Hemorrhagic septicemia is a disease of water buffalo and cattle in tropical regions caused by specific serotypes of Pasteurella multocida. Asymptomatic, pneumonic, and disseminated (endotoxemic) forms occur, often with peracute distress and high mortality. However, antimicrobial treatment very early in disease can reduce mortality. Definitive diagnosis requires the isolation of P multocida serotypes B:2 or E:2 or detection by molecular capsular and somatic serotype assays.
Hemorrhagic septicemia (HS) is an acute, highly fatal form of pasteurellosis that affects mainly water buffalo, cattle, and bison. It is a World Organization for Animal Health (OIE)–listed animal disease and is considered the most economically important bacterial disease of water buffalo and cattle in tropical areas of Asia, particularly in India and other parts of southeast Asia where water buffalo populations are high. Disease is most devastating to smallholder farmers where husbandry and preventive practices are poor and free-range management is common. HS is also an important disease in Africa and the Middle East, with sporadic outbreaks occurring in southern Europe. The only confirmed outbreaks of HS in the Americas occurred in bison in Yellowstone National Park, most recently from 1965–1967. Natural HS occurs infrequently in pigs, sheep, and goats and has been reported in camels, elephants, rhinoceros, horses, donkeys, yaks, and various species of deer and other wild ruminants.
Etiology of Hemorrhagic Septicemia
Classical hemorrhagic septicemia as defined by the OIE is caused by Pasteurella multocida serotypes B:2 and E:2 (Carter and Heddleston classification system), which correspond to serotypes 6:B and 6:E of the Namioka-Carter classification system. Serotype B:2 has been identified in most areas where the disease is endemic, whereas serotype E:2 has been found only in Africa. Septicemic pasteurellosis that is clinically similar to HS is caused by a wide variety of other P multocida serotypes. Septicemic pasteurellosis has been reported most commonly in wild ruminants and occurs in geographic areas not affected by HS, such as the US, Europe, the UK, Australia, and Canada.
Transmission, Epidemiology, and Pathogenesis of Hemorrhagic Septicemia
It has been estimated that 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 of hemorrhagic septicemia include high temperature and humidity, concurrent infection 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 the multiple stressors present during this time and the moist conditions, which prolong the survival time of the organism in the environment.
Infection occurs by contact with infected oral or nasal secretions from either healthy carrier animals or animals with clinical disease, or by ingestion of contaminated feed or water. Infection begins in the tonsil and adjacent nasopharyngeal tissues. Subsequently, bacteremia leads to dissemination and rapid growth of bacteria in various locations, tissue injury, a host cytokine response, and release of lipopolysaccharides that results in a rapidly progressing endotoxemia. Clinical signs can appear 1–3 days after infection, and death can occur within 8–24 hours after the first clinical signs develop.
Clinical Findings of Hemorrhagic Septicemia
Hemorrhagic septicemia, water buffalo
In peracute cases of hemorrhagic septicemia that result in death within 8–24 hours, animals often have fever, hypersalivation, nasal discharge, and labored respiration; however, because of the short duration of disease, these clinical signs may easily be overlooked. Acute disease can persist for up to 3 days, and less often up to 5 days, and is characterized by fever of 104°–106°F (40°–41.1°C), apathy or restlessness and reluctance to move, hypersalivation, lacrimation, nasal discharge that begins as serous and progresses to mucopurulent. Subcutaneous swelling in the pharyngeal region that extends to the ventral neck and brisket (and sometimes the forelimbs), progressive respiratory distress, cyanosis, terminal recumbency, and sometimes abdominal pain with diarrhea are also seen.
Lesions
The characteristic lesion of hemorrhagic septicemia is swelling of the subcutis and muscle of the submandibular region, neck, and brisket by clear to blood-tinged edema fluid. Serous to serofibrinous fluid may also be present in the thorax, pericardium, and abdominal cavity. There is typically widespread congestion with petechiae and ecchymoses in tissues and on serosal surfaces, particularly in the respiratory, GI, and urinary systems.
Diagnosis of Hemorrhagic Septicemia
- Clinical diagnosis based on history and clinical signs and characteristic lesions
- Laboratory diagnosis based on culture and blood tests
Clinical diagnosis of hemorrhagic septicemia in endemic areas is based on history, lapses in vaccination, environmental conditions, and the characteristic clinical signs and lesions of disease. Although typical outbreaks of HS are not difficult to recognize in endemic regions.
A definitive diagnosis of HS is based on isolation of P multocida serotype B:2 or E:2 (or other less common serotypes recognized by the OIE as causing HS) from the blood and tissues of a patient with typical clinical signs. Various other P multocida serotypes can cause HS-like disease in cattle and water buffalo, which must be differentiated from classical HS. The passive mouse protection test using specific B:2 and E:2 immune rabbit sera has been used in Asia and Africa to identify these serotypes. More precise tests, such as indirect hemagglutination, coagglutination, counter immunoelectrophoresis, and immunodiffusion tests have also been used in some laboratories. More recently, molecular techniques, including pulsed field gel electrophoresis, Southern blots, loop-mediated isothermal amplification, and PCR-based protocols, have been used to differentiate between capsular and somatic serotypes. The PCR array techniques are most feasible for use in endemic areas and can be used with various samples, including blood, tissues, or bacteria from broth or plate cultures.
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Treatment and Prevention of Hemorrhagic Septicemia
- Antimicrobials administered early in the disease
- Vaccination
Antimicrobials are effective against hemorrhagic septicemia if administered very early in the disease. However, because HS progresses rapidly, treatment is often unsuccessful. During outbreaks, any patient with a fever should be treated with intravenous 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. However, plasmid- and chromosomal-mediated multidrug resistance seems to be increasing for some strains of P multocida, and resistance to tetracyclines and penicillin has been reported for serotype B:2.
Killed vaccines are most commonly used for prevention and include bacterins, alum-precipitated and aluminum hydroxide gel vaccines, and oil-adjuvant vaccines. In patients >3 years old, an initial two doses, 1–3 months apart, are recommended, followed by booster vaccinations once or twice yearly. The oil-adjuvant vaccine provides protection for 9–12 months and is administered annually. It is most effective when administered 1 month before the monsoon or rainy season. Although it provides the strongest immunity, it is unpopular in the field because of its viscosity and difficulty of administration. Oil-based vaccines combined with polysorbate 80 or saponin have also 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 (approximately 4–5 months with variable protective efficacy), and twice yearly booster vaccinations are recommended. It is important that the vaccines are made from the strains of P multocida circulating in the regions of intended use to obtain maximal effectiveness. Maternal immunity can interfere with vaccine efficacy in calves.
Use of intranasal live-attenuated vaccines has also been suggested as a means to increase vaccine coverage via self-vaccination of those animals in contact with vaccinated animals.
Zoonotic Risk of Hemorrhagic Septicemia
The P multocida serotypes that cause hemorrhagic septicemia have not been recovered from infections in humans. However, because many serotypes of P multocida have the potential to infect humans, appropriate precautions should be taken when dealing with suspected cases of HS or HS-like disease.
What is Hemorrhagic Septicemia (HS) in water buffalo and cattle?
Answer:
Hemorrhagic Septicemia is a highly contagious and fatal bacterial disease caused by Pasteurella multocida (serotypes B:2 and E:2). It primarily affects water buffalo and cattle, leading to sudden death due to septicemia.
FAQ’s
2. How is Hemorrhagic Septicemia transmitted among animals?
Answer:
HS spreads through direct contact with infected animals, contaminated water, feed, equipment, or inhalation of infectious droplets. Stress factors like transport, overcrowding, and weather changes can increase susceptibility.
3. What are the effective prevention methods for Hemorrhagic Septicemia?
Answer:
The most effective prevention is timely vaccination, especially before the rainy season. Good biosecurity practices, minimizing stress, maintaining proper hygiene, and isolating sick animals also help control the disease.
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