Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DISEASE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1994

Trinucleotide repeats in neurologic diseases: an hypothesis concerning the pathogenesis of Huntington's disease, Kennedy's disease, and spinocerebellar ataxia type I.

Three neurodegenerative diseases, Huntington's disease (HD), Kennedy's disease (hereditary spinobulbar muscular atrophy, SBMA), and type 1 spinocerebellar ataxia (SCA-1) have been found to share a common genetic defect: an unstable region of repeated CAG trinucleotides which are thought to be translated into a polyglutamine moiety. The unstable repeat regions occur near the N-termini of the predicted proteins for HD and SBMA, but the location of the CAG repeat region is not known for SCA-1. Each disease is notable for a relatively circumscribed region of central nervous system pathology, and the lack of predicted similarity of the abnormal proteins makes a common mechanism related to the function of each protein unlikely. In order to reconcile the similar genetic abnormalities with the disparities in phenotypes, we suggest a common thread with regard to the pathogenesis of neuronal death. We hypothesize that the mechanism of neurotoxicity in these diseases occurs not through the production of abnormal proteins, but by the generation of abnormal posttranslational cleavage products. These products, in part consisting of abnormally large polyglutamine moieties, act to disturb the cellular and mitochondrial milieu such that energy metabolism is impaired, rendering specific regions of the nervous system vulnerable, and resulting in the clinical phenotypes of HD, SBMA, and SCA-1. We offer this interpretation of recent genetic findings from a neurobiologic perspective, in addition to suggesting testable hypotheses concerning potential disease mechanisms.

Base Sequence↗
PubMed1999

Mammary Paget's disease: evidence of diverse origin of the disease with a subgroup of Paget's disease developing from the superficial portion of lactiferous duct and a discontinuous pattern of tumor spread.

The pattern of spread of intraductal carcinoma associated with mammary Paget's disease has not been well studied. The purpose of this study was to examine the site of origin and the pattern of tumor spread with a three-dimensional view by serial sectioning of the tissue blocks from 19 cases of Paget's disease. Intraductal carcinoma in the superficial portion of the lactiferous ducts was seen in continuity with the overlying epidermis with Paget's disease in all 19 cases. In seven cases that had adequate tissue sampling, five showed a continuous pattern of the intraductal carcinoma within the superficial as well as the deep breast tissue. In the remaining two cases, a portion of benign duct was identified between the intraductal carcinoma in the superficial lactiferous duct and the deep breast tissue. This discontinuous pattern of spread of the intraductal carcinoma was also identified in the foci of carcinoma in deep tissue. In the five cases in which the tumor involved the skin and only the superficial portions of the lactiferous duct, the leading edge of the intraductal carcinoma was seen orientated in the direction of the nipple towards the deep breast tissue. Our study of Paget's disease demonstrated that in addition to tumor spread along the lactiferous ducts from intraductal carcinoma in the deep tissue towards the nipple, there was a group of Paget's disease arising from the nipple. These lesions included: (i) lesions limited to the areolar tissue; and (ii) lesions with intraductal carcinoma involving the duct system in both superficial and deep breast tissue with and, possibly, without skip areas pattern of spread. Although certain cases of Paget's disease may appear superficial, an independent associated carcinoma in deep breast tissue has to be ruled out.

Breast Neoplasms↗
PubMed1995

Desmosomal dissolution in Grover's disease, Hailey-Hailey's disease and Darier's disease.

Proteins involved in the formation of desmosomes and simpler adherens junctions were studied in three types of non-immune acantholytic diseases; specifically, four cases of Grover's disease (GD), one case of Hailey-Hailey's disease (HHD) and one case of Darier's disease (DD), and these were compared to two cases of immune-mediated acantholytic disease pemphigus vulgaris (PV). The proteins studied included: 1. The intracellular desmosomal proteins, desmoplakin I and II and plakoglobin; 2. The intercellular desmosomal proteins, desmoglein and CD44; and 3. vinculin, which is a major intracellular protein of the simpler aherens junctions. In GD, HHD and DD, immunostaining showed a loss of desmoplakin I and II and plakoglobin from the desmosomes, and a diffuse staining in the cytoplasm. In contrast, in pemphigus vulgaris, these proteins seemed intact and were localized to dot-like spots on the cell surface. Also, desmoglein, and CD44 were slightly affected in GD, and moderately affected in HHD and DD. Absence of desmosomal attachment plaques, the lack of labeling with desmoglein in the affected desmosomes and a diffusion of the labels into cytoplasm were demonstrated with electron microscopy using an immunogold technique. In PV, desmoglein III is one of the target antigens for the autoantibodies in this disease and was only partially preserved in a small number of lesional cells, while CD44 was mostly preserved. Vinculin was intact in GD, HHD and DD, but was lost in PV. This study, our previous work, and that of others, suggest that: 1. In GD, HHD and DD, the proteins of the desmosomal attachment plaque are primarily affected; 2. In PV, the intercellular glycoproteins are primarily involved; and 3. Simple adherens junctions are intact in GD, HHD and DD, but are damaged in PV.

Acantholysis↗
PubMed1999

Economic impact of Alzheimer's disease in the United Kingdom. Cost of care and disease severity for non-institutionalised patients with Alzheimer's disease.

BACKGROUND: While the costs associated with Alzheimer's disease have been shown to be significant, there are few data relating cost of care to severity of the disease. AIMS: We aimed to compare the costs associated with different severities of Alzheimer's disease with those incurred by control subjects over a three-month period. METHOD: In this cross-sectional, multicentre, naturalistic analysis, non-institutionalised patients with Alzheimer's disease (128), their care-givers (128), and 56 matched controls were interviewed once to establish resource use over the previous three months. Patients were stratified into three severity groups according to their Mini Mental State Examination score. Costs were calculated from the perspective of society as a whole. RESULTS: Over the three-month period, total mean cost per control subject (387 Pounds) was minor compared with mean cost incurred by patients with mild (6616 Pounds), moderate (10,250 Pounds) and severe (13,593 Pounds) Alzheimer's disease. Indirect cost, mainly time spent by care-givers, was the main cost component in all groups (68.6%), followed by direct medical costs (24.7%). CONCLUSIONS: The cost of care for an Alzheimer's disease patient is directly related to the severity of the patients illness.

Aged↗
PubMed1998

Risk factors and cardiovascular diseases associated with asymptomatic peripheral arterial occlusive disease. The Limburg PAOD Study. Peripheral Arterial Occlusive Disease.

OBJECTIVES: To describe the risk-factor profile and cardiovascular comorbidity of asymptomatic peripheral arterial occlusive disease (PAOD). DESIGN: A cross-sectional survey. Asymptomatic PAOD was defined as an ankle-brachial pressure index < 0.95, measured on two consecutive occasions, without intermittent claudication. Logistic regression analyses were performed to investigate independent associations between age, gender, smoking status, hypertension, obesity, diabetes, hypercholesterolaemia, physical activity, a family history of cardiovascular disease, the occurrence of ischaemic heart disease and cerebrovascular disease (CeVD) and asymptomatic PAOD. SETTING: 18 general practices in the province of Limburg, the Netherlands. SUBJECTS: A total of 3650 subjects, aged 40-78 years. MAIN RESULTS: Asymptomatic PAOD was present in 8.6% (n = 314) and symptomatic disease in 3.8% (n = 138) of the participants. Age, smoking status, hypertension, and diabetes were significantly associated with asymptomatic PAOD. The ratio of asymptomatic to symptomatic PAOD was higher among the younger age groups. Male gender, hypertension and smoking status were stronger associated with symptomatic PAOD compared with asymptomatic PAOD. Asymptomatic subjects had more IHD and CeVD comorbidity compared with the healthy population. CONCLUSION: Our findings suggest that the risk-factor profile and cardiovascular comorbidity of asymptomatic subjects is comparable to claudicants. Preventive efforts could be made to diminish the influence of especially smoking, diabetes and hypertension in asymptomatic subjects.

Adult↗
PubMed2002

Prior bowel resections, perianal disease, and a high initial Crohn's disease activity index are associated with corticosteroid resistance in active Crohn's disease.

OBJECTIVES: Some patients with Crohn's disease (CD) do not respond to corticosteroid therapy. Furthermore, corticosteroids frequently cause side effects. Thus, predictive parameters for treatment refractoriness would be helpful for treatment decisions. METHODS: A total of 300 patients with active CD (i.e., with a Crohn's Disease Activity Index [CDAI] >200) entered the study. Treatment started with 60-100 mg/day prednisolone equivalent, which was then tapered to 10-15 mg/day within 6 wk and maintained at that dose for another 4 wk. After 10 wk of treatment, response to steroids was defined by a CDAI <150, steroid resistance by a CDAI always > or =150 and steroid dependency by a relapse after dose reduction. Of 239 eligible patients, 196 were responders, 26 were steroid resistant, and 17 were steroid dependent. RESULTS: Prior bowel resections, a high initial CDAI, and perianal disease were associated with steroid resistance. Of the steroid resistant patients 53.9% were bowel-resected compared to 20.4% of the responders (relative risk = 3.63; 95% CI = 1.79-7.36). Perianal disease was observed in 42.3% of steroid resistant patients versus 21.9% of responders (relative risk = 2.28; 95% CI = 1.12-4.66) and initial CDAI was 347+/-91 in resistant patients versus 301+/-81 in responders (p < 0.05). Parameters for steroid dependent patients were not significantly different from those of responders. CONCLUSIONS: In this study (thus far the largest study for the evaluation of predictive factors for treatment refractoriness to corticosteroids in CD), only prior bowel resection, perianal disease, and a high initial CDAI were found to be predictive of resistance to steroid treatment.

Adrenal Cortex Hormones↗
PubMedDate not supplied

A comparison of the onset of protection induced by Newcastle disease virus strain B1 and a fowl poxvirus recombinant Newcastle disease vaccine to a viscerotropic velogenic Newcastle disease virus challenge.

Four-week-old specific-pathogen-free white rock chickens were immunized with either a commercial recombinant fowl poxvirus-vectored Newcastle disease vaccine (FPN) expressing the hemagglutinin-neuraminidase and fusion protein genes of Newcastle disease virus (NDV) strain B1 or live NDV B1. Vaccinates and controls were challenged by eyedrop and intranasal (E/I) route with a viscerotropic velogenic NDV at 14 days postvaccination to determine the time of clearance of challenge virus. In a subsequent experiment, chickens were challenged at 3, 6, or 10 days postvaccination to determine the onset of immunity. Chickens that received a recommended field dose (1x) or a 0.01x dose of FP-N subcutaneously (s.c.) and were seropositive by hemagglutination-inhibition test at 14 days postvaccination cleared the challenge virus by 14 days postchallenge. Clinical Newcastle disease and high challenge virus titers in tissues were seen only in seronegative FP-N 0.01x dose vaccinates and controls. In a comparison of vaccination with FP-N (1x, 10(4,9) median tissue culture infective dose) s.c., B1 (10(6) median egg infective dose [EID50]) s.c., or B1 (10(6) EID50) E/I, chickens vaccinated at 6 or 10 days before challenge with all vaccines were protected against clinical disease, but only those vaccinated with B1 E/I 10 days before challenge were protected against infection with the challenge virus. Vaccination at 3 days before challenge with B1 E/I provided early protection, but severe nervous signs developed later and reduced overall protection to 60%, whereas disease in chickens vaccinated with B1 s.c. and FP-N s.c. 3 days before challenge was similar to the challenge controls.

Animals↗
PubMed1977

[Perfusion scintigraphy of the myocardium in cardiological diagnosis. Coronary diseases, primary myocardial diseases and rheumatic heart valve diseases].

In 123 patients perfusion scintigrams were compared with the data of clinical investigation, right and left heart catheterisation and coronary arteriography. The intracoronary application of radioactive labelled human-albumin-microspheres and human-microaggregates were without any complications. The patients suffered from coronary heart diseases, primary myocardial diseases and rheumatic valvula heart diseases. There was a good correlation between the myocardial perfusion defect and the degree of coronary artery stenoses. Furthermore an excellent correlation was found between perfusion defects and levocardiographic findings: left ventricular aneurysms, akinetic or hypokinetic areas and the ejection fraction of the left ventricle. All myocardial infarctions were detected by a perfusion defect in the scintigrams. In 16 cardiacsurgery-patients large myocardial perfusion defects were found to be myocardial scars. In primary myocardial diseases perfusion scintigraphy is an effective method of detecting pathological myocardial patterns. The degree of perfusion defects correlates excellently with the levocardiographic findings. It seems that in rheumatic valvular diseases perfusion-scintigraphy is a method to discover rheumatic myocardial abnormalities--probably scar tissue. In comparison with thallium scintigrams it was shown that extensive myocardial failures (aneurysms) can be represented by both nuclear medical procedures but that perfusion scintigraphy is more sensitive and correlates more closely to the levocardiogram findings.

Angiography↗
PubMed2003

No disease-associated mutations found in the coding sequence of the canine polycystic kidney disease gene 1 in Bull Terriers with polycystic kidney disease.

The aim of this study was to identify possible disease-associated mutations in the canine homologue of the polycystic kidney disease gene 1 (PKD1) in Bull Terriers with autosomal dominant polycystic kidney disease. Messenger RNA was obtained from the blood or renal tissue of five Bull Terriers with the disease and four close relatives without the disease. Reverse transcription, PCR and 3' rapid amplification of cDNA ends were used to amplify the coding and 3' untranslated regions of this transcript. Comparison of PKD1 sequence between the affected and unaffected Bull Terriers, revealed six polymorphisms, but no disease-associated mutations.

Animals↗
PubMed1976

Immunological studies on Behçet's and Harada's diseases. I. Cell-mediated immunity in Behçet's and Harada's diseases. II. HL-A antigens associated with Behçet's disease.

Behçet's and Harada's diseases were studied for cell-mediated immunity, utilizing leukocyte migration inhibition test (agarose droplet method). Patients with Behçet's disease during an attack showed cellular hypersensitivity to their aqueous humor, vitreous humor, and synovial fluid, but not to the normal tissue extracts of humans, such as oral mucous membrane, skin, retina and uvea, nor to their peripheral blood leukocytes. The patients with Harada's disease, in whom uveitis was recurrent and depigmentation present in various parts of the body, showed cellular hypersensitivity to bovine uveal extract. It is probably that in Behçet's disease cellular hypersensitivity is the result of inflammatory processes rather than being an important pathogenic mechanism, whereas in Harada's disease it is implicated in the pathogenesis of the disease process.

Behcet Syndrome↗
PubMedDate not supplied

Disease activity in systemic lupus erythematosus: report of the Consensus Study Group of the European Workshop for Rheumatology Research. II. Identification of the variables indicative of disease activity and their use in the development of an activity score. The European Consensus Study Group for Disease Activity in SLE.

A European Consensus Group study, involving 29 centres from 14 countries, was performed in order to reach agreement on the definition of disease activity in systemic lupus erythematosus (SLE) and to construct a new disease index. Data on 704 lupus patients were collected and analysed, using univariate and multivariate statistical procedures, to select those clinical and laboratory features of the disorder which best correlate with the global assessment of disease activity assigned to the patients by the physician of each participating centre. A combination of 15 clinical and laboratory variables was shown to be the best predictor of disease activity in SLE. A European Consensus Lupus Activity Measurement (ECLAM) was then formulated. This index included the 15 selected variables, weighted (with some adjustments) according to their respective regression coefficients in the multivariate model. ECLAM appears to be an effective instrument for scoring patients with different degrees of disease activity. This is the first SLE disease activity index based on data from a very large number of lupus patients followed at a large number of lupus centres in different countries. It might therefore very well serve as a standardised measure for future European clinical studies. Final assessment of the validity, reliability and sensitivity of this index is now underway.

Europe↗
PubMed1996

Meningococcal disease prevention and control strategies for practice-based physicians. Committee on Infectious Diseases, American Academy of Pediatrics. Infectious Diseases and Immunization Committee, Canadian Paediatric Society.

Localized outbreaks of meningococcal disease in the United States and Canada continue to cause serious alarm within communities as a result of the fulminating pattern of the disease, high mortality rate, and high incidence among adolescents. The increasing number of outbeaks since 1991 has raised questions about the management and prevention of further cases during an outbreak. The purpose of this statement is to guide primary-care physicians in their role in infection control and prevention of both sporadic cases and outbreaks of invasive meningococcal disease. This statement provides information on the epidemiology of meningococcal disease, including definitions of sporadic, secondary, and coprimary cases, clusters of cases, and outbreaks. Data are presented on identification of cases, disease risk of contacts, and agents for chemoprophylaxis, and recommendations are given for: (1) risk assessment of contacts, (2) administration of chemoprophylaxis, (3) appropriate use of meningococcal vaccine, (4) appropriate use of the microbiology laboratory, (5) the necessity for timely and appropriate reporting of invasive meningococcal disease to local public health authorities, and (6) information on counseling and public education that may be helpful during an outbreak to minimize public anxiety. An additional section, "Information for Sharing," which uses a question-and-answer format and which may be helpful to parents and community and health care workers during an outbreak, is also provided.

Adolescent↗
PubMed1989

Neuronal RNA in Pick's and Alzheimer's diseases. Comparison of disease-susceptible and disease-resistant cortical areas.

Comparative neuronal RNA analyses were conducted in disease-prone (frontal association, Brodmann's area 9) vs relatively disease-resistant (primary visual, occipital area 17) cortex of patients with autopsy-proved Pick's disease (PD) and Alzheimer's disease (AD). Azure B-RNA staining and scanning-integrating microdensitometry were used to determine total RNA contents of pyramidal neurons in layers 3 and 5. In both PD and AD (1) significant (15% to 47%) RNA loss was detected in neurons of both cortical areas and layers relative to those of aged, nondemented controls, and (2) RNA loss was not markedly enhanced in the damaged frontal cortex relative to that in the preserved occipital cortex. Neuronal RNA depletion was generally more marked in PD than AD. However, this impairment does not appear to be related to the formation of classic neuropathological abnormalities in either disease.

Aged↗
PubMed2000

Risk-adapted therapy for clinical stage I-II Hodgkin's disease: 7-years results of radiotherapy alone for low-risk disease, and ABVD and radiotherapy for high-risk disease.

Treatment outcomes were documented for 204 adult patients with clinical Stage I-II Hodgkin's disease who were treated with risk-adapted ABVD (doxorubicin, bleomycin, vinblastine and dacarbazine) and radiotherapy (RT) at the Toronto-Sunnybrook Regional Cancer Centre between 1984 and 1994. Forty-nine patients with clinical Stage I disease (excluding bulky mediastinal presentations) and 50 patients with a combination of clinical Stage IIA disease, age 50 years or less, and favourable pathology (lymphocyte predominant or nodular sclerosing histology) were identified as low risk and treated with RT alone to 35 Gy. One hundred and five high-risk patients were treated with chemotherapy (86 with ABVD) followed by RT to 25 Gy. The 7-year cause-specific, overall and disease-free survivals were 95%, 90% and 75% respectively for the low-risk cohort, and 91%, 90% and 88% respectively for the high-risk cohort. In-field relapses accounted for 50% of the failures in both groups. Sixteen of 24 (67%) patients with RT failure and 6/14 (43%) with combined modality therapy (CMT) failure were salvaged. Twenty-eight per cent of the patients treated with RT and 21% of those treated with CMT developed hypothyroidism by 7 years. Fatal complications were recorded in 6% of the low-risk patients managed with RT and 8% of high-risk patients managed with CMT. Septic death and second malignancy accounted for the majority of treatment-related fatalities. Risk-adapted therapy emphasizing RT alone for selected patients with favourable prognostic factors and CMT based on ABVD provides excellent long-term disease control. Further treatment refinements, including the wider application of CMT with lower doses of chemotherapy and RT, will be required to reduce the rate of fatal complications to more acceptable levels.

Adult↗
PubMed2001

Clinical trials in Alzheimer's disease. Calculating Alzheimer's Disease Assessment Scale-cognitive subsection with the data from the consortium to establish a registry for Alzheimer's disease.

The database of the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) is a seminal work in the field of cognitive dysfunction and Alzheimer's disease. This 24-center study of 1,094 patients with Alzheimer's disease who received no treatment for their cognitive dysfunction and 463 normal control subjects is rich in neurobehavioral data and contains extensive imaging and neuropathologic findings. However, the Alzheimer's Disease Assessment Scale (ADAS) was not administered as part of the CERAD study, which limits the study's applicability to modern drug trials, in which the ADAS-cognitive subsection (ADAS-cog) is a popular end point. The purpose of this investigation was to develop a derived ADAS-cog score from the neurobehavioral data obtained from subjects during their evaluation in the CERAD study. Two calculated ADAS-cog scores were developed. The first was based on clinically mapping the items on the ADAS-cog to assessments that were performed in the CERAD study. The second was based on rescaling the Mini-Mental Status Exam (MMSE), using published results correlating the ADAS-cog to the MMSE. Standard characteristics of both calculated ADAS-cog scores were calculated and compared with each other and with the literature. Both calculated ADAS-cog scores performed comparably to published characteristics of the ADAS-cog. The clinically based calculated ADAS-cog outperformed the rescaled MMSE. Using the CERAD database, it is now possible to model the progression of an untreated (placebo) population of patients with Alzheimer's disease and correlate it to a study using ADAS-cog.

Aged↗
PubMedDate not supplied

Imaging-based measures of disease progression in clinical trials of disease-modifying drugs for Alzheimer disease.

The authors review and assess imaging-based strategies for measuring the rate of progression of Alzheimer disease (AD). Such techniques may be useful in addition to the behavioral instruments typically used in these studies and may be more sensitive to treatment-related change. MEDLINE searches obtained relevant published literature. Articles were reviewed with particular attention to assessments of rate of disease progression and the effects of investigational drugs. Authors studied a variety of techniques, including volumetric magnetic resonance imaging, functional MRI, fluorodeoxyglucose positron emission tomography, and several target-specific radiopharmaceuticals. In cross-sectional as well as small longitudinal trials, many of these show promise not only in diagnosis, but also as measures of disease progression. The effects of drugs that provide symptomatic relief on these measures have not been fully characterized. Even less is known about the effects of investigational drugs that may slow disease progression. Several neuroimaging techniques have been studied that could improve the ability of clinical trials to quantify the rate of progression of AD. Clinical trials of investigational drugs would benefit from more systematic validation of image-based outcome measures. Several choices of imaging techniques are available. An understanding of the relationship between a statistically significant effect size in an imaging marker and a clinically significant change in rate of disease progression will require additional studies.

Aged↗
PubMed1997

Methioninase: a therapeutic for diseases related to altered methionine metabolism and transmethylation: cancer, heart disease, obesity, aging, and Parkinson's disease.

Methionine metabolism and transmethylation are central to the metabolism and differentiation of all known cells. In enkaryotic organisms, methionine metabolism and transmethylation are of paramount importance in modification and regulation of proteins, lipids, and nucleic acids. The differential methylation of genes regulates their expression in the myriad of cells in eukaryotic organisms. Disruption and abnormalities in methionine metabolism and transmethylation seems to be associated with the major diseases of mankind, including cancer, heart disease, aging, obesity, and Parkinson's disease. In this review, we describe how aberrant and abnormal methionine metabolism and transmethylation are related to these major diseases. Most importantly, we review and hypothesize how the developing therapeutic recombination methioninase (rMETase) can be utilized to cure or prevent all of these diseases.

Aging↗
PubMedDate not supplied

Field trial in commercial broilers with a multivalent in ovo vaccine comprising a mixture of live viral vaccines against Marek's disease, infectious bursal disease, Newcastle disease, and fowl pox.

A multivalent in ovo vaccine (MIV) was tested for safety and efficacy in a commercial broiler complex. The MIV comprised five replicating live viruses including serotypes 1, 2, and 3 of Marek's disease virus (MDV), an intermediate infectious bursal disease virus (IBDV) and a recombinant fowl poxvirus (FPV) vector vaccine containing HN and F genes of Newcastle disease virus (NDV). The performance of MIV-vaccinated broilers was compared with that of hatchmates that received turkey herpesvirus (HVT) alone (routinely used in ovo vaccine in the broiler complex). The chickens that hatched from the MIV-injected and HVT-injected eggs were raised under commercial conditions in six barns. Barn 1 housed 17,853 MIV-vaccinated chickens and each of the barns 2-6 housed 18,472-22,798 HVT-vaccinated chickens. The HVT-vaccinated chickens were given infectious bronchitis virus (IBV) and NDV vaccines at hatch and at 2 wk of age. The MIV-vaccinated chickens received IBV vaccine at hatch and IBV + NDV at 2 wk of age. The relative values of hatchability of eggs, livability and weight gain of chickens, and condemnation rates at processing were comparable between the MIV and the HVT groups (P > 0.05). Chickens from the MIV- and the HVT-vaccinated groups were challenged with virulent viruses under laboratory conditions. The resistance of vaccinated chickens against Marek's disease could not be assessed because of high natural resistance of unvaccinated commercial broilers to virulent MDV. The relative resistances of the MIV- and the HVT-vaccinated groups, respectively, against other virulent viruses were as follows: IBDV, 100% for both groups; NDV, 81% vs. 19%; FPV, 86% vs. 0%. The successful use of MIV under field conditions expands the usefulness of the in ovo technology for poultry.

Animals↗