J APPL POULT RES 2008. 17:556-558. doi:10.3382/japr.2008-00063
© 2008 Poultry Science Association
Clinical and Histopathological Survey of Lesions Similar to Pox Skin Lesions in Three Flocks of a Large Commercial Layer Farm
H. Moayyedian1,
A. Mirmohammad-Sadeghi and
R. Hasanshahi
Department of Clinical Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran
1 Corresponding author: hamid_moayyedian{at}yahoo.com
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SUMMARY
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In this study, we report an outbreak of fowl pox disease in a large commercial layer farm in Iran. Three flocks of this farm were affected. Flock A (23 wk of age), flock B (44 wk of age), and flock C (71 wk of age) showed cutaneous lesions. Beak necrosis was seen at the posterior part of the upper or lower beak. Also, some vesicles were seen in combs, wattles, and eyelids. Beak and comb lesions were scraped and stained with Wright’s staining for histopathological examination. Samples showed hyperplasia of epidermis but no Bollinger bodies were seen. Histopathologically, the epidermis had marked hyperplasia (acanthosis) caused by the swelling and increased number of cells in the stratum spinosum. Clinical observations, as well as histopathological findings, led to a diagnosis of fowl pox disease.
Key Words: beak • comb • eyelid • scrape • staining
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DESCRIPTION OF PROBLEM
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Pox is a common viral disease of commercial poultry (chickens and turkeys) as well as of pet and wild birds. Of the approximately 9,000 bird species, about 232 in 23 orders have been reported to have acquired a natural pox virus infection [1]. Fowl pox is an economically important disease of commercial poultry because it can cause decreased egg production and increased mortality. Pox is a slow-spreading disease characterized by the development of discrete nodular proliferative skin lesions on the nonfeathered parts of the body (cutaneous form) or fibrinonecrotic and proliferative lesions in the mucous membrane of the upper respiratory tract, mouth, and esophagus (diphtheritic form) [2]. A concurrent systemic infection may also occur. Avian pox viruses infect birds of both sexes and all ages and breeds [3]. Fowl pox in commercial poultry is worldwide in distribution. The incidence, however, is variable. In high-density areas where multiple-age birds are raised under confined conditions, the disease tends to persist for a long time despite preventive vaccinations. The case report frequency has recently increased and involves newly affected bird species, indicating that this virus is an emerging disease [4]. In our area, it is an unusual or novel manifestation of the disease, because it has all of the signs except Bollinger bodies. Mosquitoes are considered to be an important vector for the spread of fowl pox virus in these flocks. An increase in fowl pox cases has been seen to match the mosquito season [5].
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FIELD REPORT
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In this study, we report an outbreak of fowl pox disease in a large commercial layer farm in Iran. Three flocks of this farm were affected. Flock A (23 wk of age), flock B (44 wk of age), and flock C (71 wk of age) showed cutaneous lesions (Figure 1a to 1f
). Each flock consisted of 240,000 layers in 8 houses. All flocks were Hy-Line except one-half of flock B, which was Bovans. Beak necrosis was seen at the posterior part of the upper or lower beak (Figure 1a, 1b, and 1c). When necrosis formed a complete ring surrounding the beak, the beak was dropped (Figure 1b). Some vesicles and necroses were seen in combs (Figure 1d and 1e) and wattles and eyelids (Figure 1f). Morbidity was relatively high (10%) except in Bovans in flock B, which had low morbidity (2%). Mortality was normal except for the birds that died because their beaks were dropped and they were unable to eat. Surprisingly, morbidity in 1 cage was 90 to 100%, but in an adjacent cage, it was 0%. Morbidity of comb necrosis was similar to beak necrosis, and if the comb apex was affected, the upper part of the comb was dropped (Figure 1d). Egg production did not decrease in any of the affected flocks. Clinical signs lasted about 4 to 6 wk, and after that, lesions disappeared completely. The flocks had been vaccinated against pox 2 times, at 7 and 13 wk of age. Other vaccines consisted of B1, inactivated binary (Newcastle disease + avian influenza), H120, D78, LaSota, coryza, avian influenza, inactivated 3-fold (Newcastle disease + infectious bronchitis + egg drop syndrome), and avian encephalomyelitis. At first we were suspicious of mycotoxins, because clinical signs, especially beak necrosis, were similar to ergotism. However, based on laboratory tests, the feed had no mycotoxins. The postmortem examination of birds did not reveal specific lesions. Beak and comb lesions were scraped and then fixed in 10% buffered formalin, embedded in paraffin, sectioned at 5 µm, and stained with Wright’s staining for histopathological examination [6]. Samples showed hyperplasia of epidermis, but no Bollinger bodies were seen in spite of specific examination for them. We found other histologic lesions except Bollinger bodies, which can lead to fowl pox. The nodules ranged from 2 to 4 mm in diameter, which is the characteristic lesion of the cutaneous form of pox in chickens. Histopathologically, the epidermis had marked hyperplasia (acanthosis) caused by the swelling and increased number of cells in the stratum spinosum [7]. These cells showed ballooning degeneration. Pustular lesions had superficial crusts consisting of hemorrhages, necrotizing cells, and bacteria colonies under the crustation. Lymphocyte and histiocyte infiltration was also noted in the dermis. Occasionally, fibroblast proliferation and fibrosis were observed in the areas, using Wright’s staining [8]. No pathological lesions were found in the liver, spleen, and kidney.
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Figure 1. (a) Upper beak necrosis; (b) upper beak dropped; (c) ring form of beak necrosis; (d) comb apex dropped because of necrosis; (e) comb vesicles; (f) eyelid vesicles.
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DISCUSSION
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Clinical observations, as well as histopathological findings, led to a diagnosis of fowl pox disease. Proliferative and necrotic dermatitis were noted in the affected birds. Mosquitoes feed on a viremic bird or contaminated lesion and then feed on a healthy bird, transmitting the virus. It is believed that mosquitoes can harbor the virus for a month or more. Stable flies have been shown to transmit the virus experimentally. Blowfly larvae have been found in lesions, indicating that it is possible that these insects may also play a role in transmission. Blowflies could lay eggs in necrotic lesions, become contaminated, and then contact broken skin of a noninfected bird. Our observation happened in summer, when the mosquitoes were commonly found. This farm had 2 other flocks far from these 3 flocks, and because manure management was different in those 2 flocks, no mosquitoes were seen there and, as a result, we did not observe an outbreak of fowl pox disease in those 2 flocks. No successful treatment is available at present. Antibiotics can be administered to control secondary bacterial infections, particularly in birds with respiratory and gastrointestinal lesions. Also one of our colleagues reported fowl pox in a commercial layer farm in Tehran exactly resembling our clinical and histopathological examinations.
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CONCLUSIONS AND APPLICATIONS
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- Some strains of fowl pox virus can affect the birds in spite of proper vaccination.
- Apparently, this form of pox disease does not affect bird performance, but the main problem is the beak necrosis that can affect the ability of the bird to eat.
- Age may not be important in regard to resistance.
- It appears that the expected histopathologic characteristics of pox disease may not be present in this new form of pox, as are other characteristics.
- Because of the important role of mosquitoes in transmission of this disease, mosquito control is essential.
- It appears that we will need new vaccines from new strains of fowl pox viruses.
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REFERENCES AND NOTES
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- Bolte, A. L., J. Meurer, and E. F. Kaleta. 1999. Avian host spectrum of avipox viruses. Avian Pathol. 28:415–432.[CrossRef][Web of Science]
- Docherty, D. E., R. I. Long, E. L. Flickinger, and L. N. Locke. 1991. Isolation of poxvirus from debilitating cutaneous lesions on four immature grackles (Quiscalus sp.). Avian Dis. 35:244–247.[CrossRef][Web of Science][Medline]
- Ciganovich, E. A. 1999. Pages 163–170 in Field Manual of Wildlife Diseases: General Field Procedures and Diseases of Birds. United States Geological Survey, Washington, DC.
- Ritchie, B. W. 1995. Pages 285–311 in Avian Viruses: Function and Control. Winger’s Publishing, Lake Worth, FL.
- Tripathy, D. N., and W. M. Reed. 2003. Pox. Page 259 in Diseases of Poultry. 11th ed. Y. M. Saif, ed. Iowa State University Press, Ames.
- Woodruff, C. E., and E. W. Goodpasture. 1929. The infectivity of isolated inclusion bodies of fowl pox. Am. J. Pathol. 5:1–10.[Web of Science]
- Woodruff, C. E., and E. W. Goodpasture. 1930. The relation of the virus of fowl-pox to the specific cellular inclusions of the disease. Am. J. Pathol. 6:713–720.[Web of Science]
- Ledingham, J. C. G., and M. B. Aberd. 1931. The aetiological importance of the elementary bodies in vaccinia and fowl pox. Lancet 221:525–526.
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SUMMARY
DESCRIPTION OF PROBLEM
