
Infectious Lecture 4th Year 17-10-2016 Dr.Osamah Muwafk
1
PASTEURELLOSIS :
It is include:
1- Septicemic pasteurellosis of cattle (hemorrhagic septicemia
or barbone), commonly associated with infection by P.
multocida type 1 or B, is the classical disease of southern
Asia characterized by a peracute septicemia and a high
mortality rate.
2- Pneumonic pasteurellosis of cattle, commonly associated
with infection by Mannheimia (formerly Pasteurella)
haemolytica biotype A serotype 1, and P multocida biotype
A, is a common disease in Europe and the western
hemisphere.
3- Pasteurellosis of sheep, and goats, usually associated with
infection by M. haemolytica.
Septicemic Pasteurelosis of Cattle (Hemorrhagic Septicemia,
Barbone) :
ETIOLOGY :
1- Hemorrhagic septicemia is associated with two specific
serotypes of P. multocida. The Asian serotype is designated
B:2 and the African serotype is E:2
2- occurs in cattle, yaks, camels, and water buffalo.
3- the most susceptible age group is 6 months to 2 years of age.
4- morbidity and case-fatality rates vary between 50% and
100%.
5- In endemic areas, adult animals develop a naturally acquired
immunity.
6- Outbreaks of the disease are often associated with wet humid
weather during the rainy season.

Infectious Lecture 4th Year 17-10-2016 Dr.Osamah Muwafk
2
7- the causative organism persists on the tonsillar and
nasopharyngeal mucosae of carrier animals.
8- Spread occurs by the ingestion of contaminated foodstuffs.
9- the organism does not survive on pasture for more than 24
hours.
PATHOGENESIS :
1- The portal of entry of infection is thought to be the tonsils.
2- A fulminating septicemia occurs, which is associated with the
capsular material of the organism.
3- The effects of the septicemia are most severe in the
respiratory tract, heart, and gastrointestinal tract.
4- In cattle and buffalo there is rapid translocation of bacteria
from the respiratory tract to the blood, liver, and spleen,
suggesting that the bacteria are able to invade via the mucosal
epithelial layers.
CLINICAL FINDINGS:
1- acute septicemia clinically characterized by:
a- a sudden onset of fever (41-42°C, 106-107°F)
b- profuse salivation
c- submucosal petechiation
d- severe depression
e- death in about 24 hours.
f- on range lands, animals may be found dead without any
clinical signs having been observed.
2- Localization may occur in subcutaneous tissue, resulting in the
development of warm, painful swellings about the throat,
dewlap, brisket or perineum

Infectious Lecture 4th Year 17-10-2016 Dr.Osamah Muwafk
3
3- severe dyspnea may occur if the respiration is obstructed. In the
later stages of an outbreak.
CLINICAL PATHOLOGY:
1- Culture and detection of bacteria.
2- Serology.
NECROPSY FINDINGS:
1- generalized petechial hemorrhages, particularly under the
serosae.
2- edema of the lungs and lymph nodes.
TREATMENT:
1- sulfadimidine
2- The NSAID flunixin meglumine can ameliorate the
inflammatory response to endotoxin, and treatment with
flunixin meglumlne has been shown to improve outcome in
individual animals.
CONTROL:
1- vaccine composed of killed organisms in an adjuvant base
containing paraffin and lanolin.
2- Immunity after vaccination appears to be solid for at least 12
months.

Infectious Lecture 4th Year 17-10-2016 Dr.Osamah Muwafk
4
PNEUMONIC PASTEURELLOSIS OF CATTLE (SHIPPING
FEVER PNEUMONIA):
is an entity within the bovine respiratory disease complex,
characterized clinically by acute bronchopneumonia with toxemia
and pathologically by lobar, anteroventrally distributed, exudative
pneumonia in which fibrin is usually a prominent part of the
exudate and fibrinous pleuritis is common
ETIOLOGY:
1- Mannheimia (Pasteurella) haemolytica biotype A serotype 1.
2- Eleven serotypes have been demonstrated.
3- Pneumonic pasteurellosis is a common disease of young
growing cattle.
4- The morbidity may reach 35%, the case fatality rate may range
from 5-10%.
5- occurs most commonly in young growing cattle from 6 months
to 2 years of age.
6- Transmission occurs by the inhalation of infected drop lets
coughed up or exhaled by infected animals.
PATHOGENESIS:
1- Exposure of healthy cattle to stressors such as viral infection,
change in management practices and environmental changes
leads to an explosive growth and selective colonization by M.
haemolytica A 1 in the upper respiratory tract .
2- When the large numbers of organisms enter and colonize the
lung they interact with alveolar macrophages with decreasing
clearance mechanism.

Infectious Lecture 4th Year 17-10-2016 Dr.Osamah Muwafk
5
3- Four virulence factors have been associated with M.
haemolytica: Fimbriae, A polysaccharide capsule, Endotoxin
(lipopolysaccharide) and Leukotoxin.
CLINICAL FINDINGS:
1- In the feedlot, the disease usually occurs within 10-14 days
after the animals have been stressed.
2- Animals found dead without any previous warning signs may
be the first indication of an outbreak
3- Affected cattle are depressed and their respirations are rapid
and shallow.
4- There may be a weak protective cough, which becomes more
pronounced and frequent if they are urged to walk.
5- Those that have been ill for a few days will appear gaunt
because of anorexia.
6- A mucopurulent nasal discharge, a crusty nose, and an ocular
discharge are common.
7- Outbreaks of the disease in feedlots may last for 2-3 weeks.
8- fever of 40-41 ºC.
9- In the early stages there are loud breath sounds audible over the
anterior and ventral parts of the lungs.
10- As the disease progresses these breath sounds become louder
and extend over a greater area; crackles become audible,
followed by wheezes in a few days, especially in chronic cases.
11- The course of the disease is only 2-4 days.
NECROPSY FINDINGS
1- There is marked pulmonary consolidation, usually involving at
least the anteroventral third of the lungs.

Infectious Lecture 4th Year 17-10-2016 Dr.Osamah Muwafk
6
2- A catarrhal bronchitis and bronchiolitis, and a fibrinous
pleuritis are usually present and may be accompanied by a
fibrinous pericarditis.
3- The lung is firm and the cut surface usually reveals an irregular,
variegated pattern of red, white, and gray tissue due to
hemorrhage, necrosis, and consolidation.
Differencial diagnosis:
1- viral interstitial pneumonia
2- Lungworm pneumonia
3- Epidemic acute interstitial pneumonia (fog fever)
4- Infectious bovine rhinotracheitis
5- Contagious bovine pleuropneumonia
TREATMENT:
1- Antimicrobial therapy:
a- oxytetracycline,
trimethoprim-sulfadoxine,
the
sulfonamides, and penicillin, Florfenicol.
b- Tilmicosin single subcutaneous injection at 10 mg/kg BW
c- Enrofloxacin 2.5-5. 0 mg/kg BW subcutaneously daily for 3-
5 days
d- Ceftiofur 4.4-6.6 mg/kg administered subcutaneously.
2- Anti-inflammatory agents
A- Corticosteroids and nonsteroidal anti-inflammatory drugs
(NSAIDs)
3- Expectorants

Infectious Lecture 4th Year 17-10-2016 Dr.Osamah Muwafk
7
TETANUS:
ETIOLOGY:
1- An exotoxin, tetanospasmin,
2- is produced by Clostridium tetani growing under anaerobic
conditions.
3- The organism forms spores that can persist in soil for many
years.
4- The spores are resistant to many standard disinfection
procedures, including steam heat at 100°C (212°F) for 20
minutes
5- but can be destroyed by heating at 115°C (239°F) for 20
minutes.
6- most common in closely settled areas under intensive
cultivation.
7- It occurs in all farm animals, mainly as individual, sporadic
cases.
8- case fatality rate is over 80% in young ruminants, but the
recovery rate is high in adult cattle.
9- C. tetani organisms are commonly present in the feces of
animals, especially horses.
10- The portal of entry is usually through deep puncture wounds
PATHOGENESIS:
1- The tetanus bacilli remain localized at their site of introduction
and do not invade surrounding tissues.
2- They proliferate and produce tetanolysin and tetanospasmin in
a lowering of the local tissue oxygen tension.
3- Tetanolysin promotes local tissue necrosis.

Infectious Lecture 4th Year 17-10-2016 Dr.Osamah Muwafk
8
4- Tetanospasmin diffuses to the systemic circulation, is bound to
motor end-plates and travels up peripheral nerve trunks.
5- Cause disinhibition of gamma motor neurons result in a state of
constant muscular spasticity.
6- Death occurs by asphyxiation due to fixation of the muscles of
respiration.
CLI NICAL FINDINGS:
1- The incubation period varies between 3 days and 4 weeks
2- Initially, there is an increase in muscle stiffness, accompanied
by muscle tremor.
3- There is trismus with restriction of jaw movements.
4- prolapse of the third eyelid.
5- stiffness of the hind limbs causing an unsteady, straddling gait.
6- the tail is held out stiffly, especially when backing or turning.
7- hyperesthesia with exaggerated responses to normal stimuli.
8- Falling occurs with the limbs still in a state of tetany and the
animal can cause itself severe injury.
DIFFERENTIAL DIAGNOSIS:
1- All species:
a- Strychnine poisoning
b- Meningitis
2- Horses
a- Hypocalcemic tetany (eclampsia)
b- Acute laminitis
c- Hyperkalemic periodic paralysis
d- Myositis, particularly after injection in the cervical
region
3- Ruminants

Infectious Lecture 4th Year 17-10-2016 Dr.Osamah Muwafk
9
a- Hypomagnesemia - cows, sheep and calves
b- White muscle disease
c- Polioencephalomalacia
d- Enterotoxemia
TREATMENT:
1- The main principles in the treatment of tetanus are to:
a- Eliminate the causative bacteria by the parenteral
administration of penicillin in large doses.
b- Neutralize residual toxin using Tetanus antitoxin.
c- Control muscle spasms until the toxin is eliminated or
destroyed by using Chlorpromazine (0.4-0.8 mg/kg body
weight (BW) intravenously, 1.0 mg/kg BW intramuscularly,
three or four times daily).
d- Maintain hydration and nutrition.
e- Provide supportive treatment.
BLACKLEG
ETIOLOGY
1- True blackleg, the clostridial myositis of skeletal muscles.
2- is associated with Clostridium chauvoei.
3- a Gram-positive, spore- forming, rod-shaped bacterium.
4- The spores are highly resistant to environmental changes and
disinfectants and persist in soil for many years.
5- The disease is enzootic in particular areas, especially when they
are subject to flooding
6- The case fatality rate in blackleg approaches 100%.
7- Source of infection is a soil

Infectious Lecture 4th Year 17-10-2016 Dr.Osamah Muwafk
10
8- transmission through Infection of skin wounds at shearing and
docking and of the navel at birth
9- Typical blackleg of cattle has a seasonal incidence, with most
cases occurring in the warm months of the year.
PATHOGENESIS:
1- Trauma is inciting factor.
2- Toxin formed by the organism produces a severe necrotizing
myositis locally in skeletal muscles
3- systemic toxemia that is usually fatal.
4- In cattle and sheep atypical outbreaks of sudden death occur in
which the lethal lesion is a clostridial cardiac myositis
CLINICAL FINDINGS:
A- Cattle
1- If the animal is observed before death there is severe lameness
2- pronounced swelling of the upper part of the affected leg.
3- On closer examination the animal will be found to be very
depressed
4- complete anorexia and ruminal stasis,
5- high temperature (41°C, 106°F)
6- pulse rate (100- 20/min) .
7- Pyrexia is not present in all cases
8- In the early stages the swelling is hot and painful to the touch
9- but soon becomes cold and painless,
10-
edema and emphysema can be felt.
11-
The skin is discolored and soon becomes dry and cracked.
B- Sheep
1- When blackleg lesions occur in the limb musculature in
sheep

Infectious Lecture 4th Year 17-10-2016 Dr.Osamah Muwafk
11
2- there is a stiff gait
3- disinclined to move because of severe lameness in one
limb
4- The lameness may be severe enough to prevent walking
in some animals but be only moderate in others.
ECROPSY FINDINGS:
1- Cattle found dead of blackleg are often in a characteristic
position; lying on the side with the affected hind limb stuck out
stiffly.
2- Incision of the affected muscle mass reveals dark red to black,
swollen tissue with a rancid odor and thin, sanguineous fluid
containing bubbles of gas.
DIFFERENTIAL DIAGNOSIS:
1- Malignant edema.
2- Anthrax
3- Lightning strike
4- Bacillary hemoglobinuria
5- Other causes of sudden unexpected death.
TREATMENT
1- Penicillin Large doses (40 000 IU/kg BW) should be
administered, commencing with crystalline penicillin
intravenously and followed by longer-acting preparations
2- surgical debridement of the lesion