Department of Pathology Faculty of veterinary medicine

Mechanism of bacteria- induced injury: Mechanism of bacteria- induced injury:  Intracellular bacteria  Extracellular bacteria

Intracellular bacteria  Damage the host tissues by: invasion to host cells and may form toxins.

Extracellular bacteria  Damage the host tissues by : their ability to adhere to the host cells and produce toxins. their ability to adhere to the host cells and produce toxins.

Bacterial toxins Bacterial toxins  Endotoxines  Exotoxines

Endotoxines  (a) Lipopolysaccharide ( LPS ) in nature. (b) Structural components of the outer cell wall (b) Structural components of the outer cell wall of gm –ve bacteria. of gm –ve bacteria. (c) Non specific toxines.  (d) Their biological activity include induction of fever, septic Shock, and acute respiratory fever, septic Shock, and acute respiratory distress syndrome. distress syndrome.

Exotoxines  Harmful product secreted by bacteria.  Specific for each bacteria.  Includes different Enzymes as; Leucocidins, Hemolysins, Hyalourinidase, Coagulases,and Fibrinolycins.

Inflammatory Response To Bacterial agents Inflammatory Response To Bacterial agents  Suppurative Polymorphnuclear Inflammation.  Mononuclear inflammation.  Granulomatous inflammation.  Necrotizing inflammation.

Suppurative Polymorphnuclear Inflammation  Neutrophils attracted to pyogenic bacteria which release chemo attractants that evoke this response.

Mononuclear inflammation  Mononuclear cells is a  i) Common features of All chronic inflam. Process. As in Leptospira inflam. Process. As in Leptospira  ii) In response to intracellular bacteria & spirochetes in acute bacteria & spirochetes in acute inflam. Process. inflam. Process.

Granulomatous inflammation  Distinctive form of mononuclear inflam. Evoked by slow dividing infectious agents as M. tuberculosis. M. tuberculosis.

Necrotizing inflammation  Rapid and Severe tissue damage in which cell death is the dominant feature evoked by v.strong toxins which secreted from C. perfringens. C. perfringens.

Pasteurellosis Definition:  A group of diseases affecting different species of An.  caused by; P. multocida P. hemolytica. P. hemolytica.

Pasteurellosis Cattle:  Hemorrhagic septicemia.  Pneumonic pasteurellosis.  Meningitis in calves.  Mastitis in cows.

Pasteurellosis Sheep:  Septicemia.  Enzootic pneumonia.  Mastitis in ewes.

Pasteurellosis  Poultry: Fowl cholera.  Horse: Hemorrhagic septicemia.  Rabbit: Snuffles.  Man and Rodents: Tularemia ( P. tularenses)

Hemorrhagic septicemia  Definition: *Per acute fatal disease of cattle *Caused by P.multocida *Characterized by (i) Fibrinohemorrhagic interstitial Pneumonia. (i) Fibrinohemorrhagic interstitial Pneumonia. (ii) Hemorrhagic gastroenteritis. (ii) Hemorrhagic gastroenteritis.

Hemorrhagic septicemia  Pathogenesis  The organism is a normal inhabitant in the nasopharyngeal mucosa.  Impaired local or systemic defense mechanism ( stress,transportation,bad environment,crowding)  Proliferation of the m.o Invasion of the mucosa to blood Septicemia 

Hemorrhagic septicemia  Lesions: 1. Per acute edematous form Characterized by subcutaneous edema of the throat and brisket resulting in asphyxia and death. 2. Petechial hemorrhages all over the serous membranes. 3. Accumulation of bloody stained fluid ( serosanguinous fluid ) in body cavities. 4. Swollen and hemorrhagic L.N. 5. Fibrinohemorrhagic interstitial pneumonia. 6. Acute hemorrhagic gastroenteritis.

Hemorrhagic septicemia

Pneumonic pasteurellosis (shipping fever)(OAT CELL Pnumonia )  Definition: *Severe acute disease of cattle *Caused by P. hemolytica. *Characterized by fibrinous or fibrinonecrotic bronchopneumonia (lobar) *Usually following transportation (shipping fever)

Pneumonic pasteurellosis  Pathogenesis: *Impaired defense mechanism (transportation) Proliferate in nasopharynx then Invade the lung *The m.o release endotoxines ( leukotoxin) and (cytotoxins ) Capillary thrombosis, necrosis and fibrinous pneumonia. *Leukotoxin & Cytotoxin affect leucocyte w’ accumulate in the inflamed alveoli transforming them into oat like plant ( oat cells).

Pneumonic pasteurellosis  Lesions (i) MACRO: 1-Reddish black to grayish brown consolidated areas in the cranioventral region of the lungs. 2-Gelatinous thickening of the interlobular septa. 3-Areas of necrosis with white boundaries &deep central red zone. 4-Marbling appearance of the lung as a result of septal edema and congestion intermixed with different stages of pneumonia (red and grey hepatization), necrotic areas, and normal areas.

Pneumonic pasteurellosis

Lobar pneumonia(Pasteurellosis)

Lung hepatization(Pasteurellosis)

Pneumonic pasteurellosis  (ii) MICRO:  Severe fibrinous pleuropneumonia with 4 stages  Severe thickening of the interlobular septa with serofibrinous exudates & dilated bl.vs.  Vasculitis&Thrombosis of capillaries& arterioles  Areas of coagulative necrosis with macrophages inside the alveoli (oat shaped cells) ( PATHOGNOMONIC LESIONS ) OAT CELL PNEUMONIA

Lung hepatization (Pasteurellosis)

(OAT CELL Pnumonia )

Mycoplasmosis  Definition: A group of diseases affecting different species of animals caused by Mycoplasma organism.

Mycoplasmosis  Goats: * Contagious Caprine PleuroPneumonia. ( C.C.P.P ) *Poly arthritis.  Sheep and swine: * Enzootic pneumonia.

Mycoplasmosis  Cattle:  Contagious Bovine PleuroPneumonia ( C.B.P.P ).  Mycoplasmal bronchitis and pneumonia in calves (Cuffing pneumonia)  Poly arthritis in calves.  Abortion in cows.

Contagious Bovine PleuroPneumonia (CBPP)  Definition: * Contagious infectious disease of cattle *Characterized by  (i) Fibrinous pleuropneumonia in acute cases.  (ii) Sequestra formation in subacute and chronic cases.

Contagious bovine pleuropneumonia  Cause: Mycoplasma mycoides bovis ( Small Colony )

Contagious bovine pleuropneumonia R.O.I : Deep Inhalation of infected droplets as upper respiratory tract is quite resistant.

Contagious bovine pleuropneumonia  Pathogenesis : 1- Mycoplasma inhaled deeply into the small bronchioles inflammation of bronchial wall invasion of the interlobular Connective tissue septa inflam.followed by edema then…………… spread to alveoli ………then secrete toxin w’ lead to …….. acute vasculitis, thrombosis & necrosis.

Pathogenesis : 2- Necrosed area become demarcated &surrounded by f.c.t Sequestrum 3. Mycoplasma remain viable in sequestra for years and severe coughing rupture of the fibrous capsule of the sequestra liberating organism to lymph space reinfection of the animal occurred or expelled outside and infect or other animals.

Contagious bovine pleuropneumonia  Lesions (i) MACRO: 1. Severe fibrinonecrotic pneumonia (caudal lobes) with fibrinous pleuritis. 2. Gelatinous thickening of the interlobular septa. 3. Dilated lymphatics (beaded appearance). 4. Typical marbling appearance in acute stages. 5. Sequestra formation ( PATHOGNOMONIC LESION ) (necrotic areas surrounded by C.T. capsule).

Contagious bovine pleuropneumonia

 Lesions (ii) MiCRO: a- Fibrinous pleuropneumonia. b- Marked distension of interlobular septa with serofibrinous exudates & dilated Bl.vs & lymphatics c- Marked dilatation of lymphatics. d- Vasculitis and thrombus formation in capillaries and arterioles. e- Sequestra formation.

Contagious Caprine PleuroPneumonia (CCPP) * Acute disease of goats similar to CBPP of cattle Caused by Mycoplasma Capri * But Differs in :  No widening of interlobular septa.  No sequestra formation.  Marbling is less common.  Pericarditis, & Septicemia are common.  The exudates in the chest is more thick and tend to clot easily.

Fibrinous pleuricy with adhesions(CCPP)

Mycoplasmal bronchitis and pneumonia in calves(Cuffing pneumonia)  Definition: * Mycoplasmal disease of calves * Characterized by (i) Chronic catarrhal bronchitis and bronchiolitis (ii) Development of lymphofollicular sheath around air ways giving the name of cuffing pneumonia.

Mycoplasmal bronchitis and pneumonia in calves(Cuffing pneumonia)  Cause: Mycoplasma dispar R.O.I: Inhalation of infected droplets.

(Cuffing pneumonia)  Lesions (i) MACRO: Patch purple red atlectatic foci in the cranio ventral region. (ii) MICRO:  Catarrhal bronchitis and bronchiolitis.  Peribronchial and peribronchiolar accumulation of lymphocytes and plasma cells (cuffing).  Interstitial pneumonia.

(Cuffing pneumonia)

Strangles (Shipping fever of equines) Adenitis equerium  Definition: Acute contagious disease of young equines (2m – 5y ) * Characterized by: (i) Suppurative inflammation of the upper respiratory tract. (ii) Abscessation of the retropharyngeal and submaxillary L.N (iii) Systemic dissemination to internal organs.

Strangles  Cause: Streptococcus equi produce (hemolycin & leucocydin).  R.O.I: Inhalation.

Strangles  Pathogenesis: Inhalation of the M.O nasal mucosal penetration lymphatics regional lymph nodes.

Strangles  Lesions  Purulent rhinitis, pharyngitis, laryngitis, and sinusitis.  Purulent bilateral creamy yellow nasal discharge.  Chronic empyemia of paranasal sinus and guttural pouch if inflam. Extend from nasal cavity.  Catarrhal conjunctivitis.

Strangles

Lesions  Suppurative inflammation of the submaxillary and retropharyngeal L.N which may ruptured:  (i) On skin To Outside.  (ii) On Trachea To Lung (supp.pneumonia)  (iii) On Blood To Circulation (metastatic abscess)

Strangles

 Complications: The disease is not fatal unless complicated by : 1- Suppurative bronchopneumonia, pleuritis and peritonitis with abscessation in different organs. 2-Damage of recurrent laryngeal nerve paralysis Roaring disease.

Strangles  Complications: 3- Purpura hemorrhagica (Petechial fever) resulting from intoxication and allergy (arthus reaction). characterized by sub acute edema and hemorrhage allover serous membranes. 4- Septicemia, pyaemia, valvular endocarditis and meningitis.

Colibacillosis  Definition : Infectious disease of man and animals.  Cause : E.coli.

Colibacillosis  Pathogenesis : The organism produce the disease by 5 mechanisms :  1-Enterocyte-adherent Colibacillosis  2-Enterotoxic colibacillosis  3-Enterotoxaemic colibacillosis  4-Enteroinvasive colibacillosis  5-Septicemic colibacillosis

Colibacillosis  Pathogenesis :  1- Enterocyte-adherent Colibacillosis E.coli colonizing the surface of enterocytes without producing toxins.

Colibacillosis  Pathogenesis  2 -Enterotoxic colibacillosis E.coli colonizing the mucosa producing enterotoxines diarrhea

Colibacillosis  Pathogenesis 3-Enterotoxaemic colibacillosis  E.coli colonizing small intestine Produce toxins w’ has a pathogenic effect in ts. Other than gut. Increase permeability of blood vessels (edema disease of swine)

Colibacillosis  Pathogenesis  4-Enteroinvasive colibacillosis E.coli invade intestinal epithelium Acute exudative enteritis Endotoxaemia.

Colibacillosis  Pathogenesi  5-Septicemic colibacillosis E.coli produce bacteraemia, endotoxaemia and localization in different organs.

i.Enterotoxic colibacillosis  Definition: The major cause of neonatal diarrhea in calves, pigs and lambs. Also cause diarrhea in man. * It occurs in the 1 st. 2-3 days of life as the older resist the adhesion of coli by antibodies in milk

i.Enterotoxic colibacillosis

 Pathogenesis : The organism adheres to the surface of enterocytes enterotoxines hyper secretion of sodium chloride and water from crypt Absorption by villi Secretory diarrhea occurs.

i.Enterotoxic colibacillosis  Macro: Non specific  Microscopic appearance : 1) Degeneration of enterocytes in ( jejunum & ileum ) villous atrophy (Enterocytes become cuboidal). 2) Fusion of intestinal villi. 3) Neutrophiles in intestinal lumen.

i.Enterotoxic colibacillosis  Diagnosis:  Bacterial isolation for L.N & other organs.  Presence of gm –ve bacilli in smear of ileal scraping.  Electron microscopy.  Flurescent Ab test for frozen Ts.

ii.Enteroinvasive colibacillosis  Pathogenesis :  Affect Age < 2w  E.coli invade the enterocytes of the lower small and large intestine producing acute exudative enteritis and endotoxaemia.

ii.Enteroinvasive colibacillosis  P.M. lesions :  1. Congestion of lower parts of S.I & caecum.  2. Mucosal erosions and ulcers.  3. Fluid content of intestine tenged with blood.

ii.Enteroinvasive colibacillosis

 Microscopic appearance :  Enterocytes become cuboidal or flattened (villous atrophy).  Congestion and edema of lamina propria with neutrophilic infiltration.  Thrombosis of proprial capillaries and submucosal lymphatics.

iii.Septicemic colibacillosis  Definition: Generalized Systemic infection with E.coli mainly occurs in calves either as peracute,acute, or subacute. Route of infection : (a) Navel in neonates OR (b) Upper respiratory tract and nasopharynx.

iii.Septicemic colibacillosis  P.M. lesions : (i) Omphalitis. (ii) Pneumonic lung. (iii) Firm spleen.

iii.Septicemic colibacillosis  Microscopic appearance (i) Per (more) acute cases. (ii) Acute cases. (iii) Subacute and chronic cases.

iii.Septicemic colibacillosis  Microscopic appearance :  Per(more) acute cases  due to endotoxemia-----vascular permeability hemorrhage & thrombosis  P/M lesions: 1- Picture of septicemia. 2- Abomasal ulcers.  Micro: Edema, Congestion & Thrombosis in lung and other ts.

Microscopic appearance:  Acute cases 1- Interstitial pneumonia with fibrinous exudate and Neutrophiles in alveoli. 2- Neutrophiles in the hepatic sinusoids and lungs. 3-Fibrinous thrombi in hepatic sinusoids, glomeruli and pulmonary capillaries. 4- Focal interstitial nephritis (white spotted kidney).

Microscopic appearance:  Subacute and chronic cases 1- Fibrinous Pleuritis, Peritonitis, and Pericarditis. 2- Mucopurulent to hemorrhagic sinusitis in lambs. 3- Fibrinopurulent arthritis & meningitis.

Salmonellosis Definition:  * An infectious disease of man  and animals.  * Characterized by septicemia,  Gastroenteritis and enterocolitis.

Salmonellosis   Cause : Gram – ve organism ( S.typhimurium, entritides and duplin).  Route of infection : Ingestion of contaminated materials.

Salmonellosis  Predisposing factors :  Stress (starvation, transportation, crowdness, parturition etc.).  Young animals susceptible to septicemic form whereas adults are carriers.

Salmonellosis Pathogenesis : Ingestion of M.O Enterocyte M.O by macrophages in L.P Cross the mucosa Lymphatics Blood stream Septicemia ( Fatal in young animals ) Bacteraemia Liver, spleen, gall bladder

Salmonellosis Pathogenesis : In Carriers M.O remain localized in Gut L.N & Payer's patches till stress factors.  The organism secretes both: Cytotoxins Deg. & necrosis of enterocytes Endotoxins Vascular damage (vasculitis) & thrombosis. 

Salmonellosis   Forms : (i) Septicemic, (ii) Acute or Enteric, (iii) Chronic.  Sheep : (i) Fibrinohemorrhagic enteritis (ii) Septicaemia. (iii) Abortion and death of ewes.  Cattle : Not Occur Less Than 1w In Contrast To colibacillosis.

Salmonellosis Cattle : ( i)Per acute Septicemic form Ch’Ch’: *Septicaemia, * Meningioencephalitis * Polyarthritis.

Salmonellosis (ii) Acute or enteric form i. Intestine  Post mortem lesions : - Fibrinonecrotic or fibrinohemorrhagic enteritis ( ileum, jejunum and colon ). - Enlarged mesenteric lymph nodes.  Microscopic appearance : - Fibrinonecrotic or fibrinohemorrhagic enteritis. - Thrombosis of proprial capillaries ( vasculitis). - Necrosis of payer's patches.

(Salmonellosis) micro previousquit

Fibrinonecrotic enteritis (Salmonellosis) micro previousquit

Fibrinonecrotic enteritis (Salmonellosis) previousquit gross more

Fibrinonecrotic enteritis (Salmonellosis) previousquit gross

Salmonellosis  (ii)Acute or enteric form ii. Liver  Pathognomonic lesion is the presence of paratyphoid nodules in the liver (focal areas of coagulative necrosis surrounded by macrophages)  Similar nodules are found in kidneys, spleen, lymph nodes and bone marrow.  Fibrinous cholecystitis.

Paratyphoid nodule (Salmonellosis) previousquit

Paratyphoid nodule (Salmonellosis) previousquit

Salmonellosis (iii) Chronic form Ch’Ch’: * Bronchopneumonia * purulent synovitis  N.B : Salmonella is an important cause of abortion in cattle in the majority of cases and the abortion is not associated with disease in the DAM.

Salmonellosis Horse : (i) Septicemic form *Occurs in foals 1-6 month Characterized by Septicemic lesions as in cattle.

Salmonellosis  (ii)Acute or enteric form * Occurs in older animals. Characterized by diarrhea, fever and recovery.  P.M and microscopic findings are similar to those in cattle but involves cecum and colon ( Fibrinohemorrhagic typhlocolitis)

Salmonellosis (iii) Chronic form Ch’Ch’: Ulcerative typhlocolitis

Necrobacillosis Definition:  * Infectious disease of animals.  * Characterized by necrotizing lesions in the alimentary tract and liver.

Necrobacillosis * Different conditions produced by the organism in different animals: i- calf diphtheria in calves. ii- ulcerative enteritis in foals. iii- Fistulus withers in horses. iv- necrotic stomatitis, foot rot and liver necrosis in cattle and sheep.

foot rot previousquit Micro

foot rot previousquit Micro

Necrotic Stomatitis previousquit Micro

Necrotic Stomatitis previousquit Micro

Necrobacillosis   Cause : Fusobacterium necroforum.  Route of infection : Secondary invasion following mucosal damage ( oral wound, trauma, eruption of teeth) (predisposing causes).

Necrobacillosis Pathogenesis :  The organism invade the damaged mucosa and produce  Endo&Exo toxine Necrosis.

Necrobacillosis Spread of infection:  Aspiration of necrotic material lung Gangrenous Pneumonia.  Ingestion of necrotic material Oesophagus Stomach Intestine.  Emboli Circulation Necrotic lesions in different organs.

Necrobacillosis Spread of infection:  Hepatic necrobacillosis observed in lambs and calves following omphalophlebitis or as a complication after ruminitis in cattle.  Infection of vagina and uterus after parturition as contamination after inflammatory genital ds.

Necrobacillosis  P.M lesions :  Large well demarcated yellowish gray dry areas of necrosis surrounded by a hyperaemic zone on the tongue, gum, palate,cheeks and pharynx.  Necrotic areas project above the mucosal surface Sloughs Deep ulcer

Necrobacillosis previousquit Micro

Hepatic necrobacillosis previousquit Micro

Hepatic necrobacillosis previous quit

Pulmonary necrobacillosis previous quit

Necrobacillosis  Microscopic appearance :  Structureless area surrounded by hyperaemic zone and leucocytes, later by thick capsule of granulation tissue.

Hepatic necrobacillosis previousquit Gross High power

Hepatic necrobacillosis previousquit Gross High power

Leptospirosis Definition: Acute infectious septicemic disease of cattle, dog and man. Ch’Ch’: septicemia, hepatitis, Icterus, nephritis, meningitis & abortion in swine & ruminant

Leptospirosis   Cause : Leptospira icterohemorrhagica, Pomona and canicola ( spiral m.o.).  Route of infection : ( i) Ingestion, (ii) Abraded skin, (iii) Intrauterine ( transplacental ).

Leptospirosis Pathogenesis :  M.O penetrates the mucosa blood Septicaemia If animal not die during septicemia Localization Liver Icterus  Kidney Interstitial nephritis Localization  Pregnant uterus Abortion

Leptospirosis  Cattle  P.M lesions :  Lesions of septicaemia ( petechial hemorrhages on serous membranes and S/C edema & hemorrhage,ect…………)  Liver enlarged, anemic, bile stained and showed hemorrhage and necrotic foci.  Kidney showed grayish foci of interstitial reaction.  Aborted fetuses showed advanced autolysis & putrifaction.

Leptospirosis

 Dog  P.M lesions :  Liver showed atrophy and fibrosis.  Subcapsular hemorrhages in the kidney. In chronic cases the capsule become adherent.

Leptospirosis Cattle Microscopic appearance :  1. Necrosis of hepatic cells around central vein with hyperplastic kupfer cells containing hemosiderin.  2. Cellular infiltration of portal area while bile canaliculi distended with bile.  3. Interstitial nephritis with tubular  degeneration and necrosis.  4. Placentitis and meningitis.

Leptospirosis

Dog Microscopic appearance :  1- Dissociation of hepatic cells which appear Dark and atrophied.  2- Regeneration evidenced by cytomegally, binucleation & mitoses  3- Kidney showed similar changes as in cattle but more chronic with decreased interstitial exudate and increased fibrosis.

Anthrax (splenic fever ) Definition:  Highly septicemic infectious disease of man and animals.  Characterized by septicemia and sudden death.

Anthrax (splenic fever ) Cause : Bacillus anthracis, spore forming Gram + ve bacilli. Route of infection : (i) Inhalation, (ii) Wound infection, (iii)Vaccination(if the vaccine is not sufficiently attenuated). (iv) Ingestion

Anthrax (splenic fever ) Pathogenesis : 1- Ingestion Pharynx Regional L.N Lymphatics Blood Septicemia 2. The organism produce toxin Endothelial injury Hemorrhage. 3. The organism acts on the respiratory center Asphyxia Death. 4. The capsule of the organism has a fibrinolytic properties (unclotted blood).

Anthrax (splenic fever )  Forms : (i) Septicemic form In Cattle and Sheep. *Ch’Ch’ sudden death and dark tarry unclotted blood oozing from the natural body orifices. 1. Petechial and echymotic hemorrhages on serous membranes. 2. Subcutaneous edema and hemorrhage. 3. Serosanguinous fluid in body cavities.

Anthrax (splenic fever )  Forms : (i) Septicemic form 4. Lymph nodes swollen, edematous and hemorrhagic. 5. Liver and kidney degeneration (pale and friable). 6. Spleen is markedly enlarged (spleenomegally), PATHOGNOMONIC LESION.

Anthrax (splenic fever )  Forms : (ii) Localized form  In horse, pigs and dogs: Pharyngitis, lymphadenitis and Edema of face, neck, and Throat.  In man : Cutaneous anthrax Malignant carbuncle Respiratory anthrax ( via spores inhalation ) wool sorter's disease.

Anthrax (splenic fever )

Clostridial diseases Group of diseases caused by Clostridia organisms, gram + ve, spore forming bacteria. 1.Black disease (Infectious necrotic hepatitis) 2.Bacillary hemoglbinurea 3.Black leg ( black quarter ) 4.Gas gangrene (malignant edema) 5.Tetanus (lock jaw) 6.Enteric Clostridial infections (Enterotoxaemia)

Clostridial diseases 1.Black disease (Infectious necrotic hepatitis)Definition: *Infectious disease of sheep,goat,Cattle&horse * Caused by : C. novyi. Type B Characterized by necrotic hepatitis and dark skin.

1.Black disease ( Infectious necrotic hepatitis) Cause : C. novyi Route of infection : Ingestion of food and water contaminated with spores.

1.Black disease ( Infectious necrotic hepatitis) Pathogenesis : Ingestion of spores Infestation of the animal with fasciola intestine liver necrosis circulation localization in histeocytes of liver germination suitable anaerobic condition exotoxines multiplication liver necrosis

1.Black disease ( Infectious necrotic hepatitis) P.M Lesions 1.Black coloration of skin due to venous congestion of subcutaneous tissue. 2. Pathognomonic lesion is the presence of yellowish white areas of hepatic necrosis surrounded by hyperaemic zone. 3. Subendocardial hemorrhage in left ventricle. 4. Hemorrhage and congestion of abomasums.

1.Black disease ( Infectious necrotic hepatitis)

Clostridial diseases 2. Bacillary hemoglbinureaDefinition: * Highly fatal infectious disease of cattle & sheep *Caused by C. hemolyticum spores. *Characterized by hepatic necrosis and intravascular hemolysis.

2. Bacillary hemoglbinurea Cause : C. hemolyticum Route of infection : Ingestion of food and water contaminated with spores.

2. Bacillary hemoglbinurea Pathogenesis : Ingestion of spores Infestation of the animal with fasciola intestine liver necrosis circulation localization in histeocytes of liver suitable anaerobic condition multiplication Exotoxines Remain in kupffer cells and produce intravascular hemolysis

2. Bacillary hemoglbinurea Signs: Icterus and hemoglbinurea P.M Lesions  Liver contains well demarcated areas of necrosis surrounded by hyperaemic zone.  Mottling of the kidney due to hemoglobin.  Serous cavities contain straw colored fluid with fibrin.

2. Bacillary hemoglbinurea

Clostridial diseases  3. Black leg ( black quarter )Definition: Infectious disease of cattle and sheep * Caused by C. chuvoei. *Characterized by emphysematous and edematous swelling of subcutaneous tissue with necrosis of muscles specially of hind quarter, Gangrene, Toxemia and Death.

3. Black leg (black quarter) Cause : C. chuvoei. Route of infection : Ingestion.

3. Black leg (black quarter) Pathogenesis : Ingestion of spores Infestation of the animal with fasciola intestine muscular fatigue circulation localization in skeletal muscles germination suitable anaerobic condition multiplication Exotoxines Muscle necrosis Gangrene & Toxemia

3.Black leg (black quarter) P.M Lesions  Early or wet stage : Muscles are necrosed appear dark red and separated by serohemorrhagic exudate.  Late or dry stage : i) Muscles are dark red or nearly black (due to the formation of h2s) with gases ii) Signs of toxemia

3.Black leg (black quarter)

Micro  1. Extensive coagulative necrosis (zenker's necrosis) of muscle fibers with edema and hemorrhage.  2. Vasculitis and formation of gas bubbles between the necrotic muscle fibers.

Clostridial diseases 4. Gas gangrene OR malignant edemaDefinition: * Infectious disease of cattle, sheep & equine * Caused by Separate or mixture of C.chauvoei, perfringes or septicum. * Characterized by edematous and crepitating swelling of muscles.

4. Gas gangrene OR malignant edema Cause : Separate or mixture of C.chauvei, perfringes or septicum. Route of infection : Deep wound infection (castration, shearing).

4. Gas gangrene OR malignant edema Pathogenesis :  Deep wound infection (anaerobic conditions) Germination of spores Multiplication Exotoxines Muscle necroses.

4. Gas gangrene OR malignant edema

Clostridial diseases 5. Tetanus (lock jaw)Definition: * Infectious disease of man and animals. Characterized by stiffness of muscles and closure of jaw.

Clostridial diseases 5. Tetanus (lock jaw) Cause : C. tetani. Route of infection : Deep wound.

Clostridial diseases 5. Tetanus (lock jaw) Pathogenesis :  Deep wound infection (anaerobic conditions) Germination of spores Multiplication Neurotoxins (tetanospasmin) inhibit the release of neurotransmitter glycin Stiffness of muscles (maseter and facial) death due to asphyxiation (spasm of diaphragmatic muscles)

Tetanus (lock jaw)

Clostridial diseases 5. Tetanus (lock jaw) PM lesions : Not characteristic.

Clostridial diseases 6. Enteric Clostridial infections (Enterotoxaemia)  Group of enteric diseases in cattle & sheep caused by 5 different toxigenic types of C.perfringens:  C. perfringens type A (& toxin) Gas gangrene ( malignant edema ).  C. perfringens typeB (B toxin) Lamb dysentery  C. perfringens type C (B toxin) Struck  C. perfringens type D (E toxin ) Pulpy kidney, Braxy like ds, Blind staggers.  C. perfringens type E (i toxin) Hemorrhagic enteritis

Clostridial diseases 6. Enteric Clostridial infections ( Enterotoxaemia) Action Of C.perfringens exotoxins:  & toxin: - Lecithinase /act on cell membrane/ cause hemolysis or cell necrosis.  B toxin: - Causing necrotizing enteritis & paralyzing effect on intestine.  E & i toxin: Produced as protoxin w’ get activated by proteolytic Enzymes.

Clostridial diseases 6. Enteric Clostridial infections ( Enterotoxaemia) C. Perfringens type C (Struck)  * Disease of Adult sheep, goat & feed lot cattle.  * Symptoms: Sudden death.  * PM lesions: Hemorrhagic enteritis ( jejunum & ilium) with toxemia.

C.Perfringens type C(Struck)

Clostridial diseases 6. Enteric Clostridial infections ( Enterotoxaemia) C. Perfringens type B (Lamb dysentery)  Affects lambs day, calves less than 10 days and foals 2 days.  Symptoms: Sudden death// Abdominal pain// Passage of semi fluid feces mixed with blood.

Clostridial diseases 6. Enteric Clostridial infections ( Enterotoxaemia) C. Perfringens type B (Lamb dysentery) P.M lesions :  Extensive hemorrhagic enteritis.  Single then confluent ulceration intestinal perforation peritonitis.  Congestion and edema of mesenteric lymph nodes.  Signs of toxemia.  Microscopic appearance :  Hemorrhagic enteritis and necrosis which extends to muscular layer and peritoneum. 

Clostridial diseases 6. Enteric Clostridial infections ( Enterotoxaemia) C. Perfringens type D (Pulpy kidney-overeating disease)  Definition : * Disease of sheep,Goat and sometimes calves. * Usually associated with overload or sudden change in diet to grains or C,H,O.  Symptoms : 3 forms can be recognized: Per acute Sudden death. Acute Salivation and coma. Subacute Neurological signs. Adult Diarrhea

Clostridial diseases 6. Enteric Clostridial infections ( Enterotoxaemia) C.Perfringens type D (Pulpy kidney-overeating disease) Pathogenesis :  Over feeding with carbohydrates fermentation Acidosis (favorable media for the organism to proliferate) Epsilon toxin circulating blood Endothelial injury Edema & hemorrhage in brain and kidney. 

Clostridial diseases 6. Enteric Clostridial infections ( Enterotoxaemia) C. Perfringens type D (Pulpy kidney-overeating disease) P.M lesions :  Edema in serous cavities.  Subendocardial hemorrhage of left ventricle,  Kidney congested and soft (pulpy) due to degeneration and rapid autolysis ( NOT IN ADULT)  SYMMETRIC Encephalomalacia (not in goats).

C. Perfringens type D (Pulpy kidney-overeating disease)

Clostridial diseases 6. Enteric Clostridial infections ( Enterotoxaemia) C.Perfringens type D (Pulpy kidney-overeating disease) Microscopic appearance :  Kidney : Degeneration and necrosis of proximal convoluted tubules.  Brain: Edema and hemorrhage around capillaries symmetric encephalomalacia.

Listeriosis Definition: * Infectious disease of man and animals. * Caused by Lesteria monocytogenes. * Characterized by Septicemia, Encephalitis, and Abortion. * Seasonal ds. As it occurs in winter and early spring.

Listeriosis Cause : Lesteria monocytogenes. Route of infection : Ingestion.  BEHAVE AS 3 SEPARATE DISEASES AS IT HAVE 3 FORMS  Forms : 1. Abortion 2. Septicemia 3. Encephalitis.

Listeriosis Forms : (i) Abortion syndrome  Abortion in cattle and sheep occurring during the last 3 months of pregnancy.  Early Uterine infection Late uterine infection Fetal death (septicemia) Dystocia (difficult parturition) Autolysis and Expulsion Metritis and Septicemia of dam Retained placenta (due to metritis)

Listeriosis Forms : P.M lesions : (i) Abortion syndrome  Fetus Necrotic foci in liver and spleen.  Placenta Necrosis of placenta which is covered by purulent exudate.

Listeriosis Forms : (ii) Septicemic form *Occurs in early neonatal life and *Characterized by milliary abscesses w’ are:- very numerous in liver. less numerous in heart and other organs

Listeriosis Forms : (iii) Encephalitic form * The M.O invade the brain stem. * Very severe in medulla & pons. Signs : *Deviation of head to one side where the animal moves in circles (Circling ds.). *Paralysis of masticatory ms. & pharynx. *Unilateral paralysis of the 7 th nerve resulting in drooping of an ear, eyelid and lips. * Unilateral endopthalmitis ( inflammation of ocular cavity)

Listeriosis Forms : PM lesions:  Meninges are thickened by greenish edema.  Grayish foci of softening in C/S of medulla. Micro :  Micro abscesses in brain.  Vasculitis in white matter  perivascular cuffing  meningitis.  Areas of malacia (softening) due to thrombosis.

Brucellosis Definition: * Infectious disease of animals & man. * Caused by brucella. * Ch’Ch abortion.  Cause: Brucella species.  Route of infection : 1. Ingestion 2. Conjunctiva 3. Intact or broken skin 4. Coitus.

Brucellosis Pathogenesis :  M.O Regional L.N Blood Localization Female Male & Female Male Pregnant Spleen Synovial structures Lymphoid tissue uterus Mammary gland (tendovaginitis) testis&Accessory gland (arthritis) (prostate & seminal vesicles) placental necrosis (Bursitis) Formation of granulomes Abortion (Epithelioid cells surrounded by lymphocytes and plasma cells) * Localization of brucella organism in different organs depends on the presence of its carbohydrate content ( erythritol ) as a source of energy for the growth of the M.O. * whenever the organism localized, granuloma develops.

Brucellosis Abortion in cattle  Occurs in the 7 th & 8 th m of gestation.  In severe cases, abortion or premature birth occurs.  In mild cases, calf delivered either viable or not viable.

Brucellosis P.M lesions : (i) Placenta  Edema of intercotyledonary area (between fetal membranes and uterine mucosa) with coagulative necrosis of maternal (caruncle) and fetal (cotyledon) portions of the placentome.  Placenta becomes leathery with brown thick exudate on the chorionic surface.  In animals previously infected with brucellosis, fibrosis of fetal and maternal portions of the placentome results in retained placenta.

Brucellosis P.M lesions : (i) Placenta Micro :  Edema and cell infiltration of the intercotyledonary area.  Vasculitis due to endotoxines.  areas of coagulative necrosis in fetal and maternal portions of the placentome.

Brucellosis P.M lesions : (ii) Fetus  Catarrhal or fibrinous bronchopneumonia.  Fibrinous inflammation of serous membrane. Micro :  Catarrhal or fibrinous bronchopneumonia.  Necrotizing arteritis.  Granuloma with giant cell formation in the spleen and L.N.

Brucellosis P.M lesions : ( iii) Udder (Bang's disease)  Characterized by focal interstitial mastitis. (iv) Bull  Orchitis, seminal vesiculitis and prostatitis.  Orchitis characterized by areas of necrosis which liquefies into pus surrounded by C.T. capsule.

Vibriosis (Campylobacter fetus) Definition:  * Infectious disease of cattle and sheep.  * Ch’ch’ ; Abortion and infertility. Cause: Campylobacter fetus var venerealis in cattle.  Campylobacter fetus var intestinalis in sheep.

Vibriosis (Campylobacter fetus) In Cattle: Signs  * Abortion 4-6 months of gestation.  * Temporary sterility or repeat breeding due to early  embryonic death.

Vibriosis (Campylobacter fetus) In Cattle: R.O.I  *By coitus and artificial insemination.  * Bulls can act as carriers by carrying  the organism in the penile mucosa up to 4-5 years.  * M.O can survive in vaginal mucosa for longer periods.

Vibriosis (Campylobacter fetus) In Cattle: Lesions  Gross and microscopic  picture is similar to those of brucellosis but less severe.

Vibriosis (Campylobacter fetus) In Sheep: Pathogenesis: Ingestion Bacteremia  Localization in gut,bile,or uterus of pregnant ewes

Vibriosis (Campylobacter fetus) In Sheep: Signs  Abortion 4 months of gestation  ( late).

Vibriosis (Campylobacter fetus) In Sheep: Lesions  *DAM Endometritis, Cervisitis, and Vaginitis  *Placenta Placentitis as in brucellosis. *Fetus Multiple areas of hepatic necrosis with depressed center.