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PubMed1988

Chronic enteric virus infection in two T-cell immunodeficient children.

Enteric virus infections were studied in two children with congenital T-cell immunodeficiency. One patient (LC) with cartilage hair hypoplasia developed persistent diarrhea and malabsorption following acute gastroenteritis. Electron microscope (EM) examination of feces revealed excretion of rotavirus for more than 450 days with concurrent astrovirus infection for at least 225 days, associated with the persistent diarrhea. Prolonged infection with poliovirus type 2 following vaccination had previously been noted in this patient. The second patient (DT), with the CHARGE association and DiGeorge syndrome, had two episodes of loose stools. EM of fecal extracts demonstrated rotavirus excretion for at least 66 days following the initial episode. Virus-specific immune responses were assayed in these two patients. LC showed a poor serum neutralizing antibody response to polio vaccination, no detectable antibody response (by immune EM and ELISA) to rotavirus, and no detectable antibody response to astrovirus (by immune EM). Rotavirus specific cell mediated immunity was also not detectable. DT showed no detectable serum antibody response to rotavirus (by ELISA). Rotavirus isolates from both patients were found to be group A viruses and were further analyzed by polyacrylamide gel electrophoresis. Atypical genome profiles, with multiple additional bands between segments 3-7 of the normal rotavirus profile, were obtained throughout the course of each illness, including the earliest specimens available (day 41, LC; day 7, DT). These results indicate that chronic virus infection of the gut can occur in patients with T-cell immunodeficiency. Such chronic infection may be associated with persistent diarrhea and can cause considerable problems of management.

Antibodies, Viral↗

PubMed2004

Genetic variability of hepatitis C virus in chronically infected patients with viral breakthrough during interferon-ribavirin therapy.

Little is known about hepatitis C virus (HCV) breakthrough during antiviral therapy, although it would help in understanding HCV resistance to current antiviral treatments. To analyse the implication of virological factors and the vigour of humoral immune responses in this phenomenon, we studied nine chronic hepatitis C patients with a viral breakthrough during IFN/ribavirin combination therapy, as well as five responders and five non-responders. The IRES and regions coding for the capsid protein, the PePHD domain of envelope glycoprotein E2 and the NS5A and 5B proteins were amplified by RT-PCR before treatment, before and during breakthrough, and after treatment. The major variant sequence was obtained by direct sequencing. The heterogeneity of quasispecies was studied by SSCP in all patients and sequencing after cloning in seven genotype 1b-infected patients. Humoral responses against HCV epitopes were also analysed. The major sequences of IRES, PePHD, and NS5B remained stable during treatment, regardless of the treatment response. However, the capsid protein and the regions flanking PePHD showed sequence variations in breakthrough patients, although no specific mutation was identified. The variable V3 region of NS5A, but not the PKR-binding domain and the ISDR, seemed to be associated with differences in response to treatment. The analysis of HCV quasispecies revealed no characteristic pattern during treatment in breakthrough patients, whose HCV genome profiles looked most similar to that of non-responders. The humoral response was similar between groups. In conclusion, viral breakthrough does not seem to be due to selection of resistant strains with signature mutations.

Adult↗

PubMed2006

PDGFRalpha, PDGFRbeta and KIT expression/activation in conventional chondrosarcoma.

Chondrosarcomas represent 20% of all primary bone sarcomas, and many studies have attempted to unravel molecular targets for future development of new therapies. The aim of this study was to investigate the expression/activation of PDGFRalpha, PDGFRbeta and KIT receptor tyrosine kinases (RTKs) as potential therapeutic targets in conventional central primary chondrosarcomas (CCS). The expression of PDGFRalpha, PDGFRbeta and KIT RTKs was detected in 16 CCSs using immunohistochemistry (IHC), and their level of expression and activation status were analysed by immunoprecipitation and western blot experiments. PDGFRalpha, PDGFRbeta and KIT cDNAs were screened to verify the presence of activating mutations and the presence of the cognate ligands was analysed by means of RT-PCR. RTK gene amplification was further studied by means of fluorescence in situ hybridization (FISH) analysis. The immunophenotyping and biochemical analyses showed that the CCSs co-expressed PDGFRalpha and PDGFRbeta, with the latter showing definitively greater protein expression and phosphorylation levels. PDGFRbeta was expressed but not activated in control healthy joint cartilage, in line with no PDGFB detection. Conversely, the KIT gene product did not seem to play a relevant role. These findings, in the absence of activating mutations or an abnormal genomic profile and the presence of PDGFA and PDGFB expression, are consistent with an autocrine/paracrine loop activation of the corresponding receptors. The CCS gene profile described here offers a rationale for the use of RTK inhibitors alone or in combination with chemotherapy, and supports further investigation of RTKs and their downstream signals.

Bone Neoplasms↗

PubMed2005

Genetics and prevention of oesophageal adenocarcinoma.

Gastric cancer has been declining for more than half a century, whereas the incidence of oesophageal cancer is increasing rapidly. The histopathological subtype is also changing with a predominance of oesophageal adenocarcinoma compared with squamous carcinoma. The reasons for these epidemiological changes are not clear, although population-based data have implicated gastro-oesophageal reflux disease as a risk factor. In susceptible individuals reflux of duodeno-gastric contents can lead to the development of a columnar-lined oesophagus, commonly called Barrett's oesophagus. This can then progress to adenocarcinoma via a metaplasia-dysplasia-carcinoma sequence. At the current time, the mortality from oesophageal adenocarcinoma exceeds 80% at 5 years. Therefore, endoscopic surveillance programmes have been generally recommended for patients with Barrett's oesophagus in an attempt to detect early, curable lesions. Unfortunately these programmes are cumbersome and costly and have not yet been proved to reduce population mortality. In order to improve patient outcomes we need to be able to identify patients at high risk and to understand the triggers for disease progression. There is mounting evidence that there is an underlying genetic susceptibility to Barrett's oesophagus and oesophageal adenocarcinoma. However, this is likely to be as a result of multiple low penetrance susceptibility genes which have yet to be identified. Once patients are identified as having Barrett's oesophagus their chance for developing adenocarcinoma is in the order of 0.5%-1% per year. The histological assessment of dysplasia as a predictor of cancer development is highly subjective. Therefore multiple, specific somatic mutations in the tissue have been investigated as potential biomarkers. The most promising markers to date are the presence of aneuploidy, loss of heterozygosity of p53 and cyclin D1 overexpression. However, a study of evolutionary relationships suggest that mutations occur in no obligate order. Combinatorial approaches are therefore being advocated which include genomic profiling or the use of a panel of molecular markers in order to define the common molecular signatures that can then be used to predict malignant progression. An alternative approach would be to use markers for the final common pathway following genetic instability, which is the loss of proliferative control. We have demonstrated an increase in the expression of a novel proliferation marker, Mcm2, which occurs during the malignant progression of Barrett's oesophagus. These Mcm2-expressing cells are detectable on the surface, and hence a cytological approach may be applicable. In view of the role of reflux components in the pathogenesis of Barrett's oesophagus the effect of acid and bile on the cell phenotype have been studied. These studies have demonstrated that pulsatile acid and bile exposure induce cell proliferation. The mechanism for the hyperproliferative response appears to involve p38 mitogen activated protein kinase (MAPK) pathways as well as protein kinase C (PKC) and cyclo-oxygenases. A clinical implication of the laboratory studies is that suppression of acid and bile may need to be profound in order to suppress cell proliferation and, by inference, ultimately prevent the development of dysplasia. There is some support for this concept from short-term clinical studies, and a large randomised chemoprevention trial is being instigated which will evaluate the effect of proton pump inhibitors with or without aspirin. Given the epidemic increase in oesophageal adenocarcinoma and the dismal 5-year mortality rate, a radical approach is necessary to prevent cancer development in individuals with pre-malignant lesions.

Adenocarcinoma↗

PubMed1986

A new type of atypical rotavirus in pigs.

Two independent isolates of an unusual type of rotavirus were obtained from over 900 faecal samples obtained from piglets with diarrhoea. Genome profiles, containing eleven segments, were not characteristic of group A electropherotypes and corresponded to an atypical virus. The profiles were, however, distinct from those of other previously described atypical porcine rotaviruses. Serological comparisons showed that the two isolates were related, but unrelated to other known groups of porcine rotavirus. The new isolates were passaged in gnotobiotic piglets in which they caused mild clinical signs of enteritis. A survey of porcine sera from the United Kingdom indicated a widespread distribution of antibody to this virus in pigs aged 10 weeks and over.

Animals↗

PubMed2026

Defining and managing high-risk acute myeloid leukemia (AML) in 2026.

Acute myeloid leukemia (AML) remains a highly heterogeneous malignancy in which outcomes are particularly poor for patients classified as having high-risk disease. Traditionally, high-risk AML has been defined by adverse baseline genetic features, including complex cytogenetics, TP53 alterations, and mutations associated with secondary or therapy-related disease. However, this static, genetics-centered definition is increasingly insufficient in the modern therapeutic era. Emerging evidence supports a more dynamic and context-dependent model in which risk is shaped not only by molecular architecture but also by treatment intensity, patient fitness, measurable residual disease (MRD), and evolving resistance mechanisms. Advances in genomic profiling have refined risk stratification frameworks, including ELN 2022 for intensively treated patients and the ELN 2024 classification for those receiving less-intensive therapies. In parallel, MRD has emerged as a powerful biomarker that reclassifies patients during treatment, identifying those with persistent, therapy-resistant disease despite morphologic remission. Biologically, high-risk AML is driven by the interplay of clonal evolution, epigenetic plasticity, leukemic stem cell persistence, and protective microenvironmental and immune interactions, all of which contribute to relapse. Therapeutically, the landscape has expanded to include targeted agents, venetoclax-based combinations, and transplantation strategies, yet outcomes remain limited in key high-risk subsets, particularly TP53-mutated disease and post-venetoclax relapse. Accordingly, current strategies emphasize rational combination therapies, MRD-guided treatment adaptation, and approaches targeting both leukemic cells and their supportive niches. In 2026, high-risk AML is best understood as a dynamic, treatment-context-dependent state. Improving outcomes will require integration of precision diagnostics, biologically informed therapy, and adaptive strategies designed to anticipate and overcome resistance.

Humans↗

PubMed2000

Inter- and intra-site genetic diversity of natural field populations of rice tungro bacilliform virus in the Philippines.

The genetic structure of rice tungro bacilliform virus (RTBV) populations within and between growing sites was analyzed in a collection of natural field isolates from different rice varieties grown in eight tungro-endemic sites of the Philippines. Total DNA extracts from 345 isolates were digested with EcoRV restriction enzyme and hybridized with a full-length probe of RTBV, a procedure shown in preliminary experiments capable of revealing high levels of polymorphism in RTBV field isolates. In the total population, 17 distinct EcoRV-based genome profiles (genotypes) were identified and used as indicators for virus diversity. Distinct sets of genotypes occurred in Isabela and North Cotabato provinces suggesting a geographic isolation of virus populations. However, among the sites in each province, there were few significant differences in the genotype compositions of virus populations. The number of genotypes detected at a site varied from two to nine with a few genotypes dominating. In general the isolates at a site persisted from season to season indicating a genetic stability for the local virus population. Over the sampling time, IRRI rice varieties, which have green leafhopper resistance genes, supported similar virus populations to those supported by other varieties, indicating that the variety of the host exerted no apparent selection pressures. Insect transmission experiments on selected RTBV field isolates showed that dramatic shifts in genotype and phenotype distributions can occur in response to host/environmental shifts.

Agriculture↗

PubMed2006

Probing the adaptive response of Escherichia coli to extracellular Zn(II).

The adaptive response of Escherichia coli cells to differing intracellular and extracellular Zn(II) concentrations was evaluated by two-dimensional gel electrophoresis and peptide identifications. Twenty-one Zn(II)-responsive proteins, which were previously not known to be associated with Zn(II), were identified. Most of the proteins were related to cellular metabolism and include membrane transporters and glycolytic and TCA-associated enzymes. The expression levels of no known Zn(II) transporters were identified with these studies. The results of these studies suggest a role of Zn(II) in the expression levels of several E. coli proteins, and the results are discussed in light of recent genomic profiling studies on the adaptive response of E. coli cells to stress by Zn(II) excess.

Cell Growth Processes↗

PubMed2004

Proteomics in cancer screening and management in gynecologic cancer.

Biomarkers are used routinely for population screening, disease diagnosis and prognosis, monitoring of therapy, and prediction of therapeutic response. Unfortunately, most biomarkers have low sensitivity and specificity and little predictive value. Novel techniques for better screening and early diagnosis of ovarian cancer are urgently needed. Proteomics, the study of the cellular proteins and their activation states, integrates some fundamental techniques, including high-throughput protein purification and profiling, genomic and proteomic databases, and mass spectrometry. In oncology, proteomics will contribute greatly to our understanding of gene functions in tumor development and provide information in clinical applications. This article reviews proteomic techniques and their potential applications in gynecologic cancer screening and management.

Biomarkers, Tumor↗

PubMed1989

Sequence analysis of the major outer membrane protein gene of an ovine abortion strain of Chlamydia psittaci.

The major outer membrane protein (MOMP) gene from an ovine abortion strain of Chlamydia psittaci (S26/3) has been cloned and sequenced. The gene shows the features of other chlamydial MOMPs but comparison with the previously reported sequence for the ovine abortion isolate A22/M has revealed substantial sequence divergence which is clustered into the same four intramolecular regions as the sequence variation found between C. trachomatis serovars. Subsequent restriction enzyme analysis of A22/M DNA has shown that it has an avian-type genomic profile and thus the comparison is between types rather than between strains.

Abortion, Veterinary↗

PubMed2026

Multimodal risk assessment for oral potentially malignant disorders: Integrating patient-centered and specimen-derived data.

BACKGROUND: Oral potentially malignant disorders exhibit heterogeneous malignant transformation risk that clinical approaches fail to adequately predict. Histopathologic dysplasia grading, the reference standard of risk assessment, is associated with poor interobserver reliability and limited prognostic discrimination. It is necessary to define other potential patient- and tissue-associated risk modifiers to improve patient-specific disease prediction. TYPES OF STUDIES REVIEWED: PubMed was queried for patient- and specimen-derived factors as they relate to oral cancer and oral potentially malignant disorders, with preference for systematic review and meta-analysis articles published within the past 5 years. When not available, guidelines from the American Cancer Society, National Cancer Institute, or other national organizations or the most recent best articles were referenced to support the data presented. RESULTS: Within patient-associated factors, validated measures of tobacco and alcohol exposure, clinical lesion characteristics, systemic health factors including metabolic syndrome components, comorbidity risk, and dental health indexes were found. Within specimen-derived data, tissue-based analyses encompassing histopathology and advanced molecular profiling (genomic, epigenomic, transcriptomic, spatial approaches), blood-based germline and somatic mutation analysis, and saliva-based microbiome characterization and inflammatory biomarker assessment were addressed. PRACTICAL IMPLICATIONS: Malignant transformation reflects intersecting patient and specimen risk pathways that affect each patient differently; no single modality captures this complexity. Realizing precision prognostication in oral precancer will require coordinated expansion and standardization of data collection across research groups. This review is intended to guide covariate selection for prospective study design, improve reproducibility, and ultimately enable the development of validated multimodal risk prediction tools for clinical deployment.

Humans↗

PubMed2004

Antibiotic-resistant Propionibacterium acnes on the skin of patients with moderate to severe acne in Stockholm.

The objective was to study the prevalence and antibiotic susceptibility patterns of Propionibacterium acnes strains isolated from patients with moderate to severe acne in Stockholm, Sweden and to determine the diversity of pulsed-field gel electrophoresis types among resistant P. acnes strains. One hundred antibiotic-treated patients and 30 non-antibiotic-treated patients with moderate to severe acne participated in the investigation. Facial, neck and trunk skin samples were taken with the agar gel technique. The susceptibility of P. acnes strains to tetracycline, erythromycin, clindamycin and trimethoprim-sulfamethoxazole was determined by the agar dilution method. The genomic profiles of the resistant strains were determined by pulsed-field gel electrophoresis. In the group of patients treated with antibiotics, resistant P. acnes strains were recovered in 37%, while in the non-antibiotic group of patients the incidence of resistant strains was 13%. Thus antibiotic-resistant P. acnes strains were significantly more often isolated from antibiotic-treated patients with moderate to severe acne than from non-antibiotic-treated patients (odds ratio, 3.8; P=0.01). There was a genetic diversity among the P. acnes strains. Forty-four different patterns of SpeI DNA digests were detected and two predominant clones were found. P. acnes strains exhibited different antibiotic susceptibility patterns and identical genotypes or vice versa. A person can be colonized with different strains with varying degrees of antibiotic resistance. The risk of increased resistance of P. acnes must be considered when treating acne patients with antibiotics, and especially long-term therapy should be avoided.

Journal Article↗

PubMed2026

Determinants of nucleic acid quality in formalin-fixed paraffin-embedded bladder urothelial carcinoma specimens: effects of specimen type, fixation conditions, and storage time.

Formalin-fixed paraffin-embedded (FFPE) tissue is the principal substrate for cancer genomic profiling, yet pre-analytical factors affect nucleic acid quality. In our workflow, transurethral resection (TUR) specimens of bladder urothelial carcinoma are fixed promptly but exposed to electrocautery, whereas robot-assisted radical cystectomy specimens are refrigerated overnight before fixation; we compared nucleic acid quality between these specimen types. We analyzed 56 FFPE primary bladder urothelial carcinoma specimens (33 TUR, 23 cystectomy). DNA quality was assessed by the DNA Integrity Number (DIN) and short-to-long cycle threshold ratio (S/L Ct ratio), and RNA quality by the RNA Integrity Number (RIN) and percentage of RNA fragments ≥200 nucleotides (DV200), with group comparisons, Spearman correlations, and multivariable regression (specimen type, fixation duration, storage time). The median DIN (4.4 vs. 3.8, p = 0.004) and S/L Ct ratio (0.943 vs. 0.894, p < 0.001) were higher in TUR than cystectomy specimens; the RIN was also higher (1.9 vs. 1.7, p = 0.040), though low in both groups, and DV200 did not differ (50.3% vs. 47.7%, p = 0.934). In multivariable analysis, TUR specimen type independently predicted higher DIN (β = +0.460, p = 0.040) and S/L Ct ratio (β = +0.442, p = 0.009), whereas longer storage time independently decreased the S/L Ct ratio (β = -0.513, p < 0.001) and RIN (β = -0.352, p = 0.010). In our institutional workflow, TUR specimens showed higher DNA quality metrics than robot-assisted radical cystectomy specimens subjected to overnight refrigerated pre-fixation delay, whereas this workflow-associated advantage did not clearly extend to DV200-defined RNA fragment-length quality. Storage time was associated with selected aspects of nucleic acid deterioration.

Humans↗

PubMed2004

Unique ligation properties of eukaryotic NAD+-dependent DNA ligase from Melanoplus sanguinipes entomopoxvirus.

The eukaryotic Melanoplus sanguinipes entomopoxvirus (MsEPV) genome reveals a homologous sequence to eubacterial nicotinamide adenine dinucleotide (NAD(+))-dependent DNA ligases [J. Virol. 73 (1999) 533]. This 522-amino acid open reading frame (ORF) contains all conserved nucleotidyl transferase motifs but lacks the zinc finger motif and BRCT domain found in conventional eubacterial NAD(+) ligases. Nevertheless, cloned MsEPV ligase seals DNA nicks in a NAD(+)-dependent fashion, while adenosine 5'-monophosphate (ATP) cannot serve as an adenylation cofactor. The ligation activity of MsEPV ligase requires Mg(2+) or Mn(2+). MsEPV ligase seals sticky ends efficiently, but has little activity on 1-nucleotide gap or blunt-ended DNA substrates even in the presence of polyethylene glycol. In comparison, bacterial NAD(+)-dependent ligases seal blunt-ended DNA substrates in the presence of polyethylene glycol. MsEPV DNA ligase readily joins DNA nicks with mismatches at either side of the nick junction, except for mismatches at the nick junction containing an A base in the template strand (A/A, G/A, and C/A). MsEPV NAD(+)-dependent DNA ligase can join DNA probes on RNA templates, a unique property that distinguishes this enzyme from other conventional bacterial NAD(+) DNA ligases. T4 ATP-dependent DNA ligase shows no detectable mismatch ligation at the 3' side of the nick but substantial 5' T/G mismatch ligation on an RNA template. In contrast, MsEPV ligase joins mismatches at the 3' side of the nick more frequently than at the 5' side of the nick on an RNA template. The complementary specificities of these two enzymes suggest alternative primer design for genomic profiling approaches that use allele-specific detection directly from RNA transcripts.

Amino Acid Sequence↗

PubMed2026

Acute leukemia therapy at a crossroads: from conventional chemotherapy to the era of precision medicine.

Since the discovery of cytotoxic agents in the mid-20th century, acute leukemia has consistently served as a model for oncology research. As the Human Genome Project and subsequent genomic profiling elucidated the landscape of somatic mutations and cytogenetic aberrations driving leukemogenesis, the development of molecularly targeted therapies has dramatically accelerated, yielding significant improvements in patient outcomes. In acute myeloid leukemia (AML), the emergence of selective inhibitors targeting high-frequency alterations such as FLT3, NPM1, and IDH1/2 has redefined the standard of care, demonstrating superior efficacy when combined with conventional intensive chemotherapy or hypomethylating agents. Simultaneously, for acute lymphoblastic leukemia (ALL), in addition to the significant improvements achieved by tyrosine kinase inhibitors (TKIs) for BCR-ABL-positive ALL, the advent of CD19- or CD22-targeted monoclonal antibodies and CAR-T cell therapies has marked an epoch-making milestone, representing a major paradigm shift in the management of relapsed or refractory cases. Bridging these two distinct lineages, menin inhibitors have emerged as a novel class of agents targeting a common pathogenic mechanism in KMT2A-rearranged AML/ALL and NPM1-mutated AML, exhibiting promising antileukemic activity across these subtypes. In this review, we describe the evolution of leukemia therapy-highlighting historical trajectory across AML, APL, and ALL from uniform cytotoxic chemotherapy to molecularly targeted agents, antibody-based therapies, and chemo-free paradigms, while outlining future perspectives for precision hematology.

Acute lymphoblastic leukemia↗

PubMed2006

Cytogenetic and molecular genetic changes in malignant mesothelioma.

Malignant mesothelioma (MM) results from the accumulation of a number of acquired genetic events, especially deletions, which lead to the inactivation of multiple onco-suppressor genes in a multistep cascade mechanism. Past asbestos exposure represents the major risk factor for MM, and the link between asbestos fibers and MM has been largely proved by several epidemiologic and experimental studies. Asbestos fibers induce DNA and chromosomal damage. Most MM cases have shown multiple chromosomal abnormalities. Chromosomal losses are more common than gains. The most common cytogenetic abnormality in MM is a deletion in 9p21, the locus of CDKN2A, a tumor suppressor gene (TSG). The deletion of CDKN2A is a negative prognostic factor in MM. Loss of TSG CDKN2A/p14(ARF) is also common in MM and mutations in NF2 occur in approximately half of the cases. Despite the ban on asbestos use in Western countries, the incidence of MM is increasing, and asbestos is still used in developing countries. This epidemiologic situation calls for further research. Ongoing studies are already applying high-throughput genomic profiling methods in MM. Genetic alterations observed in MM may be useful in differential diagnosis between lung cancer and MM, as diagnostic markers or therapeutic targets, and as indicators of premalignancy for primary prevention and health surveillance.

Asbestos↗

PubMed2026

Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools.

Ketogenic diet (KD) is used for the treatment of drug-resistant childhood epilepsy and has been proposed to improve outcomes in neurodegenerative diseases. However, the mechanisms by which KD alters brain circuitry remain unclear. Here, we investigated the impact of KD on hippocampal function through integrative analysis of gene expression and neurotransmission. We found that KD induces extensive transcriptional reprogramming, including altered expression of numerous synaptic genes. Proteomic and genomic profiling revealed significant changes in histone modifications, particularly at promoters of KD-regulated genes. Electrophysiological recordings showed that KD reduces excitatory synaptic gain and short-term plasticity at CA3-CA1 synapses, dampening the summation of excitatory inputs and enhancing the summation of inhibitory inputs. These functional changes were driven, in part, by a reduction in the readily releasable vesicle pool at excitatory synapses under KD. Together, our findings demonstrate that KD drives transcriptional remodeling of hippocampal circuits, leading to synaptic adaptations that may underlie its anti-epileptic and neuroprotective effects.

Animals↗

PubMed2004

Isolation and characterisation of an Indian strain of Mycoplasma mycoides subsp. mycoides type LC from a case of caprine arthritis.

Isolation and characterisation of an Indian strain of Mycoplasma mycoides subsp. mycoides LC from a case of caprine arthritis is reported in the study. The isolate was identified based on biochemical, digitonin sensitivity and growth inhibition tests. The virulence of the organism was studied by pathogenicity test in mice and goat. The antigenic and genomic profile of the isolate was compared with that of the standard strain (Y-Goat). Using different sets of primers, polymerase chain reaction was employed for rapid detection of the strain.

Animals↗