HEMORRHAGIC SEPTECEMIA (HS) 

HEMORRHAGIC SEPTECEMIA (HS) 

2. HEMORRHAGIC
SEPTECEMIA(HS)

7. Haemorrhagic Septicemia
Pasteurellosis, Shipping fever,
Stockyards disease,
Stockyardis pneumonia,
Barbone disease

8. Hemorrhagicsepticemiaisahighlyfatalacute
septecemiacbacterialdiseasethatmainly
affectscattle,buffalo,Camel,sheep,goatand
pigsofAsia,AfricaandtheMiddleEast.

9. It occurs mainly due to
•stress, such as inclement weather or pasture,
•driving transportation, shipping animals to long distance,
•endoparasite burden,
•wet weather,
•low space close confinement in cold and humid season. In
areas where animals have lowimmunitydeveloped

10. TheHSdiseaseischaracterizedby
•highriseofbodytemperature,
•deppression,
•multiplehemorrhages,
•difficult breathing, mostly open mouth breathing
(pneumonia, pleuritis(a condition in which the pleura —two large, thin layers of tissue that
separate your lungs from your chest wall —becomes inflamed) and pericarditis(inflammationof
thepericardium
•neckswelling,
•excessivesalivationfromthemouth
•severenasaldischarge,andanimalshows
reluctancetomove.

11. 3 forms of HS
•1 OEDAMATOUS OR THROAT FORM
•2 PECTORAL OR LUNGS FORM
•3 ABDOMENTAL FORM

12. ETIOLOGY
Hemorrhagic septicemia is caused by
certain members of Pasteurella
multocidaGram-,non motilepencillin
sensitive coccobacillus in the family
Pasteurellaceae.
The Asian serotype is designated B:2 and the
survive on pasture for more than 24 hours.

13. TRANSMISSION
•HS bacteria resides at nasopharngealregion.
•Hemorrhagic septicemia can be transmittedby
ingestion or inhalation, either during direct
contact or via fomites such as contaminated
feed and water.
•The causative organisms are thought to spread
mainly in respiratory secretions, but they can also
be found in other secretions and excretions,
including feces and urine.

14. Both morbidity and case-fatality rates vary
between 50% and 100%, and animals that
recover require a long convalescence(the
period in which the body recovers from a illness).
Morbidity will depend on the immune
status of the herd, either acquired naturally
or induced by vaccination.

15. •HS is listed on list B of the World
Organization for Animal Health-Office
International des Epizooties (OIE), which
includes “transmissible diseases that are
considered to be of socioeconomic and/or
public health importance within countries

16. INCUBATION PERIOD
•The incubation period is thought to be 3-5 days in most
cases, although it can be much shorter (e.g., a few
hours)

17. •The portal of entry of infection is thought to be the tonsils.
A fulminating septicemia occurs, which is associated with the
capsular material of the organism and its endotoxin.
In acute and per acute cases death ensues within 8 to 24
hours of appearance of the first clinical signs.
The effects of the septicemia are most severe in the
respiratory tract, heart, and gastrointestinal tract.
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.
PATHOGENESIS

18. CLINICAL FINDINGS
The disease is an acute septicemia and is clinically characterized by a
sudden onset of fever (41 to 42°C [106–107°F]),
followed by profuse salivation,
submucosal petechiaL haemorrhage,
severe depression, difficulty in breathing, open mouth breathing, throat
edemaand death within 24 hours.
On range lands, animals may be found dead without any clinical signs
having been observed.
Inflammation at localize area may occur in subcutaneous tissue,
resulting in the development of warm, painful swellings about the
throat, dewlap, brisket, or perineum, and severe dyspnea may occur if
the respiration is obstructed.

19. DIGNOSIS
A definitive diagnosis of HS isbased onisolation of
P multocida serotypefrom the bloodand tissues
of a patient with typical clinical signs.
Gram strain of smears from blood,liver,lungs from
dead animals

20. OPEN MOUTH BREATHING
-HIGH GRADE FEVER ARE THE MAIN
CLINICAL SIGNS OF HS

21. NECROPSY FINDINGS

22. At necropsy, the gross findings are usually limited to generalized
petechial hemorrhages, particularly under the serosae, and edema and
congestionof lung with patchy or extensive consolidation.
Subcutaneous infiltrations of gelatinous fluid may be present, and in a
few animals there are lesions of early pneumonia and a hemorrhagic
gastroenteritis(inflammationof the stomach andintestines).
Thickening of the interlobular septa may be prominent.
Lymph nodes in the thoracic region are enlarged and hemorrhagic.
Isolation of the causative bacteria is best attempted from heart, blood,
and spleen samples.

23. The differential diagnoses for HS include
many other conditions causing peracute
death.
Blackleg • Anthrax • Lightning strike •
Acute salmonellosis
• Atypical interstitial pneumonia
DIFFERENTIAL DIAGNOSIS

24. TREATMENT
Injection Ceftifur sodium
Injection Prednisolone
Injectin Fluxin Meglumine
Injection Phenramine meleate
Injection Lasix
Tracheotomy

25. TREATMENT
Whatever antimicrobial is chosen, an initial intravenous loading
dose is required to reach bactericidal concentrations in blood as
fast as possible.
Antimicrobial therapy Penicillin G sodium/potassium (22,000
IU/kg initial IV then IM every 12h).
Procaine penicillin (22,000 IU/kg IM every 12h or 44,000 IU/kg
IM every 24h after initial IV loading dose of penicillin G sodium/
potassium).
Oxytetracycline (10 mg/kg initial IV then IM every 24 for 4 days.

26. CONTROL
Hemorrhagic septicemia can be eradicated from nonendemic
areas by animal movement control, quarantines, tracing of
contacts, culling of infected and exposed animals, and
disinfection of the premise.
Although treatment may be successful when initiated early in
the course of the disease, up to 20% of surviving animals are
estimated to become clinically unapparent shedders, thereby
creating a host reservoir.
In endemic areas the condition is mainly controlled by
vaccination.

27. Removing identified carrier animals, avoiding stress by
providing adequate feed supply, and avoiding
overcrowding, particularly during the rainy season, can
further reduce the risk of clinical disease and transmission
of the infection.
Treatment of animals that were in contact with clinical herd
mates may be suitable to limit morbidity and mortality rates
during an outbreak.
CONTROL