Biomedical subjects

A M Fadly

Publications and source records attributed to A M Fadly.

At least 55 records · Page 3Linked to original sources

PubMed1975

Antigenic characterization of the inclusion body hepatitis virus.

Proof that inclusion body hepatitis of chickens (IBHC) is caused by a virus (IBHV) was established in 1973. Characterization of IBHV has been conducted by employing the standard criteria for virus classification. The results have indicated that IBHV is a member of the avian adenovirus group. However, no antigenic relationship was found between IBHV and two other avian adenovirus isolates (CELO and Indiana C) as observed by hemagglutination (HA) and virus-serum neutralization tests. Another adenovirus isolate was found to be serologically different from IBHV (Tipton strain) but it incited typical IBHC in susceptible chicks. A novel antigen, detectable by the agar gel immunodiffusion test, was demonstrated in livers from chicks infected experimentally with IBHV. This antigen was able to give a specific precipitin reaction with serums from chickens previously exposed to IBHV. Repeated embryo passage of IBHV lowered its pathogenicity for susceptible chickens. Protection of chickens against IBHV challenge was obtained by vaccination with high embryo passage IBHV (Tipton strain). It was also found that subcutaneous administration of the vaccine virus induced a better immune response than the eye-drop route as observed by the virus-serum neutralization index obtained.

Adenoviridae↗

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High virus titer in feather pulp of chickens infected with subgroup J avian leukosis virus.

Subgroup J avian leukosis viruses (ALVs), which are a recombinant virus between exogenous and endogenous ALVs, can spread by either vertical or horizontal transmission. Exogenous and endogenous ALVs can be detected in feather pulp. In this study, virus titers in feather pulp of chickens infected with subgroup J ALV were compared with those of plasma and cloacal swab. All of the broiler chickens inoculated with subgroup J ALV at 1 day old were positive for virus from feather pulp during the experimental period of between 2 wk and 8 wk of age. Virus titers in feather pulp of some broiler chickens infected with subgroup J ALV were very high, ranging from 10(7) to 10(8) infective units per 0.2 ml. Virus titers in feather pulp were usually the highest among the samples of plasma, cloacal swab, and feather pulp tested. In another experiment in which layer chickens were inoculated with subgroup J ALV at 1 day old, virus was detected in feather pulp from 2 wk until 18 wk of age, and virus persisted longer in feather pulp than in plasma. Almost all of the layer chickens tested were positive for virus by polymerase chain reaction (PCR) with DNA extracted from feather pulp samples at 2, 4, and 10 wk of age, and the PCR from feather pulp was more sensitive than virus isolation from plasma, cloacal swab, and feather pulp. All above results indicate that samples of feather pulp can be useful for virus isolation and PCR to confirm subgroup J ALV infection.

Animals↗

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Isolation and some characteristics of a subgroup J-like avian leukosis virus associated with myeloid leukosis in meat-type chickens in the United States.

Several subgroup J-like avian leukosis viruses (ALV-Js) were isolated from broiler breeder (BB) and commercial broiler flocks experiencing myeloid leukosis (ML) at 4 wk of age or older. In all cases, diagnosis of ML was based on the presence of typical gross and microscopic lesions in affected tissues. The isolates were classified as ALV-J by 1) their ability to propagate in chicken embryo fibroblasts (CEF) that are resistant to avian leukosis virus (ALV) subgroups A and E (C/AE) and 2) positive reaction in a polymerase chain reaction with primers specific for ALV-J. The prototype strain of these isolates, an isolate termed ADOL-Hc1, was obtained from an adult BB flock that had a history of ML. The ADOL-Hc1 was isolated and propagated on C/AE CEF and was distinct antigenically from ALV of subgroups A, B, C, D, and E, as determined by virus neutralization tests. Antibody to ADOL-Hc1 neutralized strain HPRS-103, the prototype of ALV-J isolated from meat-type chickens in the United Kingdom, but antibody to HPRS-103 did not neutralize strain ADOL-Hc1. On the basis of both viremia and antibody, prevalence of ALV-J infection in affected flocks was as high as 87%. Viremia in day-old chicks of three different hatches from a BB flock naturally infected with ALV-J varied from 4% to 25%; in two of the three hatches, 100% of chicks that tested negative for virus at hatch had evidence of viremia by 8 wk of age. The data document the isolation of ALV-J from meat-type chickens experiencing ML as young as 4 wk of age. The data also suggest that strain ADOL-Hc1 is antigenically related, but not identical, to strain HPRS-103 and that contact transmission of ALV-J is efficient and can lead to tolerant infection.

Animals↗

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Avian leukosis virus subgroup J infection profiles in broiler breeder chickens: association with virus transmission to progeny.

Profiles of infection with avian leukosis virus subgroup J (ALV-J) and factors that predict virus transmission to progeny were studied. Eggs from an infected broiler breeder flock were hatched at the laboratory. The flock was reared in a floor pen, transferred to laying cages at 22 wk, and inseminated to produce fertile eggs. A cohort of 139 chickens was tested at frequent intervals over a 62-wk period for virus, viral antigens, or antibodies in plasma, cloacal swabs, egg albumen, and embryos. Virus was detected in 7% of chicks at hatch but spread rapidly so that virtually all chicks became infected between 2 and 8 wk of age. Mortality due to myeloid leukosis and related tumors was 22%. Over 40% of the chicks developed persistent infections, whereas the remainder experienced transient infections. Five types of infection profiles were recognized. Novel responses included hens that were positive for virus intermittently or started late in life to shed viral antigens into the cloaca. ALV-J was isolated from 6% of 1036 embryos evaluated between 26 and 62 wk. However, over 90% of the virus-positive embryos were produced between 29 and 34 wk of age. Of 80 hens that produced embryos, 21 produced at least one infected embryo and were identified as transmitters. All but one transmitter hen would have been detected by a combination of viremia, cloacal swab, and albumen tests conducted between 18 and 26 wk. However, virus was transmitted to embryos from hens that were not persistently viremic or that rarely shed viral group-specific antigen into the albumen of their eggs. Intermittent patterns of both antigen shedding and virus transmission to embryos were observed in some hens. These results validate current screening procedures to identify potential transmitter hens and provide some suggestions for improvement but also show that identification of all transmitter hens by such procedures is unlikely. Thus, eradication programs based solely on dam testing may be less effective than those where dam testing is combined with procedures to mitigate early horizontal transmission in progeny chicks.

Animals↗

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Response of B congenic chickens to infection with infectious bursal disease virus.

Six congenic lines of chickens that differ from the parental inbred line RPRL-15I5 for genes in the major histocompatibility (B) complex were used to study the influence of the B haplotypes on the response of chickens to infection with virulent infectious bursal disease virus (IBDV) at 1 day or 4 weeks of age, and on the antibody response to vaccination with live or inactivated oil-emulsion (OE) IBDV vaccines at 7 weeks of age. IBDV-induced immunodepression and lesions in the bursa, spleen, and thymus in chickens infected with virus at 1 day of age were of the same degree of severity, regardless of line of chickens used. The response of blood cells to the mitogens phytohemagglutinin-M and concanavalin A was elevated in chickens infected with IBDV at 1 day of age. In an experiment conducted to study the effect of the B haplotype on IBDV infection in 4-week-old chickens, B congenic line C-12 (B12B12) showed the highest susceptibility to clinical IBD, with mortality of 79%. No detectable difference in the serological response to vaccination with live or OE IBDV vaccines was noted among chickens of various congenic lines. We conclude that the B haplotypes may influence IBDV-induced mortality, but not immunodepression or severity of lesions in lymphoid organs, or the antibody response to live or OE IBDV vaccines.

Animals↗

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Influence of maternal antibody on avian leukosis virus infection in White Leghorn chickens harboring endogenous virus-21 (EV21).

Slow-feathering (SF) white leghorn dams harboring the endogenous viral gene ev21, which encodes for complete endogenous virus-21 (EV21), and rapid-feathering (RF) dams lacking EV21 were immunized with a live field strain of avian leukosis virus (ALV) subgroup A. One group of SF dams and one group of RF dams were not immunized and were maintained to produce chicks lacking maternal ALV antibody. When the SF dams were crossed with line 15B1 males, the resulting male progeny were SF, EV21-positive, and the females were RF, lacking EV21 or congenitally infected with EV21. EV21-positive and -negative progeny of immunized and unimmunized SF and RF dams were exposed to ALV at hatching. Viremia, antibody development, cloacal shedding, and tumors in chickens lacking EV21 were compared with those in chickens with EV21. Congenital transmission of EV21 from SF dams to RF female chicks was significantly higher in immunized dams than in unimmunized dams. Maternal ALV antibody delayed infection with ALV and reduced viremia and cloacal shedding of virus in progeny. The effect of maternal antibody on ALV infection was much more pronounced in progeny lacking EV21 than in progeny harboring EV21. The data suggest that the development of ALV infection and tumors may be influenced by status of infection with EV21 and by the immune status of dams.

Animals↗

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The oncogenic potential of some avian adenoviruses causing diseases in chickens.

The oncogenic potentials of three different strains of avian adenoviruses (the Tipton strain of the inclusion body hepatitis virus, the DPI-2, and the Indiana C viruses) were investigated in newborn hamsters. Animal inoculations were via two routes, subcutaneous and intracerebral. All three viruses proved nononcogenic for the hamsters observed over a period of 225 days. However, lesions of hepatitis similar to those of inclusion body hepatitis of chickens were seen in three hamsters inoculated with the DPI-2 virus.

Adenoviridae↗

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Immunity to infectious bronchitis virus from spray vaccination with derivatives of a Holland strain.

Study was made of the protection of chickens from spray vaccination with different modifications of a Holland (H) strain of infectious bronchitis virus (IBV). Noted in each trial were the virus-serum-neutralizing antibody titers induced and the virulence of the vaccine virus at different passage levels. Protection against respiratory signs was good from challenge with a homologous virus serotype as well as with 5 heterologous IBV isolates. This occurred from vaccinating day-old chicks possessing homologous IBV antibodies as well as vaccinating susceptible 4-week-old chickens. The tracheal virus shed-rate following challenge was considered low (20% or less) with 4 of the challenge viruses. The challenge virus shed-rate was somewhat higher from vaccination at one day old than from vaccination at 4 weeks; the virus-serum-neutralization titers were lower, or even insignificant, with early-age vaccination. The immunogenicity and virulence of the vaccine virus was apparently reduced in the higher embryo passages employed. None of the vaccine derivatives was considered virulent under these conditions.

Aerosols↗

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Vaccination and revaccination with a Holland (H) strain of infectious bronchitis virus.

One-day-old chickens possessing maternally derived immunity to Massachusetts-type infectious bronchitis virus (IBV) were vaccinated by the eyedrop route with a Holland (H) IBV strain of the Massachusetts type. Vaccination was done with the 72nd and 92nd passages in chicken embryos. Attenuation of the virus was done in the authors' laboratory. Four weeks postvaccination the immunity was challenged with 8 different IBV serotypes. A broad spectrum of protection from respiratory signs was obtained in each of the challenged groups (compared with unvaccinated controls). With 5 of the challenge viruses, protection against tracheal virus shed was good (70% or greater). Revaccination at 4 weeks old by the aerosol route with the 53rd and 72nd passages did not greatly enhance protection. However, the virus-serum-neutralizing (VN) titers with Massachusetts-type IBV as an indicator were high, and an anamnestic response was demonstrated at 8 weeks of age. The VN titers observed at 4 weeks old were generally low and did not correlate necessarily with the protection engendered.

Aerosols↗

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Role of the bursa of Fabricius in the pathogenicity of inclusion body hepatitis and infectious bursal disease viruses.

Chickens were chemically bursectomized with cyclophosphamide at 3 days old, and studies made of the effects of infection by inclusion body hepatitis virus (IBHV) and infectious bursal disease virus. In another experiment, 3-week-old chickens were infected with infectious bursal disease virus before inoculation with IBHV. Interference with the bursa of Fabricius by cyclophosphamide or by infectious bursal disease virus enhanced the pathogenicity of IBHV. In contrast, cyclophosphamide effects on the bursa protected chickens against infectious bursal disease.

Animals↗

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Low incidence of lymphoid tumors in chickens continuously producing endogenous virus.

A flock of 258 male and 243 female chickens of a cross of Regional Poultry Research Laboratory lines 15B and 7(2) were kept in a filtered-air positive-pressure house and observed for tumors from 100 to more than 729 days of age. These birds produced high titers of a subgroup E endogenous virus from the middle of the embryonic incubation period through the end of the experiment. No neoplasms were observed in the males. The females had two neoplasms indistinguishable from lymphoid leukosis and three other neoplasms not involving lymphoid cells. No evidence was found of infection with exogenous lymphoid leukosis viruses, Marek's disease virus, reticuloendotheliosis virus, or adenovirus (isolated on the isolation farm). Inoculation of another sample of this cross with a lymphoid leukosis virus of subgroup A resulted in 88% mortality with neoplasms (mostly lymphoid leukosis) by 167 days of age. The conclusion is that high levels of spontaneously produced endogenous virus do not induce high levels of neoplasms in chickens susceptible to lymphoid leukosis.

Alpharetrovirus↗

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Hemorrhagic enteritis of turkeys: influence of maternal antibody and age at exposure.

The effect of maternal antibody (MAB) to hemorrhagic enteritis (HE) on the response of turkeys to infection with virulent and avirulent strains of HE virus (HEV) was examined. The influence of age at exposure and treatment with HEV antibody on development of clinical HE also was studied. MAB protected poults from clinical HE for up to 6 weeks of age. MAB also interfered with vaccination against the disease for at least 5 weeks after hatching, as indicated by absence of HEV antigen in spleens and by poor seroconversion at 6 days and at 3 weeks post-vaccination, respectively. The incidence of clinical HE in MAB-negative poults was significantly higher in poults inoculated with virus at 15 days of age or older than in poults inoculated at 1-13 days of age. Further, MAB-negative poults embryonally inoculated with virulent or avirulent strains of HEV did not develop disease; these poults developed antibody and resisted challenge with virulent virus at 6 weeks of age. Poults treated with HE antibody within 1 hour of challenge or at 1, 3, or 5 weeks before challenge with virulent virus were protected against lesions and mortality induced by HEV. These results suggest that MAB may influence susceptibility of turkeys to infection with HEV for at least 5 to 6 weeks after hatching, unlike the case with most other viral infections of poultry. The results confirm that early age resistance to clinical HE is independent of MAB and suggest that such resistance persists for up to 13 days of age. The data also suggest that turkeys lacking MAB can be immunized against HE by embryo vaccination.

Age Factors↗

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Effect of bursal cell number on the pathogenesis of infectious bursal disease in chickens.

The pathogenesis of infectious bursal disease (IBD) in chickens neonatally chemically bursectomized (CB) by cyclophosphamide and subsequently inoculated with various numbers of bursal cells was examined. CB chickens inoculated with at least 62.5 X 10(6) bursal cells were as susceptible to IBD clinical manifestations (as determined by gross and microscopic evaluation of bursal tissues, virus recovery from spleen, and antibody titer) as intact chickens following inoculation with virus at 5 weeks of age. In contrast, CB chickens inoculated with 2.5 X 10(6) or fewer bursal cells were refractory to the IBD clinical manifestations compared with intact chickens or CB chickens inoculated with 62.5 X 10(6) or more bursal cells. Results from this study suggest that the availability of a large number of bursal cells is an essential factor in the development of IBD.

Animals↗

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Avian leukosis virus (ALV) infection, shedding, and tumors in maternal ALV antibody-positive and -negative chickens exposed to virus at hatching.

Chickens highly susceptible to avian leukosis virus (ALV) infection and tumors, with and without ALV subgroup A maternal antibody (MAB), were infected with a field strain of ALV subgroup A at hatching. Viremia, antibody development, cloacal and albumen shedding, and tumors in chickens with MAB (MAB+) were compared with those in chickens lacking MAB (MAB-). At 18 weeks of age, the incidence of viremia was significantly lower in MAB+ chickens than in MAB- chickens; further, MAB significantly reduced the proportion of tolerantly infected (viremic antibody-negative) chickens. Cloacal shedding of ALV at 22 weeks of age and shedding of ALV group-specific (gs) antigen in albumen of eggs from all laying hens at 30-32 weeks of age were significantly lower in MAB+ hens than in MAB- hens. The incidence of ALV-induced tumors was lower in MAB+ chickens than in MAB- chickens, significantly so in one of three trials conducted. These results suggest that MAB may influence the development of viremia, antibody, and shedding of ALV following massive exposure to virus at hatching.

Animals↗

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Some observations on the response of ring-necked pheasants to inoculation with various strains of cell-culture-propagated type II avian adenovirus.

The response of ring-necked pheasants to inoculation with three strains of cell-culture-propagated type II avian adenovirus was examined. Marble spleen disease (MSD) virus of pheasants and both avirulent and virulent strains of hemorrhagic enteritis virus (HEV) of turkeys all induced typical gross and microscopic splenic lesions of MSD; neither MSD-associated lung lesions nor mortality were noted in inoculated pheasants, regardless of strain of virus used. Pheasants inoculated with a cell-culture-propagated avirulent strain of HEV were properly immunized against challenge with virulent HEV, as indicated by seroconversion and by protection against virus-induced splenic lesions. We conclude that these strains of type II avian adenovirus are comparable in pathogenicity for pheasants and cannot be distinguished. Further, absence of MSD-associated lung lesions and mortality in pheasants maintained under controlled laboratory conditions suggest that other environmental factors are probably involved in induction of such lesions and mortality in field cases of MSD.

Adenoviridae↗

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Effects of chemically or virus-induced immunodepression on response of chickens to avian leukosis virus.

The effects of chemically or virus-induced immunodepression on the infection profile (development of viremia and antibody) and shedding of avian leukosis virus (ALV) were studied in progeny chickens of experimental or commercial breeder flocks. Chickens were infected with ALV subgroup A by contact at hatching and by oral inoculation at 4-5 weeks of age. In the first experiment, chickens were inoculated with a virulent strain of infectious bursal disease virus (IBDV) at 1 day or 6 weeks of age. In the second experiment, chickens were neonatally treated with cyclophosphamide (CY), or were inoculated with strain T of reticuloendotheliosis virus (REV) at hatching, or were inoculated with strain JM of Marek's disease virus (MDV) at 2 weeks of age. The infection profile and cloacal shedding of ALV in chickens exposed to ALV and inoculated with immunodepressive viruses or CY were compared with those in hatchmates exposed only to ALV. In two of four chicken lines tested in the first experiment, shedding of ALV, as determined by virological assays of cloacal swabs at 22 weeks of age, was significantly higher in chickens infected with IBDV at 1 day of age than in uninfected hatchmates. The rate of shedding of ALV in one of these two lines was also significantly higher in chickens infected with IBDV at 6 weeks of age than in uninfected chickens. Further, the frequency of ALV-antibody detection at 22 weeks of age was significantly lower in chickens of these two lines infected with IBDV at 1 day of age than in uninfected chickens. In the second experiment, neonatal treatment with CY significantly increased the frequency of viremic chickens of both experimental and commercial flocks. The frequency of ALV-viremic chickens at 22 weeks of age was considerably higher in the REV- and MDV-inoculated groups (54% and 44%, respectively) than in control hatchmates (29%), but only in chickens of the commercial line. These findings suggest that chemically or virus-induced immunodepression may lead to an increase in rates of viremia and shedding of ALV in chickens infected with virus after hatching, especially in certain genetic lines.

Animals↗

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Observations on an enzyme-linked immunosorbent assay for the detection of antibodies against avian leukosis-sarcoma viruses.

In the detection of antibodies against exogenous subgroup A avian leukosis viruses (ALVs) using a representative subgroup A virus, concordance between enzyme-linked immunosorbent assays (ELISAs) and serum neutralizations ranged from 83 to 95%. In ELISAs, subgroup A- and subgroup B-specific neutralizing antisera were equally reactive against ALVs of subgroups A, B, and E. Conversely, little cross-reactivity of high-titered subgroup E antisera was observed against subgroup A viruses. Significant cross-reactivities of spontaneously induced subgroup E-neutralizing antisera were observed when tested against a representative subgroup B ALV. Because some normal chickens spontaneously mount antibodies against infectious endogenous viruses, misleading results may be obtained if subgroup B or E ALVs are the source of target antigens in ELISAs.

Alpharetrovirus↗

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Further studies on in vitro and in vivo assays of hemorrhagic enteritis virus (HEV).

Isolation of hemorrhagic enteritis virus (HEV) from spleens of infected turkeys in the MDTC-RP19 lymphoblastoid cell line was compared with detection of HEV antigen in the same spleens using the agar gel precipitation (AGP) test. A concordance of 80% was found between the two assays. Virus isolation had a sensitivity of 84% and a specificity of 88% compared with the AGP test. RP19 cells were also susceptible to infection with several other avian adenoviruses, but such infection was easily differentiated from that of HEV by a fluorescent-antibody (FA) test. Turkeys required 10(2) tissue-culture-infectious doses (TCID) to develop HE-specific lesions and 10(5) TCID to be killed. On the other hand, as little as 10 TCID of apathogenic HEV protected the poults against challenge with virulent HEV. The enzyme-linked immunosorbent assay (ELISA) for detection of HEV antibody was improved by using virus-infected RP19 cells as antigen. The ELISA appears to be more sensitive than the serum-neutralization test.

Animals↗