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Fatal Disease (fatal + disease)

Distribution by Scientific Domains

Medical Sciences	63%
Life Sciences	27%

Selected Abstracts

A Geometric Approach to Comparing Treatments for Rapidly Fatal Diseases

BIOMETRICS, Issue 1 2006
Peter F. Thall
Summary In therapy of rapidly fatal diseases, early treatment efficacy often is characterized by an event, "response," which is observed relatively quickly. Since the risk of death decreases at the time of response, it is desirable not only to achieve a response, but to do so as rapidly as possible. We propose a Bayesian method for comparing treatments in this setting based on a competing risks model for response and death without response. Treatment effect is characterized by a two-dimensional parameter consisting of the probability of response within a specified time and the mean time to response. Several target parameter pairs are elicited from the physician so that, for a reference covariate vector, all elicited pairs embody the same improvement in treatment efficacy compared to a fixed standard. A curve is fit to the elicited pairs and used to determine a two-dimensional parameter set in which a new treatment is considered superior to the standard. Posterior probabilities of this set are used to construct rules for the treatment comparison and safety monitoring. The method is illustrated by a randomized trial comparing two cord blood transplantation methods. [source]

The immune response to Naegleria fowleri amebae and pathogenesis of infection

FEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 2 2007
Francine Marciano-Cabral
Abstract The genus Naegleria is comprised of a group of free-living ameboflagellates found in diverse habitats worldwide. Over 30 species have been isolated from soil and water but only Naegleria fowleri (N. fowleri) has been associated with human disease. Naegleria fowleri causes primary amebic meningoencephalitis (PAM), a fatal disease of the central nervous system. The pathogenesis of PAM and the role of host immunity to N. fowleri are poorly understood. Strategies for combating infection are limited because disease progression is rapid and N. fowleri has developed strategies to evade the immune system. The medical significance of these free-living ameboflagellates should not be underestimated, not only because they are agents of human disease, but also because they can serve as reservoirs of pathogenic bacteria. [source]

Effect of Clostridium perfringens epsilon toxin on MDCK cells

FEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 2 2001
Erika Borrmann
Abstract Epsilon toxin is one of the major lethal toxins produced by Clostridium perfringens type D and B. It is responsible for a rapidly fatal disease in sheep and other farm animals. Many facts have been published about the physical properties and the biological activities of the toxin, but the molecular mechanism of the action inside the cells remains unclear. We have found that the C. perfringens epsilon toxin caused a significant decrease of the cell numbers and a significant enlargement of the mean cell volume of MDCK cells. The flow cytometric analysis of DNA content revealed the elongation of the S phase and to a smaller extent of the G2+M phase of toxin-treated MDCK cells in comparison to untreated MDCK cells. The results of ultrastructural studies showed that the mitosis is disturbed and blocked at a very early stage, and confirmed the toxin influence on the cell cycle of MDCK cells. [source]

LDL-receptor mutations in Europe,

HUMAN MUTATION, Issue 6 2004
George V.Z. Dedoussis
Abstract Familial hypercholesterolemia (FH) is a clinical definition for a remarkable increase of cholesterol serum concentration, presence of xanthomas, and an autosomal dominant trait of either increased serum cholesterol or premature coronary artery disease (CAD). The identification of the low-density lipoprotein (LDL)-receptor (LDLR) as the underlying cause and its genetic characterization in FH patients revealed more insights in the trafficking of LDL, which primarily transports cholesterol to hepatic and peripheral cells. Mutations within LDLR result in hypercholesterolemia and, subsequently, cholesterol deposition in humans to a variable degree. This confirms the pathogenetic role of LDLR and also highlights the existence of additional factors in determining the phenotype. Autosomal dominant FH is caused by LDLR deficiency and defective apolipoprotein B-100 (APOB), respectively. Heterozygosity of the LDLR is relatively common (1:500). Clinical diagnosis is highly important and genetic diagnosis may be helpful, since treatment is usually effective for this otherwise fatal disease. Very recently, mutations in PCSK9 have been also shown to cause autosomal dominant hypercholesterolemia. For autosomal recessive hypercholesterolemia, mutations within the so-called ARH gene encoding a cellular adaptor protein required for LDL transport have been identified. These insights emphasize the crucial importance of LDL metabolism intra- and extracellularly in determining LDL-cholesterol serum concentration. Herein, we focus on the published European LDLR mutation data that reflect its heterogeneity and phenotypic penetrance. Hum Mutat 24:443,459, 2004. © 2004 Wiley-Liss, Inc. [source]

Childhood melanoma: update and treatment

INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 9 2005
Phung M. Huynh MD
Childhood melanoma is a rare but potentially fatal disease that is important to include in the differential diagnosis of any pigmented lesion in a child. The best prognosis is achieved with early diagnosis and definitive surgical excision. Adjuvant chemotherapy and immunotherapy are options for those with more advanced tumors. Melanoma in children must be treated as aggressively as in adults because childhood melanoma may be equally devastating. [source]

Thrombotic thrombocytopenic purpura: 24 years of experience at the American University of Beirut Medical Center

JOURNAL OF CLINICAL APHERESIS, Issue 3 2004
Ali Shamseddine
Abstract Thrombotic thrombocytopenic purpura (TTP) is a hematological syndrome defined by the presence of thrombocytopenia and microangiopathic hemolytic anemia without a clinically apparent etiology. Patients may also suffer from fever in addition to neurological and renal impairment. Treatment should be initiated as soon as possible, otherwise this rare disease can be fatal. The main treatment options include therapeutic plasma exchange, fresh frozen plasma infusion, and adjuvant agents such as steroids and antiplatelet drugs. A search of patient records was carried out at the American University of Beirut Medical Center looking for patients who developed TTP over a 24-year period extending from 1980 to 2003. Relevant information was collected and analyzed. A total of 47 records were found. All presented with anemia and thrombocytopenia, 83% had neurological symptoms, 61.7% had fever and 34% had renal impairment. All patients were treated with a multimodality regimen including therapeutic plasma exchange, FFP infusion, steroids, antiplatelet agents, vincristine and others. 38 (81%) cases achieved complete remission. Out of these, 12 (31.6%) relapsed and responded to treatment. Patients who did not receive plasma exchange were more likely to relapse (P = 0.032). A second relapse was observed in 6 cases. The overall mortality rate from TTP over 24 years was 21.3%. TTP remains a fatal disease. A high index of suspicion should, therefore, always be present. Treatment options should be further developed and patients should directly be referred to tertiary care centers. J. Clin. Apheresis 19:119,124, 2004. © 2004 Wiley-Liss, Inc. [source]

Spontaneous amyloidosis in twelve chimpanzees, Pan troglodytes

JOURNAL OF MEDICAL PRIMATOLOGY, Issue 5 2001
Gene B. Hubbard
Spontaneous amyloidosis was diagnosed in 11 male and 1 female chimpanzees and confirmed histologically and immunohistochemically. The chimpanzees were ,15 years of age when first diagnosed and averaged 22.4 years of age. The average survival time after diagnosis of systemic amyloidosis was 1.86 years with a standard deviation of 4.06 years (n=7). The chimpanzees with amyloidosis were asymptomatic except for hepatomegaly, which became more detectable with age. Significant increases in clinical chemistry values, as compared with referenced normals and established normals, of blood urea nitrogen (BUN), asparate aminotransferase (AST), gamma-glutamyltransferase (GGT), globulin, total protein, creatinine phosphokinase (CPK), sedimentation rate, and triglycerides were found in animals 7 years of age or older with amyloidosis. These serum chemistry values, while increased in chimpanzees with amyloidosis, were generally within normal limits. Immunohistochemistry for both amyloid A protein and amyloid P component-labeled extracellular amyloid in all chimpanzees with amyloidosis was determined. Amyloid was deposited primarily in the liver. Amyloidosis in the chimpanzee is a chronic, intractable, progressive, fatal disease, and appears to be similar to secondary amyloidosis in other species. [source]

Acute mesenteric venous thrombosis due to protein S deficiency in a pregnant woman

JOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 4 2009
p Atakan Al
Abstract Acute mesenteric venous thrombosis is a rare and potentially fatal disease, which often occurs in medically compromised elderly patients. Isolated mesenteric venous thrombosis may be encountered in young women who have underlying hypercoagulable disease. We report a case of mesenteric venous thrombosis in a young pregnant woman in whom protein S deficiency was diagnosed at a later stage. The patient underwent extensive bowel resection. On follow-up she had developed an obstruction on the intestinal anastomosis. The anastomosis was revised, but the patient died of intervening complications 3 months after the operation. Early management of acute mesenteric venous thrombosis relies on early diagnosis, which requires a high index of suspicion. The condition must be considered during evaluation of persistent abdominal pain in pregnant women with hypercoagulable disorder. [source]

Parkinsonism,dementia complex of Guam

MOVEMENT DISORDERS, Issue S12 2005
John C. Steele MD
Abstract On Guam and in two other Pacific locales, indigenous residents and immigrants are prone to familial neurodegeneration that manifests as atypical parkinsonism, dementia, motor neuron disease, or a combination of these three phenotypes. This progressive and fatal disease of the Mariana islands, the Kii peninsula of Japan, and the coastal plain of West New Guinea is similar and the pathological features have close affiliation with universal tauopathies, including progressive supranuclear palsy, Alzheimer's disease, and amyotrophic lateral sclerosis. The Chamorros of Guam call the disease lytico-bodig, and neuroscientists refer to it as the amyotrophic lateral sclerosis/Parkinsonism,dementia complex. During recent decades, its prevalence has declined progressively, and the age at onset has steadily increased. In 2004, motor neuron disease, once 100 times more common than elsewhere is rare, atypical parkinsonism is declining, and only dementia remains unusually common in elderly females. The cause of this obscure malady remains uncertain, despite 60 years of international research, but its ending implicates environmental influences rather than genetic predisposition. © 2005 Movement Disorder Society [source]

Infection of T lymphocytes in Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis in children of non-Asian origin

PEDIATRIC BLOOD & CANCER, Issue 2 2009
Karin Beutel MD
Abstract Background Epstein-Barr virus (EBV) is one of the most frequent triggers of hemophagocytic lymphohistiocytosis (HLH). EBV-associated HLH (EBV-HLH) and ectopic infection of T cells has been particularly described in patients from Far East Asia. Procedure In a cohort of 12 children with EBV-HLH treated in Germany, the EB viral load was detected by real-time polymerase chain reaction in plasma and peripheral blood mononuclear cells (PBMC). Virological and clinical data were analyzed retrospectively. Results Among the 12 mainly German patients, children with underlying immunodeficiencies as well as otherwise healthy individuals were affected. The clinical course ranged from a steroid-responding to a fatal disease despite intensive treatment. Increased EBV copy numbers in plasma and/or PBMC were found in all patients. Serial measurements reflected the course of the disease. Cell-type specific viral load was determined in seven patients and revealed EBV-infection of T cells in all of them. In contrast to the reported Asian patients a significant viral load was also found in B cells. Conclusions T cell infection appears to be a typical feature of EBV-associated HLH irrespective of patients ethnic background and the clinical course. Evaluation of cell-type specific infection should be considered when targeted therapy is applied. Pediatr Blood Cancer 2009;53:184,190. © 2009 Wiley-Liss, Inc. [source]

Malaria: clinical features and recommended management

PRESCRIBER, Issue 21 2006
DTM+H, Dan Wootton MRCP
Malaria is a life-threatening disease and its syndromes vary depending on the infecting species and previous exposure. Here, the authors look at the importance of prompt diagnosis and administration of appropriate treatment and discuss the role of the GP in managing this potentially fatal disease. Copyright © 2006 Wiley Interface Ltd [source]

Modulation of proteins in Naegleria fowleri amebae by bacteria

THE JOURNAL OF EUKARYOTIC MICROBIOLOGY, Issue 2 2005
ANGELA E. FRITZINGER
Naegleria fowleri are free-living amebae found in soil and freshwater habitats that cause a fatal disease in humans called Primary Amoebic Meningoencephalitis. In the natural environment, amebae feed on bacteria. In the infected host, the amebae lyse and ingest nerve tissue. Proteins that lyse and degrade bacteria and mammalian cells have been described and are termed as naegleriapores or pore-forming proteins (PFP). In order to prevent autolysis from PFPs, Naegleria may have developed mechanisms that enable the amebae to survive in the presence of cytolytic molecules. Recently, we have established that N. fowleri express a "CD59-like" surface protein, but the function of this protein in amebae has not been elucidated. In mammalian cells, CD59 is a complement,regulatory protein that inhibits complement-mediated lysis of cells expressing this protein. In the present study, expression of the "CD59-like" protein in response to bacteria and bacterial toxins was investigated. Co-culture of N. fowleri with log phase Escherichia coli or Pseudomonas aeruginosa resulted in differential expression of the "CD59-like" protein. Treatment of the amebae with bacterial toxin also affected expression of the protein. Scanning and transmission electron microscopy demonstrated morphological changes in N. fowleri following co-incubation with the bacteria. Under all conditions examined, the amebae remained intact and viable. The results of our study implicate a possible protective role of the "CD59-like" protein in response to bacterial predators and bacterial toxins. [source]

Calciphylaxis: Is There a Role for Parathyroidectomy?,

THE LARYNGOSCOPE, Issue 4 2000
Mark D. Kriskovich MD
Abstract Objective Calciphylaxis, a rare disorder typically affecting renal failure patients, results in vascular calcification with subsequent skin necrosis, gangrene, and often death from sepsis. Parathyroid hormone is thought to act as a tissue sensitizer leading to these soft tissue changes. As such, parathyroidectomy is often advocated to control this complicated condition. A discussion of calciphylaxis does not exist in the otolaryngology literature, and head and neck surgeons performing parathyroidectomy should be aware of this phenomenon. This study evaluates the success of parathyroidectomy in reversing the ill effects of calciphylaxis in both our patient population and the literature. Study Design Retrospective study and review of the literature. Methods Five patients with calciphylaxis treated at our institution were evaluated for mortality, surgical and perioperative complications, wound healing, and predictors of patient outcomes. Results Two patients died from sepsis and infectious complications of their calciphylaxis shortly after surgery. Of the three survivors, two later died (15 and 18 mo after surgery) from causes not directly related to calciphylaxis. The other long-term survivor required partial amputation of a leg for osteomyelitis. There was one operative complication, a wound infection requiring antibiotic therapy, drainage, and packing. Postoperative hypocalcemia required treatment in two patients. Immediate perioperative survival was more likely in patients with leukocyte counts less than 20,000 cells/mL. Conclusions Calciphylaxis is a serious disease and patients often succumb to sepsis and infectious complications. Patients with extremely high leukocyte counts from coexistent infections may have a worse prognosis. Although a conclusive effective therapy does not exist, parathyroidectomy can be safely performed and may benefit some patients with what is often an otherwise fatal disease. The literature to date generally confirms our findings. [source]

Genetic Admixture in Brazilians Exposed to Infection with Leishmania chagasi

ANNALS OF HUMAN GENETICS, Issue 3 2009
Nicholas A. Ettinger
Summary Visceral leishmaniasis (VL) in northeast Brazil is a disease caused by infection with the protozoan Leishmania chagasi. Infection leads to variable clinical outcomes ranging from asymptomatic infection to potentially fatal disease. Prior studies suggest the genetic background of the host contributes to the development of different outcomes after infection, although it is not known if ancestral background itself influences outcomes. VL is endemic in peri-urban areas around the city of Natal in northeast Brazil. The population of northeast Brazil is a mixture of distinct racial and ethnic groups. We hypothesized that some sub-populations may be more susceptible than others to develop different clinical outcomes after L. chagasi infection. Using microsatellite markers, we examined whether admixture of the population as a whole, or markers likely inherited from a distinct ethnic background, differed between individuals with VL, individuals with an asymptomatic infection, or individuals with no infection. There was no apparent significant difference in overall population admixture proportions among the three clinical phenotype groups. However, one marker on Chr. 22 displayed evidence of excess ancestry from putative ancestral populations among different clinical phenotypes, suggesting this region may contain genes determining the course of L. chagasi infection. [source]

Variant Creutzfeldt-Jakob Disease: implications for the health care system

AUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH, Issue 4 2005
R. A. Dunstan
The recognition of the first cases of variant Creutzfeldt-Jakob Disease in the United Kingdom (UK) in 1996 and the realisation that this new disease represented the human form of the cattle disease BSE has prompted a considerable investment in research, particularly in the UK, Europe and the United States (US). Much has been learnt about this disease but much is still unknown. Infectivity is not destroyed by conventional sterilisation and disinfection treatment methods. This, combined with the widespread distribution throughout the lymphoid system as well as the central nervous system, raises the spectre of transmission through both surgical and ophthalmological procedures. Reports in 2004 of two likely transfusion-transmitted cases of vCJD suggest the probability of infection through blood transfusion and tissue transplantation. The risk of hospital-based and community-based transmission has not been quantified. To complicate matters even further, there is no suitable ante-mortem screening test or effective treatment for this fatal disease. The incubation period prior to onset of clinical disease is many years and there is good evidence for the existence of subclinical infection and infectivity during this stage. The extent of under-diagnosis and misdiagnosis is probably significant, adding to the risk of human-to-human transmission. [source]

Clinicopathological findings associated with feline infectious peritonitis in Sydney, Australia: 42 cases (1990,2002)

AUSTRALIAN VETERINARY JOURNAL, Issue 11 2005
JM NORRIS
Objectives To review the clinicopathological findings in naturally-occurring, histopathologically confirmed cases of feline infectious peritonitis in client-owned cats in Sydney, Australia, with the purpose of identifying factors assisting in the diagnosis of this complex disease syndrome and to characterise the disease as it occurs in this region. Design Retrospective clinical study: the clinical records of all cats with histopathologically confirmed feline infectious peritonitis at the University Veterinary Centre Sydney and a private cat hospital in Sydney between 1990 and 2002 were reviewed for signalment, history, physical findings, diagnostic test results and the distribution of histological lesions throughout the body at necropsy. Results Forty-two cats met the inclusion criteria. Significant features of this study that unique to the contemporary literature are i) the over-representation of certain breeds (Burmese, Australian Mist, British Shorthaired, and Cornish Rex) and the under-representation of other breeds (Domestic Shorthaired, Persian); ii) the overrepresentation of males; iii) the tendency for effusive disease in Australian Mist cats and non-effusive disease in Burmese; iv) the even age distribution of disease seen in cats older than 2 years-of-age; and v) the presence of fulminant immune-mediated haemolytic anaemia in two cats in this study. Conclusion The study highlights the diverse range of clinical manifestations and the complexities experienced by clinicians in diagnosing this fatal disease. Some aspects of the epidemiology and clinical manifestations of feline infectious peritonitis appear different to the disease encountered in Europe and North America, most notably the over-representation of specific breeds and the presence of immune-mediated haemolytic anaemia. [source]

iNOS activity is critical for the clearance of Burkholderia mallei from infected RAW 264.7 murine macrophages

CELLULAR MICROBIOLOGY, Issue 2 2008
Paul J. Brett
Summary Burkholderia mallei is a facultative intracellular pathogen that can cause fatal disease in animals and humans. To better understand the role of phagocytic cells in the control of infections caused by this organism, studies were initiated to examine the interactions of B. mallei with RAW 264.7 murine macrophages. Utilizing modified kanamycin-protection assays, B. mallei was shown to survive and replicate in RAW 264.7 cells infected at multiplicities of infection (moi) of , 1. In contrast, the organism was efficiently cleared by the macrophages when infected at an moi of 10. Interestingly, studies demonstrated that the monolayers only produced high levels of TNF-,, IL-6, IL-10, GM-CSF, RANTES and IFN-, when infected at an moi of 10. In addition, nitric oxide assays and inducible nitric oxide synthase (iNOS) immunoblot analyses revealed a strong correlation between iNOS activity and clearance of B. mallei from RAW 264.7 cells. Furthermore, treatment of activated macrophages with the iNOS inhibitor, aminoguanidine, inhibited clearance of B. mallei from infected monolayers. Based upon these results, it appears that moi significantly influence the outcome of interactions between B. mallei and murine macrophages and that iNOS activity is critical for the clearance of B. mallei from activated RAW 264.7 cells. [source]

Clinical presentation, pathological features and natural course of metastatic uveal melanoma (MUM) as an orphan and commonly fatal disease

ACTA OPHTHALMOLOGICA, Issue 2009
R VAN GINDERDEUREN
Purpose Uveal melanoma (UM) is a rare disease characterized by an unpredictable course and variable outcome ranging from cure by local treatment to the occurrence of untreatable metastasis. The current project is focused on the characteristics of the metastatic phenotype of the disease Methods We performed data collection from 76 pts with MUM treated in Leuven between 1957-2008. Statistical analysis involved nonparametric technics, Kaplan Meyer and log rank test Results The median age at diagnosis of UM was 58 yrs (range 30-94). Common initial treatments were surgery (71%), brachytherapy (20%) and external beam RT (7%). Synchronous metastasis was found in only 9% of cases, all others had metachronous disease after a median interval of 40 mo (range, 7-420). Metastasis in >1 organ, was seen in 47% of cases. The most frequent metastatic site was the liver (96%), followed by lung, subcutaneous, bone and brain lesions. The median OS from diagnosis of UM was 46 months (range, 2-182), and only 4,5 months in pts with MUM (range, 1-128). 65% of MUM pts qualified for further treatment, The most common drugs given were DTIC, cisplatin, tamoxifen or phase I agents. Patient benefit (PR+SD) was seen in 16/45 pts (36%), including 2 PR Conclusion In this orphan disease with female predominance metastasis occurs late, is mainly found to the liver, and is associated with high morbidity, as >1/3 of pts do not qualify for further therapy. Advances in MUM can only be achieved by networking of sites interested in this tumour type with systematic collection of data and tissue to improve our understanding of the molecular biology of the disease [source]

Fatal Mediterranean spotted fever in Greece

CLINICAL MICROBIOLOGY AND INFECTION, Issue 6 2010
A. Papa
Clin Microbiol Infect 2010; 16: 589,592 Abstract Forty-five days after the first confirmed and fatal Crimean,Congo haemorrhagic fever (CCHF) case in Greece in 2008, a female patient with similar signs and symptoms (high fever, thrombocytopaenia) and resident of the same area, was admitted to the University General Hospital of Alexandroupolis. Before admission, she had visited a local hospital where a cephalosporin was prescribed. A rash manifested over subsequent days, which was misdiagnosed as an allergy to the drug. Upon admission to the University Hospital, she was given further antibiotics, including doxycycline; a few hours later, ribavirin was added because CCHF was suspected. After the patient's death, rickettsiosis caused by Rickettsia conorii conorii (Meditteranean spotted fever; MSF) was diagnosed. Extremely high values of interleukin (IL)-1ra, IL-6, interferon-,-inducible protein-10, monocyte chemoattractant protein-1 and an absence of tumour necrosis factor-, were observed. MSF is a potentially severe and even fatal disease resembling viral haemorrhagic fevers that has to be included in the differential diagnosis of febrile syndromes combined with thrombocytopaenia, even when a tick bite is not reported, and an eschar is absent. Physicians have to be aware of MSF in patients with severe disease who are returning from the Mediterranean area. [source]

Ancient Weapons for Attack and Defense: the Pore-forming Polypeptides of Pathogenic Enteric and Free-living Amoeboid Protozoa,

THE JOURNAL OF EUKARYOTIC MICROBIOLOGY, Issue 5 2004
MATTHIAS LEIPPE
ABSTRACT Pore-forming polypeptides have been purified from several amoeboid protozoans that are well-known human pathogens. Obligate enteric parasites, such as Entamoeba histolytica, and free-living but potentially highly pathogenic species, such as Naegleria fowleri, contain these cytolytic molecules inside cytoplasmic granules. Comprehensive functional and structural studies have been conducted that include isolation of the proteins from their natural sources, monitoring of their biological activity towards different targets, and molecular cloning of the genes of their precursors. In the case of the most prominent member of the protein family, with respect to protozoans, the three-dimensional structure of amoebapore A was solved recently. The amoebic pore-forming polypeptides can rapidly perforate human cells. The antibacterial activity of amoebapores and of related polypetides from free-living protozoa points to a more vital function of these molecules: inside the digestive vacuoles they combat growth of phagocytosed bacteria which are killed when their cytoplasmic membranes are permeabilized. The concommitant activity of these proteins towards host cells may be due to a coincidental selection for an efficient effector molecule. Nonetheless, several lines of evidence indicate that these factors are involved in pathogenesis of fatal diseases induced by amoeboid protozoa. [source]

Oral vaccines: new needs, new possibilities

BIOESSAYS, Issue 6 2007
Mohd Azhar Aziz
Vaccination is an important tool for handling healthcare programs both in developed and developing countries. The current global scenario calls for a more-efficacious, acceptable, cost-effective and reliable method of immunization for many fatal diseases. It is hoped that the adoption of oral vaccines will help to provide an effective vaccination strategy, especially in developing countries. Mucosal immunity generated by oral vaccines can serve as a strong first line of defense against most of the pathogens infecting through the mucosal lining. Advances in elucidating the mechanism of action of oral vaccines will facilitate the design of more effective, new generation vaccines. There are promising developments in the use of different agents to effectively deliver the vaccine candidate. It is hoped that ongoing research may be able to set another cardinal point, after polio vaccine, in eradicating infectious diseases. BioEssays 29:591,604, 2007. © 2007 Wiley Periodicals, Inc. [source]