Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Emerging infectious diseases are caused by old, new, and mutant microorganisms. Emergence of these pathogens can be attributed to changes in the characteristics and risk factors of patients, the widespread use of antibiotics, changes in the environment, the role of xenotransplantation, and international travel. In the United States, the incidences of C. difficile, cyclosporiasis, enterohemorrhagic E. coli gastroenteritis, Hantavirus, hepatitis C virus infection, and Lyme disease have increased significantly over the past two decades. Malassezia pachydermatis, extended spectrum beta lactamase (ESBL), Gram negative bacilli, and antibiotic resistant Enterococci, S. aureus, S. pneumoniae, and M. tuberculosis have also emerged prominently. Although not yet seen in the United States, variant Creutzfeldt-Jakob disease has made a great emotional impact on this country. Identifying, treating, and controlling emerging infectious disease and pathogens have created enormous challenges.
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PMID:Emerging infectious diseases and pathogens. 1031 33

Oman is generally hot and dry, but the Salalah region in southern Dhofar province is relatively cool and rainy during the summer monsoon, and has a distinctive pattern of infection. Important, notifiable infections in Oman include tuberculosis, brucellosis (endemic in Dhofar), acute gastroenteritis, and viral hepatitis: 4.9% of the adults are seropositive for hepatitis B surface antigen and approximately 1.2% for hepatitis C virus. Infection with human immunodeficiency virus is uncommon, and leprosy, rabies, and Crimean-Congo hemorrhagic fever are rare. Between 1990 and 1998, the incidence of malaria, (>70% due to Plasmodium falciparum) decreased from 32,700 to 882 cases. Cutaneous and visceral leishmaniasis (caused by Leishmania tropica and L. infantum, respectively) and Bancroftian filariasis occur sporadically. Intestinal parasitism ranges from 17% to 42% in different populations. A solitary focus of schistosomiasis mansoni in Dhofar has been eradicated. There are major programs for the elimination of tuberculosis, leprosy, and malaria, and to control brucellosis, leishmaniasis, sexually transmitted diseases, trachoma, acute respiratory infection in children, and diarrheal diseases. The Expanded Program on Immunization was introduced in 1981: diphtheria, neonatal tetanus, and probably poliomyelitis have been eliminated.
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PMID:Infectious and tropical diseases in Oman: a review. 1067 71

The duration of immunodeficiency following marrow transplantation is not known. Questionnaires were used to study the infection rates in 72 patients surviving 20 to 30 years after marrow grafting. Furthermore, in 33 of the 72 patients and in 16 donors (siblings who originally donated the marrow) leukocyte subsets were assessed by flow cytometry. T-cell receptor excision circles (TRECs), markers of T cells generated de novo, were quantitated by real-time polymerase chain reaction. Immunoglobulin G(2) (IgG(2)) and antigen-specific IgG levels were determined by enzyme-linked immunosorbent assay. Infections diagnosed more than [corrected] 15 years after transplantation occurred rarely. The average rate was 0.07 infections per patient-year (one infection every 14 years), excluding respiratory tract infections, gastroenteritis, lip sores, and hepatitis C. The counts of circulating monocytes, natural killer cells, B cells, CD4 T cells, and CD8 T cells in the patients were not lower than in the donors. The counts of TREC(+) CD4 T cells in transplant recipients younger than age 18 years (at the time of transplantation) were not different from the counts in their donors. In contrast, the counts of TREC(+) CD4 T cells were lower in transplant recipients age 18 years or older, even in those with no history of clinical extensive chronic graft-versus-host disease, compared with their donors. The levels of total IgG(2) and specific IgG against Haemophilus influenzae and Streptococcus pneumoniae were similar in patients and donors. Overall, the immunity of patients surviving 20 to 30 years after transplantation is normal or near normal. Patients who received transplants in adulthood have a clinically insignificant deficiency of de novo-generated CD4 T cells, suggesting that in these patients the posttransplantation thymic insufficiency may not be fully reversible.
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PMID:Immunity of patients surviving 20 to 30 years after allogeneic or syngeneic bone marrow transplantation. 1173 50

In the first half of the 20th century, improved living conditions, preventive measures, vaccines and antibiotics led to a marked reduction in morbidity and mortality from infectious diseases. It was predicted that the conquest of all infectious diseases was imminent. However, 50 years later, in 1999, they were still the major cause of disease worldwide, and caused nearly one third of all deaths (a total of 55.9 million). The eradication of smallpox in the 1970s and the approaching eradication of poliomyelitis represent major achievements. The prevalence of measles, pertussis and tetanus neonatorum is also markedly reduced, but still 1.5 million children in developing countries die each year because of lack of vaccines. Malaria and tuberculosis are re-emerging. Tuberculosis and HIV/AIDS are the diseases with known aetiology that cause most deaths, altogether 5 million each year. Respiratory and gastrointestinal infections cause 6.5 million deaths annually. Infections in the immunocompromised host have become a "trade mark" of today's advanced medicine. Almost every year, new diseases related to new micro-organisms are described; over the last 30 years, approximately 40 new diseases/micro-organisms have been diagnosed. Among the best known are HIV/AIDS, peptic ulcer caused by Helicobacter pylori, Legionnaires' disease, borreliosis (Lyme disease), hepatitis C, gastroenteritis caused by rotavirus, and Ebola haemorrhagic fever. Antimicrobial resistance development of micro-organisms has become one of the major health problems worldwide; a number of preventive measures are being introduced.
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PMID:[Microorganisms strike back--infectious diseases during the last 50 years]. 1180 14

Vibrio vulnificus is a Gram-negative, motile, curved bacillus of the family Vibrionaceae that is a rare cause of gastroenteritis, septicemia, and wound infections in humans. V. vulnificus is halophilic, flourishes in warm temperatures, and is part of the bacterial flora of the marine environment. The location of our health care setting, on the Gulf of Mexico, has given us the opportunity to observe a wide variety of clinical presentations of infections caused by this organism. In the first case, a 27-year-old man struck by lightning while windsurfing was found pulseless in the water and was resuscitated. The patient subsequently developed cardiac arrhythmias, respiratory failure, and necrotizing fasciitis, blood cultures yielded V. vulnificus. After antibiotic therapy and several fasciotomies, the patient recovered. The second case was that of a 43-year-old Asian man employed as an oyster shucker who presented with complaints of redness, tearing, and photophobia of the right eye. The diagnosis of corneal ulcer secondary to V. vulnificus was made after culture of the right eye revealed the organism. The third case involved a 46-year-old man who presented with complaints of abdominal pain, nausea, chills, and bullous lesions on the lower extremities. He developed disseminated intravascular coagulation, and cultures of the lesions on his lower extremities showed V. vulnificus. Initially, the patient denied any exposure to raw seafood or seawater, but he eventually remembered eating raw oysters 3 days before his illness. The fourth case is that of a 32-year-old, human immunodeficiency virus-positive, hepatitis C-positive woman with cirrhosis who presented with productive cough, chills, fever, and red spots on her extremities and buttocks. Blood cultures revealed V. vulnificus and the patient was treated with antibiotics and improved clinically. These four cases illustrate the wide range of clinical presentations associated with this organism.
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PMID:Varied clinical presentations of Vibrio vulnificus infections: a report of four unusual cases and review of the literature. 1498 56

Over the last fifteen years there have been five pandemics of norovirus (NoV) associated gastroenteritis, and the period of stasis between each pandemic has been progressively shortening. NoV is classified into five genogroups, which can be further classified into 25 or more different human NoV genotypes; however, only one, genogroup II genotype 4 (GII.4), is associated with pandemics. Hence, GII.4 viruses have both a higher frequency in the host population and greater epidemiological fitness. The aim of this study was to investigate if the accuracy and rate of replication are contributing to the increased epidemiological fitness of the GII.4 strains. The replication and mutation rates were determined using in vitro RNA dependent RNA polymerase (RdRp) assays, and rates of evolution were determined by bioinformatics. GII.4 strains were compared to the second most reported genotype, recombinant GII.b/GII.3, the rarely detected GII.3 and GII.7 and as a control, hepatitis C virus (HCV). The predominant GII.4 strains had a higher mutation rate and rate of evolution compared to the less frequently detected GII.b, GII.3 and GII.7 strains. Furthermore, the GII.4 lineage had on average a 1.7-fold higher rate of evolution within the capsid sequence and a greater number of non-synonymous changes compared to other NoVs, supporting the theory that it is undergoing antigenic drift at a faster rate. Interestingly, the non-synonymous mutations for all three NoV genotypes were localised to common structural residues in the capsid, indicating that these sites are likely to be under immune selection. This study supports the hypothesis that the ability of the virus to generate genetic diversity is vital for viral fitness.
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PMID:Rapid evolution of pandemic noroviruses of the GII.4 lineage. 2036 Sep 72

Noroviruses are the principal cause of epidemic gastroenteritis worldwide. Multiple reports have concluded that the major capsid proteins of GII.4 strains, which cause 80% of norovirus infections worldwide, are evolving rapidly, resulting in new epidemic strains. Surrogate neutralization assays using sera from outbreaks and from immunized mice suggest that, as with influenza virus, antigenic variation maintains GII.4 persistence in the face of human population herd immunity. To test this hypothesis, mice were hyperimmunized with virus-like particles (VLPs) representing an early (GII.4-1987) and a contemporary (GII.4-2006) GII.4 strain. Anti-GII.4-1987 IgG monoclonal antibodies (MAbs) strongly reacted with GII.4 VLPs derived between only 1987 and 2002. Ligand binding blockade was more efficient with GII.4-1987 and GII.4-1997 VLPs than with GII.4-2002. Anti-GII.4-2006 IgG MAbs recognized either a broad panel of GII.4 VLPs (1987 to 2006) or a subset of contemporary (2004 to 2006) VLPs. Most 2006 antibodies did not recognize or only poorly recognized GII.4 VLPs of 2007 or 2008, documenting rapid antigenic evolution of GII.4 capsids. Generally, 2006 MAbs blocked homotypic VLP-ligand binding but were unable to block VLPs representing strains primarily circulating during or earlier than 2002. These analyses demonstrate that both subtle and significant evolutionary change has occurred within antibody epitopes between epidemic strains, providing direct evidence that the GII.4 noroviruses are undergoing antigenic variation, likely in response to herd immunity. As with influenza virus, HIV, and hepatitis C virus, norovirus antigenic variation will significantly influence the design of efficacious vaccines and immunotherapeutics against these important human pathogens.
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PMID:Norovirus GII.4 strain antigenic variation. 2098 May 8

Human herpes virus 6 (HHV-6) infects > 95% of humans. Primary infection which occurs mostly during the first 2 years of life in the form of roseola infantum, non-specific febrile illness, or an asymptomatic illness, results in latency. Reactivation of latent HHV-6 is common after liver transplantation. Since the majority of human beings harbor the latent virus, HHV-6 infections after liver transplantation are most probably caused by endogenous reactivation or superinfection. In a minority of cases, primary HHV-6 infection may occur when an HHV-6-seronegative individual receives a liver allograft from an HHV-6-seropositive donor. The vast majority of HHV-6 infections after liver transplantation are asymptomatic. Only in a minority of cases, when HHV-6 causes a febrile illness associated with rash and myelosuppression, hepatitis, gastroenteritis, pneumonitis, and encephalitis after liver transplantation. In addition, HHV-6 has been implicated in a variety of indirect effects, such as allograft rejection and increased predisposition to and severity of other infections, including cytomegalovirus, hepatitis C virus, and opportunistic fungi. Because of the uncommon nature of the clinical illnesses directly attributed to HHV-6, there is currently no recommended HHV-6-specific approach prevention after liver transplantation. Asymptomatic HHV-6 infection does not require antiviral treatment, while treatment of established HHV-6 disease is treated with intravenous ganciclovir, foscarnet, or cidofovir and this should be complemented by a reduction in immunosuppression.
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PMID:Impact of human herpes virus 6 in liver transplantation. 2116 Oct 19

Human noroviruses are a major cause of food-borne illness, accountable for 50% of all-etiologies outbreaks of acute gastroenteritis (in both developing and developed countries). There is no vaccine or antiviral drug for the prophylaxis or treatment of norovirus-induced gastroenteritis. We recently reported the inhibitory effect of 2'-C-methylcytidine (2CMC), a hepatitis C virus polymerase inhibitor, on the in vitro replication of murine norovirus (MNV). Here we evaluated the inhibitory effect of 2CMC on in vitro human norovirus replication through a Norwalk virus replicon model and in a mouse model by using AG129 mice orally infected with MNV. Survival, weight, and fecal consistency were monitored, and viral loads in stool samples and organs were quantified. Intestines were examined histologically. 2CMC reduced Norwalk virus replicon replication in a dose-dependent manner and was able to clear cells of the replicon. Treatment of MNV-infected AG129 mice with 2CMC (i) prevented norovirus-induced diarrhea; (ii) markedly delayed the appearance of viral RNA and reduced viral RNA titers in the intestine, mesenteric lymph nodes, spleen, lungs, and stool; (iii) completely prevented virus-induced mortality; and (iv) resulted in protective immunity against a rechallenge. We demonstrate for the first time that a small-molecule inhibitor of norovirus replication protects from virus-induced disease and mortality in a relevant animal model. These findings pave the way for the development of potent and safe antivirals as prophylaxis and therapy of norovirus infection.
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PMID:The viral polymerase inhibitor 2'-C-methylcytidine inhibits Norwalk virus replication and protects against norovirus-induced diarrhea and mortality in a mouse model. 2398 82

Originally developed and commercialized as an antiprotozoal agent, nitazoxanide was later identified as a first-in-class broad-spectrum antiviral drug and has been repurposed for the treatment of influenza. A Phase 2b/3 clinical trial recently published in The Lancet Infectious Diseases found that oral administration of nitazoxanide 600mg twice daily for five days reduced the duration of clinical symptoms and reduced viral shedding compared to placebo in persons with laboratory-confirmed influenza. The same study also suggested a potential benefit for subjects with influenza-like illness who did not have influenza or other documented respiratory viral infection. From a chemical perspective, nitazoxanide is the scaffold for a new class of drugs called thiazolides. These small-molecule drugs target host-regulated processes involved in viral replication. Nitazoxanide is orally bioavailable and safe with extensive post-marketing experience involving more than 75 million adults and children. A new dosage formulation of nitazoxanide is presently undergoing global Phase 3 clinical development for the treatment of influenza. Nitazoxanide inhibits a broad range of influenza A and B viruses including influenza A(pH1N1) and the avian A(H7N9) as well as viruses that are resistant to neuraminidase inhibitors. It is synergistic with neuraminidase inhibitors, and combination therapy with oseltamivir is being studied in humans as part of ongoing Phase 3 clinical development. Nitazoxanide also inhibits the replication of a broad range of other RNA and DNA viruses including respiratory syncytial virus, parainfluenza, coronavirus, rotavirus, norovirus, hepatitis B, hepatitis C, dengue, yellow fever, Japanese encephalitis virus and human immunodeficiency virus in cell culture assays. Clinical trials have indicated a potential role for thiazolides in treating rotavirus and norovirus gastroenteritis and chronic hepatitis B and chronic hepatitis C. Ongoing and future clinical development is focused on viral respiratory infections, viral gastroenteritis and emerging infections such as dengue fever.
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PMID:Nitazoxanide: a first-in-class broad-spectrum antiviral agent. 2510 73


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