Haemorrhagic septicaemia: Its significance, prevention and control
Rajeev Ranjan, Jitendra K Biswal and Smrutirekha Mallick
ICAR-National Institute on Foot and Mouth Disease, Bhubaneswar-751003, Odisha
Summary: Hemorrhagic septicemia (HS) is an acute and highly fatal septicemia bacterial disease caused by Pasteurella multocida of cattle and buffaloes. P. multocida is susceptible to mild heat (55°C), most hospital disinfectants. Outbreaks mostly occur during pre or post monsoon. In India, during the past four decades it has been found that HS accounted for 46–55% of all bovine deaths. The expected annual economic loss due to HS varies from ₹ 58.63 billion to ₹ 175.72 billion. Cattle and water buffaloes are the principal hosts of HS, and it is widely considered that buffaloes are the more susceptible. P. multocida is spread by direct contact with infected animals and indirect contact (fomites). All ages are affected and the morbidity rate can be high. The case fatality rate is nearly 100% unless the animal is treated very early. The Pasteurella organisms remain as commensal in the terminal bronchiole and alveoli. The organisms cannot invade the lungs due to the pulmonary defense mechanism. A fever, dullness, and reluctance to move are the first signs. Following these signs, salivation and nasal discharge appear, and edematous swellings are seen in the pharyngeal region and then spread to the ventral cervical region and brisket. Visible mucous membranes are congested, and respiratory distress occurs, and death occurs due to hypoxia and toxemia 6–24 hours after the first signs are seen. Animals can be cured only if they have been treated in the very early stages of the disease with suitable antimicrobials. Vaccination is a major control measure in the endemic and epidemic areas. The most commonly used vaccine of HS in endemic area is oil adjuvant vaccine is recommended.
Introduction: Hemorrhagic septicemia is a particular form of pasteurellosis caused by Pasteurella multocida, an acute and highly fatal septicemia mainly in susceptible cattle and buffaloes. Livestock owners generally fear this disease while they view foot-and-mouth disease and other major infectious disease in the continent merely as a “nuisance”. In susceptible animals, the clinical signs often progress rapidly from dullness and fever to death within hours. Because the disease develops so quickly, few animals can be treated in time, and recovery is rare. Subclinical carriers can introduce hemorrhagic septicemia into a herd. Young animals are mainly affected in endemic regions, and outbreaks are particularly common during rainy weather, when the organism can spread readily. In areas where cattle have no immunity, severe disease is expected to occur in all ages. In Hindi this disease is called as Galaghotu, in Odiya it is called as ‘Sahana’.
Etiology: This is a bacterial disease caused by Pasteurella multocida subsp. multocida, which belongs to Order: Pasteurellales. Family: Pasteurellaceae. This is a Gram-negative coccobacillus residing mostly as a commensal in the upper respiratory tract of animals. In a new classification, Pasteurella multocida strains causing most Pasteurella infections, including hemorrhagic septicemia, are called P. multocida subspecies multocida. P. multocida is susceptible to mild heat (55°C), most hospital disinfectants. During the monsoon rains, it is thought that the organisms can survive for hours and probably days in the moist soil and water.
Epidemiology: Haemorrhagic septicaemia (HS) is a major disease of cattle and buffaloes characterized by an acute, highly fatal septicaemia with high morbidity and mortality. Outbreaks mostly occur during before or after monsoon (high humidity and high temperatures). It was Booliger, who investigated a fatal disease in Cattle in 1978.
Economic losses: HS is a disease of utmost economic importance particularly in Asia and to a lesser extent in Africa. In Asia the susceptible animal population consists of 432 million cattle and 146 million buffaloes, which constitute 30% and 95% of the world’s cattle and buffalo population, respectively. In India where the production of milk is highest in Asia, around 50% of the milk comes from the more susceptible buffaloes. In India, during the past four decades it has been found that HS accounted for 46–55% of all bovine deaths. During the twelve years period since 1974 to 1986 it accounted for 58.7% of the aggregate of deaths due to five endemic diseases, viz. foot-and-mouth disease (FMD), rinderpest, black quarter, anthrax and HS. Most estimates of losses take into account only direct losses, i.e. value of animals that die of HS. Annual loss in India is estimated to be 40, 000 cattle and buffaloes while in term of currency expected annual economic loss due to HS varies from ₹ 58.63 billion to ₹ 175.72 billion. The maximum losses occur in case of buffaloes followed by cross bred and indigenous cattle. A true estimate of losses should take into account a variety of factors which constitute indirect losses. These are listed below:
- Loss of productivity – milk, meat, draught power, and cost of alternate sources of draught power.
- Impairment of the reproductive potential of the animals.
- A reliable differential diagnosis as there is tendency during the Monsoon to attribute any mortality to HS. Thus a possible over-estimation of these losses should be taken into account. However, it must also be borne in mind that reported losses constitute only a fraction of the actual losses. This is bound to be so since HS is a disease that occurs in situations where husbandry practices are poor and therefore disease reporting system will also be poorly developed.
Host Range: Cattle and water buffaloes (Bubalus bubalis) are the principal hosts of hemorrhagic septicaemia, and it is widely considered that buffaloes are the more susceptible. Although outbreaks of hemorrhagic septicaemia have been reported in sheep, goats and swine, it is not a frequent or significant disease. Hemorrhagic septicemia has also been reported in bison (Bison bison), African buffalo (Syncerus caffer), camels, elephants, horses, donkeys and yaks. Systemic pasteurellosis has been reported in various species of deer including fallow deer (Dama dama), sika deer (Cervus nippon) and chital deer (Axis axis), as well as elk (Cervus elaphus canadensis), pronghorn (Antil ocapra americana) and other wild ruminants. Laboratory rabbits and mice are highly susceptible to experimental infection. There are no reported cases of human infection. Cattle, water buffalo, and bison appear to be the reservoirs of infection.
Transmission: P. multocida is spread by direct contact with infected animals and indirect contact (fomites). Close herding and wetness, as occurs during the rainy season, appear to contribute to spread. The source of the infection is infected animals or carriers. The carrier state may be greater than 20 percent shortly after an outbreak, but within 6 weeks the rate is usually less than 5 percent. The causal agent does not survive for more than 2 to 3 weeks in the soil or on pastures. Cattle and buffalo become infected when they ingest or inhale the causative organism, which probably originates in the nasopharynx of infected animals. In endemic areas, up to 5% of cattle and water buffalo may normally be carriers. The worst epidemics occur during the rainy season, in animals in poor physical condition. Stresses such as a poor food supply are thought to increase susceptibility to infection, and close herding and wet conditions seem to contribute to the spread of the disease. P. multocida can survive for hours and possibly days in damp soil or water; viable organisms are not found in the soil or pastures after 2–3 weeks. Nasal secretions: organisms are also not consistently present in sick animals. Biting arthropods do not seem to be significant vectors.
Incubation Period: The influence of extrinsic factors in the development of the clinical pasteurelloses, and particularly in hemorrhagic septicemia, has been noted by many workers. When favorable circumstances for the growth and multiplication of P. multocida in the animal body occur, severe septicemia develops within a few hours. However, the organisms may be harbored for varying periods in a small percentage of carrier animals without any clinical sign. The perpetuation of the disease from year to year or season to season is generally attributed to the carrier state. The immune status of the animal is thought to influence the severity of the disease. Cattle or buffalo artificially inoculated subcutaneously with lethal doses (approximately 20,000 bacilli) show clinical signs within a few hours and succumb within 18 to 30 hours.
Morbidity and Mortality
The morbidity rate depends on environmental conditions, herd management, the animals’ immunity and other factors. Although hemorrhagic septicemia can be seen at any time of the year, close herding and wet conditions contribute to the spread of the disease; the worst epidemics occur during the rainy season. Stressors such as poor nutrition increase an animal’s susceptibility to clinical disease, and also stimulate shedding of the organism from carriers. All ages are affected where hemorrhagic septicemia is not endemic, and the morbidity rate can be high. In endemic regions, outbreaks often occur when healthy carriers are introduced into a herd. In these areas, most adults have some immunity to the organism, and clinical cases tend to occur in young animals between the ages of 6 months and 2 years. However, massive epizootics are sometimes seen. The case fatality rate is nearly 100% unless the animal is treated very early; few animals survive once the clinical signs have become apparent. A few spontaneous recoveries may be seen, especially late in an outbreak. Up to 20% of the survivors can become carriers for a short period after an outbreak; by 6 months, the carrier rate is 5% or less. Buffaloes are thought to be more susceptible to illness than cattle, with higher morbidity and mortality rates. Susceptibility to systemic pasteurellosis may vary among the Cervidae. In a series of outbreaks at a deer park in Denmark, more than 300 clinical cases occurred in fallow deer (Dama dama), but only a single death due to this disease observed in a sika deer (Cervus nippon). Red deer (Cervus elaphus) in the park were unaffected.
Pathogenesis: The Pasteurella organisms remain as commensal in the terminal bronchiole and alveoli. The organisms cannot invade the lungs due to the pulmonary defense mechanism. But, due to stress as imposed upon by predisposing factors like malnutrition, long transportation, climatic changes, the organisms assume the virulent role and thereby bring about changes in the lung and the lung is unable to clear the pathogens. Carter in 1973 remarked that the organisms are efficient in destroying bovine mononuclear leukocytes of blood and macro-phages of lungs. From the death macrophages pharmacologically active amines like histamine and prostaglandin as well as some fibroblastic elements are released. These substances used to bring about inflammatory changes in the lung parenchyma and help in the deposition of fibrin. The changes thus produced in the lungs comprise of fibrinous bronchopneumonia. Consolidation of the lungs produces high bronchial sound (moist rales). Death occurs due to hypoxia and toxemia.
Diagnosis:
Clinical diagnosis: Most cases in cattle and buffalo are acute or per acute with death occurring from 6 to 24 hours after the first recognized signs sometimes animals may survive as long as 72 hours. A fever, dullness, and reluctance to move are the first signs. Following these signs, salivation and nasal discharge appear, and edematous swellings are seen in the pharyngeal region (fig. 1) and then spread to the ventral cervical region and brisket. Visible mucous membranes are congested, and respiratory distress occurs, and the animal usually collapses and dies 6–24 hours after the first signs are seen. Widely distributed hemorrhages, edema, and general hyperemia are the most obvious tissue changes observed in infected animals. In almost all cases there is an edematous swelling of the head, neck, and brisket region. Incision of the edematous swellings reveals a coagulated sero- fibrinous mass with straw colored or blood-stained fluid. Buffaloes are generally more susceptible to HS than cattle and show more severe forms of disease with profound clinical signs. In the recent past, HS has been identified as a secondary complication in cattle and buffalos following outbreaks of foot and mouth disease (FMD). Case fatality approaches 100% if treatment is not followed at the initial stage of infection.
Laboratory diagnosis:
Samples: P. multocida is not always found in blood samples before the terminal stage of the disease, and is not consistently present in nasal secretions. In freshly dead animals, a heparinised blood sample or swab should be collected from the heart within a few hours of death, and a nasal swab. If a necropsy is not feasible, blood samples can be taken from the jugular vein by aspiration or incision; blood samples should be placed in a standard transport medium and transported on ice packs. Spleen and bone marrow provide excellent samples for the laboratory, as these are contaminated relatively late in the post-mortem process by other bacteria. A variety of diagnostic techniques have been developed over the years for HS. These include:
- Blood smear, culture and biological tests for isolation of the causative agent. Mouse isolation may prove necessary as samples are often heavily contaminated when they reach the diagnostic laboratory. A mouse colony is therefore necessary in such laboratories.
- Biochemical and serological tests (capsular such as rapid slide agglutination and indirect haemagglutination tests or somatic such as agar gel precipitation test) for identification of P. multocida and determination of serotypes. An ELISA test has recently been developed in Australia, however it fails to differentiate between the Asian (B:2) and African (E:2) types. This is not a serious limitation in Asia as only B:2 type of P. multocida has been encountered so far. Thus ELISA can be a good test for screening a large number of cultures from a collection in a laboratory where the turnover is high.
- Non serological tests for presumptive identification of serotypes (e.g. acriflavine flocculation test, hyaluronidase test).
- Molecular methods such as PCR, ribotyping or restriction endonuclease analysis which have an epidemiological significance because they enable strain differentiation within serotypes and hence some epidemiological inferences, for investigations extending beyond routine diagnosis.
Differential diagnosis: This disease is must be differentiated from other etiological factors which leads to sudden death seen with peracute and acute hemorrhagic septicemia likes lightning, snakebites, blackleg, rinderpest, and anthrax.
- Shipping fever is often mistakenly confused for HS, but has a multifactorial etiology (often Mannheimia haemolytica), is not septicaemic, and does not cause multisystemic petechial haemorrhages
- The peracute nature of the disease and the extensive oedema and haemorrhage make it difficult to differentiate from blackleg and anthrax
- Acute salmonellosis, mycoplasmosis, and pneumonic pasteurellosis should also be considered
Treatment: HS is a primary bacterial disease and, theoretically, could be effectively treated by the wide range of antibiotics currently available. However, treatment is constrained by a host of practical considerations. Animals can be cured only if they have been treated in the very early stages of the disease. The conditions for an early detection of the disease and hence its effective treatment are usually lacking in primitive husbandry systems. In organized farms, however, early detection and effective treatment are achieved through regular checking of rectal temperatures of in-contact animals. Antimicrobial sensitivity/ susceptibility testing (AST) are particularly necessary for P. multocida for which resistance to commonly used antimicrobial agents has occurred. The following agents have proven their clinical efficacy: penicillin, amoxicillin (or ampicillin), cephalothin, ceftiofur, cefquinome, spectinomycin, florfenicol, tetracycline, sulfonamides, trimethoprim/sulfamethoxazole, erythromycin, tilmicosin, enrofloxacin (or other floroquinolones), amikacin and norfloxacin. In initial phase of the disease intravenous administration of sulphonamides i.e. sulphamethazine @150 mg/kg body weight for 3 days. The treatment may be rendered with antimicrobial sensitive to the microorganisms and symptomatic treatment with anti-inflammatory drugs may be required as suggested by the Veterinarian.
Prevention and control:
Measures during an outbreak: Vaccination is a major control measure in the face of a new epidemic. Various vaccine types have been developed among which the broth bacterin, the oil adjuvant vaccine, the double emulsion vaccine and a live vaccine. During an outbreak, one should resort to immediate whole herd vaccination, irrespective of previous vaccination history. The most commonly used vaccine of HS in endemic area is oil adjuvant vaccine is recommended. Sanitary measures include early detection and isolation of new cases and their immediate treatment with antibiotics, deep burial of carcasses or incineration, and the prevention of movements of animals to disease free areas.
Measures in endemic zones: Vaccination on a routine prophylactic basis preferably two to three months before the high-risk season (monsoon). Awareness of the disease among farmers backed up by a good disease reporting/disease information system. Segregation of animals from endemic and non-endemic areas to avoid contact with carriers.
Prevention of spread across borders: It has been said above that HS was an endemic disease unlikely to spread in a way such as it easily crosses borders. However, import of animals from an area of unknown status vis-à-vis HS to a free area should comply with some practical procedures which should take into account the high percentage of carriers that occur in endemic areas than was earlier believed, and the persistence of the carrier status for long periods. Briefly, these are:
- Ensure that the animals originate from a region where no outbreaks of HS have occurred for a minimum period of one year;
- Carry out an indirect haemagglutination (IHA) testing (a test which can reveal recent infection) on the animals to be exported as well as on a random sample of in-contacts in the country of origin whenever possible;
- Hold animals under observation for 2–3 weeks before transport (while carrying out the above testing);
- Quarantine them for the same period of time upon arrival to destination and;
- Vaccinate all animals at the end of the quarantine period. Whenever animals are exported from HS endemic countries, even after observing all the above precautions, it is important to vaccinate all susceptible stock in the importing country that are likely to come into contact with the imported animals. Whilst these above-mentioned measures may be feasible and meaningful in island situations, the Asian continent has to contend with many land borders, across which considerable unquarantined animals may be moving.
