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Avian Spirochetosis
Overview of Avian Spirochetosis
Etiology, Epidemiology, and Transmission
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Topics in Avian Spirochetosis
  • Overview of Avian Spirochetosis
         
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        Overview of Avian Spirochetosis(Avian borreliosis)

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        Avian spirochetosis is an acute, febrile, septicemic, bacterial disease that affects a wide variety of birds.

        Etiology, Epidemiology, and Transmission

        The causal organism, Borrelia anserina, is an actively motile spirochete, ~0.2–0.3 μm × 8–20 μm, and consists of 5–8 loosely arranged coils. Cultivation in vitro is difficult. Borrelia will grow on Barbour-Stoenner-Kelly medium, but loses virulence after 12 passages. It can also be propagated in embryonating duck or chick embryos or in young ducks or chicks.

        Spirochetosis is found in temperate or tropical regions, wherever the biologic vectors are found. The most common vector is Argas persicus, the “cosmopolitan” fowl tick, but other Argas spp transmit the disease in different geographic areas. In the western USA, a highly efficient vector is A sanchezi.

        Diverse immunologic and serologic types of B anserina have been demonstrated in many areas. Recovery from one type confers solid immunity against the homologous types for ≥1 yr, but not against heterologous strains. Relapses, such as occur with some human Borrelia infections, are unknown in B anserina infection of birds; any reinfection can be attributed to a heterologous type.

        Generally, an infected Argas tick can transmit the disease at every feeding and maintains the infection throughout larval, nymphal, and adult stages. The ticks also transmit the infection transovarially, ie, the F1 larvae are infective. Ticks remain infected despite feeding on chicks hyperimmune to B anserina or on chicks with high blood levels of chemotherapeutic agents effective against Borrelia. Other vectors (lice, mosquitoes, some species of ticks, inanimate objects) can transmit the spirochete mechanically to a susceptible host whenever the piercing apparatus becomes contaminated with blood that contains Borrelia. Ingestion of bile-stained fecal droppings containing the spirochete, contamination of feed or water, and cannibalism during spirochetemia can result in infection. After the bite of an infected tick, the incubation period is ~3–12 days.

        Clinical Findings

        Marked enlargement and mottling of the spleen is the most characteristic lesion. Signs are highly variable, depending on the virulence of the spirochete, and may be absent. Signs include listlessness, depression, somnolence, moderate to marked shivering, and increased thirst. Young birds are affected more severely than older ones. During the initial stages of the disease, there is usually a green or yellow diarrhea with increased urates. The course of the disease is 1–2 wk. Mild strains are common. However, in many tick-infested geographic areas, morbidity can approach 100% and mortality may be 33–77%. Egg production in layers or breeders may be reduced by 5–10%, with a higher number of small eggs.

        Lesions

        An enlarged spleen with petechial or ecchymotic hemorrhages, not unlike spleens in marble spleen disease of pheasants (see Hemorrhagic Enteritis/Marble Spleen Disease), is present. However, a contrasting situation may be seen in Mongolian pheasants, in which the spleen is reported to be small and pale. Occasionally, the liver may be swollen and contain focal areas of necrosis. Kidneys may be enlarged and pale. A green, catarrhal enteritis is common.

        Diagnosis

        Diagnosis depends on demonstration of Borrelia in the blood, either as actively motile during darkfield microscopy, or as stained spirochetes in Giemsa-stained blood smears. In young birds, the Borrelia may reach vast numbers per oil-immersion field and persist for several days. Older birds usually have low numbers of Borrelia that are detected only with difficulty, or not at all, and that persist for only 1–2 days. Anemia is common and results in increased numbers of immature RBC.

        Agar-gel diffusion and various serologic tests have been described but are of questionable value due to diverse serotypes that exist in some localities. Specific agglutinins clump the spirochetes in successively larger clumps during the terminal stages of the disease. Agglutinationlysis then begins to disintegrate these clumps, and spirochetal degradation products are liberated, which may result in pyrexia. Death occurs most often 1–3 days after Borrelia disappear from the bloodstream. Spirochetal antibodies are readily detected in yolks of eggs laid by infected hens.

        Treatment and Control

        Several antibacterial agents are effective. The most widely used are penicillin derivatives, but the streptomycins, tetracyclines, and tylosin are also effective. The antibiotics can be completely effective if begun when the number of spirochetes per oil-immersion field is low or moderate; however, if large numbers of spirochetes are present in the bloodstream, the sudden liberation of large quantities of spirochetal degradation products can result in higher mortality than no treatment.

        Control must be directed against the biologic vector. Argas ticks are notable for their long lifespan, ability to survive for extended periods without a blood meal, efficiency in transmitting the spirochete, and ability to remain securely hidden in cracks and crevices often beyond the effective reach of pesticides. Accordingly, control is difficult. A combination of tick eradication and immunization is the most effective means of control.

        Immunization can be highly successful and, next to eradication of the biologic vector, is the preferred method of control. Bacterins prepared from local strains of Borrelia have been used with success. Vaccines may be prepared from formalin- or phenol-inactivated material from lysates of blood, tissues, embryos, or eggs infected with B anserina, and may be lyophilized or liquid. Whole-egg propagated bacterins are usually given in 1 or 2 IM injections. Little if any cross-protection is afforded to different serotypes. Birds normally have protective immunity after recovering from natural infection.

        Last full review/revision March 2012 by Larry R. McDougald, PhD

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