Thursday, November 20, 2008

Recovery and Preservation of Goat Follicular Oocytes


Embryo-transfer has become the fastest method of genetic improvement of farm animals. In vitro maturation and in vitro fertilization (IVF) of follicular oocytes are the recent advances of embryo transfer, these are the important tools to study gamete physiology. From these techniques embryos can be obtained in abundant quantity, production of transgenic animal, embryo sexing, embryo splitting and multiplication of embryos in vitro on lines of superior offspring is possible by these methods.

The oocytes can be obtained from living animals as well as from slaughtered animals also. If those are collected from immature living animals and from immature slaughtered animals, in vitro matured, in vitro fertilized and transferred to the recipient the generation interval can be reduced. If the oocytes collected from varies of slaughtered animal the utility of that animal even after slaughter is improved. This also formulate low cost supply of follicular oocytes which can be matured, cultured and fertilized in vitro.

Material and Methods

Thirty three pairs of goat ovaries were obtained from, local slaughter house Parbhani immediately after slaughter: Paired ovaries were brought to the laboratory in a thermos flask containing 0.9 per cent normal saline at a room temperature: Normal saline is supplemented with Inj-Benzyl penicillin - 400 IU per m1' of saline: Inj-Streptomycin 200 mg/ml and 0.25 mg Nystatin. The pair of ovaries in various stages of oestrous cycle were classified as per (Zemjanis, 1970) into early luteal stage, luteal state and follicular stage. After recovery of oocytes, the good quality oocytes were selected and 65 oocytes were preserved in Ham’s F-10 medium with 10 per cent and 73 oocytes were preserved in 15 percent serum level at 5°C temperature for 24 hours. The ovaries were wahsed with normal saline and placed in a sterile petridish containing medium. The follicles measuring above 3mm in diameter were punctured with. The help of needle (19 guage) and contents were allowed to flow freely into the medium. The whole pertridish containing culture medium was observed under streoscopic microscope at 25 x in order to locate occytes.

Result and Discussion

The average numbers of follicles between 3-5 mm size in early luteal, luteal, and follicular stages were 4.30 + 0.37, 6.00 + 0.57 and 5.20 + 0.40; 3.00 + 1.00, 4.00 + 0.40 and 5.50 ± 0.22 respectively for 10 percent serum level and 15 percent serum level present findings are in agreement with those of Parkale (1987) an d Giri (1992) who reported them as 4.70, 4.95 and 4.32, 3.28, 4.33 and 4.02 respectively for corresponding stages of oestrous cycle in buffaloes. The present findings for early luteal and luteal stages are lower and for follicular stage in agreement with those. of Thakre (1993) who reported them as 5.60+ 0.35, 5.52 + 0.40 and 5.24 + 0.28 the corresponding stages of *estrous cycle in goat.
The overall average number of follicles per pair of ovaries irrespective of oestrous, stages and follicular sizes were 6,00+1.07 and 5.27+0.83 respectively, which are in agreement with those reported by Thakre (1993). These findings are higher than those reported by Parkale (1987) and Giri (1992) as 4.65 and 4.04 respectively.
Differences in the number of follicles may be due to differences in species, breeds, climatic conditions and endocrine profile etc of animals studied by different workers.
The average recovery rate follicular oocytes in early luteal, luteal and follicular stage for 10 per cent and 15 per cent serum levels was 73.33, 63.18 and 72.42] 66.66, 72.22 and 78.84 per cent respectively which are found to be higher than observations made by Giri (1992) and are in agreement with Thakare (1993) who reported them as 47.83, 58.24 and 47.20 and 76.84 per cent respectively which is in accordance with Lambert (1983) who reported 72-79 per cent by laproscopy method. The present findings are significantly higher than that reported by Leibfred and First (1979), Parkale (1987) and Giri (1992) who reported lower recovery rate of follicular oocytes as 50.00, 50.00 and 50.92 per cent respectively.
In the present study in Ham’s F-10 medium 65 medium 65 oocytes for 10 per cent serum level and 73 oocytes for 15 per cent serum level were preserved at 5oC for 24 hours, it was observed that there was no significant change recorded in the morphology of oocytes.


1. Giri, C.G. (1992): Characterisation and morphological in vitro maturation of bulffalo follicular oocytes in different culture media. M.V.Sc. Thesis, Kokan Krishi Vidapith,Dapoli.
2. Lambert R.D. : Sirad, M.A. Benard, C; Beland, R.; Riouz J.E. Lecierc, P : Manard D.P. and Bedoya M. (1986): In vitro fertilization of bovine oocytes matured in vitro and collected at laproscopy. Heriogenology 25 (1): 117.
3. Leidfired, L. and First, N.L. (1979): Characterization of bovine follicular oocytes and their ability to mature in vitro J. Anim Sci. 48 (1): 76-86.
4. Parkale, D.D. (1987): Studies on buffalo (bos bubalis) avaries, follicles and follicular oocytes with special references to culture of oocytes in vitro M.V.Sc. Thesis, Kokan Krishi Vidyapith Dapoli.
5. Thakare N.V. (1993): Studies on recovery, characterization and morphological in vitro maturation of goat follicular oocytes in different culture media. M.V. Sc. Thesis, M.A.U. Parbhani.

by : Khillare, K.P.
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Study on Pathogenicity of the Aspergillus species in experimentally immunosuppressed mice


Recent years have witnessed dramatic changes in man’s environment and his immune defenses. Increasing incidence of secondary infections due to opportunistic fungi such as Aspergillus has been noted. Members of the genus Aspergillus are ubiquitous in nature and can survive under various conditions. Aspergillus, a conidia bearing fungus cause multiple diseases in human. These diseases include invasive aspergillosis, aspergilloma, different forms of hypersensitivity diseases, etc. The rising incidence of these infections in patients has been attributed to the widespread use of multiple antibacterial antibiotics, corticosteroids, irradiation, cytotoxic and other immunosuppressive drugs in clinical practice, increased incidence of acquired immunodeficiency syndrome (AIDS), autoimmune diseases and diabetes, coupled with stressful life styles. The literature abounds with reports of pathogenic potential of the Aspergillus species and the role of various predisposing factors on the susceptibility of host to these opportunistic fungal infections, demonstrated in experimental animals (Sidransky et al., 1965, Ford and Friedman, 1967, Sandhu et al., 1970, White, 1977, Thurston et al., 1979, Hassan and Selim, 1983, Chattopadhyay et al., 1994, Atasever et al., 2004, etc.). But todate not much work has been done on the pathogenic potential of Aspergillus isolated from processed and ready to eat milk product. This study was undertaken to study the pathogenicity of a strain of Aspergillus isolated from khoa and to observe that whether cortisone would alter the susceptibility of mice to the pathogen after the intraperitoneal administration of spores of Aspergillus spp.

Material and Methods

Aspergillus spp. was isolated from a khoa sample procured from a retail shop in Mhow. The fungus was tested for its pathogenicity in the immunocompromised host. Spore suspension for inoculation was prepared by growing the organism on Potato dextrose agar medium at 22oC until profuse sporulation had occurred, usually in 4 to 6 days. The spores were harvested by addition of sterile normal saline with 0.1% of Tween 80 and shaking with glass beads. Tween 80 was added to spore suspension to avoid their clumping. Large particles were allowed to sediment under gravity and the supernatant spore suspension was decanted. After counting in a hematocytometer chamber a definite number of spores were used for inoculation.

Swiss albino mice weighing about 18-20g, bred in the small animal house of Institute of animal health and biological products, Mhow, were purchased for the study. Treated mice received 5 mg hydrocortisone, subcutaneously for 2 days before the spores were injected. 5 x 106 number of spores were injected in mice via intraperitoneal route. Untreated control mice were injected with same number of spores via same route at the same time as the cortisone treated mice.

Mice with and without treatment by cortisone were also inoculated with spores previously heated at 103oC for 24 hours. Their non-viability was confirmed by failure to grow on potato dextrose agar medium.

The rooms and cages used for housing the animals were thoroughly cleaned time to time. The animals were reared under strict hygienic conditions during and before infecting them. All the animals were adjudged to be healthy. The animals were provided with food and water ad libitum. The animals were observed daily for any morbidity or mortality. The mice died were necropsied within a short time.


On intraperitoneal inoculation of spores of Aspergillus spp. in mice, the mortality was found in mice pretreated with hydrocortisone. Deaths occurred between three to ten days after exposure to spores of Aspergillus spp. Untreated or non - immunosuppressed mice were resistant to infection. On necropsy, lesions of visceral aspergillosis were observed. The parietal and serosal peritoneum appeared moist. Adhesions between visceral organs were found. Yellowish grey colour granulomas or abscesses were found in liver and kidneys. Heat killed spores produced no evident lesions in control or experimental mice.


Mice are normally resistant to infection with Aspergillus and other saprophytic fungi. Hence, they are suitable animals for testing the possible role of cortisone drug in reducing resistance (Sidransky and Friedman,1959).In choosing the immunosuppressive regimen, corticosteroids were selected because of their profound effect on macrophage function, immobilization of phagocytes, stabilizing their lysosomes, diminished phagocytosis, low antibody production or impairment of antigen-antibody interaction in accordance with Louria and Brown (1960), Weissmann (1964) and Spreadbury et al. (1989).

The result of this study, which reveal that the administration of cortisone enhances the susceptibility of mice to the spores of Aspergillus spp. Being injected intraperitoneally, are consistent with earlier reports of Sidransky et al. (1972). Also, in conformity with his observations on Aspergillus sp., the fungal infection in the cortisone treated mice was found confined to the liver and kidney. Cortisone treatment would seem to impair the defenses, which prevent conidial germination, and also presumably those defenses that remove the conidia, which germinate. It therefore appears that host defenses exist in these organs and are inhibited by the cortisone treatment.


1. Atasever, A., Uyanik, F., Cam, Y. and Gumussoy, K.S. (2004): Indian Vet. J., 81: 979.
2. Chattopadhyay, S.K., Vanamayya, P.R., Sharma, A.K., Meur, S.K., Sikdar, A. and Parihar, N.S. (1994): Indian Journal of Veterinary Pathology, 18: 125.
3. Ford, S. and friedman, L. (1967): Journal of Bacteriology, 94: 928.
4. Hassan, M.N. and Selim, S.A. (1983): Arch. Exper. Vet. Med., 5: S. 687.
5. Louria, D.B. and Browne, H.G. (1960): Annals of the New York Academy of Science, 89: 39.
6. Sandhu, D.K., Sandhu, R.S., Demodaran,V.N. and Randhawa, H.S. (1970): Sabouraudia, 8: 32.
7. Sidransky, H. and Friedman, L. (1959): Amer. J. Path., 35: 169.
8. Sidransky, H., Verney, E., and Pittsburgh, H.B.A. (1965): Arch. Path., 79: 299.
9. Sidransky, H., Epstein, S.M., Verney, E. and Horowitz, C. (1972): American Journal of Pathology, 69: 55.
10. Spreadbury, C.L., Krausz, T., Pervez, S. and Cohen, J. (1989): Journal of Medical and Veterinary Mycology, 27: 5.
11. Thurston, J.R., Cysewski, S.J., Richard, J.L. (1979): Am. J. Vet. Res., 40: 1443.
12. Weissmann, G. (1964): Lysosomes, 24: 594.

by : Chhabra, D.1 and Dhakad, N.K.2
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Avian Influenza infection in Human

Avian Influenza (“Flu”)

Avian influenza is an infectious disease of birds caused by type A strains of the influenza virus. The devastating form of influenza in chickens was recognized as a distinct disease entity as early as 1878 in Italy. The isolation of an avian influenza virus in 1901 preceded the discovery of mammalian and human influenza viruses, but it was not until 1955 that it was recognized that avian and mammalian influenza viruses are closely related.

Avian influenza A viruses - subtypes

Avian species can be infected by each of the 15 HA (Haemagglutinin) and nine NA (Neura-minidase) subtypes of influenza A viruses recognized up to now, in apparently any possible combinations. To date all outbreaks of the highly pathogenic form have been caused by influenza A viruses of subtypes H5 and H7. Highly pathogenic viruses possess a tell-tale genetic “trade mark” or signature - a distinctive set of basic amino acids in the cleavage site of the HA - that distinguishes them from all other avian influenza viruses and is associated with their exceptional virulence.

Natural Host and Reservoir

The reservoir of influenza A virus is in aquatic birds, especially ducks, shorebirds and gulls. Influenza A viruses appear well adapted to wild aquatic birds that are considered to be their natural hosts, and in which disease signs rarely appear. Considerable circumstantial evidence has long suggested that wild waterfowl introduce avian influenza viruses, in their low pathogenic form, to poultry flocks, but do not carry or directly spread highly pathogenic viruses. This role may, however, have changed very recently. The die-off of more than 6000 migratory birds, infected with the highly pathogenic H5N1 virus that began at the Qinghai Lake nature reserve in central China in late April 2005, was highly unusual and probably unprecedented. Prior to that event, wild bird deaths from highly pathogenic avian influenza viruses were rare, usually occurring as isolated cases found within the flight distance of a poultry outbreak.

Susceptible Host

The host range of influenza virus is generally unpredictable. Domestic poultry including chickens and turkeys are particularly susceptible to epidemics of rapidly fatal influenza. Influenza A viruses have been isolated from humans and from several other mammalian species. Domestic swine and Humans are now considered as mixing vessel since they are susceptible to infection with both avian and mammalian viruses, thus resulting in emergence of novel subtype.

Transmission among birds

Large amounts of virus are secreted in bird droppings, contaminating dust and soil. Airborne virus can spread the disease from bird to bird causing infection when the virus is inhaled. Contaminated equipments, vehicles, feed, cages or clothing-especially shoes can carry the virus from farm to farm. The virus can also be carried on the feets and bodies of animals, such as rodents, which act as “mechanical vectors” for spreading the disease. Direct or indirect contact of domestic flocks with wild migratory waterfowl has been implicated as a frequent cause of epidemics. Live bird markets have also played an important role in the spread of epidemics.

Disease in Birds

Infection causes a wide spectrum of symptoms in birds, ranging from mild illness to a highly contagious and rapidly fatal disease resulting in severe epidemics. The later is known as “highly pathogenic avian influenza” (HPAI). This form is characterized by sudden onset, severe illness and rapid death, with a mortality that can approach 100 percent. If the birds survive for more than 48 hrs, there is cessation of egg laying, respiratory distress, lacrimation, sinusitis, diarrhea, edema of the head, face and neck and cyanosis of unfeathered skin, particularly the comb and wattles. To date, all outbreaks of the highly pathogenic form of avian influenza have been caused by viruses of the H5 and H7 subtypes. Recent research has shown that H5 and H7 viruses of low pathogenicity can, after circulation for sometimes short periods in a poultry population, mutate into highly pathogenic viruses. Low pathogenic avian influenza (LPAI) viruses cause only mild disease or asymptomatic infection.

Flu and its significance to Humans

Influenza viruses are normally highly species-specific, meaning that viruses that infect an individual species (humans, certain species of birds, pigs, horses, and seals) stay “true” to that species, and only rarely spill over to cause infection in other species. Of the hundreds of strains of Avian influenza A viruses, only four are known to have caused human infections: H5N1, H7N3, H7N7, and H9N2. In general, human infection with these viruses has resulted in mild symptoms and very little severe illness, with one notable exception: the highly pathogenic H5N1 virus.

Scenario Before 1997

Despite the warnings to the poultry industry about these viruses, only influenza A H1N1, H2N2, H3N2 viruses have caused widespread respiratory illness in humans in the 20th century including pandemics in 1918, 1957 and 1968 heralding the emergence of each human subtype respectively.

The pandemics had its first recognizable wave in the spring of 1918, with descriptions of outbreaks in the United States, Europe and Asia by the end of April. Sequence and phylogenetic analysis of the completed 1918 gene segments suggest that the haemagglutinin and neuraminidase gene segments were derived from an avian influenza source but not directly. The HA and NA gene segments of the 1918 virus have acquired a number of changes from the avian consensus that suggests to us that the precursor to the pandemic strain spent some period of time, perhaps 5 to 10 year, adapting and evolving in a mammalian host.

In 1957, the Asian pandemic virus (H2N2) had acquired the HA, NA and PB1 gene from an avian virus, while in 1968, the Hong Kong pandemic strain (H3N2) had acquired the HA and PB1 gene from an avian source, retaining the NA from the preceding H2N2 subtype. The mechanism of emergence of subtypes in 1957 and 1968 (Reassortment of genes with avian influenza virus) is different from its first pandemic 1918.

Thus pandemic strains possessing novel HA derived from avian or animal influenza viruses, with or without other accompanying avian virus genes, sporadically emerge in humans and have the potential to cause a pandemic of influenza if the virus is capable of transmitting among a human population that lacks immunity to the novel HA. Indeed, reassortment viruses, harbouring a combination of avian and human viral genomes have been responsible for major pandemics of human influenza.

Mixing vessel

Swine have long been considered a likely mixing vessel in which avian and human viruses may reassort, since these animals possess respiratory epithelium that bear cell surface sialyloligosacharides that are preferentially recognized by avian (sialic acid (SA) a 2,3 galactose) and human influenza viruses (SA a 2, 6 galactose). Largely because of these differences in receptor specificity, avian influenza viruses were not considered to be able to directly infect humans and cause influenza like respiratory illness.

Scenario after 1997

However in the late 1990’s two subtypes of avian influenza emerged that caused respiratory infections in humans. In 1997, a high pathogenicity avian H5N1 influenza virus circulated among poultry on farms and in retail markets in Hong Kong. The H5N1 viruses were transmitted to humans, causing 18 documented cases of respiratory disease, including six deaths. In 1998-99, a second influenza A virus subtype, H9N2, was isolated from humans with respiratory disease.

This event established for the first time that these avian influenza viruses were to be considered a risk to public health. The relatively high rates of H5 and H9 antibody seroprevalence among Hong Kong poultry workers highlight the potential for avian viruses to transmit to humans, particularly those with occupational exposure. Such transmission increases the likelihood of reassortment between a currently circulating human virus and an avian virus and thus the creation of a strain with pandemic potential. All human cases have coincided with outbreaks of highly pathogenic H5N1 avian influenza in poultry.

All evidence to date indicates that close contact with dead or sick birds is the principal source of human infection with the H5N1 virus. Especially risky behaviours identified include the slaughtering, defeathering, butchering and preparation for consumption of infected birds. In a few cases, exposure to chicken faeces when children played in an area frequented by free-ranging poultry is thought to have been the source of infection. Faeces from infected ducks may have contaminated swimming in water bodies where the carcasses of dead infected birds have been discarded or which or other birds might be another source of exposure. In some cases, investigations have been unable to identify a plausible exposure source, suggesting that some as yet unknown environmental factor, involving contamination with the virus, may be implicated in a small number of cases.

Situation in India

The first outbreak of Avian Influenza occurred in domestic poultry on 18th February 2006 in Navalpur village in Maharashtra. Over 1.5 lakh birds were killed in Maharashtra and the loss was estimated at Rs.20 crore. The strain reported was H5N1.The reported outbreaks continued through April 2006.On 25th July 2007; an outbreak occurred in backyard poultry, the first report since April 2006 in Chingmeirong village, East Imphal District of Manipur. Samples tested at the High Security Animal Disease Laboratory in Bhopal and the National Institute of Virology in Pune confirm that the samples are positive for H5N1 strain of Avian Influenza.

The Ministry of Health and Family Welfare has informed WHO that no human cases of H5N1 infection have been detected to date. Tests conducted on samples taken from persons under investigation and their close contacts have yielded no positive results as of today.

In India, as in all countries experiencing their first outbreaks of highly pathogenic H5N1 avian influenza, WHO strongly recommends that patient samples be sent to WHO collaborating laboratory for diagnostic confirmation. Certainty about the status of human cases in a newly affected country is important for accurate risk assessment.

In addition, analyses conducted by WHO approved laboratories can yield information about the possible evolution of the virus and clues about how the virus may have arrived in the country. Genetic and antigenic studies of circulating viruses also help ensure that work on the development of a pandemic vaccine strays on track.


Outbreaks caused by the H5N1 strain are presently of the greatest concern for human health. In assessing risks to human health, it is important to know exactly which avian virus strains are causing the outbreaks in birds. All available evidence points to an increased risk of transmission to humans when outbreaks of highly pathogenic avian H5N1 influenza are widespread in poultry. There is mounting evidence that this strain has a unique capacity to jump the species barrier and cause severe disease, with high mortality, in humans. There is no evidence, to date that efficient human to human transmission of H5N1 strain has occurred and very often. Efficient transmission among humans is a key property of pandemic strains and a property that the avian H5N1 and H9N2 viruses apparently lacked. The biological and molecular basis for effective aerosol transmission among humans is not known. The virus can improve its transmissibility among humans via two principal mechanisms. The first is a “reassortment” event, in which genetic material is exchanged between human and avian viruses during co-infection of a human or pig. Reassortment could result in a fully transmissible pandemic virus, announced by a sudden surge of cases with explosive spread.

The second mechanism is a more gradual process of adaptive mutation, whereby the capability of the virus to bind to human cells increases during subsequent infections of humans. Adaptive mutation, expressed initially as small clusters of human cases with some evidence of human-to-human transmission, would probably give the world some time to take defensive action, if detected sufficiently early.

As the number of human infections grows, the risk increases that a new virus subtype could emerge, triggering an influenza pandemic. Humans as well as swine must now be considered a potential mixing vessel for the generation of such a virus. This link between widespread infection in poultry and increased risk of human infection is being demonstrated right now in Asia.

However, urgent control of all outbreaks of avian influenza in birds - even when caused by a strain of low pathogenicity - is of utmost importance. Research has shown that certain, avian influenza virus strains, usually of low pathogenicity can rapidly mutate (within 6 to 9 months) into a highly pathogenic strain if allowed to circulate in poultry populations. Altogether, more than half of the laboratory-confirmed cases have been fatal. H5N1 avian influenza in humans is still a rare disease, but a severe one that must be closely watched and studied, particularly because of the potential of this virus to evolve in ways that could start a pandemic. The challenge for all of us is to gain an under-standing of how just 10 or 11 proteins of these viruses to replicate and be transmitted not only bet-ween hosts of one species but also between species.


1. Katz, J.M., (2003):Avian Diseases 47: 914-920.
2. Kawaoka, Krauss, S., and Webster, R.G., (1989):Journal of Virology 63: 4603- 4608.
3. Li, K.S., Journal of Virology77(12): 6988- 6994.
4. Murphy, F.A., Gibbs, E.P.J., Horzinek, M.C., and Studdert, M.J., Veterinary Virology, 3rd Edition, Academic Press, New York: 466- 468.
5. Taubenberger, J.K., (2003): Avian Diseases 47:789-791.
6. Toshihiro Ito, J. Jour. of Virology 72(9): 7367- 7373.

by : Mohan. M1, Trevor Francis Fernandez2 and Feroz Mohammed.M.S.3
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Use of PVC sheet for Repair of fracture in Eagle


The fracture of wing is not so common condition in free-range birds. This may sometime occur because of trauma or accidents as wing bones are thin and brittle with large medullary canal (Bennett and Kuzma, 1992). It is very difficult to put bandage over such bones as it increases weight of the wings that disturbs the normal posture and balance of bird. The present paper deals with the efforts to decrease weight of bandage, at the same time given full rigidity and toughness using PVC sheet as plastering material.

History and Observation

An adult male eagle was presented at Pet clinic and care centre, Akola, with the history of trauma due to unknown cause and was unable to fly. Bird was restless and trying to fly but was not able to fly. After clinical observation, the case was diagnosed as a compound fracture of humerus bone of left wing. There was swelling of area due to blood clot. The skin was opened and piece of sharp ends of fractured bone could be seen. Hence it was decided to operate the bird using some new technique other than described elsewhere (Martin and Ritchie, 1994).

Surgical Treatment:

The feathers around the fractured area were plugged out. Local anaethesia at about 3-5 ml (2% procaine HCl) was infiltrated locally around the growth (Hoque, 2001). The area was washed and cleaned with normal saline and was painted with antiseptic. The fractured ends then aligned properly and kept in opposition. After putting cotton bandage, 2mm thick PVC sheet of size 4"×1" was made pliable by putting it in the hot water for2-4 min. for allowing proper fitting over bone. These two plates were tied over using sutured nylon (by passing through skin) and a knot was applied as three pairs. Then the wing was bandaged to restrict the movement of wing . Before applying bandage, the wound was powdered with antibiotic, ampicillin. On third day, the bandage was opened and the site was dressed with antiseptic and 50 % hydrogen peroxide (H2O2) and the powder was dusted around the stitches for next 10 gays. On removal of plates on 25th day, complete healing of the area was revealed and bird was able to fly.


1. Bennett, R.A. and Kuzma, A.B. (1992): Joul. Zoo wildl Med 23 (1): 5-23.
2. Hoque, M., Maith, S.K. Singh G. R. Arora, B. M. and Pratap, K.(2001): Intas Polivet. 2 (11): 266-267.
3. Martin, H. D. and Ritchie B.W. (1994). Orthopedic surgical techniques. In Ritchie BW, Harrison GJ, Harrison (eds.) Avian Medicine: Principles and application. Wingers Publishing, Inc. Lake Worth, FL pp1137-1169.

by : G. P. Manjulkar1, P. R. Zade2 and V. P. Pathak3
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A case report of Pigeon Pox-Histopathologic Diagnosis

Avian pox is a well-known disease in chickens, turkeys, pigeons, and canaries, and it has been identified in more than 60 wild bird species (Tripathy, 1991). Avian pox is a transmissible disease that is spread by several kinds of vectors: biting arthropods such as mosquitoes and mites, and aerosols generated from infected birds, or the ingestion of contaminated food or water. The disease has two forms: cutaneous and diphtheritic. Pigeon pox is a slowly developing disease resulting in morbidity and mortality among all age groups and sexes. The disease may be complicated with parasitism or poor condition of the flock. A case of cutaneous form of pigeon pox is presented.

Case History and Discussion

During March 2006, two local breed of pigeons were brought by local people to the dispensary with the history that they were found dead and lying along the roadside. On examination, they were found to be dehydrated and emaciated in nature. Several 0.5-1 cm diameter coalescing, round, yellowish, rough and firm masses were found at the eyelids, beak, and the mouth, and some were superficially ulcerated. Diphtheritic lesions were not found in birds. Histologic sections of skin containing the nodular lesions had cords and large clusters of markedly hypertrophic and hyperplastic epidermal stratified squamous epithelium, surrounded by dense fibroblastic stroma. Lesions consisted of swollen and pale keratinocytes with a foamy, vacuolated cytoplasm and single, round, dense eosinophilic intracytoplasmic viral inclusions (identified as Bollinger bodies). Inclusions distended the cell cytoplasm, producing cell necrosis. Some of them had clear, unstained, central rounded spaces. The superficial epidermis of the lesions was ulcerated with eosinophilic, amorphous keratinaceous crusts and necrosis.

On the basis of necropsy results, histopathologic features, and the presence of viral intracytoplasmic inclusions in epidermal cells, a diagnosis of poxvirus infection was made. In some cases, the diagnosis of a pox virus infection can be suspected by external clinical examination and gross lesions (Heuschele, 1986), but it is necessary to confirm the disease in the cutaneous form by the presence of characteristic Bollinger bodies in epithelial cells of epidermis observed in histopathologic analysis, by electron microscopy for viral particles in epidermal cells, or by virus isolation (Heuschele, 1986 and Randall and Reece, 1996). In this bird, gross lesions were compatible with an avian pox diagnosis, and this fact was confirmed by the histopathologic analysis performed on bird. An outbreak of pigeon pox involving eight local golla breed of pigeons in rural areas of Bareilly district was reported. Deaths in a few cases was recorded which might have been aided by heavy parasite load (Rajendra Singh et al., 1990).

Mortality and morbidity due to poxvirus infection may be very high in pigeons (Tripathy, 1991). Nevertheless, Pox virus is not fatal in all infected individuals, but it can reduce viability and predispose affected birds to predation, secondary infection, and accident (Reece, 1989). Thus Pox virus infection was an important, if not the direct, cause of death in bird.

by : M. Mohan and Trevor Francis Fernandez
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A new Polyherbal formulation to control bacterial enteritis in poultry: a case study in Salmonella enteritidis induced experimental model

by: K.K.Baishya, Shivi Maini and K.Ravikanth

1) Veterinary Officer, Kashipur, Uttaranchal, India.
2) Scientist, Ayurvet Limited, Vill. Katha, P.O.Baddi, Dist. Solan (H.P.), India.


An experiemental study was conducted in day old 150 VenCobb chicks to evaluate efficacy of polyherbal formulation in induced bacterial enteritis with Salmonella enteritidis.
Birds were randomly divided into three groups: negative control, infected and untreated control & prophylactically treated group with AV/ADC/16 (14th-28th days). Salmonella infection was induced on day 21st. A significant decrease in overall growth, productivity, feed conversion and mortality was evident in untreated infected group in addition to severity of clinical signs. However, prophylactic administration of herbal formulation reduced mortality and clinical symptoms were mild to negligible. No negative effect on growth & performance was observed in treated group III.

Keywords: enteritis, polyherbal, antidiarrhoeal, performance.

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Epidemiological studies (parasitological, serological and molecular techniques) of Trypanosoma evansi infection in camels

Epidemiological studies (parasitological, serological and molecular techniques) of Trypanosoma evansi infection in camels (Camelus dromedarius) in Egypt

Ahmed Abdel-Rady

Department of Animal Medicine, Infectious diseases,
Faculty of Veterinary Medicine, Assiut University, Assiut, Egypt


Trypanosomosis in camel caused by Trypanosoma evansi is still a serious problem in camel husbandry causes considerable economic losses in many camel-rearing regions of the world. In the present study 193 camels clinically suspected for surra were examined parasitologically by Giemsa stained blood smear (GSBS) and haematocrit centrifugation technique, serologically for detection of anti-trypanosomal antibodies by card agglutination test for trypanosomes (CATT), and for DNA amplification, by Polymerase chain reaction (PCR), with primers yielding a 177 bp PCR product for the specific detection of Trypanozoon parasites. Out of 193, eight camels were positive by GSBS (4.1%) while 12 were positive with haematocrit centrifugation technique (6.2%). Detection of anti-trypanosomal antibodies with CATT yielded 84 positive samples (43.5%). Using PCR 110 out of 193 were positive (56.9 %). PCR technique is accurate, more sensitive and specific method for diagnosis of trypanosome infected camels than parasitological techniques; it overcomes the problem of specificity and can detect low parasitemic camels in chronic cases. The PCR proved to be the best test used for detection of camel trypanosomosis in Egypt.

Keywords: Camels, Trypanosomosis, Stained Blood smear, Haematocrit centrifugation technique (HCT), Card agglutination test (CATT), Polymerase chain reaction (PCR)


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Monday, November 3, 2008

Studies on potential fowl cholera vaccine

The avian disease fowl cholera has consistently plagued the poultry industry for many years and has led to excessive monetary losses. Although better management of layer birds and use of inactivated and live vaccines have been in place, fowl cholera remains an inadequately controlled problem. In fact, the use of some of the current vaccines has resulted in fowl cholera outbreaks within the flock. Thus, the poultry industry has a need for a safe, rationally attenuated vaccine against fowl cholera. Therefore a study was initiated with the main objective, in the short-term, to further the development of a rationally attenuated live vaccine against fowl cholera using the P. multocida X-73 mutant in which the genes pnhA and pnhB have been inactivated.
Preliminary studies suggest that X-73 mutant was attenuated for virulence. The recombinant pnhA protein from P. multocida (strain X-73) was successfully isolated and purified. Biochemical and enzymatic studies of the purified pnhA confirmed that this protein was a Nudix hydrolase, more specifically, classified as a dinucleoside oligophosphate pyrophosphatase.
pnhA has properties very similar to other dinucleoside oligophosphate pyrophosphatase, and the preferred substrate target for the enzyme is diadenosine pentaphosphate.
Further studies of the complemented X-73 mutant using the chicken embryo-lethatlity assay showed an incomplete restoration of virulence. The complemented X-73 mutant contains a functional pnhA gene, but an inactivated pnhB gene. From our studies it was assumed that a functional pnhB gene was necessary to restore virulence within the mutant and that the function of pnhA in pathogenesis requires a functional pnhB protein.
Due to unforeseen problems with the stability of the X-73 mutant, bird trials and thus vaccine assessment was not performed in this study.
The pnhA protein is the first Nudix hydrolase identified within the Pasteurellaceae family. Nudix hydrolases have been shown to play a role in the pathogenesis of other bacterial pathogens. The X-73 mutant has potential as a trial vaccine, which may control fowl cholera, but further work beyond the extent of this project is needed to further develop the X-73 mutant.
Vaccine development for this disease is important because the disease has been controlled by the use of antibiotics which are costly and P. multocida has the potential to become resistant to the antibiotics in use.

Source: Carmel Ruffolo, Ph.D., Department of Biological Science, University of Wisconsin-Parkside, Kenosha, WI, USA.

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