Ahmed M.A. Alsaidya , PhD Lecturer , Department of Pathology and Poultry Diseases College of Veterinary Medicine, University of Mosul, Mosul, Iraq https://orcid.org/ https://www.researchgate.net/profile/ Morbid Anatomy | Part I | 4th year 2019 Actinobacillosis (Wooden tongue) It is a chronic suppurative inflammatory disease of ruminants, caused by actinobacillus ligniersi, characterized by inflammation of soft tissue of the head especially tongue (localized firm swelling of dorsum), less commonly pharyngeal lymph nodes, facial skin, nares and esophageal groove. It is sporadic and self-limiting disease. Etiology : Actinobacillus ligniersi (normal commensal organism in the oral flora of the cattle), • Gram negative coccobacilli or pleomorphic rods. • form sulfur granules as white or yellow-white cheesy accumulation of the organism. Predisposing factor : Oral mucosa injuries by fibrous feed materials or by foreign bodies and during oral manipulation by hand of owner or veterinarian. Pathogenesis : • The organisms are present in the mouth and upper respiratory tract. • Local infection by the organism causes an acute inflammatory reaction in the tongue and the subsequent development of granulomatous lesions in which necrosis and suppuration occur, often with the discharge of pus to the exterior. Spread to regional lymph nodes is usual. • Lingual involvement in cattle causes interference with prehension and mastication due to acute inflammation in the early stages and distortion of the tongue at a later stage. • Visceral involvement is recorded. Clinical signs : • Incubation period is unknown, morbidity and mortality rate is low and course of the disease is long. • The onset of glossal actinobacillosis is usually acute, the affected animal being unable to eat for a period of about 48 hours. There is excessive salivation and gentle chewing of the tongue. Part I | Morbid Anatomy | Dr. Ahmed Alsaidya Page | 1 • On palpation the tongue is swollen and hard, particularly at the base, the tip often appearing to be normal. • Nodules and ulcers are present on the side of the tongue and there may be an ulcer at the anterior edge of the dorsum. • In the later stages when the acute inflammation is replaced by fibrous tissue, the tongue becomes shrunken and immobile and there is considerable interference with prehension. Macroscopic & Microscopic appearance : The organism A. lignieresi invades the injured areas in the mouth, pharynx or intestines etc., to enter different kinds of tissues (especially soft tissues) to produce the lesions. The granulomas developing in these organs contain several colonies of the organisms. Grossly, these are firm, hard and the colonies of the organisms look like yellowish white specks on the cut surfaces of the granulomas. Finger like clubs or projections abutting the bacterial colonies are surrounded by cellular granulation tissue consisting of epithelioid cells, a few giant cells and leucocytes. Fibroblasts form masses of fibrous tissue beyond these infiltrating inflammatory cells. The granulomatous growth of the tissue marked by inflammation and abscessation in this infection contains foci of pus having clubs radiating from the centres of the masses called rosettes. Microscopically, these rosettes are surrounded by giant cells, epithelioid cells and neutrophiles. The organisms can be found between these clubs and stain blue in the sections staind by Ziehl-Neelsen's method. The clubs stain Red with carbol fuchsin , and these clubs stain Pink with eosin and hematoxyline . Diagnosis : 1. Clinical signs 2. History of the disease 3. Demonstration of organisms in the tissue sections 4. Demonstration of the Rosettes 5. Culture and identification of the organisms Differential diagnosis : 1. Actinomycosis 2. Nocardiosis 3. Staphylococcus infection 4. Tubercullosis Part I | Morbid Anatomy | Dr. Ahmed Alsaidya Page | 2 Actinomycosis (Lumpy Jaw ) It is a chronic infectious debilitating disease of cattle mainly, caused by actinomyces bovis, characterized by rarefying osteomyelitis of jaw bones. and formation of bony cavities filled with pus in head bones particularly the mandible and maxilla. Etiology : • Actinomyces bovis is the primary cause • Actinomyces bovis is common inhabitant (flora) of the mouth and digestive tract, Gram positive, grow in branching filaments (crushed preparation of sulfur granules from pus or tissues), coccoid, or filament rods have distinct cell walls. Pathogenesis : • The diseases caused by Actinomyces bovis, which is a soil born bacteria • Trauma to the oral mucosa and eruption of teeth allow the organisms to inter the osseous tissue . • The lesions in the tissues of animals infected with A. bovis are of a granulomatous kind and the organisms are found embedded in the granulation tissue or found as granules in the pus of suppurative lesions. The swollen lesions may discharge sticky honey like exudates containing minute hard yellowish white granules called sulphur granules. • In the jawbones a rarefying osteomyelitis is produced. • The lesion is characteristically pyogranulomatous, necrosis and loss of the bone , with scare formation and multiple fistulae are characteristic. • Involvement of the jaw causes interference with prehension and mastication. • Rarely, localization occurs in other organs, caused apparently by hematogenous spread from these primary lesions. Lesions : large mass of granulomatus and osteoid growth protroded skin The discharge of pus is small in amount and consists of sticky, honey-like fluid containing minute, hard, yellow white granules (Sulfur granules). Granulomatous lesions containing pockets of pus may be found in the esophageal groove, the lower esophagus and the anterior wall of the reticulum. Spread from these lesions may cause a chronic, local peritonitis. Suppurative osteitis is found in the maxillae. A mass of granulation tissue with soft purulent centres is found in the medullary cavity of the maxillae. Several sulphur granules are seen in such purulent centres. The bone adjacent to these growths becomes absorbed and rarefied and the formation of a new bone on its outside forms what is called lumpy jaw. Sinuses leading to the surface of the skin with discharge of pus develop in such affected areas (maxillary region). Part I | Morbid Anatomy | Dr. Ahmed Alsaidya Page | 3 Microscopically, the stained sections of the lesions of actinomycosis show a granular center as a mass of Gram positive filaments matted together to form a mycelium(rosettes like) . This mycelium is surrounded by a zone of shiny and radiating clubs , followed by layer of neutrophils surrounded by giant cells , epithelioid cells and finally fibrous connective tissue. The colonies of actinomyces may become calcified in cases of long standing. Diagnosis : its depended on 1. Clinical signs 2. Gross and microscopic lesions , using gram stain to identified the G+ organisms in tissue 3. Demonstration of the organism in smears of fresh unfixed material stained by Grams stain 4. Demonstration of the (Mycelium ) or Rosettes with shiny , refractile , radiating clubs in the fresh pus . Differential diagnosis : 1. Actinobacillosis 2. Nocardiosis 3. Staphylococcus infection. Part I | Morbid Anatomy | Dr. Ahmed Alsaidya Page | 4 Black Leg (Black Quarter) Definition It is a highly fatal and febrile bacterial disease caused by Clostridium chauvoei in ruminants (particularly cattle) and characterized by swollen and emphysematous or crepitating lesions of the muscles and subcutaneous tissues in some region in the bodies such as the shoulder or the hind quarter of the affected animals. (The infectious myositis is the most marked lesion.) . Etiology Cl. chauvoei , Gram positive, spore-forming bacteria and may have central or subterminal spores ,The organisms exist in the soils and are also found in large numbers in the local muscle lesions and exudates around such lesions. Susceptible animals Although blackleg has been found in cattle as young as 2 months old, most losses occur in cattle between 6 months and 2 years of age. Occasionally, losses are seen in adult cattle. Generally, the best conditioned animals are affected, with most losses occurring where there is an abundance of feed. Pathogenesis Toxins and neuraminidase produced by the causative bacteria are believed to play a significant role in pathogenesis of diseases. The bacteria enters by ingestion and then gains entrance to the body through small punctures in the mucous membrane of the digestive tract. Bacterial spores are eaten in contaminated feed or soil. The spores then enter the bloodstream and lodge in various organs and tissues, including muscles. Here they lie dormant until stimulated to multiply, possibly by some slight injury to the animal. The injury reduces blood flow to the area, thereby reducing the supply of oxygen to the tissues. In the absence of oxygen, the spores germinate and multiply. As they grow, the bacteria produce toxins which destroy surrounding tissues. The toxins are absorbed into the animal’s bloodstream which makes the animal acutely sick and causes rapid death. Part I | Morbid Anatomy | Dr. Ahmed Alsaidya Page | 5 Clinical signs It occurs as an acute disease usually with a fatal ending. Animals are found dead without showing signs of illness. There is a characteristic extension of the limbs a short time after death of the affected animals. Lameness is noticed in the sick animals. High temperature ,increased pulse rate are seen in the sick animals. Sheep reveal myositis, lameness and depression in the cases of Cl.