Professional Documents
Culture Documents
APPLIED PREVENTIVE
VETERINARY MEDICINE
Synonyms:
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).
Etiology:
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).
Jibachha's Applied Preventive medicine
3
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
factor.
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.
Transmission:
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.
Jibachha's Applied Preventive medicine
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.
Pathogenesis:
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
5
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.
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
poisoning.
Treatment:
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).
9
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.
Jibachha's Applied Preventive medicine
10
References:
Arif Zafar, M.G., Muhammad, Zafar Iqbal and M. Riaz, 2009. Effects of Hypertonic Saline Solution on
Clinical Parameters, Serum Electrolytes and Plasma Volume in the Treatment of Haemorrhagic
Septicaemia in Buffaloes. Pakistan Veterinary journal, 30 (2): 95-99.
Ahrar Khan, Muhammad Kashif Saleemi, Muhammad Zargham Khan, Shafia Tahseen Gul,
Muhammad Irfan and Muhammad Shahbaz Qamar, 2011. Haemorrhagic Septicaemia in Buffalo
(Bubalus bubalis) Calves Under Sub-Tropical Conditions in Pakistan. Pakistan J. Zool., vol. 43(2), pp.
295-302.
Ataei, S., Burchmore, R., Hodgson, J.C., Finucane, A., Parton, R. and Coote, J.G., 2009. Identification of
immunogenic proteins associated with protection against haemorrhagic septicaemia after
vaccination of calves with a live-attenuated area derivative of Pasteurella multocida B:2. Res. Vet.
Sci., 87: 207-210.
Bain, R.V.S., 1963. Haemorrhagic septicaemia, FAO agriculture studies No. 62, FAO, Rome.
Bastianello, S. S., and Jonker, M.R., 1981. Septicaemia pasteurellosis J. S. Afri. Vet. Assoc., 52: 99-104.
Benkirane, A. and De Alwis, M.C.L., 2002. Haemorrhagic septicaemia, its significance, prevention
and control in Asia. Vet. Med. Czech., 47: 234240.
Burtis, C.A., & E. R. Ash wood, 1999. Tietz Textbook of Clinical Chemistry, 3rd edn, Saunders
Company, London, pp. 494"497.
Cannon, M., Harford, S. and Davies, J., 1990. A comparative study on the inhibitory actions of
chloramphenicol,thiamphenicol and some fluorinated derivatives, Antimicrobial. Chemotherapy.,
26: 307317.
Captain, C. M., Herrero, I. A., Patel, R., Ishitani, M.B.and Boyce, T.G., 2002. Wound infection with
Neisseria weaveri and a novel subspecies of Pasteurella multocida in a child who sustained a tiger
bite. Clin. Infect. Dis., 34: 7476.
Carter, G.R. and De Alwis, M.C.L., 1989. Haemorrhagic septicaemia. In: C., Adlam and J. M. Rutter.
(eds.) Pasteurella and Pasteurellosis. Academic Press. London. pp. 131-160.
Carrol, E.J., Schalm O.W., Lasmanis J., 1964.Experimental coliform (Aerobactor
aerogenes)mastitis:characteristics of endotoxin and its role in pathogenesis. Am. J. Vet. Res.25:720776.
Carty, B., Chiers, K., Schwarz, S., Kehrenberg, C., De Costere, A. and De Kruif, A., 2005. Fatal
peritonitis caused by Pasteurella multocida capsular type F in calves. J. clin. Microbiol., 43: 1480
1483.
Jibachha's Applied Preventive medicine
11
Dagleish, M.P., Hodgson, J.C., Ataei, S., Finucane, A., Finlayson, J., Sales, J., Parton, R. and Coote,
J.G.,2007. Safety and protective efficacy of intramuscular vaccination with a live area derivative of
Pasteurella multocida B:2 against experimental Haemorrhagic septicaemia in calves. Infect. Immun.,
75.
D e Alwis, M.C.L., 1982. Pasteurella multocida serotype 6: B from an elephant. Sri Lanka vet. J., 30.
De Alwis, M.C.L, 1984. Haemorrhagic septicaemia in cattle and buffaloes. Office International des
Epizooties Revue Scientifique ET Technique, 3, 707-730.
De Alwis, M.C.L., 1990. Haemorrhagic septicaemiaa general review. Trop. Anim. Health. Prod. 22:
195-194.
De Alwis, M.C.L., 1999. Haemorrhagic septicaemia. Australian Centre for International Agricultural
Research (ACIAR) Monograph No 57, Canberra, Australia, pp: 1-34.
Deldar, A., Naylor J.M., Bloom J.C., 1984. Effect of Escherchia coli endotoxin on leukocyte and platelet
count, fibrinogen concentration, and blood colostrums-fed and colostrums-deficient neonatal
calves. Am. J. Vet. Res.45:670-677.
Farooq, U., Husain, M., Irshad, H., Badar, N., Munir, R. and Ali, Q., 2007. Status of haemorrhagic
septicaemia based on epidemiology in Pakistan. r :Pak. Vet. J., 27: 67-72.
Ganheim, C., C. Hulten, U. Carlsson, H. Kindahl, R. Niskanen & K. P. Waller, 2003. The acute phase
response in calves experimentally infected with bovine viral diarrhoea virus and/or Mannheimia
haemolytica. Journal of Veterinary Medicine B, 50, 183"190.
Griel, L.C., Zarkower A., Eberhart R.J., 1975. Clinical and clinicalpathological effects of Escherchia coli
endotoxin in mature cattle. Can. J. Comp. Med.39:1-6
Hajikolaei, M.R.H., Ghorbanpour, M., Seyfi-Abdshapouri, M.R., Rasooli, A., Moazeni-Jula, G.R. and
Ebrahimkhani, D., 2008. Study on the prevalence of Pasteurella multocida carriers in slaughtered
cattle and relationship with their immunity status at Ahvaz abattoir. J. Vet. Res., 63: 25-29.
Harper, M., Boyce, J.D. and Adler, B., 2006. Pasteurella multocida pathogenesis: 125 years after
Pasteur. FEMS Microbiol. Lett. 265: 110.
Horadagoda, N.U., DeAlwis, M.C.L., Gomis, A. I.U., Vipulasiri, A.A., and Molligoda, S.C.1989.
Experimental Haemorrhagic septicaemia: Clinical, bacteriological and pathological studies. Symp.
Buffalo Res., Sri Lanka. pp 46.
Horadagoda, A.P.D., Eckersall, J. C. Hodgson, H. A. Gibbs & G. M. Moon, 1994. Immediate responses in
serum TNF alpha and acute phase protein concentrations to infection with Pasteurella haemolytica
A1 in calves. Research in Veterinary Science, 57, 129"132.
Jibachha's Applied Preventive medicine
12
Horadagoda, N.U.J. C., Hodgson, G. M. Moon, T. G. Wijewardana, and P. D. Eckersall, 2001. Role of
endotoxin in the pathogenesis of haemorrhagic septicaemia in the buffalo. Microbe. Pathol. 30:171178.
Kazimi, S.E. and Anwarr-ul-Haq, 1981. Susceptibility of buffalo calves to pasteurellosis. Pak. Vet. J.,
13:116.
Khan, A.U., Saddique, R. Ahmad and H. Khan, 2006. Serosurveillance of Haemorrhagic septicaemia
in cattle and buffaloes in district Malakand, NWFP. J Agric Biol Sci, 1: 11-14.
Khin, M.N., Zamri-Saad M. and Noordin, M.M., 2010. Pathological changes in the lungs of calves
following intratracheal exposure to Pasteurella multocida B: 2. Pertanika J. Trop. Agric. Sci., 33:
113117.
Kristinsson, G. and Adam, H.M., 2007. Pasteurella multocida infections. Pediat. Rev., 28: 472-473.
Kumar, H.V., Mahajan, S. Sharma, et al., 2007. Concurrent pasteurellosis and classical swine fever in
Indian pigs. J Swine Health Prod.; 15(5):279283.
Mahmood, A.K., MA Sheikh, S Akhtar, G Nabi and HB Rashid, 2007. Duration of maternally derived
antibodies against pasteurella multocida in cow calves. Pak Vet J, 27: 92-94.
Molna, H.A., Dela Pena, E., Camer, G.and Padilla, M.A., 1994. An outbreak of haemorrhagic
Septicaemia among carabaos in Northern Samer. Philippine J. Vet. Med., 31: 27-33.
Momin, R.R., Pethkar, D.K., Jiaswal, T.N. And Jhala, V. M., 1987. Haemorrhagic Septicaemia: A
General Review Vet. J, 64: 896-897.
Nazif, S.A., Rezakhani, M. Koohimoghadam, M. Ansari-Lari and Z. Esmailnezhad, 2008. Evaluation of
serum hapatoglobin in clinically healthy cattle and cattle with inflammatory disease in Shiraz, A
tropical area in southern Iran, Bulgarian Journal of Veterinary Medicine, 11, No 2, 95-101
OIE, 2000. World Organization for Animal Health Manual of diagnostic tests and vaccines for
terrestrial animals. Haemorrhagic septicaemia. Rev. Sc. Tec., 3: 589-578.
Paape, M.J., Miller, R.H. and Ziv, G., 1990. Effects of florfenicol, chloramphenicol and thiamphenicol
on phagocytosis, chemiluminescence, and morphology of bovine polymorph nuclear neutrophil
leukocytes, J. Dairy Sci. 73: 17341744.
Pedersen, K., Hammer, A.S., Sorensen, C.M.and Heuer, O.E., 2009. Usage of antimicrobials and
occurrence of antimicrobial resistance among bacteria from mink. Vet. Microbiol., 133: 115-122.
Quinn, P.J., Carter, M.E.; Markey, B., Carter, G. R. and Mosby, R., 1999. Clinical veterinary
Microbiology. Edinburgh, London and New York. pp. 254-8.
Radostits, O.M., C.C., Gay, KW Hinchcliff and PD Constable, 2007. Veterinary Medicine: A Textbook of
diseases of cattle, horses, sheep, pigs and goats. 10th Ed, WB Saunders Co, Philadelphia, USA.
Jibachha's Applied Preventive medicine
13
Rimler, R.B., and Rhoades, K.R., 1994. Hyaluronidase and chondroitinase activity of Pasteurella
multocida serotype B: 2 involved in haemorrhagic septicaemia. Vet. Rec., 134: 6768.
Rivers, E, B. Nguyen, S. Havstad, J. Ressler, A. Muzzin, B. Knoblich, E. Peterson and M. Tomlanovich,
2001.Early goal-directed therapy in the treatment of severe sepsis and septic shock. New Engle J
Med, 345: 1368- 1377.
Sams, R.A., 1994. Florfenicol: chemistry and metabolism of a novel broad-spectrum antibiotic. In:
Proceedings of the XVIII World Buiatrics Congress, Bologna, Italy, and pp. 1317.
Saini, S.S., Sharma, D.R., Gill, B.S., Kwarts, M.S., Singh, J., Sarma, J.K., Dhillon, S.S. and Ramneek, R.,
1991. Re-emergence of haemorrhagic Septicaemia in Punjab. Indian J. Anim. Sci., 61: 1178-1180.
Shafarin, M.S., Zamri-Saad, M., Khairani, S.B. and Saharee, A.A., 2009. Pathological changes in the
respiratory tract of goats infected by Pasteurella multocida B: 2. J. comp. Pathol. 140: 194-197.
Sheikh, M. A., Anzam M. and Shakoori A.R., 1996. Observations on haemorrhagic septicaemia in
Pakistan livestock. Journal of Veterinary Medicine, Series B, 43, 293-304.
Shoaib, Ashraf, Awais Omer, Muhammad Ijaz, Umer Naveed Chaudry and Muhammad Muddassir.
Ali, 2009. Efficacy of Florfenicol Against Haemorrhagic Septicaemia in Buffalo Calves, Pakistan J.
Zool. Suppl. Ser., No.9, pp. 119-122.
Singh, A.K., 2010. Haemorrhagic
farmers.www.cabdirect.org/abstract.
septicaemia
in
cattle,
case
of
worry
to
Skinner, J.G., R.A.L. Brown & L. Roberts, 1991. Bovine haptoglobin response in clinically defined
field conditions. The Veterinary Record, 128, 147-149.
Tabatabaei, A.M., Moazzeni jula, G.R., Jabbari, A.R.and Esmailzadeh, M., 2007. Vaccine efficacy in
cattle against Haemorrhagic septicaemia with live attenuated area mutant of Pasteurella multocida
B: 2 strain. J. Cell Anim. Biol., 1: 62-65.
Wassenaar, T.M. and Silley, P., 2008. Antimicrobial resistance in zoonotic bacteria: lessons learned
from hostspecific pathogens. Anim. Hlth. Res. Rev., 9: 177-186.
Wijewantha, E.A. and Karunaratne, T.G, 1986. Haemorrhagic septicaemia. Cornell Vet., 58: 462-465.
Zafar, M.A., G Muhammad, MH Husain, T Ahmad, A Yusuf and I Sarfaraz, 2009. Comparative efficacy
of hypertonic saline and normal saline solutions in experimentally induced endotoxic shock in dogs.
Pak Vet J, 29: 115-120.
Zafar, M.A., Muhammad, G., Iqbal, Z. and Riaz, M., 2010. Effects of hypertonic saline solution on
clinical parameters, serum electrolytes and plasma volume in the treatment of haemorrhagic
septicaemia in buffaloes. Pak. Vet. J., 30: 95-99.
14