8. 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.
9. Exotoxines
Harmful product secreted by
bacteria.
Specific for each bacteria.
Includes different Enzymes as;
Hemolysins, Leucocidins,
Coagulases,and Hyalourinidase,
Fibrinolycins.
12. 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.
14. 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.
20. Hemorrhagic septicemia
Definition:
*Per acute fatal disease of cattle
*Caused by P.multocida
*Characterized by
(i) Fibrinohemorrhagic interstitial Pneumonia.
(ii) Hemorrhagic gastroenteritis.
21. 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
22. 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.
25. 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)
26. 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).
27. 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.
33. 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
40. Mycoplasmosis
Cattle:
Contagious Bovine PleuroPneumonia
( C.B.P.P ).
Mycoplasmal bronchitis and pneumonia
in calves (Cuffing pneumonia)
Poly arthritis in calves.
Abortion in cows.
41. 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.
44. 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.
45. 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.
46. 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).
52. 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.
53. 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.
55. 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.
56. Mycoplasmal bronchitis and pneumonia
in calves(Cuffing pneumonia)
Cause:
Mycoplasma dispar
R.O.I:
Inhalation of infected droplets.
57. (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.
63. 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.
70. 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)
79. 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.
80. 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.
89. 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
91. 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.
92. 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.
94. 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.
95. 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.
98. 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.
99. 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.
102. 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.
103. 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).
104. Microscopic appearance:
Subacute and chronic cases
1- Fibrinous Pleuritis, Peritonitis, and
Pericarditis.
2- Mucopurulent to hemorrhagic sinusitis in
lambs.
3- Fibrinopurulent arthritis & meningitis.
107. Salmonellosis
Cause :
Gram – ve organism
( S.typhimurium, entritides and duplin).
Route of infection :
Ingestion of contaminated
materials.
108. Salmonellosis
Predisposing factors :
Stress
(starvation, transportation,
crowdness, parturition etc.).
Young animals
susceptible to septicemic form
whereas adults are carriers.
109. 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
110. 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.
111. 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.
113. 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.
118. 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.
121. 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.
123. 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)
127. 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.
134. Necrobacillosis
Spread of infection:
Aspiration of necrotic material
Gangrenous Pneumonia.
Ingestion of necrotic material
Stomach Intestine.
Emboli Circulation
different organs.
lung
Oesophagus
Necrotic lesions in
135. 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.
136. 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
152. 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.
155. 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.
158. Anthrax(splenic fever)
Cause :
Bacillus anthracis, spore forming Gram + ve
bacilli.
Route of infection :
(i) Inhalation,
(ii) Wound infection,
(iii)Vaccination(if the vaccine is not sufficiently
attenuated).
(iv) Ingestion
159. 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).
160. 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.
161. 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.
162. 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 .
171. 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)
172. 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.
174. 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
175. 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.
180. 2.Bacillary
hemoglbinurea
Pathogenesis :
Ingestion of spores
Infestation of the animal with fasciola
liver necrosis
intestine
circulation
localization in histeocytes of liver
Exotoxines
Remain in
suitable anaerobic condition
multiplication
kupffer cells and produce
intravascular hemolysis
181. 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.
184. 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.
186. 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
187. 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
190. 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.
191. 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.
192. 4.Gas gangrene OR
malignant edema
Cause :
Separate or mixture of
C.chauvei, perfringes or septicum.
Route of infection :
Deep wound infection (castration ,
shearing)
.
196. Clostridial diseases
5. Tetanus (lock jaw)
Definition:
* Infectious disease of man and
animals.
Characterized by stiffness of
muscles and closure of jaw.
198. 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)
203. 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
204. 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.
205. 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.
208. 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.
209. 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.
210. 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
211. 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.
212. 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).
215. 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 .
216.
217.
218. 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.
220. 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)
221. 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.
222. 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
223. 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)
224. 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.
225.
226. 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.
227. Brucellosis
Pathogenesis :
Localization
Female
M.O
Pregnant
Spleen
uterus
Mammary gland
Regional L.N
Male & Female
Synovial structures
(tendovaginitis)
(arthritis)
placental necrosis
Blood
Male
Lymphoid tissue
testis&Accessory gland
(prostate & seminal vesicles)
(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.
228. 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.
229. 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.
230. 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.
231. 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.
232. 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.
236. 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.