Hemorrhagic Septicemia (HS)
Also known as
Hemorrhagic septicemia (HS) is one of the most economically important pasteurelloses. In cattle and buffaloes it is associated with several serotypes of Pasteurella multocida.
This highly fatal disease occurs mainly in cattle and buffaloes but has also been reported in goats, African buffalo, camels, horses and donkeys, pigs and wild elephants. Two different serotypes have caused septicemic disease in antelope and elk, and one was associated with the disease in bison.
South Asia is the area of highest prevalence and incidence of HS, possibly due to radical changes in weather between seasons, animal debilitation caused by seasonal scarcities of forage and the pressures of work that draft animals are asked to do.
The disease also occurs in the Middle East and Africa but to a lesser extent, and predisposing conditions are not as clearly defined as in South Asia. Sporadic outbreaks occur in southern Europe. The only confirmed outbreaks of HS in the Americas occurred in bison in Yellowstone National Park, most recently from 1965–1967.
In India from 1974–1986, HS was responsible for the highest mortality rate of any infectious diseases in buffaloes and cattle, and was second in morbidity rate (number of animals affected) in the same animals. When compared to foot and mouth disease, rinderpest, anthrax and blackleg, HS accounted for 58.7% of the deaths due to these five endemic diseases.
In Pakistan, HS is a disease of great economic importance and considered by farmers to have more negative consequences than foot and mouth disease--due to higher mortality rate and the greater economic impact.
HS is the most economically important bacterial disease of water buffalo and cattle in tropical areas of Asia, particularly in Southeast Asia’s large population of water buffalo. This disease is most devastating to small farmers where husbandry and preventive practices are poor and free-range management is common.
Many cases are peracute (very severe and quickly fatal) resulting in death within 8 to 24 hours. These animals often have fever, excessive salivation, nasal discharge, and difficult respiration, but because of the short duration of disease these signs may not be seen.
Acute cases can persist up to 3 days (sometimes 5 days), characterized by fever of 104° to 106°F, apathy or restlessness and reluctance to move, excessive salivation, watery eyes, nasal discharge that begins as clear and progresses to thick mucus, subcutaneous swelling in the throat area that extends to the lower neck and brisket (and sometimes the forelegs), progressive respiratory difficulty, bluish skin and mucous membranes due to lack of oxygen in the tissues, terminal recumbency (unable to get up), and sometimes abdominal pain with diarrhea.
The incubation periods (time between exposure and observable disease) for buffalo calves 4 to 10 months of age varies with the route of infection. The incubation period is 12 to 14 hours for experimental subcutaneous infections, approximately 30 hours for orally induced infections, and 46 to 80 hours for natural exposure (contact with an infected animal).
Progression of the disease in buffaloes and cattle is divided into three phases. Phase one is characterized by fever, with rectal temperature of 104–106 °F, loss of appetite and depression. In phase two the animal exhibits increased respiration rate (40–50 breaths per minute), labored breathing, clear nasal discharge (turning thick and white as the disease progresses), salivation and edema spreading to brisket and forelegs.
In phase three, the animal is down and can’t get up, with continued acute respiratory distress and terminal septicemia (“blood poisoning). The three phases overlap when disease course is short. In general, buffaloes have a more acute onset of disease than cattle, with shorter duration.
Predisposing factors include close contact with infected or carrier animals and the stress of monsoon or wet seasons. After initial replication in the tonsils, bacteria soon multiply throughout the animal. Recovered animals may remain as carriers (with no outward signs of disease) and serve as a reservoir of infection.
Herd immunity is high after an outbreak, and no new cases occur until susceptible new animals enter the herd or come into contact with carriers, or birth of new naïve animals. In these situations, further disease outbreaks may occur.
- Excess salivation
- Swelling in the throat area which spreads to the neck and brisket regions
- Congested mucus membranes
- Rapid breathing
- Respiratory distress
- Death usually within 6 hours of onset of clinical signs
Hemorrhagic septicemia is caused by several types of Pasteurella multocida. Unlike other Pasteurella species which serve as secondary opportunistic invaders, this species is a primary pathogen.
Serotype E:2 has been associated with outbreaks in Africa and type B:2 has been associated with outbreaks in Asia. Serotype E:2 was reported in Senegal, Mali, Guinea, Ivory Coast, Nigeria, Cameroon, the Central African Republic and Zambia. Many outbreaks of HS in Africa have now been associated with serogroup B, and serogroup E has been associated with outbreaks in Asia.
Natural routes of infection are inhalation and/or ingestion. Experimental transmission has succeeded using intranasal aerosol spray or oral drenching. Subcutaneous inoculation results in rapid onset of the disease and a shorter clinical course.
When HS is introduced for the first time into a geographic area, morbidity and mortality rates are high, approaching 100% unless animals are treated in the very early stages of disease.
Three factors affect global distribution of HS: climate conditions, husbandry practices and species of animal. The disease is almost non-existent where climatic conditions are mild and dairy breeds are used. In contrast, on the warmer dry plains, where there are seasonal heavy rains and indigenous cattle, buffaloes and zebu cattle, the disease is endemic. Occasional sporadic outbreaks occur in areas with topography, climate and animals in between these extremes.
The tonsils of up to 5% of healthy water buffalo and cattle are colonized by small numbers of P. multocida serotype B:2 or E:2, which can be shed during periods of stress. Common stressors associated with outbreaks include high temperature and humidity, concurrent infection (such as blood parasites or foot and mouth disease), poor nutrition, or work stress. Although outbreaks can occur at any time, disease is most prevalent during the rainy season.
Increased outbreaks associated with high rainfall are most likely due to moist conditions and multiple stressors present during this time. Moisture prolongs survival of the pathogen in the environment. Infection occurs by contact with infected oral or nasal secretions from healthy carrier animals or animals with clinical disease, or by ingestion of contaminated feed or water.
Infection begins in the tonsils and adjacent tissues. Subsequent bacteremia (bacteria in the bloodstream) leads to dissemination and rapid growth of bacteria in various locations of the body. Tissue damage and host response lead to endotoxemia (endotoxins from these bacteria are present in the bloodstream).
There is a very high death rate, but animals that recovery have immunity to the same or different strains of P. multocida. Some of these animals become healthy carriers that serve as a source of infection for future outbreaks.
Although typical outbreaks of HS are not difficult to recognize in endemic regions, several other diseases can look the same. Acute salmonellosis, anthrax, and noninfectious toxicities should also be considered. Sporadic cases are more difficult to diagnose clinically and might be confused with sudden death from other causes like blackleg, lightning strike, or snakebite. A definitive diagnosis of HS is based on isolation of the pathogen from blood and tissues of an animal with typical signs.
Killed vaccines are commonly used for prevention. In animals younger than 3 years old, an initial two doses given 1 to 3 months apart is recommended, followed by booster vaccinations once or twice yearly. The oil-adjuvant killed vaccine provides protection for 9 to 12 months and is given annually. It provides the best immunity, but is unpopular because of its viscosity (too thick to go through a small needle) and difficulty of administration.
Oil-based vaccines combined with saponin have been used in attempts to increase the ease of administration or immune protection. The commonly used alum-precipitated and aluminum hydroxide gel vaccines have shorter durations of immunity, and twice yearly booster vaccinations are recommended.
It is important that vaccines are made from the strains of P. multocida circulating in the regions of intended use. Attenuated or modified-live vaccines have been used with some success. A live vaccine prepared from a P. multocida of fallow deer origin seems effective and is recommended for use in Southeast Asia by the Food and Agricultural Organization (FAO) of the United Nations. Various modified-live vaccines made from either purified or recombinant bacterial components have also been used experimentally.
Penicillin, ampicillin or oxytetracycline are often administered at label dose rates, or sulphadimadine (100 milliliters orally) and injection of oxytetracycline for 3 days continuously.
These antimicrobials are effective against HS if administered very early in the disease, but because HS progresses rapidly, therapy is usually not begun soon enough and is often unsuccessful. During outbreaks, any animal with a fever should be treated with IV antimicrobials as soon as possible to quickly obtain systemic bactericidal antimicrobial concentrations.
Various sulfonamides, tetracyclines, penicillin, gentamicin, kanamycin, ceftiofur, enrofloxacin, tilmicosin, and chloramphenicol have been used effectively to treat HS but multi-drug resistance seems to be increasing for some strains of P. multocida, and resistance to tetracyclines and penicillin has been reported for serotype B:2.
Prognosis is poor unless antimicrobial therapy is instigated very early in the disease process. The majority of animals will die after clinical signs have developed—even with intensive treatment.