Department of Pathology Faculty of veterinary medicine

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



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.


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.


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.)







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)

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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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Pulmonary necrobacillosis

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Necrobacillosis

Microscopic appearance: Structureless area

surrounded by hyperaemic zone and leucocytes ,

later by thick capsule of granulation tissue.


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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.


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


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).


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.


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.


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 .








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)


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.


Cause : C. novyi

Route of infection : Ingestion of food and

water contaminated with spores.


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


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.




2. Bacillary hemoglbinurea

DefinitionDefinition:: * Highly fatal infectious

disease of cattle & sheep *Caused by C. hemolyticum

spores.*Characterized by hepatic

necrosis and intravascular hemolysis .


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.




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.


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) 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.


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).


Pathogenesis: Deep wound infection

(anaerobic conditions) Germination of spores Multiplication Exotoxines Muscle necroses.




5. Tetanus (lock jaw)DefinitionDefinition::

*Infectious disease of man and animals.

Characterized by stiffness of muscles and closure of jaw.


5. Tetanus (lock jaw)

Cause : C. tetani.

Route of infection : Deep wound.


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)


5. Tetanus (lock jaw)

PM lesions : Not

characteristic.


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


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.



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)


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.


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.


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


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 .



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)



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 .


(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.


(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.


(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.

Documents

Department of Pathology Faculty of veterinary medicine