department of pathology faculty of veterinary medicine
TRANSCRIPT
Department of Department of PathologyPathology
Faculty of veterinary medicineFaculty of veterinary medicine
Mechanism of Mechanism of bacteria-induced injurybacteria-induced injury::
Intracellular bacteriaIntracellular bacteria
Extracellular bacteriaExtracellular bacteria
Intracellular Intracellular bacteriabacteriaDamage the host Damage the host
tissues by: tissues by: invasion to host invasion to host cells and cells and maymay form form toxinstoxins..
Extracellular Extracellular bacteriabacteria Damage the host Damage the host tissues bytissues by ::
their ability to their ability to adhere to the host adhere to the host cells and cells and produceproduce toxinstoxins..
Bacterial toxinsBacterial toxinsEndotoxinesEndotoxines
ExotoxinesExotoxines
EndotoxinesEndotoxines((aa ) ) Lipopolysaccharide Lipopolysaccharide ) ( LPS) ( LPS in in
naturenature.. ((bb ) ) Structural components of the Structural components of the
outer cell wall outer cell wall of gm –ve bacteriaof gm –ve bacteria..
((cc)) NonNon s pecific toxines s pecific toxines . .((dd ) ) Their biological activity include Their biological activity include
induction of induction of
feverfever,, septic Shock septic Shock,, and acute and acute respiratoryrespiratory
distress syndromedistress syndrome..
ExotoxinesExotoxinesHarmful product Harmful product
secreted by secreted by bacteriabacteria.. SpecificSpecific for each for each
bacteriabacteria . . Includes different Includes different
Enzymes asEnzymes as;; LeucocidinsLeucocidins,, HemolysinsHemolysins,, HyalourinidaseHyalourinidase,, CoagulasesCoagulases,and ,and FibrinolycinsFibrinolycins..
Inflammatory Response To Inflammatory Response To Bacterial agentsBacterial agents SuppurativeSuppurative Polymorphnuclear Polymorphnuclear InflammationInflammation..
MononuclearMononuclear inflammation inflammation..GranulomatousGranulomatous
inflammationinflammation.. NecrotizingNecrotizing inflammation inflammation . .
Suppurative Suppurative Polymorphnuclear Polymorphnuclear InflammationInflammation
NeutrophilsNeutrophils attracted attracted to to pyogenicpyogenic bacteria bacteria which release which release chemochemo attractants that attractants that evoke this responseevoke this response . .
Mononuclear Mononuclear inflammationinflammation Mononuclear cells is aMononuclear cells is a------------
i) i) Common features of All Common features of All chronicchronic
inflam. Process. inflam. Process. As in As in LeptospiraLeptospira
ii) ii) In response to In response to intracellularintracellular bacteria bacteria & & spirochetes spirochetes in in
acuteacute inflam. Processinflam. Process..
Granulomatous Granulomatous inflammationinflammation Distinctive form of Distinctive form of mononuclear mononuclear inflam. Evoked by inflam. Evoked by slow dividing slow dividing infectious agents asinfectious agents as
M. tuberculosisM. tuberculosis..
Necrotizing Necrotizing inflammationinflammation RapidRapid and and SevereSevere tissue tissue
damage in which damage in which cell cell death death is the dominant is the dominant feature evoked by feature evoked by v.strong toxins v.strong toxins which which secreted fromsecreted from
C. perfringensC. perfringens . .
Pasteurellosis DefinitionDefinition : :
A group of diseases A group of diseases affectingaffecting different different
species of Anspecies of An . .caused bycaused by; ; P. multocidaP. multocida
P. hemolyticaP. hemolytica..
Pasteurellosis CattleCattle : :
Hemorrhagic septicemiaHemorrhagic septicemia ..
Pneumonic Pneumonic pasteurellosispasteurellosis..
Meningitis in Meningitis in calvescalves . .Mastitis in Mastitis in cowscows..
Pasteurellosis SheepSheep::
SepticemiaSepticemia . .Enzootic Enzootic
pneumoniapneumonia . .Mastitis in Mastitis in ewesewes..
PasteurellosisPoultry: Fowl cholera.
Horse: Hemorrhagic septicemia.
Rabbit: Snuffles.Man and Rodents :
Tularemia ( P. tularenses)
Hemorrhagic Hemorrhagic septicemiasepticemiaDefinitionDefinition::
**Per acute fatal disease of Per acute fatal disease of cattlecattle
**Caused by P.multocidaCaused by P.multocida **Characterized byCharacterized by
((ii ) ) Fibrinohemorrhagic interstitial Fibrinohemorrhagic interstitialPneumoniaPneumonia . .
((iiii ) ) Hemorrhagic gastroenteritis Hemorrhagic gastroenteritis..
Hemorrhagic Hemorrhagic septicemiasepticemia 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 septicemiaHemorrhagic septicemiaLesions:
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 septicemiaHemorrhagic septicemia
Hemorrhagic Hemorrhagic septicemiasepticemia
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:
11--Reddish black to grayish brown Reddish black to grayish brown consolidated areas in the consolidated areas in the cranioventral cranioventral regionregion of the lungsof the lungs..
22--Gelatinous thickening of the interlobular Gelatinous thickening of the interlobular septasepta..
33--Areas of necrosis with white boundaries Areas of necrosis with white boundaries &deep central red zone&deep central red zone..
44--Marbling appearance Marbling appearance of the lung as a of the lung as a result of septal edema and congestion result of septal edema and congestion intermixed with different stages of intermixed with different stages of pneumoniapneumonia (red and grey hepatization)(red and grey hepatization), , necrotic areasnecrotic areas, , and normal areasand normal areas..
Pneumonic pasteurellosis
Pneumonic pasteurellosis
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)
Lung hepatization (Pasteurellosis)
(OAT CELL Pnumonia)
MycoplasmosisDefinition:
A group of diseases affecting different species of animals caused by Mycoplasma organism.
MycoplasmosisGoats:
* 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 pleuropneumoniaR.O.I:
Deep Inhalation of infecteddroplets as upper respiratorytract 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
Contagious bovine pleuropneumonia
Contagious bovine pleuropneumonia
Contagious bovine pleuropneumonia
Contagious bovine pleuropneumonia
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 lymphofollicularsheath
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)
(Cuffing pneumonia)
(Cuffing pneumonia)
(Cuffing pneumonia)
Strangles(Shipping fever of equines)
Adenitis equeriumDefinition: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 internalorgans.
StranglesCause:
Streptococcus equi produce (hemolycin & leucocydin).
R.O.I: Inhalation.
StranglesPathogenesis:
Inhalation of the M.O nasal mucosal penetration lymphatics regional lymph nodes.
StranglesLesions
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
Strangles
Strangles
LesionsSuppurative inflammation of
the submaxillary and retropharyngeal L.N which may ruptured:
(i ) On skin T o Outside.(ii )On Trachea To Lung
(supp.pneumonia)(iii ) On Blood T o Circulation
(metastatic abscess)
Strangles
Strangles
Strangles
Strangles
Strangles
Strangles
Strangles
Strangles
StranglesComplications:
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.
StranglesComplications:
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.
ColibacillosisColibacillosisDefinition :
Infectious disease of man and animals .
CauseCause : : E.coli.
ColibacillosisColibacillosisPathogenesis:
The organism produce the disease by 5 mechanisms:
1-Enterocyte-adherent Colibacillosis
2-Enterotoxic colibacillosis 3-Enterotoxaemic
colibacillosis 4-Enteroinvasive colibacillosis
5-Septicemic colibacillosis
ColibacillosisColibacillosisPathogenesis: 1-Enterocyte-adherent
Colibacillosis
E.coli colonizing the surface of enterocytes without producing toxins.
ColibacillosisColibacillosisPathogenesis
2-Enterotoxic colibacillosis
E.coli colonizing the mucosa
producing enterotoxines diarrhea
ColibacillosisColibacillosisPathogenesis
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)
ColibacillosisColibacillosisPathogenesis4-Enteroinvasive
colibacillosis E.coli invade intestinal
epithelium Acute exudative enteritis Endotoxaemia.
ColibacillosisColibacillosisPathogenesi
5-Septicemic colibacillosis E.coli produce bacteraemia,
endotoxaemia and localization in different organs.
i.Enterotoxic colibacillosisDefinition:
•The major cause of neonatal diarrhea in calves , pigs and lambs.
Also cause diarrhea in man .
*It occurs in the 1st. 2-3 days of life as the older resist the adhesion of coli by antibodies in milk
i.Enterotoxic colibacillosis
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 ) E nterocytes
(become cuboidal . 2 )Fusion of intestinal villi .3 )Neutrophiles in intestinal
lumen.
i.Enterotoxic colibacillosisDiagnosis :
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
ii.Enteroinvasive colibacillosis
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 colibacillosisDefinition:
• 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 & thrombosisP/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
cases1- Fibrinous Pleuritis, Peritonitis,
and Pericarditis.
2- Mucopurulent to hemorrhagic sinusitis in lambs.
3- Fibrinopurulent arthritis & meningitis.
Salmonellosis DefinitionDefinition : :
*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 PathogenesisPathogenesis ::
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
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 formCh’Ch:’
*Septicaemia, *Meningioencephalitis
*Polyarthritis.
Salmonellosis (ii )Acute or enteric formi. 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
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Fibrinonecrotic enteritis
(Salmonellosis)
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Fibrinonecrotic enteritis (Salmonellosis)
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Fibrinonecrotic enteritis
(Salmonellosis)
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Salmonellosis (ii)Acute or enteric formii. 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)
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Paratyphoid nodule (Salmonellosis)
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Salmonellosis (iii )Chronic formCh’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 formCh’Ch:’
Ulcerative typhlocolitis
Necrobacillosis
DefinitionDefinition : : *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
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foot rot
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Necrotic Stomatitis
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Necrotic Stomatitis
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Necrobacillosis
Cause : Fusobacterium necroforum.Route of infection :
Secondary invasion following mucosal
damage ( oral wound, trauma, eruption of teeth )
( predisposing causes.)
Necrobacillosis PathogenesisPathogenesis ::
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
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Hepatic necrobacillosis
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Hepatic necrobacillosis
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Pulmonary necrobacillosis
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Necrobacillosis
Microscopic appearance: Structureless area
surrounded by hyperaemic zone and leucocytes ,
later by thick capsule of granulation tissue.
Hepatic necrobacillosis
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Hepatic necrobacillosis
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Leptospirosis DefinitionDefinition : :
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 PathogenesisPathogenesis ::
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
Leptospirosis
Leptospirosis Dog
P.M lesions: Liver showed atrophy and
fibrosis.Subcapsular hemorrhages
in the kidney. In chronic cases the capsule become adherent.
Leptospirosis CattleMicroscopic 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
Leptospirosis
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)
DefinitionDefinition : :
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 t he vaccine is notsufficiently
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 offace, neck, and Throat.
In man : Cutaneous anthrax----------Malignant carbuncle
Respiratory anthrax ( via spores inhalation ) ---
--------------- wool sorter's disease .
Anthrax(splenic fever)
Anthrax(splenic fever)
Anthrax(splenic fever)
Anthrax(splenic fever)
Anthrax(splenic fever)
Anthrax(splenic fever)
Anthrax(splenic fever)
Clostridial diseases
Group of diseases caused by Clostridiaorganisms, 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)
DefinitionDefinition:: *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 Lesions1.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)
1.Black disease (Infectious necrotic hepatitis)
Clostridial diseases
2. Bacillary hemoglbinurea
DefinitionDefinition:: * 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 hemoglbinureaP.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
2.Bacillary hemoglbinurea
Clostridial diseases
3. Black leg ( black quarter )DefinitionDefinition::
•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 gasesii) Signs of toxemia
3.Black leg(black quarter)
3.Black leg(black quarter)
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 edema
DefinitionDefinition:: * 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
4.Gas gangrene OR malignant edema
Clostridial diseases
5. Tetanus (lock jaw)DefinitionDefinition::
*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)
Tetanus (lock jaw)
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)
C.Perfringens type C(Struck)
Clostridial diseases
6. Enteric Clostridial infections (Enterotoxaemia) C. Perfringens type B (Lamb dysentery)
Affects lambs 10-14 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)
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 DefinitionDefinition : :
*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 syndromeFetus 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 7th 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 DefinitionDefinition : :
* 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 & seminalvesicles )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 7th & 8th 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 )PlacentaEdema 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 )PlacentaMicro:
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 )FetusCatarrhal 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 )BullOrchitis, seminal vesiculitis and
prostatitis.Orchitis characterized by areas of
necrosis which liquefies into pus surrounded by C.T. capsule.
Vibriosis(Campylobacter fetus) DefinitionDefinition : :
* 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.