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Bacteria are spherical or rod shaped prokaryotic microorganisms. Pathogenic bacteria are capable to produce a diversity of diseases. Pathogenic bacteria are classified according to morphologic, cultural, biochemical and antigenic characters. In tissue most bacteria are present in interstitial tissue and on the epithelial surface (extracellular pathogens) or within the cells (facultative intracellular) as Mycobacterium and Brucella. Bacteria can also divided into gram positive or gram negative according to their staining reaction with Gram’s stain. The pathogenic or virulence of bacteria depend on several factors such as adherence, invasion, capsule, endotoxins and exotoxins. The previous factors help bacteria to invade the host, cause disease and evade the host defense. The bacteria produce diseases by different mechanisms. They may be pyogenic (pus producing), toxigenic or intracellular.
It a rapidly fatal septicemic disease of animals and man caused by a gram positive, spore forming bacterium (Bacillus anthracis). The spores can remain viable for long as 15 years in the soil. Susceptible host All animal and fowl are affected. Goat, sheep and cattle are the most susceptible host where the disease is seen as fulminant septicemic. In more resistant animals (swine) the disease is localized and confined to the regional lymph nodes. Route of infection. In human, the infection usually occurs through contact with infected animals or animals products. 1. Ingestion of contaminated food and water. 2. Inhalation is the important source for infection especially in man during handling contaminated wool (wool sorter’s disease). Moreover, cattle may also infected through inhalation dust containing spores. 3. Wound infection is seen in man causing malignant carbuncle or pustule. 4. Insufficient attenuated vaccine may cause infection. 5. By biting flies, but it is not clearly established. Pathogenesis Infection occurs through inhalation or ingestion of the spore or entry of the organism through skin. The ingested spores proliferate in the tonsil or the spore resist the gastric juice proliferated in the sub mucosal lymph space. The bacilli enter through skin proliferated in the connective tissue. The bacilli then spread by means of lymphatic to lymph nodes and further to blood stream leading to septicemia. The organism evades the immune system through building a capsule, which contain antiphagocytic substances such as glutamyl polypeptides. Moreover, the microorganism elaboration exotoxins, which consist of three components, designated as edema factor, protective factor and lethal factor. The toxin injury the endothelium leading to hemorrhage and effusion of blood in organs. Moreover, it affects the respiratory center in brain leading to asphyxia and death. A combination of lethal peptide toxin and massive amounts of anti. phagocytic capsular material kill the host, which prevent opsonization and killing of bacilli. Signs The signs in sheep and cattle are variable and the animal may be die without showing any signs. In animals with acute type of disease, anthrax recognized as febrile disease with depression, weakness, cyanosis, and subcutaneous edema in brisket, flank and throat regions and bloody discharge from natural orifice. In swine and dog pharyngitis is seen with the swelling of the throat. Lesions
1. The died animal is early bloated and the rigor mortis is never
complete (Fig.1).
2. The lesions include edema and hemorrhages in any part of the body specially serous membrane. 2. Spleen is greatly enlarged and the pulp is dark and soft or even fluid. 3. Lymph nodes are usually edematous swelling and hemorrhagic. 4. The liver and kidneys are congested besides hemorrhagic gastroenteritis. Lungs are edematous and reveals hemorrhages 5. In localized infection in swine edema and hemorrhages are seen in pharynx and cervical lymph nodes. In chronic cases the lymph nodes become enlarged, firm with yellowish foci. 6. Microscopically, presence of large number of anthrax bacilli in blood and most other tissue is seen. In spleen the tissue architecture is obscure by presence of large number of erythrocytes. The lymph follicles are seen as tiny island of trabeculi in a sea of red cells and necrotic debris. In localized infection shows localized area of necrosis surrounded by granulation tissue.
Fig.1: The died animal is early bloated and the rigor mortis is
never complete.
Fig. 2: The died animal shows enlarged darkened and softened
spleen.
Fig. 3: Blood film showing gram positive, spore forming
bacterium.
Fig. 4: Kidney of died animal showing glomeruli containing
anthrax bacilli. H&E.
The clostridium are sporulating anaerobic bacteria of large size, which found either singly or in pairs. The clostridium induced diseases through tissue invasion or without tissue invasion. In both cases the pathogenicity is due to toxin production. Several member of the genus clostridium are responsible for the following diseases in human and animals. 1. Black leg 2. Bovine bacillary hemoglobinuria 3. Malignant edema 4. Braxy 5. Black disease 6. Gas gangrene 7. Tetanus 8. Enterotoxemia 1. Black leg (quarter ill or black quarter) It is an economically important acute highly fatal disease of cattle and occasionally of other species as sheep, goat and swine characterized by gangrenous myositis , particularly of extremities. Cause The causative agent is Clostridium chauvoie a rod shape gram positive, motile, sporulating non capsule forming anaerobic microorganism. Clostridium chauvoie produces four toxin which is both necrotizing and hemolytic. Route of infection and pathogenesis Infection occurs by ingestion. Wound infection may occurs in sheep after castration and shearing. The ingested spores multiply in intestine and cross the intestine mucosa then enter general circulation and distributed to various organs and skeletal muscle. The spores remain dormant until the anaerobic environment occurs through devitalization of muscle by trauma. The microorganisms are germinate and proliferate and start to produce toxin which lead locally to myonecrosis and systemically to death. Moreover, the powerful toxin can damage capillaries produce sero. hemorrhagic exudate. The proliferating organism also able to ferment sugar and produce gas. Signs Lameness is the first signs of disease. Moreover fever, anoroxia and depression are seen. Marked swelling of the upper part of the affected; leg. In the early stages, the swelling is hot and painful soon becomes painless and cold. The swelling crepitates on pressure due to presence of gas. The skin over the swelling is discolored and soon becomes dry and cracked. The animal dies within 12-36 hours after the appearance of signs. Gross lesions: 1. The dead animal are usually lying on the affected side. The carcass is bloating and putrefaction quickly. The lesions usually involve hind quarters, shoulders, neck, back or lions and frequently tongue and heart. 2. The skin over the affected area is dark red or even black with crepitating on pressure. The black color is due to the formation of iron sulphide In cut section a serosanguineous, foul smell fluid may exude. 3. The subcutaneous tissue is red or infiltrated with yellowish gelatinous exudate intermixed with hemorrhages and gas bubbles
4. The incised affected muscles are dark red in color, swell with rancid
odor due to fermentation of glycogen (Figs 5 & 6).
5. The regional lymph nodes are enlarged and may be hemorrhagic. 6. The heart usually shows ulcerative endocarditis in the left atrium, bicuspid valve, and inner wall of the pulmonary vein. 7. Body cavities: The abdominal and thoracic cavities contain excess fluid which contains variable amounts of fibrin and is usually blood. stained. 8. Other organs: The internal organs undergo degeneration, and the postmortem decomposition with the production of gas in the liver occurs rapidly. Microscopic appearance
The muscle fibers show coagulative necrosis which infiltrated with
neutrophils and lymphocytes, cloudy swelling, and fatty change.
Moreover, the muscle fibers are separated by gas bubbles, edema, and
hemorrhage Gram positive microorganisms are observed everywhere among
the muscle fibers. The lymph nodes show hemorrhagic lymphadenitis and
emphysema (Figs. 7& 8)
Fig. 5: Black leg. Dark-red skeletal muscle of a heifer showing
hemorrhage, necrosis, edema and emphysema.
Fig. 6: Black leg disease. skeletal muscle showing dark red
hemorrhagic and emphysematous.
Fig. 7: Lymph node of cattle infected with black leg disease
showing air bubbles (emphysema). H&E.
Fig. 8: High power of the previous Fig. to show air bubbles. H&E.
2. Bacillary Hemoglobinuria (Red water disease, Infectious icterohemoglobinuria). It is an acute fatal toxemic disease characterized by hemoglobinuria and jaundice with the presence of necrotic infarcts in the liver and death within two days. It affects mainly cattle and occasional occur in sheep. Cause Clostridia haemolyticum Pathogenesis and mode of infection: Infection occurs through ingestion of feed and water contaminated with the spores. The spores multiply in intestine and then gain entry to general circulation and localized in liver and remain latent until anaerobic condition develops due damage of liver by migration of the of liver flukes or other parasites or any causative agent causing hepatic damage. Then the clostridia start to produce exotoxins (necrotizing and hemolysing), that cause further hepatic damage and infarction due to thrombosis of branches of portal vein, hemolysis of erythrocytes and death. Signs Fever, jaundice, cessation of lactation and rumination, anorexia are seen besides abdominal pain and shallow respiration. The urine is dark red Macroscopic picture Rigor mortis develops quickly. The liver is enlarged and friable and shows characteristic large one or more infracted areas. The subcutaneous tissue shows presence of gelatinous fluid and petechial or ecchymotic hemorrhages. Moreover, presence of excessive amounts of clear or turbid, blood. stained fluid in the pleural, pericardial and peritoneal cavities. Moreover, red urine is present in the urinary bladder and kidneys. 3. Malignant edema It is an acute wound infection disease characterized by febrile course of short duration with hot painful swelling at the site of infection. It is common in solipedes, sheep, swine, sometimes cattle, goat and carnivore. Cause Clostridium septicum which similar in almost all characters to C. chauvoie Mode of infection and pathogenesis Infection occurs as a sequelae of wound infection such as those occurs in shearing or docking or to parturition during which aseptic precaution are ignored. Pathogenesis Infection occurs through wound contamination. The organisms gain access to the heavy muscles and start to proliferate when the environment becomes anaerobic. Propagation proceeds until the neighboring tissue is injured by the action of exotoxins produced by the bacilli. The potent exotoxins are produced in the affected area and cause toxemia and death when absorbed into the blood stream. Clinical signs The disease animals are depressed, and show stiffness or lameness and fever. The skin over the affected area is dark in color. When infection occurs at parturition, there is swelling of the vulva accompanied by discharge of a reddish. brown fluid. Death occurs within 1. 3 days. Macroscopic picture The lesions are similar to blackleg except that hemorrhagic edema is more prominent than emphysema. Fragmentation of muscle is the basic alteration due exotoxin. Moreover, lesions of septicemia with hemorrhage are present throughout the body. 4. Braxy It is an acute toxemic and fatal disease of sheep caused by Clostridium septicum. Lambs less than one year are mostly affected. The disease occurs more in winter. Route of infection and pathogenesis Infection occurs through ingestion where the organisms gain entry to the abomasal wall when its resistance is lowered by ingestion of frost covered food or through wound caused by nematode parasites. The organisms proliferate and produce exotoxins which responsible for lesions and signs. Signs and lesions
Sudden death with few or no clinical signs is observed. The abomasal
wall is thickened, edematous and hemorrhagic (Fig. 9)
Fig. 9: Abomasum of sheep infected with braxy showing hemorrhagic
necrosis.
5. Black disease (Infectious necrotic hepatitis). It is an acute fatal toxemic disease of sheep and rarely cattle that caused by Clostridia novyi type B Mode of infection and pathogenesis: The infection and pathogenesis is similar to Clostridium haemolyticum Signs and gross lesions:
Death of the diseased animals may occur without prominent signs. The
liver is congested and enlarged. It shows characteristic multiple foci
of necrosis, these necrotic areas. The necrotic areas occur mostly under
the capsule of the diaphragmatic surface of the liver but may be more
deeply seated and can be easily missed unless the liver is carefully
sliced (Fig.10).
Subcutaneous venous congestion causes a dark discoloration of the pelt which is the reason for the name black disease. The heart shows petechial hemorrhage on the epicardium and endocardium besides hydropericardium.
Fig.10: Liver of sheep infected with black disease showing
multiple foci of necrosis.
6. Tetanus (Lockjaw)
It is highly fetal infectious disease caused by intoxication of the
nervous system with exotoxins of Clostridium tetani. And characterized
by tonic spasms of the entire body musculature or of single groups of
muscle without impairment of consciousness (Fig.11).
Pathogenesis and lesion The infection occurs through wound infection. The bacteria grow in anaerobic environment and produce exotoxins, which spread allover, the body through lymph or blood and along nerve to CNS. The organism liberates three toxin component, hemolysing tetanolysin, fibrinolysin and the most important one is neurotoxin tetanospasmin. Macroscopically, no lesions are noticed but the animal die from asphyxia due to interference with respiratory and cardiac functions by tonic spasm. The blood is dark. Rigor mortis occurs immediately after death.
Fig. 11: Sheep showing tonic spasms of the entire body
musculature or of single groups of muscle without impairment of
consciousness.
7. Enterotoxemia It is a group of infectious diseases gathered under the name of enterotoxemia, which resulted from elaboration of toxin, by Clostridium perfringens in the gastrointestinal tract of well fed lamb, kids, calf and pigs. The diseases characterized by sudden death or short period of nervous signs. Clostridia perfringens is spore forming and toxin. producing microorganism. There are five strains of C. perfringens (type A, B, C, D and E). The toxins produced are alpha, beta, epsilon and iota. A. Clostridium perfringens type A (Yellow lamb disease)
It is a disease of lamb and calf with short coarse and high mortality
(Fig.12)
Lesions
Enlarged friable liver, dark kidneys, anemia, hydropericardium and
icterus are the observed lesions (Fig.13).
Fig. 12: Calf infected with Clostridium perfringens showing high
mortality.
Fig. 13: Calf infected with Clostridium perfringens showing
hydrothorax.
B. Lamb dysentery
It is an acute fetal disease of very young lamb and calf caused by
Clostridia perfringens type B characterized by sudden death without
signs in peracute cases or severe abdominal pain, recumbency, and the
passing of brown fluid feces sometimes containing blood (Fig.14)
Lesions Hemorrhagic ulcerative enteritis is characteristic often with ulceration and peritonitis. The heart shows epicardial and endocardial petechial and ecchymotic hemorrhage beside hydropericardium. Microscopically, focal area of necrosis which involve the entire thickness of mucosa and extend to intestinal muscularis.
Figure14: Sheep infected with lamb dysentery showing blood
stained tail and hind quarter.
Fig. 15: Lamb showing hemorrhagic and ulcerative enteritis. C. Struck It is a disease of adult sheep caused by C. perfringens type C and characterized by hemorrhagic ulcerative duodenitis and jujenitis. Pathogenesis The toxin, which is absorbed from the intestine into the blood stream, damages the capillary endothelium of the epicardium and other parts of the body. The heavy feeding with milk or other heavy nutritious food in the stomach and intestine furnishes an excellent medium for the growth of the toxin. producing clostridium. Gross lesions
Hemorrhagic enteritis with blood stained contents beside petechial and
ecchymotic hemorrhages are present (Fig.16)
Fig.16: Intestine of sheep infected with struck showing hemorrhagic
enteritis besides petechial hemorrhages.
D. Pulpy Kidney It is an acute toxemic disease of lamb and sheep caused by Clostridia perfringens type D. Calf may also affected. It is characterized softness of the kidney tissue, degenerative changes of the brain and congestion of the gastrointestinal tract Mode of infection and pathogenesis Clostridium perfringens type D normally inhabits the digestive tract of sheep and probably other ruminants. Under certain conditions such as overeating, feeding on heavy grains and young cereals, heavy sucking lambs, the organism proliferate rapidly in the intestine and produces lethal quantities of toxin. Clinical signs Death occurs usually within a very short period. Depression, and off. food are observed. Clonic convulsions with frothing at the mouth and sudden death. In more prolonged cases show a green, pasty diarrhea, staggering, recumbency, and severe clonic convulsions . Gross lesions
Animal dies in a good condition with hydropericardium with sub
epicardial hemorrhage and congested intestine (Figs 17& 18).
The kidney is soft swollen and congested due to very rapid autolysis
after death. The liver is dark and congested (Fig. 19).
Microscopically, the kidneys show cloudy swelling, necrosis of the epithelium of the proximal convoluted tubules, with edema and congestion of the renal cortex and congestion of the medulla. The brain in sheep shows degenerative changes of the vascular endothelium, perivascular and pericellular edema, and necrotic foci in the basal ganglia, thalamus, internal capsule, substantial Nigeria, subcortical white matter and cerebellum. Congestion and desquamation of the epithelium are noticed. Subepicardial hemorrhage, cloudy swelling of myocardium and degeneration of the Purkinjie fibers are seen.
Fig. 17: Sheep infected with pulpy kidney showing increase amount of
pericardial fluid.
Fig. 18: Sheep infected with pulpy kidney showing congested intestine.
Fig. 19: sheep infected with pulpy kidney showing autolysed kidney.
Staphylococcal are gram. positive cocci 1m in diameter. They form clumps. Staphylococcus spp. are residents of normal skin, nasal cavity and lower gut according to individual species. The pathogenesis of diseases induced by these organisms is due to excretion of several toxins including coagylases, fibrinolysin, hyaluronidase, hemolysin and enterotoxins. Almost all species of animals show pyogenic infections of various organs and tissue particularly skin, mammary glands, lungs, joints and uterus. The important pathogenic staphylococci include S. aureus, S. epidermidis, S. intermedius and S. hyicus. 1. Botryomycosis It is a chronic pyogranulomatous lesion caused by S. aureus Susceptible host It occurs in all species particularly horse (spermatic cord following castration forming Scirrhous cord). In cattle the mammary gland may be affected leading to granulomatous staphylococcal mastitis. It also occurs in sheep, dog, cats and pig. Lesions Grossly, pyogranuloma consists of multiple firm nodules with yellowish brown purulent core. The nodule consists of centrally located abscess surround by dense granulation tissue. Sinuses usually communicate the abscesses with the exterior. |The pus contains botryomycotic granules. The metastatic lesions can be occur in lungs, liver, heart, kidneys and regional lymph nodes.
Microscopically, numerous neutrophils in center (surround the causative
agents) surrounded by granulation tissue infiltrated by epithelioid
cells, plasma cells, lymphocytes and rarely multinucleated giant cells.
The entire lesion is surrounded by fibrous tissue (Fig. 20)
Figure 20: Lung of sheep infected with staphylococcus showing caseous
necrosis surrounded with fibrous capsule. H&E.
Escherichia coli is a common member of the normal flora of the large intestine. They are gram negative rod. shaped bacteria, which colonize the intestine shortly after birth. These bacteria remain benign as long as they do not acquire genetic element encoding virulence. Strain that acquire bacteriophage or plasmid DNA encoding enterotoxins or invasion factors become virulent and can cause either watery diarrhea, or an inflammatory dysentery. The Escherichiae include many primary pathogens of importance to domestic animals characterized by enteric diseases. Three groups of E coli are associated with diarrheal diseases. E coli strains that produce enterotoxins are called enterotoxogenic E coli. Second group of E coli strains has invasive factors and cause tissue damage and inflammation. The third group called entero. pathogenic and associated with outbreak of diarrhea in newborn but not produce any recognizable toxin or invasive factors. 1. Colibacillosis It is an acute disease (mainly of young animals) caused by E. coli Rout of infection and pathogenesis The disease is seen in animals and human especially calves, piglet, lamb and foals. The infection mainly occurs through ingestion of contaminated food or water. Under certain condition (feeding error, bad management, crowding, the animals not tack colostrum and bad weather) the E coli acquired the virulence and enterotoxins factors and becomes pathogenic. A. Enterotoxic Colibacillosis The disease is the most common colibacillosis in animals. The disease is common in calves and lambs. The disease is contracted orally by ingestion of food and water contaminated with a pathogenic strain shed by an infected animal. The pathogenesis of diarrhea includes two steps: intestinal colonization followed by elaboration of enterotoxins. The microorganisms come in contact and adhere with the microvilli and produce potent enterotoxins. The toxin stimulates the increase cellular secretion by activation of adenylate cyclase. Moreover, the enterotoxin activates guanylate cyclase, which increase secretion of fluid from the intestinal mucosa, leading to diarrhea, dehydration and death. B. Enterotoxemic Colibacillosis It is observed in calves and swine due to proliferation of E. coli in the intestine with production of neurotoxin leading to vascular damage and non. inflammatory edema in gastric, colonic, palpebral, subcutaneous and central nervous system. C. Local invasive Colibacillosis
The enteric E coli penetrate and destroy the epithelial lining and
producing dysentery (Fig. 2)
D. Septic colibacillosis The affected animals show polyserositis, arthritis, meningitis and pyelonephritis due to endotoxins produced by E coli, which invade the animal through digestive and respiratory systems, pharynx or umbilicus.
Fig. 21: Calf intestine showing necrotic enteritis with thickened villi
due to infiltration with inflammatory cells. H&E
It is an acute or chronic infectious disease of cattle, sheep, swine goats, man and other species caused by members of genus Brucella and characterize by a storm of abortion in cattle between 7th to 8th months of pregnancy. Brucellae are gram negative coccobacilli, non-spore forming, non-motile and aerobic microorganisms. Causes The three species of genus Brucella are Brucella melitensis, B abortus and B suis. Moreover, B ovis recently identified as the cause of epididymitis in ram. B canis can cause of abortion in bitch. Pathogenesis and lesions The host defense depends mainly upon cell mediate immunity. Brucellae are facultative intracellular parasites, multiply mainly in monocytes and macrophages and placental trophoblasts. This characteristic dominates the pathology, clinical signs and therapy of disease. The organisms gain entry into the body through a varity of portals. Oral entry through ingestion of contaminated water and food with uterine discharge, aborted fetus and placenta represent the most common route of infection. Moreover, infection can occur through skin, conjunctiva, and respiratory tract or through coitus. The Brucella traverses the intestinal epithelium overlaying Payer’s patches through endocytosis. The bacteria establish themselves within the reticuloendothelial cells of regional lymph nodes where they multiple for a variable period leading to acute lymphadenitis which become chronic, enlargement due to hyperplasia, medullary hemorrhages besides infiltration with neutrophils and eosinophils and accumulation of plasma cells in medullary sinus without fibrosis
Later on, the bacteria enter lymphatic and get entry to general
circulation leading to bacteremia waves. The bacteria then localize in
variety of tissue with special affinity to male and female reproductive
systems, placenta, fetus and mammary gland. The bacteria also localize
in lymph nodes spleen, liver and joints (Fig. 22)
Whenever the organisms are localized, a granuloma develops. The bacteria are engulfed by phagocytic cells and multiply in their cytoplasm. Lymphocytes and plasma cells are surrounding the phagocytic cells. As the granuloma grows, caseous necrosis in the centers and large number of neutrophils enter the lesions. The entire granuloma finally encircled with fibrous connective tissue.
When the animal become pregnant the organisms invade the uterus and
multiply in chorioallantoic trophoblasts. The proliferation lead to
severe ulcerative endometritis (Fig. 23)
In animals, which have had earlier abortion, the placenta is not shed adhesion between maternal and fetal placenta due to proliferation of fibrous connective tissue. Moreover, the placental reaction in second infection is productive instead of acute necrotic in primary one.
The placenta of cow not previously infected shows coagulative necrosis
of fetal and maternal placentome, which appear as dull and granular. The
intercotyledonary chorion is edematous. A narrow zone of acute
inflammation is seen between necrotic area and adjacent tissue. Brown
thick and sticky odorless exudate occupies the intercotyledonary area
between the uterine mucosa and fetal membrane (Fig. 24)
The bovine placenta having resistance to Brucella show yellowish granular necrotic area on the surface of fetal cotyledons. The rest of chorion is opaque and thickened with a leathery consistency, which covered with sticky brownish and odorless exudate. Fibrosis is seen in caruncles and cotyledons. Chronic inflammation is shown by macrophage, lymphocytes and plasma cells. Neutrophils are numerous. Moreover cattle may show chronic interstitial mastitis, hygromatous swelling of the joints
Bull is relatively resistant to infection and may suffer from orchitis
and epididymitis (Fig. 25)
Lesions in aborted fetus
The fetal body and umbilical cord are edematous. Skin is covered with
purulent exudate and feces. The fetus shows suppurative or hemorrhagic
enteritis, suppurative bronchopneumonia (Figs 26 & 27)
Fig. 22: Cattle infected with brucellosis showing enlarged
joint.
Fig. 23: Endometrium of cattle infected with brucellosis showing
sever endometritis characterize by periglandular infiltration with round
cells. H&E.
Fig. 24: Placenta of cattle showing coagulative necrosis and
thickening of intercotyledonary space.
Fig. 25: Tests of bull infected with brucellosis showing
epididymitis.
Fig. 26: Aborted fetus showing suppurative bronchopneumonia. H&E.
Fig. 27: Aborted fetus showing coagulative necrosis of the
hepatic parenchyma. H&E.
Fig. 28: Aborted fetus showing fibrinous exudate on the serous
membrane.
Infections caused by Pseudomonas Pseudomonas mallei. P pseudomellei and P aeruginosa are the three species of Pseudomonas, which induce diseases in animals. It is a chronic respiratory disease of old equines (especially ass and mule) and humans which characterized by nasal discharge, nodules on respiratory mucosa lungs and skin. Cause Pseudomonas mallei (Malleomyces mallei, Actinobacillus mallei, or Bacillus mallei) is a non. spore forming gram negative rode shape bacilli Pathogenesis Glanders usually acute in mules and ass but chronic in horse. Infection occurs through direct transmission by ingestion of contaminated food by nasal discharge. The ingested organisms enter the intestinal lymphatic then to general circulation from which enter the pulmonary tissue causing inflammatory reaction. The inflammation in early stage is consisted from neutrophils surrounded with histiocytes and finally encircled with vascular connective tissue (young nodule). Later on, the center caseated and surrounded with epithelioid cells, few giant cells and connective tissue. During the septicemic phase fever is recorded. The organisms penetrate the bronchial wall and enter the lumen and present in secretion. Later on, the bacilli localized in the lymphatic of respiratory system and skin. Localization of bacillus in lymphatic vessels of skin lead thickened indurated lymph vessels duo to lymphangitis of small lymph vessels and perilymphangitis of the large one. The bacillus mallei is stimulated the phagocytic cells to form the nodule. At the first the center of nodule contain pus which caseated later. Ulcer is due to rupture of superficial nodules. Dogs and cats can be infected through ingestion of contaminated horsemeat. Intraperitoneal injection of infected material into male guinea pig resulted in purulent orchitis in 3 to 4 days. This experiment is called Strauss test, which used for experimental diagnosis. Signs
In acute form the disease is septicemic with high
temperature. In chronic respiratory form, copious and persistent
catarrhal or purulent nasal discharges (Fig. 29)
Skin indolent ulcer of lower extremities and lower abdomen besides thickening of superficial involvement is seen in skin form (farcy). Lesions
Deep ulcers are seen on the nasal mucosa particularly over the nasal
septum (Figs 30 &31)
The first lesion appears is pyogranulomatous gray transparent or yellowish gray nodules of 1. 3cm and similar to tuberculous nodules are seen in the pulmonary tissue and surrounded by hyperemic zone. Firstly, the nodules consisted from neutrophils surrounded with histocytes and finally encircled with vascular connective tissue (young nodule). Later on, the center caseated and surrounded with epithelioid cells, few giant cells, lymphocytes and connective tissue. Similar granulomata are seen in liver, spleen or other organs.
Moreover, acute
purulent bronchopneumonia is
seen occasionally in
few cases (Figs 32 & 33).
Skin form (farcy) is characterized by persistent ulcer connected by thickened indurated lymph vessels besides suppuration of superficial lymph nodes with discharging of thick tenacious pus. Healing may occurs with scar formation that may be break down leaving persistent unhealed ulcer.
Fig. 29: Donkey infected with glanders showing mucopurulent nasal
discharge.
Fig. 30: Microscopic picture of nasal mucosa showing necrosis and
inflammation besides thrombosis of nasal vessels. H&E.
Fig. 31: Higher power of vessel wall infiltrated and replaced by
mostly degenerate neutrophils and fibrin. H&E.
Fig. 32: Lung of donkey infected with glanders showing an
extensive pyogenic granulomatous pneumonia in a donkey.
Fig. 33: Lung showing suppurative bronchopneumonia. H&E.
It is a chronic granulomatous disease of deeper structure of tongue, oral cavity and adjacent lymph nodes of cattle, small ruminants, horse and man. The disease is characterized by formation of fibrous tissue with chronic suppuration. Cause Actinobacillus ligniersii is a small non. motile gram negative bacillus. Pathogenesis The organism affects the soft structures and spread through lymphatic to regional lymph nodes. Infection occurs in soft tissue more than bone. Infection occurs through wound infection caused by sharp object like awns. The organism initiates granulomatous inflammation around it beside diffuse fibrosis leading to enlarged firm tongue (woody tongue). The presence of eosinophilic clubs is due to combination of the product of host reaction and invading organisms. Signs
The tongue may be enlarged and protruded from the mouth (Fig. 34)
Lesions
The tongue is the most affected organ besides neighboring lymph nodes of
head, gum, palate and pharynx. The tongue is enlarged hard in
consistency beside glistening cut surface (woody tongue). Circular or
irregular granuloma of about 5cm in size of white, gray or yellowish
whites colors and firm in consistency display the normal structure are
seen. In cut section, irregular yellowish granules of 2. 3mm in diameter
called sulfur granules are seen (Figs 35 & 36).
Lesions may be found in the wall of forestomach, skin, liver and lungs. Microscopically, the granulomata consist of gram negative bacilli in the center surrounded by palisade eosinophilic club shaped structure (Indian club) appearing as rosette (Figs 37& 38). The radiating clubs followed by layer of neutrophils surrounded by epithelioid cells and finally fibrous connective tissue.
Fig. 34: Cattle infected with actinomycosis showing enlarged
tongue and protruded from the mouth.
Fig. 35: Actinobacillosis of the tongue “wooden tongue”. The
tongue is enlarged, firm and contains numerous granulomatous lesions.
Fig. 36: Actinobacillosis. Multifocal, well demarcated yellow
lesions.
Fig. 37: Tongue showing granulomata consist of gram negative
bacilli in the center surrounded by palisade eosinophilic club shaped
structure (Indian club) appearing as rosette, followed by layer of
neutrophils surrounded by epithelioid cells and finally fibrous
connective tissue. H&E.
Fig. 38: Tongue showing granulomata consist of gram negative
bacilli in the center surrounded by palisade eosinophilic club shaped
structure (Indian club) appearing as rosette followed by layer of
neutrophils surrounded by epithelioid cells and finally fibrous
connective tissue. H&E.
Hemorrhagic septicemia or shipping fever It is an acute septicemic disease of cattle and buffaloes caused by P multocida and sometimes P hemolytica and characterized by fibrinous pneumonia. It is the most important respiratory disease of cattle. Causes P multocida and sometimes P hemolytica are the causes of Pasteurellosis, but need helpful stresses to move from normal residential in the upper respiratory tract into pathogenic one in lungs. They are gram. negative facultative anaerobic rods shaped bacteria. Although the P multocida and P hemolytica are obligatory parasites, they exist as normal commensals in the oropharynx of cattle and sheep and other animals. Parainfluenza, chlamydia and mycoplasma are predisposing factors for Pasteurellosis besides shipping or exhaustion of animals. Pathogenesis Infection usually occurs through ingestion of contaminated food or through inhalation especially in animals kept in crowded barns. It is believed that Pasteurella alone not be able to cause the diseases but it is a secondary to virus or mycoplasmal infection and other predisposing causes. Under stress situation such as bad weather, shipping, dipping or association with other viruses or mycoplasmal diseases, the Pasteurella species become pathogenic and invade the tissue, entering blood and spread through the body. Pasteurellae cause their effect by combination of two mechanisms that include release of endotoxins and important exotoxins, which kill bovine macrophage and neutrophils. Death of animal results from asphyxia due to laryngeal edema and enlargement of tongue. Signs
Diseased animal shows fever muconasal discharge, severe respiratory
distress with extended head and neck besides mouth breathing and froth
on lips (Fig. 39).
Lesions
Petechial hemorrhages are noticed on serous and other organs especially
pericardium (Fig. 40)
The interlobular edema and hemorrhage are not prominent. Fibrinous
pleurisy is also noticed (Fig. 45)
Acute hemorrhagic gastroenteritis is usually present (Fig. 8)
Calves (Two to four months) show fibrinopurulent meningitis and polyarthritis. Cow shows severe fatal hemorrhagic mastitis. Pasteurellosis in sheep usually caused by P hemolytica and characterize by hemorrhages and lesions of septicemia. The lesions represented by hemorrhages in subcutaneous tissue, intramuscular, under the serous membrane. Moreover, swollen and edematous lymph nodes, necrotizing pharyngitis and bacterial emboli in the lungs. Fibrinous bronchopneumonia, similar to bovine lesions without pleural effusion, may be seen.
Fig. 39: Cattle infected with pasteurellosis showing mouth
breathing.
Fig. 40: Pasteurellosis showing subepicardial hemorrhages.
Fig. 41: Acute fibrinous pneumonia in sheep suffering from
pasteurellosis.
Fig. 42: Lung showing gross picture of gray hepatization.
Fig. 43: Lung showing fibrinous inflammation characterized by
congested interalveolar capillaries, fibrin threads in alveoli and
massive inflammatory cells. H&E.
Fig. 44: Lung showing fibrinous inflammation characterized by
congested interalveolar capillaries, fibrin threads in alveoli and
massive inflammatory cells. H&E. Circling disease It is an acute septicemic infectious disease of ruminants, man and other animals and characterizes by encephalitis in cattle, sheep, goat and human or septicemic infection with liver necrosis in monogastric animals and young calves and lambs, or abortion in pregnant cattle. Cause and susceptible animals Listeria monocytogens is a small rod shaped gram positive intracellular parasite. Rat suspected to be a reservoir. Cattle, sheep, goat, swine rabbit and fowl besides man are susceptible to infection. Route of infection and pathogenesis. The organisms are excreted through urine, feces uterine discharge and aborted fetus. Three forms of diseases are recorded. When an outbreak occurs, all animals show only one form. Meningioencephalitis or nervous form resulted from infection through nasal mucosa or conjunctiva. The microorganisms travel by ascending way through the peripheral nerve especially trigeminal nerve to the brain stem (medulla oblongata, pons and spinal cord leading to encephalitis, from which the infection extend to meninges. Ingestion of contaminated food is suspected to cause the septicemic form and abortion in pregnant animals. The ingested organisms penetrate and multiply in intestinal mucosa, destroy the cells and then release to be phagocytized by mononuclear cells. The organisms get entry to general circulation In pregnant animals abortion form resulted from localization of the organism in the uterus or through coitus, causing metritis and death of the fetus and finally abortion. Signs 1. Nervous form
These form common in cattle, sheep, goat and human. It also occurs in
swine, dog and horse. It is characterized by abnormal posturing of head
and neck, lethargy, walking aimless and in circle due to neck is pulled
to one side, blindness and facial paralysis with dropping of ear,
eyelids and lips. Finally, animal become recumbent and dies from
respiratory failure (Fig. 45).
2. Septicemic form It usually occurs in young animal as lambs, calves and piglet. The animals are dull, emaciated, with gastroenteritis. 3. Abortion form The dam shows no signs. Abortion occurs in the last quarter of gestation. Lesions 1. Nervous form The lesions can be seen only by microscopic examination and restricted to brainstem.
Early lesions are consisted of aggregation of mononuclear cells with or
without neutrophils. Later on, diffuse leukocytic infiltration and
microabbesses are seen. The Listeria monocytogens can be easily
demonstrated at the center of lesion with appropriate stain. The white
matter is edematous and showed foci of softening. (Figs 46,47& 48)
Intense meningeal lymphocytic infiltration is a characteristic accompaniment. 2. Septicemic form It characterized by focal necrosis of the liver and less frequent spleen, lymph nodes, lungs, adrenal, myocardium and gastrointestinal tract. Microscopically, the necrotic areas are infiltrated with mononuclear cells and neutrophils. 3. Abortion form Abortion can occur in cattle and sheep in the last quarter of gestation without any clinical signs in dam. The abortion occurs due to intrauterine death of the fetus. So the aborted fetus usually autolysed. The principle lesion in aborted fetus is coagulative necrosis of the liver containing stainable organisms.
Fig. 45: Sheep infected with Listeriosis ( nervous form )
characterized by abnormal posturing of head and neck, lethargy, walking
aimless and in circle, facial paralysis with dropping of ear, eyelids
and lips. Finally, animal become recumbent and dies from respiratory
failure.
Fig. 46: Sheep infected with Listeriosis nervous form showing ,
suppurative meningioencephalitis.
Fig. 47: Sheep infected with Listeriosis nervous form showing
micro abscess characterize by focal infiltration of the brain tissue by
neutrophils. H&E.
Fig. 48: Sheep infected with Listeriosis nervous form showing
perivascular lymphocytic cuffing. H&E.
Fig. 49: Liver of sheep infected with Listeriosis showing
pyogranuloma represented by focal replacement of the hepatic parenchyma
with neutrophils and macrophages. H&E.
Fig. 50: Liver of sheep infected with Listeriosis showing
subcapsular pyogranuloma. H&E.
Diseases caused by high bacteria High bacteria are usually produce lesions similar to that of mycotic infection. The high bacteria differed from fungi that they lacking eukaryotic nuclei and mitochondria. The high bacteria involve some important animal pathogens such as Actinomyces, Nocardia, Corynebacterium, Dermatophilus, Streptomyces and Mycobacterium. Infection caused by Corynebacterium organisms The member of genus Corynebacterium can induce a wide variety of diseases in human and animals. The Corynebacterium are gram positive, not acid fast microorganisms. The lesions induce by Corynebacterium are varied; the tissue reaction against some members is necrotizing, to others is suppurative and granulomatous to other.
Corynebacterium pyogens (Actinomyces pyogens) produce abscesses in
cattle, swine, sheep and goat, suppurative dermatitis, arthritis and
umbilical infection in calves, purulent mastitis and metritis in cow
beside suppurative pneumonia in cattle (Fig. 51).
Fig. 51: Skin of cattle showing suppurative dermatitis represent
by focal abscess (basophilic structure material). H&E.
Corynebacterium renale can induce suppurative inflammation in the
urinary tract of cattle (mainly cow) as pyelonephritis (Figs.52 & 53)
Fig. 52: Gross picture of kidney showing pyelonephritis.
Fig. 53: Microscopic picture of pyelonephritis showing
suppurative inflammation and accumulation of pus in pelvis which extend
into medulla. H&E.
Corynebacterium pseudotuberculosis (C ovis) is the causes of caseous lymphadenitis in sheep and goat.
It is a chronic disease of sheep and goat characterized by chronic suppurative inflammation and caseous necrosis in the lymph nodes and other organs. Cause Corynebacterium pseudotuberculosis (C ovis), gram positive diphtheroid , non. motile, non. sporulating bacilli. Susceptible hosts
Sheep and goat are the natural host. In cattle and horses,
Moreover, C ovis causes ulcerative lymphangitis in cattle (Fig. 54)
Route of infection and pathogenesis The organism gain entry wound through wound or abrasion and rarely through inhalation or ingestion. It is frequent in sheep in cases of docking, shearing, and castration. Pathogenesis: Through wound infection the microorganisms, engulfed within macrophage, get entry to lymph nodes. Moreover, entrance of microorganisms into blood results in the development of lesions in many organs like the lung, liver, kidney and spleen. The microorganisms produce exotoxin (phospholipase D) and bear toxic lipids enable microorganism to survive inside macrophages. The lesions start first as aggregation of macrophages which die and caseated later (by the action of exotoxin) an surrounded by epithelioid cells, lymphocytes and encircled by fibrous tissue. Then the epithelioid cells die and new reactive layers form outside and later necrotic. The results is spherical, onion like concentrically laminated masses. Calcification may occurs.;; Signs
The disease occurs as inapparent infection and encountered only as an
incidental finding in slaughtered house. The superficial lymph nodes,
namely, prescapular, prefemoral, supramammary and mediastinal lymph
nodes are enlarged (Fig. 55)
lesions
The affected lymph node is greatly enlarged. In cross section, the lymph
node is replaced by concentrically laminated layers of fibrous
connective tissue alternate with caseous friable mass that may be
greenish and occasionally gritty resembling the structure of onion (Fig.
56 & 57)
Lung lesions are represented by miliary suppurative foci or multiple
abscesses (Fig. 58)
Microscopically, acute focal areas of suppurative inflammation are seen
in young lambs (Figs 59 & 60)
Fig. 54: Buffalo infected with C. ovis showing gross picture of
ulcerative lymphangitis showing enlarged and thickened subcutaneous
lymph vessels.
Fig. 55: Sheep infected with caseous lymphadenitis showing
enlargement of sub mandibular lymph node.
Fig. 56: Lymph node cut section showing concentrically laminated
layers of fibrous connective tissue alternate with caseous friable mass
that may be greenish and occasionally gritty resembling the structure of
onion.
Fig. 57: Lymph node cut section showing concentrically laminated
layers of fibrous connective tissue alternate with caseous friable mass
that may be greenish and occasionally gritty resembling the structure of
onion.
Fig. 58: Lung of young lamb infected with caseous lymphadenitis
characterized by acute focal areas of suppurative inflammation. H&E.
Fig. 59: Lung of lamb infected with caseous lymphadenitis showing
suppurative inflammation.
Fig. 60: Lung showing caseous necrosis represented by replacement
of pulmonary tissue by eosinophilic and basophilic debri. H&E.
Fig. 61: Lymph node of sheep infected with caseous lymphadenitis
showing caseous necrosis represented by replacement of lymphoid tissue
by eosinophilic and basophilic debri. H&E.
Fig. 62: Lymph node of sheep infected with caseous lymphadenitis
showing calcification stained black with Von Kossa stain.
Lumpy jaw It is a chronic infectious suppurative granulomatous disease of cattle , but many species may be infected under natural infection. It is characterized by hard , irregular chronic focal suppurative inflammation in the mandible and maxilla. Cause
Actinomyces bovis, a gram. positive rod shaped anaerobe microorganism
(Fig. 63)
Route of infection The infection occurs through wound infection caused by sharp pieces of feed or foreign material. The organism is commonly present in the mouth cavity Pathogenesis Microorganisms gain entry through wound infection caused by sharp object. The microorganisms have affinity toward the hard tissue. The organism initiates granulomatous inflammation around. The presence of eosinophilic clubs is due to combination of the product of host reaction and invading organisms. If an alveolar periostitis occurs, the infection can easily be transported by the venous or lymphatic circulation, probably within the cytoplasm of the macrophages, into the bone marrow or it may invade the bone marrow by direct contact. Generalized disease involved hard tissue is recorded in dog. Lesions
Hard irregular enlargement of the mandibular and maxillary bones, which
give the disease it common name (lumpy jaw) is seen (Figs 64 & 65)
The cut surface is white and glistening results from diffuse fibrous tissue proliferation in which small abscesses is embedded. Sinus tracts may be drainage through skin or oral cavity, yellowish pus containing hard in masses called sulfur granules. Similar lesions may be seen in lungs and lymph nodes.
Microscopically, early lesion shows acute suppurative inflammation with
the accumulation of neutrophils . Later on, macrophages, lymphocytes,
fibroblasts, and later giant cells appear in the area forming The
classic lesion in this case consists of centrally located
eosinophilic bacterial colonies surrounded by radiating brightly
eosinophilic short clubs (Figs 66 ,67 & 68)
Fig. 63: A Gram positive filamentous bacilli was isolated in an
anaerobic culture.
Fig. 64: Sheep showing hard irregular enlargement of the
mandibular which give the disease it common name (lumpy jaw).
Fig. 65: Actinomycosis. Diffuse granulomas in maxilla and
formation of green yellow pus. “Sulphur granules” are found in the pus.
Fig. 66: Lung showing clustered of bacteria surrounded by
homogeneous matrix called Splendore-Hoeppli material and finally
surrounded with neutrophils .H&E.
Fig. 67: Bone showing bacterial colonies surrounded by
homogeneous matrix called Splendore-Hoeppli material and finally
surrounded with neutrophils .H&E.
Fig. 68: Lymph node showing bacterial colonies surrounded by
homogeneous matrix called Splendore-Hoeppli material and finally
surrounded with neutrophils .H&E.
Paratyphoid It is an acute or chronic infection febrile bacterial disease caused by Salmonellae and characterized either by acute septicemic form especially in young animals or by acute or chronic enteritis. In human it cause gastroenteritis, septicemia or enteric fever. Cause Salmonellae are members of family Enterobacteriaceae. Salmonellae are rod shaped non. sporulating motile facultative anaerobic bacilli. S typhimurium, S enteriditis, and S dublin are common serptypes in ruminants, S typhimurium and S cholerasuis in pigs and S typhimurium in horse. Moreover, S abortus may cause abortion in mare between 6th to 9th months of pregnancy. Susceptible host Salmonellosis is a disease of all animal species particularly young animals. The young animals show peracute septicemic or acute enteritis, but in older animals the infection is less severe or even unnoticed especially in cattle. Mode of infection Ingestion, of contaminated food with feces from either clinically ill animals or carrier, is the principle route of infection. The predisposing causes as transport, sudden change of diet, parturition, vaccination is important to salmonella organisms to become pathogenic. Pathogenesis Pathogenic salmonellae ingested in food survive passage through the gastric acid barrier and invade the mucosa of small and large intestine with production of toxins. To be fully pathogenic, salmonellae must posses a variety of virulence factors as ability to invade cells, completely lipopolysaccharide coat beside ability to intracellular replication and endotoxins elaboration. The organisms colonize the ileum and colon. Salmonella invade epithelial cells and proliferation within the epithelium and lymphoid follicle and stimulate productions of pro. inflammatory cytokines that induce acute inflammation resulting in diarrhea and ulcer and necrosis of intestinal mucosa. Many salmonellae infection not progress further. Others more pathogenic especially in young age, the bacteria spread to mesenteric lymph nodes within macrophages and can get entry to general circulation and cause systemic diseases. In animals survive the organism may be localized in various organs especially liver, spleen, gallbladder and intestine producing enteritis. Signs Three forms of disease can be observed clinically: 1. The peracute septicemic form occurs in newborn calves and foals. The diseased animals show depression, dullness, high fever, and death within 1. 2 days. Nervous signs including incoordination and convulsions can be recorded in calves infected with S dublin. 2. Acute form is the common form in adult animals. The diseased animal shows fever, with severe watery diarrhea, severe dehydration, dysentery and tenasmus. The feces contain mucus and fibrinous cast. Abortion occurs in pregnant animals. Polyarthritis are seen in survival calves. 3. Chronic form is occasionally seen in adult cattle with persistent diarrhea, severe emaciation, and intermittent fever. Gross lesions
In peracute septicemic form lesions of septicemia as extensive
submucosal and subserosal petechial hemorrhages (Fig. 69)
In acute form, enterocolitis is the principle lesions. Severe catarrhal
to hemorrhagic enteritis involve the stomach proximal part of small
intestine and extend to colon is noticed. The mucosa is hyperemic, or
hemorrhagic, thickened and often covered with yellow or gray exudate.
Microscopically, the intestinal the epithelial cells undergo
degenerative changes and necrosis (Fig. 70)
The lesions in other organs are less consistent. Mesenteric lymph nodes
are enlarged, edematous and hemorrhagic (Fig. 71)
Liver enlarged, pales, and showed many foci of necrosis (paratyphoid
nodule) besides distended gallbladder with bile (Fig. 72)
In chronic form superficial necrosis of the intestinal mucosa, which may proceed to the development of an extensive diphtheretic pseudomembrane appearing as yellowish. gray necrotic material. Microscopically, the intestinal glands are atrophied, some are dilated due to closure of the ducts with debris, and macrophages and lymphocytes infiltrate the lamina propria.
Fig. 69: General view of the digestive tract of the horse with
salmonellosis showing congestion and petechial hemorrhages.
Fig. 70: Intestine showing necrotic enteritis with dilated
lymphatic vessels. H&E.
Fig. 71: Intestine showing enlarged mesenteric lymph node.
Fig. 72: Gall bladder of sheep infected with salmonellosis
showing distended with bile.
Fig. 73: Microscopic picture of paratyphoid nodule showing
focal parenchymal necrosis of liver infiltrated with lymphocytes
(typhoid nodule).
It is a group of lesions induced by Fusobacterium necrophorum characterized by necrosis in various tissues according to animal species. Fusobacterium are gram. negative anaerobic filamentous bacilli, which may cause infection in any part of the body. Most strains are encapsulated. Fusobacterium species are prevalent on all mucosal surfaces as commensal organisms. They may have an opportunity to penetrate tissue and inducing diseases under certain conditions such as wound. Tissue necrosis and poor blood supply favoring the growth of anaerobes. The microorganisms produce enzymes, endotoxin and exotoxin that play a role in pathogenesis of disease.
In cattle, Fusobacterium necrophorum induce elevated tenacious necrotic
plaques of the pharynx, larynx and trachea which known as calf
diphtheria, pneumonia, large areas of hepatic coagulative necrosis
association with ulceration of rumen in heavily fed animals (Figs 74, 75
& 76).
Calf diphtheria is highly contagious and fatal disease of calves under 6 months. The organism gain entry through wounds. Grayish red or yellow single or multiple round or linear well circumscribed coagulative necrosis is seen on borders of tongue, inner surface of cheeks, gum, soft palate pharynx, larynx and tonsils. The lesions usually elevated over the surface and extend deeply into mucosa, submucosa, muscularis or even bone or cartilage. The necrotic tissue is surrounded by red zone, which later replaced by fibrous tissue. Removal of necrotic tissue leaves a bleeding ulcer, which heal later by cicatrization. In horse, F necrophorum is associated with necrotizing disease of animals that forced to stay for long period in deep manure and urine soaked mud. The gangrenous dermatitis starts at heel and deep structure of the frog and characterized by sharply demarcated necrosis.
Fig. 74: Liver of cattle infected with Fusobacterium necrophorum
showing multiple abscesses.
Fig. 75: Liver of cattle infected with Fusobacterium
necrophorum showing periportal coagulative necrosis. H&E.
Fig. 76: Rumen of cattle infected with Fusobacterium
necrophorum showing showing healed ulcer.
Diseases caused by streptococcal infection Streptococcal bacteria is a gram positive spherical organisms grow in pairs or chains. Members of genus streptococcal can infect animals and human producing several diseases. Moreover, streptococcal can invade wound producing local purulent inflammation. The streptococcal infection in animals leads to the following diseases: strangles, streptococcal mastitis, urogenital infection, cervical lymphadenitis of swine, streptococcal meningitis and arthritis in swine, streptococcal infection in guinea pig, neonatal streptococcal infection and pneumococcal infection in animals
It is an acute infectious disease of upper respiratory tract of young horse caused by Streptococcus equi and characterized by purulent lymphadenitis of mandibular and pharyngeal lymph nodes. Mode of infection Infection occurs through inhalation or ingestion of contaminated food and water. The disease are most common in young horses live in crowded condition. The incubation period ranged from 4 t0 8 days. Pathogenesis The microorganism multiply and colonize on nasal mucosa. It penetrate the mucous glands to reach lymph spaces of mucosa or is carried by phagocytes in lymph vessels to reach other lymph nodes. In the lymph node the streptococcal microorganisms multiply and produce toxin which attract large number of neutrophils and cause liquefactive necrosis and forming abscesses. Sometimes the organisms gain enter to general circulation and infect viscera and other lymph nodes. Signs
Fever, anoroxia, mucopurulent nasal discharge conjunctivitis followed by
edematous swelling of the pharyngeal region are noticed (Fig. 77)
Lesions
Acute catarrhal or purulent inflammation of the upper respiratory system
with abscess formation in the daring lymph nodes (Figs. 78, 79 & 80)
Metastatic abscesses are seen in lungs, kidneys, spleen and occasionally brain. Septicemia may occurs with fewer abscess. .Rupture of retropharyngeal abscess lead to empyema. Complication 1. Catarrhal bronchitis, pneumonia, pleurisy, pericarditis, pyemia and chronic valvular endocarditis. 2. Empyema in guttural pouch due to rupture of retropharyngeal lymph node. 3. Peritonitis due to rupture of mesenteric lymph nodes. 4. Abscesses in different lymph nodes. 5. Purpura hemorrhagica (Petechial fever)
It is complicated cases of strangles characterized edema and hemorrhage
on subcutaneous tissue and mucous (Fig. 81)
Fig. 77: Horse infected with strangles showing mucopurulent nasal
discharge.
Fig. 78: Horse infected with strangles showing swelling of
pharyngeal region due to suppurative inflammation of pharyngeal lymph
node.
Fig. 79: Horse infected with strangles showing swelling of
submandibular region.
Fig. 80: Horse infected with strangles showing multiple absences
in upper respiratory.
Fig. 81: Horse infected with strangles showing edema and
hemorrhages in the mucosa of nostril in case of purpura hemorrhagica.
It is a chronic granulomatous infectious disease of man and animals caused by certain organisms within the genus Mycobacterium, and characterized by the development of tubercles nodules in different organs. Causes
The disease is caused by many species of genus Mycobacterium.
Mycobacterium is a slender, curved rods acid fast bacilli (Fig. 82)
Mycobacterium bovis is the main cause of tuberculosis in animals such as cattle, buffalo, camels, sheep, goats, horses, pigs and dogs. Human can get the infection mainly through ingestion of infected milk. M tuberculosis, is the main cause of tuberculosis in human and non human primates, occasionally in dogs but rarely in other relatively resistant domestic animals such as cattle and cats M avium is the main cause of tuberculosis in birds and may account for a considerable proportion of cases of tuberculosis especially in pigs. Susceptible host and mode of infection:
Tuberculosis is seen in all species of animals and man. The incidence of
infection is higher in cattle, less in pigs and the disease rarely
occurs in sheep and horse, and uncommon in goats (Fig. 83)
The main route of infection, especially in housed domestic animals, is through inhalation of infected droplet. Infection by ingestion is more common swine, horse, birds and in young animals through drinking of infected milk. Intrauterine infection especially from cow to fetus is occasionally occurs. Pathogenesis Mycobacterium infection occurs by airborne transmission or ingestion of droplet contains viable organisms produced by sputum of infected animals. The bacilli adhere to the lining epithelium, where they induce local infiltration of neutrophils. The neutrophils are able to engulf the bacilli but are not able to kill them. The neutrophils rapidly totally disappear from the infected area due to their destruction and can not be seen in the lesion. The macrophages arrive to the site of infection and phagocytize the bacilli. The intracellular organisms resist destruction by macrophages. The mechanism by which intracellular survival may be due to prevention of phagosome. lysosome fusion, or direct cytotoxic effect of some cell wall component to macrophages or prevent acidification of phagolysosome. Accumulation of mycobacterium stimulates an inflammatory response, which mature into a granulomatous lesion.
Following the formation of the primary lesion at the site of entry in
organs, the bacilli carried to regional lymph node either freely or in
macrophages through the lymph where tubercles are formed. The lesions in
organ and regional lymph node called primary complex (Fig. 84).
Infection spread to next lymph node and lymphatic until reach the circulation, localized in an organ or various organs in large numbers. Postprimary infection can occur in animal under stress, the resistance of the body is lowered activation of infection from old encapsulated lesions resulting in formation of daughter tubercle or get entry to general circulation and localized in various organs. Gross lesion Tubercle bacilli produce characteristic lesions no matter where they localize in tissue. Lesions in tuberculosis are either proliferative (focal or diffuse) or with exudation. The proliferative is more common forming microscopic tubercles, which later diffuse to be seen by naked eye. A. The proliferative form seen either as tubercles, miliary form or caseous form
1. Tubercle or nodular form is the classical form of lesions. The
tubercle is 1. 2 cm in diameter, first gray and translucent but soon
becomes yellowish. Large tubercles are dry, grayish. white and contain
caseous masses calcified foci (Fig. 85)
2. Miliary tuberculosis is generalized form of tubercle. The lesions
are characterized by the presence of numerous number of recent tubercle
2. 3 mm in diameter, approximately of the same age and shape (Fig. 86)
3. Caseous form is characterize by a small or large areas of tissue
necrosis (Fig. 87)
B: The exudative form involve the serous membrane as tuberculous
pleuritis in dogs (Fig. 88) Microscopically, The tuberculous lesions are basically proliferative except in serous membrane is exudative. The tissue reactions to mycobacterium bacilli start as a small aggregates of neutrophils that phagocytize the bacilli. The neutrophils die and totally disappear from the area. After that the macrophages arrive and phagocytize the bacteria. The bacilli kill macrophage. Numerous monocytes and histocytes are attracted to the area under the effect of cytokines, metabolic products and disintegration of bacilli. The mononuclear cells become enlarged and pale with large vesicular nuclei and foamy cytoplasm (epithelioid cells).
Fusion of more than one epithelioid cell or by mitotic division of the
nucleus of one cell without division of the cytoplasm resulted in
formation of Langhan’s giant cells. Lymphocytes, migrating from the
adjacent blood vessels, form a dense zone around epithelioid cells.
Under the effect of bacterial toxin, unsaturated fatty acids and perhaps
also a vascular condition of the tubercle the tubercle undergoes
degenerative changes and caseous necrosis (Figs 89, 90, 91, 92& 93).
Old tubercles are encircled with fibrous tissue. Encapsulated. The necrotic portion may calcify or liquefy old tubercles. Calcification is a characteristic in some species of animals (cattle, sheep, and goats) while it is rarely or not observed (buffalo, pig, dog, and fowl). The difference of tubercle structure in different animal species. Cattle, sheep, and goat tubercles is characterized by the presence of a few number of lymphocytes, giant cells besides abundant connective tissue network and capsule. Calcification occurs frequently. The disease mainly occurs in thoracic cavity, particularly lungs and related lymph nodes. Lungs The lungs involved in about 75% of the tuberculous cases. The pulmonary lesions take three forms. A. tuberculous bronchopneumonia
The infection takes place through the air passage. The inflammatory
process starts as terminal bronchiolitis with expansion into the
alveoli. Macroscopically, catarrhal inflammation of one or more lobules
followed by pneumonia, caseation alternated with congestion and edema.
Lesions rarely form cavities (vomica) due to liquefactive necrosis (Figs
94 & 95)
B. Miliary tuberculosis It results from entry of Mycobacterium into general circulation and arrest of the organisms in pulmonary vessels. The lungs show numerous discrete gray translucent firm nodules of same size and age. C. Chronic nodular tuberculosis It results from arrest of bacilli in lymphatic or capillaries. The tuberculous lesions formed from yellow caseous or calcified foci surrounded by varying degree of fibrosis. Tuberculous pleurisy and peritonitis
It is tuberculous forms characterized by the presence localize or
diffuse area of soft grayish velvety granulation tissue on serous
membrane. The tubercle may aggregate extensive clusters similar to
pearls or grapes (Pearl disease). The center of the nodules is caseated
(Figs 96 & 97)
The spleen is involved in about 15% and the lesions is confined to the capsule. The lymph nodes involved in about 90% of the affected cases. The mammary gland involved in 1% of tuberculous cases. Three forms are seen according to anatomical distribution. Miliary tuberculous mastitis, diffuse lobular tuberculous mastitis and caseous tuberculous mastitis are seen. Alimentary tract lesions It is always secondary except in calf. They show tubercles lesion ileum and colon or in Payer’s patch. Central nervous system Lesions are frequent in calves and young cattle and present in cerebrum, cereblum and meninges In equine the tubercle is more cellular having many lymphocytes but little connective tissue ground substance besides softening of the center with rarely calcification. In swine infected with Mycobacterium bovis the tubercle characterize by abundant lymphocytes with less connective tissue and caseation and calcification. Meanwhile, the avian strain causes much less caseation and calcification and highly cellular (neoplastic like appearance). The dog’s tubercles characterized by liquefactive necrosis. The fowl tubercle shows extensive caseation without calcification besides deficient cellular elements and connective tissue framework.
Fig. 82: Mycobacterium bovis is acid fast bacilli.
Fig. 83: Cattle infected with tuberculosis showing chronic cough.
Fig. 84: Lung of cattle showing enlarged and caseated lymph node
and involvement of pulmonary tissue (primary complex).
Fig. 85: Lung of cattle showing tuberculous nodules.
Fig. 86: Liver showing gross picture of miliary tuberculosis
characterize by presence of same size and age nodules.
Fig. 87: Lung showing large caseated tuberculous nodule.
Fig. 88: Peritoneum showing pearl disease.
Fig. 89: Lymph node of cattle infected with tuberculosis showing
young nodules represented by aggregation of epithelioid cells and giant
cells. H&E.
Fig. 90: Lung showing tuberculous nodule young nodules
represented by aggregation of epithelioid cells and giant cells. H&E.
Fig. 91: Liver showing tuberculous nodules consist from caseous
necrosis, epithelioid cells and giant cells surrounded with fibrous
tissue. H&E.
Fig. 92: Lymph node showing tuberculous nodule characterize by
cassation and calcification. H&E.
Fig. 93: Lymph node showing cassation and calcification. H&E
Fig. 94: Tuberculous lung showing cavities or vomica.
Fig. 95: Bronchioles of animals infected with tuberculosis
showing involvement of the wall by tuberculous nodule. H&E.
Fig. 96: Miliary tuberculous peritonitis showing tuberculous
nodules formed from caseous necrosis surround by epithelioid cells and
giant cells surrounded by fibrous tissue. H&E.
Fig. 97: Miliary tuberculous peritonitis showing tuberculous nodules of
same size and age.
It is a chronic wasting infectious disease caused by Mycobacterium paratuberculosis and characterized by chronic catarrhal enteritis, and thickening of the intestinal mucosa. Cause Mycobacterium paratuberculosis is an aerobic, non. spore forming acid. fast bacillus. Susceptible host It is a disease of cattle and occasionally sheep and goat. Route of infection and pathogenesis Infection occurs through ingestion of contaminated food and water. The ingested microorganisms reach to small intestine mainly the terminal part of ileum, but the rest of small intestine and large intestine and mesenteric lymph nodes are involved. The mycobacterium gets entry through intestinal mucosa and phagocytizes by macrophages. The microorganisms then localize and multiply in the mucosa of the small intestine and in the mesenteric lymph nodes. In pregnant cows, infection may occur leading to congenital infection and abortion. Signs
The disease characterizes by long incubation period ranged from 2. 6
years. Emaciation accompanied with chronic diarrhea, which lasts for
several weeks or months are seen. The feces are soft, thin, homogenous
and without offensive odor (Figs 98 & 99).
Lesions The intestinal wall is thickened (4. 5times) with yellowish white rigid smooth, transversely folded mucosa that resemble the convolutions of the brain with red crest (Fig.100). These changes mainly involve the posterior part of small intestine (jugenum, ileum). It may be extend also to the large intestine. Lymph vessels in the serosa of the intestine and in the mesentery are thickened and convluted and may contain caseated or calcified nodules. The mesenteric nodes enlarged, soft with moist cut surface containing yellowish white necrotic foci. Microscopically, the lamina propria is diffusely infiltrated with lymphocytes and plasma cells and a large number of eosinophils with a very few number of epithelioid cells in early stage. Later on, the epithelioid cells increases and the other infiltrating cells are proportionally reduced. Moreover giant cells are seen (Fig.101&102). Some intestinal glands are cells compress and obliterate and others are cystic. The submucosa may involve but muscularis mucosa and muscularis remain intact. The acid. fast bacilli can be demonstrated in cytoplasm of macrophages. Lymph nodes shows granulomatous lymphadenitis. Abomasum: The abomasum shows atrophy and cystic changes of the gastric glands, besides edema and occasional hemorrhage are common in the lamina propria and submucosa. Focal areas of necrosis and erosions of the epithelium particularly over Peyer's patches are seen in small and large intestine. The lymphoid follicles and lymph nodes show necrosis of lymphocytic elements.
Fig. 98: Goat infected with Johne's disease showing emaciation.
Fig. 99: Cow infected with Johne's showing emaciation.
Fig.100: Johne's disease. Thickened and corrugated intestinal
mucosa.
Fig.101: Microscopic picture of paratuberculosis or Johne's
disease, intestine showing severely infiltrated with macrophages. H&E.
Fig.102: Microscopic picture of paratuberculosis or Johne's
disease, intestine showing severely infiltrated with macrophages. H&E.
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