on skin Caseous mass on cut of lesion, onion like concentric laminated mass Discharge of pus 92  PSEUDOTUBERCULOSIS Microscopic features Caseous necrosis surrounded by epithelioid cells, lymphocytes and covered by fibrous connective tissue Concentrically laminated mass with no giant cells Calcification 93  PSEUDOTUBERCULOSIS Diagnosis Symptoms and lesions Isolation and identification of causative organisms Demonstration of bacteria in tissue sections using special stains 94  YERSINIOSIS Yersiniosis is an infectious disease of animals caused by Yersimia sp. and characterized by abortion in cattle, necrotic hepatitis and arteritis. This is often confused with brucella induced abortions in cattle as yersimia serologically cross reacts with brucella. Etiology Yersinia enterocolitica Yersinia pseudotuberculosis 95  YERSINIOSIS Pathogenesis Yersinia have a protein ‘invasin’ on their cell wall Binds with host cell integrins Multiplication of organism inside the host cells Necrosis, pus formation and formation of nodules in liver Placentitis leading to abortion 96  YERSINIOSIS Characteristic symptoms Abortion in cattle, sheep and goat Diarrhoea in pigs 97  YERSINIOSIS Macroscopic features White/gray nodules on placenta and liver of aborted foetus Enteritis, ulcers in ileum Enlargement of mesenteric lymph nodes Necrotic foci in liver, spleen, lymph nodes and lungs 98  YERSINIOSIS Microscopic features Necrotic lesions in liver surrounded by macrophages, lymphocytes, epithelioid cells and covered by fibrous capsule Necrosis in intestines, spleen, lymph nodes 99  YERSINIOSIS Diagnosis Symptoms and lesions Isolation and identification of bacteria Immunodiagnostic tests- SAT/ELISA Demonstration of organisms in tissue sections using special stains 100  BRUCELLOSIS Brucellosis is an infectious bacterial disease of animals caused by Brucella sp. and characterized by abortion in late gestation and formation of granulomatous lesions in genital organs, joints and fetal liver. Etiology Brucella abortus Br. ovis Br. melitensis Br. canis 101  BRUCELLOSIS Synomemus: Mediterranean fever Gastric fever Bruce's septicaemia Malta fever Bang's disease" or "Bang's abortion disease“ Undulant fever 102  BRUCELLOSIS Pathogenesis Ingestion Enter through intact or abraded skin or conjunctivae After entry, organisms first localize in regional lymph nodes, where they proliferate within reticulo endothelial cells. The organisms enter and travel through the intestinal epithelial cells overlying Peyer's patches by endocytosis. Then they enter into the lymphatics. Development of bacteraemia 103  BRUCELLOSIS Pathogenesis Affinity with female and male reproductive organs, placenta, foetus, and mammary glands. Localize in lymph nodes, spleen, liver, joints, bones Proliferates intracellularly High affinity with erythritol in placenta and foetus particularly for chorio-allantoic trophoblasts This sugar also promotes growth of brucella organisms in vitro. Abortions in animals in late gestation 104  BRUCELLOSIS Pathogenesis Usually, infections with brucella are chronic, or persistent, often without clinical signs. 105  BRUCELLOSIS Characteristic symptoms Orchitis Accumulation of fluid in scrotum Abortion in late gestation (7-9 month) Retention of placenta Hygroma of knee 106 Brucellosis- swelling at carpal joint (Hygroma of knee)  BRUCELLOSIS Macroscopic features Oedema of chorion Oedema of foetus, serosan-guinous fluid in body cavity Pneumonia, necrotic foci in liver Enlargement of scrotum in males Induration of mammary gland in cows 108  BRUCELLOSIS Necrotic foci in liver Enlargement of scrotum in males Brucellosis: thickened placenta with white necrotic foci on cotyledons 110  BRUCELLOSIS Microscopic features Infiltration of phagocytic cells, epithelioid cells and lymphocytes surrounded by fibrous tissue proliferation Fetal broncho pneumonia Organism in chorionic epithelial cells In males, proliferation of fibrous tissue compresses or replaces epididymis 111  BRUCELLOSIS Diagnosis Symptoms and lesions Immunodiagnostic tests- CFT, SAT, ELISA, DIA Isolation of bacteria Demonstration of organisms in tissue sections using special stains 112  CAMPYLOBACTERIOSIS Campylobacteriosis is an infectious disease of cattle and sheep caused by Campylobacter sp. and characterized by early abortion, suppurative metritis, cervicitis and vaginitis. Etiology Campylobacter foetus Comma shaped bacteria 113  CAMPYLOBACTERIOSIS Pathogenesis Natural inhabitant of reproductive tract of bovines Preputial cavity Mucosa of glans penis Distal portion of urethra Vagina, cervix, uterus and oviduct Spreads through coitus or AI due to use of infected semen 114  CAMPYLOBACTERIOSIS Pathogenesis Bull to bull transmission occurs through artificial vagina Bacteria multiplies in the cervix Reaches to uterine horn and oviduct within 7-14 days Protected from phagocytes because it is covered with mucous Abortion at 5 month of gestation Organism impairs the supply of oxygen and nutrients 115  CAMPYLOBACTERIOSIS Characteristic symptoms Abortion in mid gestation (5 month) Mucopurulent vaginal discharge Retention of placenta 116  CAMPYLOBACTERIOSIS Macroscopic features Abortions at 4-5 month of gestation Purulent exudate in uterine discharges- yellowish Congestion of vagina Oedema in foetus Necrotic foci in liver Oedematous placenta 117 Pig, small intestine. White to tan multifocal luminal exudate within the small intestine. Pig, small intestine. Hemorrhage in the lumen of the small intestine with thickened mucosal folds.  CAMPYLOBACTERIOSIS Microscopic features Infiltration of neutrophils, macrophages & lymphocytes in uterus Enlargement of uterine glands Necrosis in placenta Suppurative endometritis, cervicitis and vaginitis 120  CAMPYLOBACTERIOSIS Diagnosis Symptoms and lesions Isolation of bacteria Immunodiagnostic tests – ELISA Demonstration of organisms in tissue sections using special stains 121  Leptospirosis Introduction Leptospirosis is an important, complex spirochetal infection of animals and humans caused by serovars of Leptospira interrogans. cause of abortion and stillbirth in farm animals but also causes acute disease (septicemia, hepatitis, nephritis, meningitis) in these and other animals. Mud fever. a type of leptospirosis occurring in the summer and autumn in Germany and Russia, caused by Leptospira interrogans; it is transmitted to humans by the field mouse and affects mainly workers in swamps or flooded fields. Called also autumn fever. 122  Leptospirosis Synonyms of Leptospirosis Stuttgart disease Canefield Fever Canicola Fever Field Fever Mud Fever Seven Day Fever Spirochetosis Swineherd Disease Weil’s disease- Man 123  Leptospirosis Etiology: Leptospira interrogans- pathogenic species – L. icterohaemorrhagiae - Man – weil’s disease – L. canicola -Dogs – L. pomona – Swine and Cattle – L.grippotyphosa - Goat Leptospira are thin (leptos = thin) spiral organisms, single and helical, with bent, hooked or curved ends motile by means of periplasmic flagella 124  Leptospirosis Incidence Worldwide distribution and affects cattle, pig, sheep, dog and man Rat – Reservoir Transmission The natural reservoir of pathogenic leptospires is the proximal convoluted tubules of the kidney and, in certain maintenance hosts, the genital tract. 1. Ingestion 2. Coitus 3. abrasions 4. Intact skin 5. In- utero 6. Man can be infected while swimming in water Transmission may be direct, that is, through contact with urine, postabortion discharges, milk, or through venereal or transplacental transmission. 125 Pathogenesis: The organism invade the blood stream and multiply producing septicaemia -Temperature rises and last for several days Animals not die during this phase, the organisms settles down in liver, kidney and pregnant uterus Acute form – Calves, piglets and lambs Sheep and goats – encephalitis occurs Jaundice – Intravascular haemolysis and hepatic necrosis Anemia , icterus, haemoglobinuria Leptospires – Found in Urine Albuminuria – Interstitial Nephritis- Focal or diffuse Gravid uterus – abortion Uraemia – Death 126 127  Clinical Signs Acute / septicaemic stage fever, haemorrhages, bloody diarrhoea, vomiting, jaundice Increased erythrocyte sedimentation rate, albuminuria, severe debilitation, often death. Peracute form few signs other than haemorrhage, is most common in puppies. The subacute / nephritic form/ Stuttgart disease characterized by typical signs of uraemia, and include "uraemic" breath, Ulcerative stomatitis, vomiting (often bloody), weight loss, dehydration, coma, and death. 128  Gross lesions Icterus, anaemia, petechiae on serous membrane Liver – Haemorrhages –near the central veins Kidney -Swollen and red , nepheitis Spleen - Haemosiderosis Acute haemorrhagic meningitis, necrosis of placenta 129 kidney from a lamb with leptospirosis. 130 Dog, lung. Petechiae are scattered throughout the lung. Dog, kidney. The cortex has a pale mottled to striated appearance consistent with tubulointerstitial nephritis. Gross lesions of interstitial nephritis associated with leptospiral infection in a pig Leptospirosis: dark, swollen kidneys suggestive of hemolytic crisis Placentitis associated with leptospiral abortion in a pig A. Severe neutrophilic and histiocytic tubulointerstitial nephritis in a dog with acute leptospirosis 136 Leptospira interrogans, dark-field microscopy, low power, microscopic agglutination test. The characteristic hooked ends (ôquestion marksö or ôinterrogation pointsö) that give the species its name are visible in nonagglutinated bacteria Leptospira, Warthin-Starry silver stain, medium power, porcine kidney. Note the large number of thread-like black bacteria within the tubule lumen of the proximal convoluted tubules.  Microscopic lesions Liver: Hyperchromatic nuclei with eosinophilic granular cytoplasm Kidney: Tubular epithelial cell degeneration followed by hydropic degeneration and necrosis, Interstitial nephritis, Infiltration of lymphocytes and plasma cells. Gastrointestinal tract : Congestion and petechiae on the mucosa Purulent necrotic laryngitis Placentitis, abortion. Leptospira can be found in the foetus. 139 Diagnosis Symptoms Demonstration of organisms in the tissue sections Microscopic agglutination test Inoculation Dark field examination of urine Tissue sections –Organisms are black in colour in silver stains – Levaditi and warthin starry stain 140  SALMONELLOSIS Synonyms – Paratyphoid Salmonellosis occurs in all animals but is more common in cattle (S. Dublin, S. typhimurium), horses (S. typhimurium), pigs (S. choleraesuis, S. typhimurium). It is rare in dogs and cats 141 Transmission Direct or indirect Contamination of feed, water and environment Ingestion of materials contaminated with faeces Carrier animals 142  Pathogenesis Entry of bacteria Adhere to intestinal epithelial cells by fimbriae or pili Invasion of epithelial cells are controlled by invasion genes in bacteria induced by low oxygen tension in intestine Attaches to intestinal cells Proliferate within enterocytes and macrophages Macrophages transport bacteria to lymphnodes Growth of bacteria within macrophages is aided by bacterial genes induced by acidic pH within macrophage phagolysosomes Multiplication occurs Infection ranges from mild enteritis or septicemia 143  Clinical signs Septicaemia – Characteristic form in new born foal, calves and guinea pigs – Depression, dullness, prostration, high fever (105˚ – 107˚) – Death within 24 – 48 hrs Acute enteritis – Common in adult animals of all species – High fever – Diarrhoea / Dysentry – Tenesmus – Abortion in pregnant animals – Mortality 75% – Recumbency – Death within 2 – 5 days 144  Chronic enteritis – Common syndrome in pigs, cattle, horses – Persistent diarrhoea with passage of spots of blood, mucus, fibrinous casts; – moderate fever. – Loss of weight -emaciation 145 Lesions Enterocolitis – Hyperaemia, thickening, hemorrhages in the mucosa of ileum and colon ulcerations Microscopical lesions – Haemorrhage, oedema, necrosis, leucocytic infiltration Multiple necrotic foci in liver, presence of paratyphoid nodules (Small aggregation of reticulo – endothelial cells) Enlargement of spleen and lymphnodes Hyperplasia of reticulo endothelial cells Septicaemia – fibrinoid necrosis of vessel walls and hyaline in glomerular capillaries Ulcerative proctitis Abortion – occurs late in gestation; Oedematous placenta with focal haemorrhage and necrosis; oedema of foetus 146 Diagnosis Isolation and identification of organisms ELISA DNA probe 147  LISTERIOSIS (Circling disease) The disease is characterised by encephalitis, systemic infection (septicaemia) or and abortion Etiology Listeria monocytogenes -Rod shaped, Gram +ve, intracellular organisms 13 serotypes on the basis of somatic and flagellar antigens 148 Host It causes disease in most species of animals (ruminants, pigs, dogs, cats), and also in humans. In wildlife, it has been reported in deer, fox and leopard. The organism is called 'monocytogenes' since it causes mononucleosis (increased number of mononuclear leukocytes in the blood) in rabbits, in the systemic form of the disease. 149 Transmission Ingestion of contaminated material Ingestion of milk Congenital Wounds in the buccal mucosa from feed, from nibbling on plantations or infection tooth cavites Infection of trigeminal nerve Organisms are excreted in feces -Source of infection 150 Pathogenesis Listeria have ability to penetrate epithelial cells like conjunctiva,urinary bladder and intestine Bacteria have a surface leucine–rich proteins called interhalins Helps in penetration in to the epithelial cells Binds to E-cadherins on host epithelial cells which acts as receptors for interhalins Organisms gains entry into cells Multiply, destroy the cells & released Phagocytosed by macrophages 151 Pathogenesis To avoid destruction escapes from phagosomes and lies freely in cytoplasm of macrophages They can survive and multiply inside normal macrophages. Moreover, L. monocytogenes can travel from cell to cell without exposure to t he extracellular fluid. Activated macrophages phagocytose & kill bacteria Transport by macrophages is thought to result in a septicaemic phase in some cases. Centripetal movement (Le., toward the centre) of organisms within the branches of the trigeminal nerve eventually makes them to reach medulla oblongata. Listeria organisms are excreted in faeces even in absence of disease 152 Clinical signs 3 different syndromes, which usually do not occur together. – 1. Encephalitis in humans, cattle, sheep, goats, and pigs – 2. Systemic infection (septicaemia) in humans, cattle, sheep, pigs, dogs and cats – 3. Abortion in humans, cattle, and sheep. Less commonly, the organism causes endocarditis and purulent lesions in other organs and tissues. 153 Clinical signs Encephalitis More common in ruminants animal's abnormal posturing (position) of the head and neck walking aimlessly in a circle ("circling disease") nystagmus (constant involuntary movement of the eyeball) blindness, and paralysis. 154 Clinical signs Systemic infection Generalized listeriosis is the most common form in monogastric animals (pigs, dogs, cats), and in human newborns and infants. The most characteristic lesion is focal necrosis of the liver. Less commonly, lesions occur in the spleen, lymph nodes, lungs, adrenal glands, myocardium, gastrointestinal tract, and brain. 155 Clinical signs Abortion Abortion is important mainly in cattle and sheep. Abortion usually occurs in the last quarter of gestation without signs of infection in the dam (mother). The foetus dies in uterus and may be severely autolyzed when expelled. If not damaged by autolysis, focal hepatic necrosis containing stainable organisms in the foetal liver is the main lesion of diagnostic value. 156 Gross Lesions Encephalitis – No gross lesions Systemic infection – The most characteristic lesion is focal necrosis of the liver. – Less commonly, lesions occur in the spleen, lymph nodes, lungs, adrenal glands, myocardium, gastrointestinal tract, and brain. Abortion – The foetus dies in uterus and may be severely autolyzed when expelled. – If not damaged by autolysis, focal hepatic necrosis containing stainable organisms in the foetal liver is the main lesion of diagnostic value. 157 Microscopic Lesions Medulla – Circumscribed mononuclear cells in perivascular areas – No tissue necrosis – Organisms are Gram +ve and demonstrated in tissue sections – Micro abscess in brain Systemic infection – More common in monogastric animals – Focal necrosis of liver (Characteristic) - Micro abscess in liver Abortion – Common in cattle and sheep – Focal hepatic necrosis with stainable organisms are seen in foetal liver 158 Liver showing diffuse vacuolation and microabscess. HE X 200 Liver showing periportal mononuclear cell infiltration. HE X 200  Liver showing moderate hepatocellular necrosis, microabscess and infiltration of inflammatory cells. HE X 200. Adrenal cortex showing microabscess. HE X 200 Brain showing focal extensive area of abscess, microabscess and multifocal perivascular cuffing. HE X 50. Diagnosis Demonstration of typical microscopical lesions. Microabscess – diffuse purulent inflammation or glial nodules Perivascular accumulation of lymphocytes Lymphocytie – leptomeningitis with Gram +ve organism Isolation and identification of bacteria in culture media 164  Colibacillosis Colibacillosis Three district pathogenetic mechanism are identified in enteropathogenic Escherichia coli (E.coli) Enterotoxic colibacillosis Caused due to colonisation of Escherichia coli on the surface of intestinal cells and production of toxins Most common in young piglets, calves, lambs during the first week of life 165 Enteroinvasive colibacillosis Less common in animals. Seen in pigs and cattle The organism penetrates the enterocytes, lamina propria and extend into mesenteric lymphnodes Enteroadherant colibacillosis Seen in pigs and calves Caused by some serotypes which do not produce toxin The organism penetrates the glycoprotein coat, adhere to mucosal cell surface and destroy microvillus 166  OEDEMA DISEASE OF SWINE Synonyms - Enterotoxaemic colibacillosis Healthy pigs are affected Clinical signs are incoordination, paralysis of limbs, diarrhoea Morbidity 35%; mortality 100% Toxin produced by bacteria is called “oedema disease toxin” (Shiga – like toxin) → enters into circulation → necrotising arteritis Oedema of stomach wall & and colon; fluid accumulation within body cavities 167 Septicaemic colibacillosis Organism invade the host through the oral cavity, respiratory system, pharynx and umblicus Produce endotoxin Signs and lesions are bacterial arthritis, polyserositis (pericarditis, pleuritis, peritonitis) meningitis, opthalmitis pyelonephritis, emboli, purulent or fibrinous exudates No diarrhoea or intestinal lesions 168  GLASSER'S DISEASE Caused by Haemophilus parasuis – a normal resident of the oropharanyx of pigs Young pigs are affected mostly after stress Clinical signs are fever, lameness, respiratory distress and neurological signs Lesions are polyserositis (pericarditis, peritonitis, pleuritis, meningitis, swollen joints) Microscopically fibrinous inflammation of all serosal surfaces 169  CONTAGIOUS PLEUROPNEUMONIA OF SWINE Caused by Haemophilus pleuropneumoniae. Endotoxins produce lesions Spreads through respiratory route by infected animals Young animals up to 6 months of age are susceptible Death with one day or two Mortality 50% Clinical signs include fever, respiratory distress, nasal discharge mixed with blood Characteristic lesions are fibrinopurulent pneumonia, fibrinous pleuritis, sequestration of lungs, meningitis and arthritis Microscopically, alveolar and interlobular oedema, dilation of lymphatics, congestion, haemorrhage and intravascular fibrinous thrombus 170  SWINE ERYSIPELAS Synonym: Diamond skin disease Definition It is contagious disease of young pigs characterized in acute cases by high fever, reddish spots on the skin and haemorrhages in the internal organs and in chronic cases by dyspnoea, arthritis, vegetative endocarditis caused by gram positive Erysipelothrix rhusiopathiae Aetiology Erysipelothrix rhusiopathiae 171 Incidence It is found in most parts of the world and in some, it may be enzootic since the organisms thrive in the soil Young pigs: 3 to 6 months old are most susceptible Also affects sheep, cattle, birds and it causes ‘Erysipeloid’ in man Transmission Through skin abrasions Alimentary tract Flies may transmit the disease 172 Pathogenesis Infection is by ingestion Organisms found in the excreta and urine of affected animals From the tonsil or intestine reach the blood circulation and proliferate cause septicaemia Toxin liberated and Injure the wall of blood vessels causing erythematous lesion on skin and haemorrhages in internal organs. Organisms settles in joints or heart valves causing arthritis and vegetative endocarditis 173 Clinical signs Acute febrile reaction with high mortality On the skin bright red erythema and urticarial swelling of rhomboid shape referred to as Diamond skin disease (abdomen, neck, ear and thighs) Progress to necrosis, crust formation and sloughing Joints - Hot, painful and swollen with lameness Heart involvement- Dyspnoea and cyanosis 174 Gross lesions Oedema and haemorrhages in serous cavities and organs due to damage of blood vessels Diamond skin lesions initially bright red later turns to dark Arthritic form- Joint capsule is enlarged, thickened, distended with fluid 175 Microscopic lesions Infiltrated with lymphoid cells and neutrophils Cardiac form- mitral or bicuspid valve shows coarse vegetation and it occlude the lumen Diagnosis Symptoms and lesions Organisms can be isolated from blood 176 Erysipelas skin lesions – Diamond skin disease Acute severe skin form of swine erysipelas with extensive small raised pink/red lesions some developing dark scabs  STRANGLES Synonym : Adenitis equorum, distemper Acute contagious disease of young horse characterized by sudden onset of fever, muco purulent inflammation of upper respiratory tract, followed by swelling and abscess formation on the submaxillary and pharyngeal lymph nodes and occasionally other parts caused by Streptococcus equi Etiology Streptococcus equi - Streptococcus – Gram positive spherical chain occuring in man and animals 179 Transmission Inhalation is the most important route of infection. Ingestion is also possible Pathogenesis Incubation period: 4 to 8 days. Infection of the pharyngeal and nasal mucosa an acute pharyngitis and rhinitis. Drainage to lymph node results in abscessation Infection spread to other organs causing suppurative process in the lung, kidney, liver, spleen, brain, tendon sheath and joints After an attack of strangles has subsided, purpura haemorrhagica (many petechial or ecchymotic haemorrhages) may occur due to the development of sensitivity to streptococcal protein. 180 Clinical signs and lesions Oedematous swelling on the pharyngeal region producing dyspnoea giving an impression that the animal is strangling Abscess containing -Cream yellow pus Spread of infection through lymph and blood – produces abscess in lung, kidney, liver, spleen and brain. Abscesses in the retropharyngeal lymph nodes may drain into the guttural pouches, leading to empyema (accumulation of pus) Death may be due to septicemia and pyaemia 181  Lesions Bilateral nasal discharge Unilateral nasal discharge in the case of glanders. Purulent inflammation of upper respiratory tract Abscesses in submaxillary and pharyngeal lymph nodes Purpura haemorrhagica is a complication of strangles showing subcutaneous oedema and haemorrhages. Demonstration of organisms in pus smears 182 Enlarged submaxillary lymphnodes Open abscess submaxillary lymphnodes Streptococcus equi infection (strangles); brain abscess, cross-sectional view, horse.  MATERIALS TO BE COLLECTED FOR DIAGNOSIS Smears and swabs from pus and discharges from nasal cavity Pieces of affected lymph nodes, lung, spleen and trachea in 10% formalin.  Genus: Pseudomonas numerous species of Pseudomonas only three are responsible for diseases of animals: – P. mallei (glanders), – P. pseudomallei (melioidosis), and – P. aeruginosa (purulent infections) 188  GLANDERS Synonym: Farcy, malleus It is a contagious disease of horses, mules and donkeys (solipeds), usually chronic in nature characterised by formation of nodules and ulcers of upper air passages, lungs and cutaneous tissue. Aetiology Burkholderia (Pseudomonas) mallei (Actinobacillus mallei ) 189 Incidence Horses, mules, donkeys, highly susceptible and man is moderately susceptible Sheep and goats may be infected. The disease is also transmissible to human beings Transmission Ingestion, inhalation and through skin invasion 190 Pathogenesis Infection is by ingestion and inhalation of organisms Penetrating the pharyngeal and intestinal mucosa Enters the general circulation and reach pulmonary capillaries Septicaemic phase with high temperature Forming emboli in the pulmonary capillaries Acute inflammatory reaction in the perialveolar and peribronchiolar area Serous exudate in the connective tissue 191 Pathogenesis Penetrate the bronchial wall and enter lumen voided along with secretions Aspirate into alveoli produce bronchopneumonia Death is caused by anoxic anoxia. Neutrophils undergo degeneration- karyorrhexis and fragments of nucleus seen as scattered manner - Characteristics of glanders in stained smears Organisms enters circulation and localized in various organs produce nodules and ulcers in skin –Cutaneous involvement called as farcy. 192 Clinical signs Acute: septicaemia with fever Chronic : Two forms due to bacteremia – Pulmonary- Chronic cough, pneumonic signs, purulent oily discharge – Cutaneous form (Farcy)- ulcers, oily pus discharge, 193 Gross lesions Lungs – Miliary nodules – Pleurisy – fibrinous deposits – Ulcers in trachea and larynx (punched out) Lymphatic glands – Swollen edematous with yellowish grey centers – Thick tortuous cords of lymph vessels (farcy cords) – Nodule formation in the lymph vessels (farcy buds) – Nodules may open and discharge oily pus with persistent ulcers farcy-pipe: A hard, cordy swelling of the subcutaneous lymphatics in farcy. 194 Microscopic lesions The pulmonary lesions are granulomatous with caseous necrotic centre surrounded by epitheliod cells, giant cells and lymphocytes Lymphangitis and lymphadenitis of the hind limbs in the form of thick tortuous cords of lymph vessels and nodule formation in lymph vessels. The vessels are dilated and tightly packed with leucocytes. Leucocytes infiltrate focally into the walls also giving them a beaded appearance. They nodules may open and discharge oily pus 195 Diagnosis Lesions Serological tests- CFT Guinea pig inoculation (Straus test- male - suppurative orchitis within 4 to 5 days) and Confirmation by intradermal mallein test. 196  Melioidosis Synonyms Pseudoglanders Whitmore's Disease Introduction Melioidosis is an infectious disease caused by a bacterium called Burkholderia pseudomallei (previously known as Pseudomonas pseudomallei) 197  Melioidosis is primarily a disease of rodents with an occasional case occurring in humans. Most mammals appear to be susceptible. In horses, clinical and necropsy findings are similar to those of glanders. Spread Ingestion by insect bites, cutaneous abrasions, Possibly inhalation. Pathogenesis and lesions similar to Glander 198  Rickettsial infections Minute, Gram – negative, obligate intracellular parasite Multiply only within cells Transmitted from one species to other by arthropod vectors in which transovarian transmission is common Rickettsia species have an affinity for growth in endothetial cells and vascular smooth muscle cells Vasculitis complicated by thrombi and haemorrhages 199  ANAPLASMOSIS Synonym: Gall sickness Definition Anaplasmosis is an acute or chronic rickettsial disease especially of adult cattle characterized by anaemia, extreme weakness, high feve