In medicine, infectious disease or communicable disease is disease caused by a biological agent such as by a virus, bacterium or parasite. This is contrasted to physical causes, such as burns or chemical ones such as through intoxication.

Basics

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Infectious diseases are the invasion of a host organism by a foreign replicator, generally microorganisms, often called microbes, that are invisible to the naked eye. Microbes that cause illness are also known as pathogens. The most common pathogens are various bacteria and viruses, though a number of other microorganisms, including some kinds of fungi and protozoa, also cause disease. Prions are borderline, and memes would not usually be considered in this scope. An infectious disease is termed contagious if it is easily transmitted from one person to another.

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NEJM — Collection Updates for Infectious Diseases

OTHER POINTS OF VIEW: When to Consider the Use of Antibiotics in the Treatment of 2009 H1N1 Influenza–Associated Pneumonia
We are now facing a pandemic caused by an epidemiologically distinct, novel virus, the 2009 pandemic influenza A (H1N1) virus (swine flu), against which few persons born since 1970 have...
OTHER POINTS OF VIEW: Antiviral Treatment for Patients Hospitalized with 2009 Pandemic Influenza A (H1N1)
With the 2009 H1N1 pandemic well under way, many clinicians are providing care to patients with influenza. Previously, although antiviral treatment was recommended,12 clinicians may not always have prescribed it...
CORRESPONDENCE: Emergence of Oseltamivir-Resistant Pandemic H1N1 Virus during Prophylaxis
Mariana Baz, M.Sc., Yacine Abed, Ph.D., Jesse Papenburg, M.D., Xavier Bouhy, B.Sc., Marie-Ève Hamelin, Ph.D., and Guy Boivin, M.D.To the Editor: Neuraminidase inhibitors (oseltamivir and zanamivir) are recommended for treatment of severe illness caused by the 2009 pandemic influenza A (H1N1) virus, and their use has also been...

BMC Infectious Diseases - Latest Articles

Destructive arthritis in a patient with chikungunya virus infection with persistent specific IgM antibodies
Denis MalvyKhaled EzzedineMaria Mamani-MatsudaBrigitte AutranHughes TolouMarie-Catherine ReceveurThierry PistoneJerome RambertDaniel MoynetDjavad Mossalayi Thu, 10 Dec 2009 00:00:00 -0000
Background: Chikungunya fever is an emerging arboviral disease characterized by an algo-eruptive syndrome, inflammatory polyarthralgias, or tenosynovitis that can last for months to years. Up to now, the pathophysiology of the chronic stage is poorly understood.Case presentationWe report the first case of CHIKV infection with chronic associated rheumatism in a patient who developed progressive erosive arthritis with expression of inflammatory mediators and persistence of specific IgM antibodies over 24 months following infection. Conclusions: Understanding the specific features of chikungunya virus as well as how the virus interacts with its host are essential for the prevention, treatment or cure of chikungunya disease.
Cryptic Leishmania infantum infection in Italian HIV infected patients
Claudia ColombaLaura SaporitoFabrizio VitaleStefano RealeGiustina VitaleAlessandra CasuccioManlio TolomeoDaniela MarantoRaffaella RubinoPaola Di CarloLucina Titone Thu, 10 Dec 2009 00:00:00 -0000
Background: Visceral leishmaniasis (VL) is a protozoan diseases caused in Europe by Leishmania (L.) infantum. Asymptomatic Leishmania infection is more frequent than clinically apparent disease. Among HIV infected patients the risk of clinical VL is increased due to immunosuppression, which can reactivate a latent infection. The aims of our study were to assess the prevalence of asymptomatic L. infantum infection in HIV infected patients and to study a possible correlation between Leishmania parasitemia and HIV infection markers. Methods: One hundred and forty-five HIV infected patients were screened for the presence of anti-Leishmania antibodies and L. infantum DNA in peripheral blood. Statistical analysis was carried out by using a univariate regression analysis. Results: Antibodies to L. infantum were detected in 1.4% of patients. L. infantum DNA was detected in 16.5% of patients. Significant association for PCR-Leishmania levels with plasma viral load was documented (p=0.0001). Conclusions: In our area a considerable proportion of HIV infected patients are asymptomatic carriers of L. infantum infection. A relationship between high HIV viral load and high parasitemic burden, possibly related to a higher risk of developing symptomatic disease, is suggested. PCR could be used for periodic screening of HIV patients to individuate those with higher risk of reactivation of L. infantum infection.
Combination antiretroviral drugs in PLGA nanoparticle for HIV-1
Christopher DestacheTodd BelgumKeith ChristensenAnnemarie ShibataAkhilesh SharmaAlekha Dash Wed, 09 Dec 2009 00:00:00 -0000
Background: Combination antiretroviral (AR) therapy continues to be the mainstay for HIV treatment. However, antiretroviral drug nonadherence can lead to the development of resistance and treatment failure. We have designed nanoparticles (NP) that contain three AR drugs and characterized the size, shape, and surface charge. Additionally, we investigated the in vitro release of the AR drugs from the NP using peripheral blood mononuclear cells (PBMCs). Methods: Poly-(lactic-co-glycolic acid) (PLGA) nanoparticles (NPs) containing ritonavir (RTV), lopinavir (LPV), and efavirenz (EFV) were fabricated using multiple emulsion-solvent evaporation procedure. The nanoparticles were characterized by electron microscopy and zeta potential for size, shape, and charge. The intracellular concentration of AR drugs was determined over 28 days from NPs incubated with PBMCs. Macrophages were imaged by fluorescent microscopy and flow cytometry after incubation with fluorescent NPs. Finally, macrophage cytotoxicity was determined by MTT assay. Results: Nanoparticle size averaged 262 + 83.9 nm and zeta potential -11.4 + 2.4. AR loading averaged 4% (w/v). Antiretroviral drug levels were determined in PBMCs after 100 mcg of NP in 75 mcL PBS was added to media. Intracellular peak AR levels from NPs (day 4) were RTV 2.5 + 1.1; LPV 4.1 + 2.0; and EFV 10.6 + 2.7 mcg and continued until day 28 (all AR > 0.9 mcg). Free drugs (25 mcg of each drug in 25 mcL ethanol) added to PBMCs served as control were eliminated by 2 days. Fluorescence microscopy and flow cytometry demonstrated phagocytosis of NP into monocytes-derived macrophages (MDMs). Cellular MTT assay performed on MDMs demonstrated that NPs are not significantly cytotoxic. Conclusions: These results demonstrated AR NPs could be fabricated containing three antiretroviral drugs (RTV, LPV, EFV). Sustained release of AR from PLGA NP show high drug levels in PBMCs until day 28 without cytotoxicity.

pubmed: 0019-9567

Genetic control of the innate immune response to Borrelia hermsii influences the course of relapsing fever in inbred strains of mice.
Benoit VM, Petrich A, Alugupalli KR, Marty-Roix R, Moter A, Leong JM, Boyartchuk VL Genetic control of the innate immune response to Borrelia hermsii influences the course of relapsing fever in inbred strains of mice. Infect Immun. 2009 Dec 7; Authors: Benoit VM, Petrich A, Alugupalli KR, Marty-Roix R, Moter A, Leong JM, Boyartchuk VL Host susceptibility to infection is controlled in large measure by the genetic makeup of the host. Spirochetes of the genus Borrelia include nearly 40 species of vector-borne spirochetes that are capable of infecting a wide range of mammalian hosts, causing Lyme disease and relapsing fever. Relapsing fever is associated with high-level bacteremia, as well as hematologic manifestations such as thrombocytopenia (i.e. low platelet numbers) and anemia. To facilitate studies of genetic control of susceptibility to Borrelia hermsii infection we performed a systematic analysis of the course of infection using immunocompetent and immunocompromised inbred strains of mice. Our analysis revealed that sensitivity to B. hermsii infections is genetically controlled. In addition, whereas the role of adaptive immunity to relapsing fever spirochetes is well documented, we found that innate immunity contributes significantly to reduction of bacterial burden. Similar to human infection, progression of the disease in mice was associated with thrombocytopenia and anemia. Histological and fluorescence in situ hybridization (FISH) analysis of infected tissues indicated that red blood cells were removed by tissue resident macrophages, a process that could lead to anemia. Spirochetes in the spleen and liver were often visualized associated with RBCs, lending support to the hypothesis that direct interaction of B. hermsii spirochetes with RBCs leads to clearance of bacteria from the bloodstream by tissue phagocytes. PMID: 19995898 [PubMed - as supplied by publisher]
Mycoplasma genitalium Rapidly Disseminates to the Upper Reproductive Tract and Knees of Female Mice Following Vaginal Inoculation.
McGowin CL, Spagnuolo RA, Pyles RB Mycoplasma genitalium Rapidly Disseminates to the Upper Reproductive Tract and Knees of Female Mice Following Vaginal Inoculation. Infect Immun. 2009 Dec 7; Authors: McGowin CL, Spagnuolo RA, Pyles RB Mycoplasma genitalium is an emerging sexually transmitted infection and is associated with notable reproductive tract syndromes in women such as cervicitis, pelvic inflammatory disease and infertility. Investigations into the causal relationships of M. genitalium and clinical disease have been hindered largely by the lack of a well-established small animal model of genital tract infection. To establish a murine model, female Swiss Webster mice were conditioned with either progesterone or estradiol and then inoculated intravaginally with M. genitalium type strain G37 or a contemporary Danish strain, M2300. Persistent lower tract infection was observed up to 77 d post-inoculation (PI). Upper reproductive tract colonization was observed as early as 3 d PI with long-term infection observed in estradiol- (65%) and progesterone-treated (18%) animals. In the upper tract, more than 90% of M. genitalium PCR-positive samples were from the uterus and oviducts. Ultimately, gross hydrosalpinx was observed 21 d to 10 weeks PI in approximately 60% of infected animals suggesting tubal occlusion. In addition, dissemination of M. genitalium to the knee tissues was observed as early as 7 d PI with persistent infection detected up to 28 d PI. Mice infected with M. genitalium also developed specific antibodies to the major antigenic outer membrane protein MgPa, elongation factor Tu, pyruvate dehydrogenase E1alpha and DnaK (Hsp70) indicating persistent infection despite a robust humoral responses to infection. These findings provide strong experimental evidence that M. genitalium can establish long-term infection of reproductive tract and joint tissues with preliminary evidence of pathological reproductive tract outcomes. PMID: 19995897 [PubMed - as supplied by publisher]
Morphine Disrupts the IL-23/IL-17 Mediated Pulmonary Mucosal Host Defense Against S. pneumoniae Infection.
Ma J, Wang J, Wan J, Charboneau R, Chang Y, Barke RA, Roy S Morphine Disrupts the IL-23/IL-17 Mediated Pulmonary Mucosal Host Defense Against S. pneumoniae Infection. Infect Immun. 2009 Dec 7; Authors: Ma J, Wang J, Wan J, Charboneau R, Chang Y, Barke RA, Roy S S. pneumoniae is a pathogen that causes serious respiratory disease and meningitis in the immunocompromised drug abuse population. However, the precise mechanisms by which drug abuse compromises the host immune defense to pulmonary S. pneumoniae infection is not fully understood. Using a well-established murine model of opiate abuse and S. pneumoniae lung infection, we explored the influence of morphine treatment on the IL-23/IL-17 axis and related innate immunity. Impairment of early IL-23/IL-17 production caused by morphine treatment was associated with delayed neutrophil migration and decreased pneumococcal clearance. Furthermore, morphine treatment impaired MyD88 dependent IL-23 production in alveolar macrophages and dendritic cells in response to in vitro S. pneumoniae cell infection. Moreover, morphine treatment significantly inhibited the S. pneumoniae induced phosphorylation of IRF3, ATF2, and NF-kappaBp65. TCRdelta deficient mice showed a decrease in IL-17 production and a severely weakened capacity to clear lung S. pneumoniae infection. Finally, morphine treatment resulted in diminished secretion of antimicrobial proteins S100A9 and S100A8/A9 during early stages of S. pneumoniae infection. In conclusion, morphine treatment causes a dysfunction in IL-23-producing dendritic cells and macrophages, and IL-17- producing gammadeltaT lymphocytes in response to S. pneumoniae lung infection. This leads to diminished release of anti-microbial proteins S100A8/A9 proteins, compromised neutrophil recruitment, and more severe infection. PMID: 19995896 [PubMed - as supplied by publisher]
Protection against lethal Neospora caninum infection in mice induced by heterologous vaccination with a mic1-3 knockout Toxoplasma gondii strain.
Penarete Vargas DM, Mévélec MN, Dion S, Sèche E, Dimier-Poisson I, Fandeur T Protection against lethal Neospora caninum infection in mice induced by heterologous vaccination with a mic1-3 knockout Toxoplasma gondii strain. Infect Immun. 2009 Dec 7; Authors: Penarete Vargas DM, Mévélec MN, Dion S, Sèche E, Dimier-Poisson I, Fandeur T Neospora caninum and Toxoplasma gondii are closely related, obligate intracellular parasites infecting a wide range of vertebrate hosts and causing abortion and neonatal morbidity and mortality. Several lines of evidence suggest that cross immunity between these two pathogens could be exploited in the design of strategies for heterologous vaccination. We assessed the ability of an attenuated strain of T. gondii (mic1-3KO) conferring strong protection against chronic and congenital toxoplasmosis to protect mice against lethal N. caninum infection. Mice immunized with mic1-3KO tachyzoites, by the oral and intraperitoneal routes, developed a strong cellular Th1 response and displayed significant protection against lethal heterologous N. caninum infection, with survival rates of 70% and 80%, respectively; whereas only 30% of the non immunized mice survived. We report here the acquisition of heterologous protective immunity against N. caninum following immunization with a live attenuated mic1-3KO strain of T. gondii. PMID: 19995895 [PubMed - as supplied by publisher]
Cytolethal Distending Toxin from Aggregatibacter actinomycetemcomitans induces DNA damage, S/G2 cell cycle arrest and caspase-independent death in budding yeast model.
Matangkasombut O, Wattanawaraporn R, Tsuruda K, Ohara M, Sugai M, Mongkolsuk S Cytolethal Distending Toxin from Aggregatibacter actinomycetemcomitans induces DNA damage, S/G2 cell cycle arrest and caspase-independent death in budding yeast model. Infect Immun. 2009 Dec 7; Authors: Matangkasombut O, Wattanawaraporn R, Tsuruda K, Ohara M, Sugai M, Mongkolsuk S Cytolethal Distending Toxin (CDT) is a bacterial toxin that induces G2/M cell cycle arrest, cell distension, and/or apoptosis in mammalian cells. It is produced by several Gram-negative species and may contribute to their pathogenicity. The catalytic subunit, CdtB, has homology with DNaseI and may act as a genotoxin. However, the mechanism how CdtB leads to cell death is not yet clearly understood. Here we used yeast as a model to study the molecular pathways involved in the function of CdtB from Aggregatibacter actinomycetemcomitans (Aa), a cause of aggressive periodontitis. We show that AaCdtB expression induces S/G2 arrest and death in a DNase-catalytic residue and nuclear-localization dependent manner in haploid yeasts. Yeast strains defective in homologous recombination (HR) repair, but not other DNA repair pathways, are hypersensitive to AaCdtB, suggesting that HR is required for survival upon CdtB expression. In addition, yeast does not harbor the substrate for the other activity proposed for CdtB function, that is phosphatidylinositol-3,4,5-triphosphate phosphatase. Thus, these results suggest that direct DNA damaging activity alone is sufficient for CdtB toxicity. To investigate how CdtB induces cell death, we examined the effect of CdtB in yeast strains with mutations in apoptotic regulators. Our results suggest that yeast death occurs independently of the yeast metacaspase, YCA1, and Apoptosis Inducing Factor, AIF1, but is partially dependent on histone H2B serine 10 phosphorylation. Therefore, we report here the evidence that AaCdtB causes DNA damage that leads to non-apoptotic death in yeast, and the first mutation that confers resistance to CdtB. PMID: 19995894 [PubMed - as supplied by publisher]
Treponema denticola suppresses expression of human beta-defensin-3 in gingival epithelial cells through inhibition of TLR2 axis.
Shin JE, Kim YS, Oh JE, Min BM, Choi Y Treponema denticola suppresses expression of human beta-defensin-3 in gingival epithelial cells through inhibition of TLR2 axis. Infect Immun. 2009 Dec 7; Authors: Shin JE, Kim YS, Oh JE, Min BM, Choi Y We previously reported that Treponema denticola, one of periodontal pathogens, suppresses the expression of human beta-defensins (HBDs) in human gingival epithelial cells. To identify the mechanisms involved in this suppression, immortalized and normal human gingival epithelial cells were infected with live or heat-killed T. denticola for 24 h, and then the expression of HBDs was examined by real-time RT-PCR. Live T. denticola suppressed the expression of HBD-3 substantially and also suppressed the expression of HBD-1 and -2. However, heat-killed bacteria did not produce a suppressive effect, but instead slightly up-regulated the levels of HBD-2 and -3. In contrast to live T. denticola, which reduced the activation of MAPK and NF-kappaB within an hour of infection, heat-killed bacteria did not show any inhibitory effect on those signaling pathways. Knock-down of toll-like receptor (TLR) 2 via RNA interference abrogated the suppressive effect of T. denticola on the expression of HBD-3. Heat-killed T. denticola but not live bacteria could activate TLR2 in CHO/CD14/TLR2 reporter cells, suggesting that T. denticola contains heat-labile inhibitor(s) of TLR2 in addition to ligands recognized by TLR2. Indeed, live T. denticola was able to inhibit TLR2 activation by Pam3CSK. In conclusion, T. denticola suppressed the expression of HBD-3 by inhibiting the TLR2 axis in gingival epithelial cells. These results may provide new insight into the pathogenesis of periodontitis caused by T. denticola. PMID: 19995893 [PubMed - as supplied by publisher]

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