Borrelia anserina infections

Preferred Scientific Name

• Borrelia anserina infections

International Common Names

• English: avian borreliosis; avian spirochaetosis; avian spirochetosis; borreliosis, avian; fowl spirochetosis; spirochaetosis; spirochetosis; spirochetosis, borrelia anserina, in birds

Local Common Names

• Brazil: borreliose aviária

Avian (fowl) spirochetosis, or borreliosis, is an acute, septicaemic disease of a variety of avian species, including chickens, turkeys, geese, ducks and pheasants, caused by the bacterium Borrelia anserina (Barnes, 1997). It is of most significance in tropical and subtropical areas; extensively reared free-range flocks are more likely to be affected than confined flocks (Kanth, 2006). The disease was first described among geese in Russia (Sakharoff, 1891). A few decades later in Brazil, Marchoux and Salimbeni (1903) incriminated the role of ticks of the genus Argas as natural vectors of the disease; this was later confirmed by several authors in all continents (Prowazek, 1909; Knowles et al., 1932; Diab and Soliman, 1977).

B. anserina was classified under different taxonomic names at the beginning of the twentieth century (Knowles et al., 1932). These differences were mostly justified by the negative results obtained in cross-immunity tests performed on laboratory birds with different geographic strains. Nowadays, it is well known that different B. anserina antigenic types exist and active immunity is serotype-specific (DaMassa and Adler, 1979; Soni and Joshi, 1980; Sambri et al., 1999). 

Post-mortem findings

The most characteristic post-mortem finding is the marked enlargement and mottling of the spleen, showing ecchymotic haemorrhages. The spleen becomes three to six times its normal size. The liver may also be enlarged, congested and friable containing minute areas of necrosis. The kidneys are enlarged and pale. Greenish mucoid enteritis is usually present.

Histopathology

The spleen shows hyperplasia of histiocytes and reticular cells, moderate depletion of lymphocytes and accentuation of the red pulp. Extensive erythrophagocytosis is evident in the sinusoidal macrophages of the spleen, in Kupffer cells of the liver and in bone marrow smears. Haemosiderosis is observed in the spleen, liver and intestines. Silver-stained spirochetes can be observed in the spleen, liver, small intestine, kidney or lungs (Bandopadhyay and Vegad, 1983; Cooper and Bickford, 1993).

Natural infection via either tick bites or ingestion of infective faeces, blood or ticks results in an incubation period of 3-12 days. Intravenous inoculation of infected blood into susceptible birds induces the disease after 24 to 48 hours (Knowles et al., 1932; Labruna et al., 1999). The most common clinical symptoms are fever, generalized weakness, ruffed feathers, loss of appetite, thirst, greenish diarrhoea, dropped head, and finally paralysis of wings and legs. Cyanosis or pallor of comb and wattles are visible. A few spirochetes may be found in the peripheral blood coincident with the initial temperature rise, thereafter increasing in concentration in 2 or 3 days, and then usually disappearing after a further 1 or 2 days. The disease course lasts for 3 to 7 days, followed by bird recovery or death. Recovered birds develop solid immunity and are not carriers of the bacterium. Under natural outbreaks, mortality rates vary from 1-2% up to almost 100%. The lowest rates occur in closed flocks where spirochetosis is endemic. The highest rates occur when susceptible flocks are placed in pens inhabited by infected ticks or when infected ticks are introduced in clean flocks by either infested birds or equipment.

Birds develop anaemia, the severity of which is maximum when spirochetemia is in decline. Studies have revealed the role of cold agglutinins and soluble immune complexes in the production of anaemia during acute spirochetosis. It is suspected that these adhere to erythrocytes, enhancing their phagocytosis by macrophages in tissues, especially in spleen (Soni et al., 1980; Joshi et al., 1982; Barnes, 1997).

Besides being the primary vector, Argas spp. ticks are also reservoirs of the bacterium in nature. B. anserina can survive trans-stadially during all tick stages and is transmitted transovarially (Zaher et al., 1977). Once infected, a tick remains infected by B. anserina for its entire life (Hoogstraal, 1985).

Argas ticks have a multi-host life cycle pattern, consisting of eggs, larvae, two to four nymphal stages and the adults (males and females). Larvae feed for 4-6 days, whereas the nymphal instars and adult ticks feed for only 20 to 50 minutes, at night, when birds are housed. Egg deposition and incubation, mating and all tick moults occur off the host, inside cracks and crevices. Each female may lay as many as 900 eggs during her entire life. These are produced in as many as seven batches with a blood meal preceding each batch of eggs. Hungry ticks leave the cracks or crevices at dark hours, and move toward a sleeping chicken. Larvae attach mainly on the underneath side of the wing web. Nymphs and adults feed mainly on the shanks. Fed ticks detach from the hosts and immediately walk and hide in cracks or crevices. As engorged ticks walk toward hidden places they usually release black faeces which are characteristic. Highly infested flocks can be carefully identified by the presence of several small black spots <1 mm wide) on the roosts and walls, especially around crack entrances. Unfed Argas ticks are able to survive without a new blood meal for several months or years.

Spirochetosis outbreaks have been reported in Californian turkey and chicken flocks where no ticks, lice or mites could be found (McNeil et al., 1949). These intriguing findings have been subject to several speculations about the transmission by mosquitoes or through contaminated faeces from wandering birds. Once introduced in a clean flock, spirochetosis can be transmitted from bird to bird by virtually any means whereby blood, excreta, or tissues from an infected live or recently dead bird come in contact with a susceptible bird (Barnes, 1997).

Most of the literature about spirochetosis was published before the 1980s, especially from the 1940s to the 1960s, when the poultry industry comprised several small enterprises, many of which could be categorized by poor sanitation conditions. New scientific reports about field spirochetosis have rarely been released. This contrast is certainly a result of modifications of poultry-rearing methods around the world in the past few decades. The industry today, as it is in most countries, is very advanced in response to globalization, industrialization, vertical integration and aggregation such that a few large agribusiness companies virtually control the poultry industry in different countries. A number of diseases that used to cause problems before this revolution in production systems no longer do so, among them avian spirochetosis. These modifications have diminished the possibilities of tick establishment into new intensively managed flocks. In many countries where spirochetosis was reported to be one of the most severe diseases affecting the poultry industry in the past, the disease became confined to small flocks kept for personal consumption of product (village chickens) or very limited local sale, with no significant economic impact to the country. Sa’idu et al. (1995) noted the drastic decline of cases of spirochetosis in Nigeria in the 1980s, when compared to the 1970s, and associated it with better housing of birds and improved management and tick control measures.

Nowadays, free-range egg production is becoming a trend in response to concerns about the welfare of poultry kept in large farm complexes. It will be interesting to see the impact of such management on the establishment of Argas populations in these modified flock systems.

B. anserina is sensitive to penicillin, tylosin, streptomycin, dihydrostreptomycin, oxytetracycline and aureomycin. Generally, a single intramuscular dose of any of these drugs is sufficient for a severely affected bird to recover (Hsiang and Packchanian, 1951; Singer, 1977; Kheir El Din et al., 1986).