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Shipping fever, Pasteurellosis (English), Bhayagute (Nepali), Galghotu (Hindi), Bhajaha, Dakaha
(Maithali), Ghurka (Bhojpuri), Ghataruwa, Jibhi (Western Nepal).
Haemorrhagic septicaemia (HS) is an acute, fatal, septicaemic major disease of cattle and buffaloes
(Farooq et al., 2007) caused by the Gramnegative bacteria Pasteurella multocida (Tabatabaei et al.,
2007). It is characterized by sudden onset, high rise in body temperature, anorexia, depression,
oedematous swelling on throat, brisket and upper dewlap region, dyspnoea, nasal discharge,
salivation and reluctance to move (Radostits et al., 2007).
The disease is caused by Pasteurella multocida, a Gram-negative coccobacillus residing mostly as a
commensal in the upper respiratory tract of animals (Quinn et al., 1999). Serotypes B: 2 and E: 2 are
two common serotypes of P. multocida associated with disease in animals in Asia and Africa,
respectively (Benkirane and De Alwis, 2002). The species P. multocida is subdivided into four
subspecies that include P. multocida, P. gallicida, P. septica and the recently described P. tigris
(Captain et al., 2002). P. multocida is a non-motile, Gram-negative bacteria, usually forming small
coccobacilli or short rods. Isolates obtained from infected tissues show a bipolar staining affinity,
while those from healthy animals are often pleomorphic. A degree of pleomorphism will also be
noted particularly in old cultures with longer rods of varying length (OIE, 2000).
The organism produces endotoxins which are responsible for all manifestations of the disease
(Horadagoda et al., 2001). These endotoxins have severe effects on central circulation and lead to
hypovolaemia. (Rivers et al., 2001).
Species Affected:
Buffaloes are more susceptible to HS than cattle (De Alwis, 1999), young animals are more
susceptible than adults (Kazimi and Haq, 1981). Experimentally confirmed that susceptibility of
rabbits and mice from P.multocida infection is high, while guinea pigs, pigeons, pigs and horses have
moderate degree of susceptibility. The susceptibility is variable in sheep and goats, while fowl and
dogs are not susceptible to HS. Swines are also susceptible. Highly fatal septicaemic pasteurellosis
was reported in camels (Momin et al., 1987) and elephants (De Alwis, 1982).
Geographical Distribution:
The disease has a major impact on the livestock industry in countries of Southern Europe, the
Middle East and Southeast Asia including China, where HS associated with serotype B: 2 are
distributed widely (Dagleish et al., 2007; Ataei et al., 2009). This same type serotype has been
reported from Egypt and Sudan.
The magnitude of the outbreak will depend on the proportion of susceptible animals in the herd or
village, diagram show such a cycle.
Fig.1. The epidemiological cycle in haemorrhagic septicaemia (De Alwis, 1984).
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Predisposing Factors:
Parasitic, viral and bacterial infections, exhaustion and over-working specially in buffaloes,
transport, successive change in nutrition, management and temperature with changes of seasons
and mode of husbandry, were reported to have an influential role in the occurrence of the disease
(Bain, 1963). Hot and humid weather is a major contributory factor in the outbreak of HS. High
environmental temperature (37C) does favour the growth of the bacteria (Hajikolaei et al., 2008).
Weather also possess stress on young calves. Scarcity of green fodder in these days is another stress
Historical Information:
Pasteurellosis of cattle was first described in 1878 by Bollinger in Germany and the causative agent
was isolated by Kitt in 1885. Rossenbusch and Merchant used pasteurella multocida as a causative
agent. Robert told that it is serotype -1 that is responsible for this disease.
The healthy carrier animals harbor the pathogen in their nasopharynx and tonsils (De Alwis, 1990),
and disseminate the disease by direct contact or through contamination of soil, water and pasture
and hence transmission of infection is through inhalation or ingestion. Carriers have a great role in
creating HS outbreaks (Wijewantha and Karunaratne, 1986). The causal agent does not survive for
more than 2 to 3 weeks in the soil or on pastures. Carrier animal may transmit the disease to their
young one through milk.
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Incubation Period:
The incubation period is usually 3 to 5 days but some animals can carry the organism for varying
periods without symptoms. In experimental infections with lethal doses, cattle or buffalo develop
clinical signs within a few hours and die within 18 to 30 hours.
Pasteurella multocida remains as commensal in bronchi, terminal bronchioles, and alveoli. This
pathogen cannot invade lungs due to defense mechanism but stresses as climatic change,
malnutrition, transport, etc. trigger the organism and lungs are unable to clear the pathogens
(Harper et al., 2006).Organisms are proficient in destructing bovine blood mononuclear leukocytes
and lung macrophages. Pharmacologically active substances like histamine, prostaglandins,
hyaluronidase, chondroitinase (inflammatory substances) as well as fibro-elastic elements are
released with the death of the macrophages (Rimler and Rhoades, 1994). Other than release of
these active substances, organism leads to septicaemia which has the most severe effect in the
respiratory tract, heart and gastro-intestinal tract (Radostits et al., 2007).
Trachea, part of respiratory system is large enough in animals that travel along the neck where
acute inflammatory reaction takes place as a result of released inflammatory substances which in
return lead to development of submandibular oedema (Harper et al., 2006; Shafarin et al., 2009).
The changes produced in the lungs comprises of bronchopneumonia which appear as consolidated
lungs (Shafarin et al., 2009) that in return produces high bronchial/respiratory sounds (rales).
Other than the release of pharmacologically active substances, there is another thought in the
development and consequences of HS that the Pasteurella multocida produces endotoxins which
are responsible for all manifestations (Horadagoda et al., 2001; Zafar et al., 2010). Death of the
animals occurs due to hypoxia and toxaemia (Khin et al., 2010)
Clinical Signs:
In cattle and buffalo:
HS is characterized by rapid onset, high fever, salivation, conjunctivitis, lacrimation, cessation of
rumination and dullness followed by sudden death in per acute conditions. In acute cases,
symptoms include dyspnoea, painful groans, respiratory distress and oedematous swelling in the
head-throat-brisket region, swollen haemorrhagic lymph nodes and fore-limbs followed by
recumbence at late stages (Bastianello and Jonker, 1981; Carter and De Alwis, 1989). The onset of
the clinical signs occurs at 30 hours after experimental inoculation and in two to three days
following natural infection (Carter and De Alwis, 1989).
The first symptom is an elevation of body temperature which usually takes place very rapidly. An
animal that 3 or 4 hours before had a temperature of 100F or 101F may be found with a
temperature of 103F to 1050F. Soon thereafter the body becomes alternately hot and cold.
Rumination, milk secretion and appetite disappear. The back is arched and constipation is
frequently present although towards the end, diarrhoea sometimes makes its appearance, the
faeces generally being tinged with blood. In some instances blood trickles from the nose or may be
found free in the urine. The pulse rate is increased and as the disease advances, becomes almost
imperceptible. There is usually a marked increase in the respiratory rate with evidence of
dyspnoea; each respiration is accompanied by a grunt. The visible mucous membranes are early
red, the small vessels standing out clearly. In white animals or in animals with white areas on their
bodies cyanosis is occasionally noted. This cyanosis appears to result from two causes, the action of
the toxin on the vascular system and the action of the toxin upon haemoglobin in which its oxygen
carrying capacity is interfered. Examination of the chest reveals areas which on percussion may be

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somewhat consolidated. On auscultation, if these areas are not too deep the inspiration bronchial
note is found shrill due to swelling of the bronchial mucous membrane. On respiration fine rales
may be heard followed by bubble which results from the presence of liquid or mucous in the
bronchial tree.
In sheep and goat:
In lambs and kids, pneumonic pasteurellosis can be acute, characterized by fever, lethargy, poor
appetite and sudden death. Sheep and goats that survive the acute stage may recover or become
chronically affected showing reduced lung capacity and weight gain efficiency and sporadic deaths
may occur.
Symptoms associated with pneumonia include fever, fast or difficult breathing, nasal discharge, and
decreased activity.
In pig:
High temperature 1040F to 1070F usually ranges in pig. Dullness, depression, anorexic and copious
nasal discharge is seen in pig. Pasteurellosis in pig is usually seen in acute form (Kumar, 2007).
Morbidity and Mortality:
Khan et al., (2006), reported that the young stock of both buffaloes and cattle have higher morbidity
(21.19%), mortality (95.25%) and case fatality rates as compared to the older ones. The exhaustion
of the maternal immunity against HS after the 60th day of life and delayed vaccination might be
attributed to the higher susceptibility of the young calves (Mahmood et al., 2007). Once clinical sign
appear, case fatality is nearly 100%. A wide range of mortality rate (5 to 90%) has been reported in
different outbreaks in India (Saini et al., 1991) and Philippines (Molna et al., 1994).
Haemorrhagic septicaemia should be suspected in animals with a rapid course of infection, and
fever and oedematous swellings in the throat, neck and brisket. A high herd incidence and high case
fatality rate are also suggestive of this disease. Sporadic cases of haemorrhagic septicaemia may be
difficult to diagnose. P. multocida is not always found in blood samples before the terminal stage of
the disease, and is not consistently present in nasal secretions.
A long bone freed of tissue should be taken from animals that have been dead for a long time, also
liver, lung, kidney, and spleen sample should be collected. Blood sample should be collect from tips
of ears (from live animal only).
1. Organism identification:
Smear from heart blood, lung, spleen and an intestinal content from dead animal is stained with
LEISHMANS STAIN. Bipolar organism is seen in smear. Smear can also be prepared in Methylene
blue stain also.

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2. Organism culture:
Sample is cultured in blood agar and BGA plate, no-haemolytic and dewdrops like colonies may be
seen. Tryptose-tryphone agar containing 0.1% sucrose and its extract make very small colony.
3. Animal inoculation:
Rabbit is most susceptible lab animal for these bacteria. Mice and guinea pigs are used generally for
this purpose. Material is inoculated through subcutaneous or intraperitoneal route, animal die
within 24 hours; having haemorrhagic lesion.
Clinical Pathology:
Shoaib Ashraf (2009), reported there was no significant difference between haematology of
diseased and healthy calves, except total leukocytic count of diseased calves was higher which got
normal after treatment.
Table No.1. Different changes in blood parameters HS infected buffalo calf.

Source: Shoaib Ashraf, 2009

Arif Zafar et al., (2009), also reported concentration of haemoglobin in HS suffering animals was
lower than the reference (reference value: 12-15 g/ dl) values. Haematocrit was also decreased
than the normal values (reference value: 30-35%) in diseased buffaloes. It is important to
remember that severe, acute inflammation can result in a leukocytosis or leukopenia. Endotoxin
exposure in cattle produces a consistent and profound leukopenia within 1 hour, followed by a
rebound leukocytosis within 24 hours (Griel et al., 1975). Both neutropenia and lymphopenia are
observed, with the neutropenia being more severe (Griel et al., 1975). Endotoxin causes an
immediate accumulation, migration, and activation of leukocytes in the microcirculation,
particularly in the alveolar capillaries (Deldar et al., 1984). Both neonatal and adult ruminants will
have profound leukopenias during the initial stage of Gram-negative bacterial infection that last for
24 48 hours before the rebound leukocytosis (Carrol et al., 1964).
ESR (Erythrocyte Sedimentation Rate - It is a non-specific screening test that indirectly measures
how much inflammation is in the body.
Table No.2.
Different changes in blood parameters in HS affected buffalo calf.

Source: Arif Zafar, 2009.


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Sodium ions (Na+) concentration increased during disease in all the animals than the normal
(reference value: 130-135 mEq/L), chloride ions (Cl) concentration also showed the same trend as
sodium ions (reference value: 95-105 mEq/L). A decrease was noted in the potassium ions (K+)
concentration during disease condition in all the animals (Arif Zafar et al., 2009).
Increase in serum sodium is seen in conditions with water loss in excess of salt loss, as in profuse
sweating, severe diarrhoea or vomiting, polyuria (as in diabetes mellitus or insipidus), hyperglucoor mineralocorticoidism, and inadequate water intake.
Decrease in sodium is seen in states characterized by intake of free water or hypotonic solutions, as
may occur in fluid replacement following sweating, diarrhoea, vomiting, and diuretic abuse.
Dilutional hyponatremia may occur in cardiac failure, liver failure, nephrotic syndrome,
malnutrition, and SIADH.
There are many other causes of hyponatremia, mostly related to corticosteroid metabolic defects or
renal tubular abnormalities. Increase in serum chloride is seen in dehydration, renal tubular
acidosis, acute renal failure, diabetes insipidus, prolonged diarrhea, salicylate toxicity, respiratory
alkalosis, hypothalamic lesions, and adrenocortical hyperfunction.
Decrease in serum chloride is seen in excessive sweating, prolonged vomiting, salt-losing
nephropathy, adrenocortical defficiency, various acid base disturbances, conditions characterized
by expansion of extracellular fluid volume, acute intermittent porphyria, etc.
Decrease in serum potassium is seen usually in states characterized by excess K+ loss, such as in
vomiting, diarrhoea, villous adenoma of the colorectum, certain renal tubular defects,
hypercorticoidism, etc. Redistribution hypokalemia is seen in glucose/insulin therapy, alkalosis
(where serum K+ is lost into cells and into urine), and familial periodic paralysis. Where incease in
serum potassium is seen in states characterized by excess destruction of cells, with redistribution of
K+ from the intra- to the extracellular compartment, as in massive hemolysis, crush injuries,
hyperkinetic activity, and malignant hyperpyrexia. Decreased renal K+ excretion is seen in acute
renal failure, some cases of chronic renal failure, Nazif et al., (2008), showed that acute respiratory
infections resulted in significant increase of serum haptoglobin (Hp) levels. Similar findings were
demonstrated in cattle with experimental infection with Pasteurella haemolytica (Ganheim et al.,
Haptoglobin (Hp) is 2-globulin, synthesized in the liver. It is one of acute phase proteins whose
serum levels increase in acute infections (Burtis & Ashwood, 1999). Skinner et al., (1991) evaluated
serum Hp in inflammations and introduced Hp as an inflammatory indicator in cattle. In apparently
healthy animals (mixed breed and age), serum Hp reference value was <0.35 g/L (Horadagoda et
al., 1994).
Post-mortem Lesion:
Post-mortem lesions following experimental inoculation were congested lungs with light petechial
haemorrhages on the heart. In acute cases, wide-spread haemorrhages over the pleural surfaces
and the parenchymal organs, oedematous and red-gray lobular inflamed lungs, oedematous lymph
nodes, pericarditis with serous haemorrhage on the left ventricle and blood stained exudates were
observed (Horadagoda et al., 1989; Farooq et al., 2007). HS also leads to fatal peritonitis in calves
(Carty et al., 2005). Trachea was congested and contained froth. Kidneys were swollen and
hyperemic. Liver seemed to be normal. There were petechial haemorrhages on the epicardium
(Ahrar Khan et al., 2011). Ahrar Khan et al., (2011) also reported edema in head, neck and interJibachha's Applied Preventive medicine

mandible region, congested trachea having froth; pneumonic lungs and lymphadenitis were present
in all carcasses of calves died of HS. Such type of lesions has been reported (De Alwis, 1999;
Benkirane and De Alwis; 2002; Farooq et al., 2007).
Differential Diagnosis:
If the condition is an acute one characterised by sudden death, other diseases likely to cause sudden
deaths, such as anthrax, rinderpest and black quarter, should be taken into account. Equally
important are the non-infectious causes of sudden death such as lightning, snakebites and acute
Treatment of HS can be successful if only antibiotics are given at the initial stages of the disease.
Various combinations of sulpha drugs and antibiotics were considered to be more effective (Sheikh
et al., 1996). P. multocida are resistance to streptomycin, tetracycline, oxacillin and trimethoprim
(Wassenaar and Silley, 2008), therefore, while treating HS case such drugs should be avoided.
The infected animal should be placed in a warm, well ventilated stall and all healthy cattle should be
segregated from infected animal. The body of the infected individual should be maintained warm by
blanketing and collapse from shock anticipated. Consequently a careful lookout must be kept for a
failing pulse-especially loss of volume and a tendency to imperceptibility. If this occurs two or five
ml. of adrenaline chloride solution (1:1000), should be administered subcutaneously and repeated
if necessary.
1. The oldest therapy recommended was intravenous treatment with sulfonamides. Intravenous
infusion of sulfadimidine sodium 33.33% at a dosage of 1 ml. per 5 pounds bodyweight (about 2.3
kg) has been practiced. However, the large volume of drug to be injected, the practical difficulties of
intravenous therapy in the type of animal involved and the consequences of leakage of the drug into
the surrounding tissues all weigh heavily against this treatment regimen (De Alwis, 1984). In initial
phase of disease intravenous administration of sulfonamides i.e. sulfamethazines @ 150mg/kg for
three days or sulfadimidines @150mg/kg for three days is recommended. Side effects of
sulfonamides are crystallization in urinary tract, cutaneous eruption, hypothyroidism and
idiosyncratic toxicosis.
2. Arif Zafar et al., (2009), reported 25 buffaloes suffering from haemorrhagic septicaemia were
treated with rapid intravenous infusion of hypertonic saline solution (7.5% NaCl) in NaCl; 2400
mmol NaCl/L) @ 4 ml/Kg BW once in combination intramuscular administration of Ceftiofur HCl @
6 mg/kg BW, and intravenous administration of ketoprofen (nonsteroidal anti-inflammatory drug)
@2 mg per kg body wt. The recovery rate from disease was 80 percent. Hypertonic saline solution
was administered once (only on the first day of treatment) in the buffaloes while ceftiofur HCl and
ketoprofen were administered after every 12 and 8 hours, respectively, for five consecutive days.
3. In one study Shoaib Ashraf et al., (2009), reported, 40 buffaloes calves of six to eighteen months
of age suffering from H. S treated with combination of florfenicol at the dosage rate of 20 mg/kg
body weight I.M. with flunixin meglumine at the dosage rate of 2.2 mg/kg B.W gave better results
with survival rate of 90%. Florfenicol is a fluorinated derivative of chloramphenicol and
thiamphenicol which has a fluorine atom instead of the hydroxyl group located at C-3 (Sams, 1994).
Florfenicol is not subject to the action of acetyltransferase, which is an enzyme used by bacteria to
develop resistance to chloramphenicol and thiamphenicol (Cannon et al., 1990; Paape et al., 1990).

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4. Penicillins are widely used in the treatment of HS because the causative organism is sensitive to
-lactam antibiotics (Kristinsson and Adam, 2007; Pedersen et al., 2009).
5. Oxytetracycline can be used @5-10 mg/kg for 3 days. Besides these treatments may extend with
chloramphenicol @10 mg /kg or ampicillin@10 mg (Singh, 2010). Side effects (SE) of tetracyclines
are renal impairment, last 2-3 weeks of ingestion in pregnant animals and up to 4 weeks of age in
neonates. Gastrointestinal symptoms are more severe with oxytetracycline among the
tetracyclines; discoloration of the teeth when used during pregnancy and drug interactions with
anti-acids, dairy products, calcium salts, iron salts, magnesium salts, zinc salts and warfarin
Endotoxins have profound effects on the circulatory system including myocardial depression,
pronounced vasodilatation and alterations in the endothelial barrier which result in hypovolaemia
and decreased cardiac output.
It is, therefore, of great importance to maintain an adequate cardiac output and blood pressure
through restoration of intravascular volume. Thus, in addition to antibiotic therapy, fluid
administration plays a vital role in the management of sepsis and septic shock (Zafar et al., 2009).
So, fluid administration is the corner stone for the management of patients suffering from
septicaemia (Rivers et al., 2001).
Along with these anti-inflammatory drugs are also given e.g. betamethasone @ 1mg/5kg or
dexamethasone @ 1mg/5kg, prednisolone @10mg/kg (should not be given in pregnant animal,
may abort) in serious condition. The non-steroidal anti-inflammatory drugs (NSAIDs) such as,
aspirin, paracetamol and phenylbutazone, meloxicam, nimesulide, ketoprofen, fluxinine @ 1mg/kg
body weight is safe for animals.
Note: Early recognition and treatment with antibiotics is essential for successful therapy. If one
treatment fails continue with other drugs.
Prevention and Control:
Vaccination of HS for prophylactic purpose must be carried out preferably two to three months
before the season (Benkirane and De Alwis, 2002). It is also recommended that during an outbreak,
one should resort to immediate whole herd vaccination, irrespective of previous vaccination
history (Benkirane and De Alwis, 2002). This strategy also failed in the present outbreak as
mortality reached to 31.48%. A live-attenuated vaccine, which would mimic the early stages of the
natural infection, might be expected to confer more solid and long-term protective immunity
(Tabatabaei et al., 2007).
HS vaccine prepared from a whole broth culture of Pasteurella multocida type B and Mannheimia
haemolytica & P. trehalosi (208 germs/ml), killed by 0.3% formalin and precipitated by 1%
aluminium potassium sulphate (both final concentration). For best results vaccinate animals at
least 21 days before the haemorrhagic septicemia season. Shake the product vigorously before use;
inject adult and calves with 2 ml SC. Immunity appears in 10 days after vaccination and lasts for 6
to 8 months. Revaccination is advised after 6 months or manufacturer instruction. Anaphylactic
reactions may
appear occasionally after vaccination of zebus; serious in & very often on some exotic cattle breeds,
particularly on animals, which have been vaccinated many times against foot-and-mouth disease,
blackleg or anthrax. Thus sensitiveness should be checked in these breeds before use. In case of
reaction, immediate injectioin of antihistamine is recommended. vaccine should store at room
temperature for 6 months; at +4C for 1 year; avoid light and heat.
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