Transcript pathology_of_bacterial_diseases._course_no._401._by_dr

Department of Pathology
Faculty of veterinary medicine
Mechanism of bacteriainduced 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.
Bacterial toxins
Endotoxines
Exotoxines
Endotoxines
(a) Lipopolysaccharide ( LPS ) in nature. 
(b) Structural components of the outer cell wall
of gm –ve bacteria.
(c) Non specific toxines.
(d) Their biological activity include induction of 
fever, septic Shock, and acute respiratory
distress syndrome.
Exotoxines
Harmful product secreted by 
bacteria.
Specific for each bacteria. 
Includes different Enzymes as; 
Hemolysins, Leucocidins,
Coagulases,and Hyalourinidase,
Fibrinolycins.
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
ii) In response to intracellular 
bacteria & spirochetes in acute
inflam. Process.
Granulomatous inflammation
Distinctive form of 
mononuclear inflam.
Evoked by slow dividing
infectious agents as
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.
Pasteurellosis
Definition:
A group of diseases affecting 
different species of An.
caused by; P. multocida 
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.
(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)
Invasion
Proliferation of the m.o 
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
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
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 )
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
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 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)
(Cuffing pneumonia)
(Cuffing 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
Strangles
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
Strangles
Strangles
Strangles
Strangles
Strangles
Strangles
Strangles
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

The organism produce the disease by 5 mechanisms :
Pathogenesis :
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 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
(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
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 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)
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Fibrinonecrotic enteritis
(Salmonellosis)
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Fibrinonecrotic enteritis
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Fibrinonecrotic enteritis
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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)
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Paratyphoid nodule (Salmonellosis)
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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
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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
Pathogenesis :
The organism invade the 
damaged mucosa and
produce
Endo&Exo toxine Necrosis. 
Necrobacillosis
Spread of infection:
Aspiration of necrotic material
Gangrenous Pneumonia.
lung
Ingestion of necrotic material Oesophagus
Stomach Intestine.
Emboli Circulation
different organs.
Necrotic lesions in 


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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Necrobacillosis
Microscopic appearance : 
Structureless area 
surrounded by hyperaemic
zone and leucocytes,
later by thick capsule of
granulation tissue.
Hepatic necrobacillosis
Gross
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Hepatic necrobacillosis
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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
Leptospirosis
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
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)
Definition:
Highly septicemic infectious 
disease of man and animals.
Characterized by septicemia 
and sudden death.
Anthrax(splenic
Cause
:
fever)
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)
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 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
multiplication
exotoxines
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)
1.Black disease
(Infectious
necrotic hepatitis)
Clostridial diseases
2. Bacillary hemoglbinurea
Definition:
* 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
Exotoxines
multiplication
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
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
intestine
Infestation of the animal with fasciola
muscular fatigue
circulation
localization in skeletal muscles
germination
multiplication
Muscle necrosis
suitable anaerobic condition
Exotoxines
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)
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
Definition:
* 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
edema
gangrene
OR
malignant
4.Gas
edema
gangrene
OR
malignant
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)
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


Struck
C. perfringens type C (B toxin)


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 :
Per acute
Acute
Subacute
Adult
3 forms can be recognized: 
Sudden death.
Salivation and coma.
Neurological signs.
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
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
1. Abortion 
2. Septicemia 3. Encephalitis.
Forms :
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
Placenta


Necrotic foci in liver and spleen.
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
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 :
Localization
Male
M.O
Pregnant
Spleen
uterus
Mammary gland
vesicles)
placental necrosis
Regional L.N
Female
Synovial structures
(tendovaginitis)
(arthritis)
Blood 
Male & Female
Lymphoid tissue
testis&Accessory gland
(prostate & seminal
(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) 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
*Fetus
Placentitis as in brucellosis.
Multiple areas of hepatic necrosis
with depressed center. •


•