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

EDITORIAL: Antimicrobial Prophylaxis for Urinary Tract Infection in Children
Alejandro Hoberman, M.D., and Ron Keren, M.D., M.P.H.Approximately one third of children who have a urinary tract infection — the most frequent serious bacterial infection in young febrile children — have vesicoureteral reflux, a congenital condition in...
EDITORIAL: Yeast Infections — Human Genetics on the Rise
Steven M. Holland, M.D., and Donald C. Vinh, M.D.We lead inextricably mycotic lives: yeasts leaven our bread, ferment our wine and beer, and inhabit our skins, mouths, and gastrointestinal tracts; however, not all is harmony. Hippocrates reported aphthous...
CASE RECORDS OF THE MASSACHUSETTS GENERAL HOSPITAL: Case 34-2009 — A 20-Year-Old Man with Sore Throat, Fever, and Rash
Charles R. Taylor, M.D., Rajesh T. Gandhi, M.D., Jason Handwerker, M.D., and Lyn M. Duncan, M.D.Dr. Robert W. McGarrah (Medicine): A 20-year-old man was admitted to this hospital because of sore throat, fever, and a diffuse rash.The patient had been well until approximately 4 weeks...

Centers for Disease Control and Prevention

Media Briefing on Antiviral Guidance and 2009 H1N1 Flu
Tue, 08 Sep 2009 12:00:00 -0500
CDC will host a press conference on its updated guidelines on antivirals as well as an update on 2009 H1N1 flu.
Weekly Update on 2009 H1N1 Flu
Wed, 02 Sep 2009 12:00:00 -0500
CDC will host a press conference to update on 2009 H1N1 Flu.
CDC to Distribute $40 Million in Recovery Act Funding to Help States Fight Healthcare-Associated Infections
Tue, 01 Sep 2009 12:00:00 -0500
The Centers for Disease Control and Prevention today announced plans to distribute $40 million to state health departments to help prevent healthcare-associated infections (HAIs).

BMC Infectious Diseases - Latest Articles

Uptake of meningococcal conjugate vaccine among adolescents in large managed care organizations, United States, 2005: Demand, supply and seasonality.
Suchita LorickDaniel FishbeinEric WeintraubPascale WortleyGrace LeeFangjun ZhouRobert Davis Tue, 03 Nov 2009 00:00:00 -0000
Background: In February 2005, the US Advisory Committee on Immunization Practices recommended the new meningococcal conjugate vaccine (MCV4) for routine use among 11- to 12-year-olds (at the preadolescent health-care visit), 14- to 15-year-olds (before high-school entry), and groups at increased risk. Vaccine distribution started in March; however, in July, the manufacturer reported inability to meet demand and widespread MCV4 shortages were reported. Our objectives were to determine early uptake patterns among target (11-12 and 14-15 year olds) and non-target (13- plus 16-year-olds) age groups. A post hoc analysis was conducted to compare seasonal uptake patterns of MCV4 with polysaccharide meningococcal (MPSV4) and tetanus diphtheria (Td) vaccines. Methods: We analyzed data for adolescents 11-16 years from five managed care organizations participating in the Vaccine Safety Datalink (VSD). For MCV4, we estimated monthly and cumulative coverage during 2005 and calculated risk ratios. For MPSV4 and Td, we combined 2003 and 2004 data and compared their seasonal uptake patterns with MCV4. Results: Coverage for MCV4 during 2005 among the 623,889 11-16 years olds was 10%. Coverage for 11-12 and 14-15 year olds was 12% and 11%, respectively, compared with 8% for 13- plus 16-year-olds (p<0.001). Of the 64,272 MCV4 doses administered from March-December 2005, 73% were administered June-August. Fifty-nine percent of all MPSV4 doses and 38% of all Td doses were administered during June-August. Conclusions: A surge in vaccine uptake between June and August was observed among adolescents for MCV4, MPSV4 and Td vaccines. The increase in summer-time vaccinations and vaccination of non-targeted adolescents coupled with supply limitations likely contributed to the reported shortages of MCV4 in 2005.
Downregulation of MIP-1alpha/CCL3 with praziquantel treatment in Schistosoma haematobiumand HIV-1 co-infected individuals in a rural community in Zimbabwe
R Zinyama-GutsireE GomoP KallestrupC ErickstrupH UllumA ButterworthS MunyatiT Mduluza Fri, 23 Oct 2009 00:00:00 -0000
Background: Chemokines have been reported to play an important role in granulomatous inflammation during Schistosoma mansoni infection. However there is less information on their role in Schistosoma haematobium infection, or on the effect of concurrent HIV-1 infection, as a potential modifying influence. Methods: To determine levels of MIP-1α/CCL3 chemokine in plasma of S. haematobium and HIV-1 co-infected and uninfected individuals in a rural black Zimbabwean community.A cohort was established of HIV-1 and schistosomiasis infection and co-infection comprising 379 participants. Outcome measures consisted of HIV-1 and schistosomiasis status and levels of MIP-1α/CCL3 in plasma at baseline and three months post treatment. An association was established between MIP-1α/CCL3 plasma levels with HIV-1 and S. haematobium infections. Results: A total of 379 adults formed the established cohort comprising 76 (20%) men and 303 (80%) women. Mean age was 33.25, range 17 - 62 years. The median MIP-1α/CCL3 plasma concentration was significantly higher in S. haematobium infected compared with uninfected individuals (p = 0.029). In contrast, there was no difference in the median MIP-1α/CCL3 levels between HIV-1 positive and negative individuals (p = 0.631). MIP-1α/CCL3 concentration in plasma was significantly reduced at three months after treatment with praziquantel (p = 000). Conclusion: The results of our study show that the MIP-1α/CCL3 levels were positively associated with S. haematobium egg counts at baseline but not with HIV-1 infection status. MIP-1α/CCL3 levels were significantly reduced at three months post treatment with praziquantel. We therefore conclude that MIP-1α/CCL3 is produced during infection with S haematobium. S. haematobium infection is associated with increased MIP-1α/CCL3 levels in an egg intensity-dependent manner and treatment of S. haematobium is associated with a reduction in MIP-1α/CCL3.
Acute sensorineural hearing loss and severe otalgia due to scrub typhus
Ji-In KangDong-Min KimJun Han Lee Thu, 22 Oct 2009 00:00:00 -0000
Background: Scrub typhus is an acute febrile illness caused by Orientia tsutsugamushi.Case presentations: We encountered a patient with sensorineural hearing loss complicating scrub typhus, and three patients with scrub typhus who complained of otalgia, which was sudden onset, severe, paroxysmal, intermittent yet persistent pain lasting for several seconds, appeared within 1 week after the onset of fever and rashesrash. The acute sensorineural hearing loss and otalgia were resolved after antibiotic administration. Conclusion: When patients in endemic areas present with fever and rash and have sensorineural hearing loss or otalgia without otoscopic abnormalities, clinicians should suspect scrub typhus and consider empirical antibiotic therapy.

pubmed: 0019-9567

Identification of a Claudin-4 residue important for mediating the host cell binding and action of Clostridium perfringens enterotoxin.
Robertson SL, Smedley JG, McClane BA Identification of a Claudin-4 residue important for mediating the host cell binding and action of Clostridium perfringens enterotoxin. Infect Immun. 2009 Nov 2; Authors: Robertson SL, Smedley JG, McClane BA The 24-member claudin protein family plays a key role in maintaining the normal structure and function of epithelial tight junctions. Previous studies with fibroblast transfectants and naturally-sensitive Caco-2 cells have also implicated certain claudins (e.g., Claudin-4) as receptors for Clostridium perfringens enterotoxin (CPE). The current study first provided evidence that the second extracellular loop (ECL-2) of claudins is specifically important for mediating the host cell binding and cytotoxicity of native CPE. Rat fibroblast transfectants expressing a Claudin-4 chimera, where the natural ECL-2 was replaced by ECL-2 from Claudin-2, exhibited no CPE-induced cytotoxicity. Conversely, CPE bound to, and killed, CPE-treated transfectants expressing a Claudin-2 chimera with a substituted ECL-2 from Claudin-4. Site-directed mutagenesis was then employed to alter an ECL-2 residue that invariably aligns as N in claudins known to bind native CPE, but as D or S in claudins that cannot bind CPE. Transfectants expressing a Claudin-4N149D mutant lost the ability to bind or respond to CPE, while transfectants expressing a Claudin-1 mutant with the corresponding ECL-2 residue changed from D to N acquired CPE binding and sensitivity. Identifying carriage of this N residue in ECL-2 as being important for native CPE binding helps to explain why only certain claudins can serve as CPE receptors. Finally, preincubating CPE with soluble recombinant Claudin-4, or Claudin-4 fragments containing ECL-2, specifically blocked the cytotoxicity on Caco-2 cells. This result opens the possibility of using receptor claudins as therapeutic decoys to ameliorate CPE-mediated intestinal disease. PMID: 19884339 [PubMed - as supplied by publisher]
Neither Mosquito Saliva nor Immunity to Saliva has a Detectable Effect on Infectivity of Plasmodium Sporozoites Injected into Mice.
Kebaier C, Voza T, Vanderberg J Neither Mosquito Saliva nor Immunity to Saliva has a Detectable Effect on Infectivity of Plasmodium Sporozoites Injected into Mice. Infect Immun. 2009 Nov 2; Authors: Kebaier C, Voza T, Vanderberg J Malaria infection is initiated when a female Anopheles mosquito probing for blood injects saliva together with sporozoites into the skin of its mammalian host. Prior studies had suggested that saliva may enhance sporozoite infectivity. Using rodent malaria models (Plasmodium berghei and P. yoelii), we were unable to show that saliva had any detectable effect on sporozoite infectivity. This is encouraging for plans to immunize humans with washed, attenuated P. falciparum sporozoites because many individuals develop cutaneous, hypersensitivity reactions to mosquito saliva after repeated exposure. If washed sporozoites have no appreciable loss of infectivity, they likely do not have decreased immunogenicity; thus vaccinees are unlikely to develop cutaneous reactions against mosquito saliva during attempted immunization with such sporozoites. Earlier studies also suggested that repeated prior exposure to mosquito saliva reduces infectivity of sporozoites injected by mosquitoes into sensitized hosts. However, our own studies show that prior exposure of mice to saliva had no detectable effect on numbers of sporozoites delivered by infected mosquitoes, the rate of disappearance of these sporozoites from the skin or infectivity of the sporozoites. Under natural conditions, sporozoites are delivered both to individuals who may exhibit cutaneous hypersensitivity to mosquito bite and to others who may have not yet developed such reactivity. It was tempting to hypothesize that differences in responsiveness to mosquito bite by different individuals might modulate the infectivity of sporozoites delivered into a milieu of changes induced by cutaneous hypersensitivity. Our results with rodent malaria models, however, were unable to support such a hypothesis. PMID: 19884338 [PubMed - as supplied by publisher]
Towards the Rational Design of a Malaria Vaccine Construct; Example of the MSP3 Family, Part II: Antigenicity Studies.
Demanga CG, Daher LJ, Prieur E, Blanc C, Pérignon JL, Bouharoun-Tayoun H, Druilhe P Towards the Rational Design of a Malaria Vaccine Construct; Example of the MSP3 Family, Part II: Antigenicity Studies. Infect Immun. 2009 Nov 2; Authors: Demanga CG, Daher LJ, Prieur E, Blanc C, Pérignon JL, Bouharoun-Tayoun H, Druilhe P Plasmodium falciparum MSP3 is a main target of protective immunity against malaria, currently undergoing vaccine development. It was shown recently to belong, together with MSP6, to a new multigene family, which C-terminal regions have a similar organisation, contain both homologous and divergent regions, and are highly conserved across isolates. In an attempt to rationally design novel vaccine constructs, we extended the analysis of antigenicity and function of region-specific antibodies, previously performed with MSP3 and MSP6, to the remaining 4 proteins of the MSP3 family using 4 recombinant proteins and 24 synthetic peptides. Antibodies to each MSP3 family antigen were found highly prevalent among malaria exposed individuals from the village of Dielmo (Senegal). Each of the 24 peptides was antigenic, defining at least one epitope mimicking that of the native proteins, with a distinct IgG isotype pattern for each, though with an overall predominance of the IgG3 subclass. Human antibodies affinity-purified upon each of the 24 peptides exerted an anti-parasite ADCI effect, which in most cases was as strong as that of IgG from protected African adults. The two regions with high homology were found to generate a broad network of cross-reactive antibodies with various avidities. A first multigenic construct was designed using the above findings and those from related immunogenicity studies in mice, and was shown to have valuable immunological properties. These results indicate that numerous regions from the MSP3 family play a role in protection and provide a rationale for the tailoring of new MSP3 derived malaria vaccines. PMID: 19884337 [PubMed - as supplied by publisher]
Virulence, Inflammatory Potential and Adaptive Immunity Induced by Shigella msbB Mutants.
Ranallo RT, Kaminski RW, George T, Kordis AA, Chen Q, Szabo K, Venkatesan MM Virulence, Inflammatory Potential and Adaptive Immunity Induced by Shigella msbB Mutants. Infect Immun. 2009 Nov 2; Authors: Ranallo RT, Kaminski RW, George T, Kordis AA, Chen Q, Szabo K, Venkatesan MM The ability of genetically detoxified LPS to stimulate adaptive immune responses is an ongoing area of investigation with significant consequences for the development of safe and effective bacterial vaccines and adjuvants. One approach to genetic detoxification is deletion of genes whose product modifies LPS. The msbB1 and msbB2 genes which encode late acyltransferases were deleted in the S. flexneri 2a human challenge strain 2457T to evaluate the virulence, inflammatory potential and acquired immunity induced by strains producing underacylated lipid A. Consistent with a reduced endotoxic potential, S. flexneri 2a msbB mutants were attenuated in an acute mouse pulmonary challenge model. Attenuation correlated with a decrease in the production of proinflammatory cytokine and chemokine release without significant changes in lung histopathology. Specific proinflammatory cytokines (IL-1beta, MIP-1alpha, and TNF-alpha) were also significantly reduced after infection of mouse macrophages with either single or double msbB mutants. Surprisingly, the msbB double mutant displayed defects in the ability to invade, replicate and spread within epithelial cells. Complementation restored these phenotypes, but the exact nature of the defects was not determined. Acquired immunity and protective efficacy were also assayed in the mouse lung model using a vaccination-challenge study. Both humoral and cellular responses were generally robust in msbB-immunized mice and afforded significant protection from lethal challenge. These data suggest that loss of either msbB gene reduces the endotoxicity of Shigella LPS, but does not coincide with a reduction in protective immune responses. PMID: 19884336 [PubMed - as supplied by publisher]
The effects of PspC on complement-mediated immunity to Streptococcus pneumoniae vary with strain background and capsular serotype.
Yuste J, Khandavilli S, Ansari N, Muttardi K, Ismail L, Hyams C, Weiser J, Mitchell T, Brown JS The effects of PspC on complement-mediated immunity to Streptococcus pneumoniae vary with strain background and capsular serotype. Infect Immun. 2009 Nov 2; Authors: Yuste J, Khandavilli S, Ansari N, Muttardi K, Ismail L, Hyams C, Weiser J, Mitchell T, Brown JS Streptococcus pneumoniae may evade complement activity by binding of Factor H (FH), a negative regulator of the alternative pathway, to the surface protein PspC. However existing data on the effects of FH binding to PspC on complement activity are conflicting, and there is also considerable allelic variation in PspC structure between S. pneumoniae strains that may influence PspC-dependent effects on complement. We have investigated interactions with complement for several S. pneumoniae strains in which the gene encoding PspC has been deleted. The degree of FH binding varied between strains, and was entirely dependent on PspC for seven strains. Data obtained with TIGR4 strains expressing different capsular serotypes suggests FH binding is affected by capsular serotype. Results of immunoblots for C3 degradation products and iC3b deposition assays suggested FH bound to PspC retained functional activity, but loss of PspC had strikingly varied effects on C3b/iC3b deposition on S. pneumoniae, with large increases on serotype 4, 6A, 6B and 9V strains, but only small increases or even decreases on serotype 2, 3, 17 and 23F strains. Repeating C3b/iC3b assays with TIGR4 strains expressing different capsular serotypes suggested that differences in the effect of PspC on C3b/iC3b deposition were largely independent of capsular serotype and depend on strain background. However, data obtained from infection in complement deficient mice demonstrated that differences between strains in the effects of PspC on complement did surprisingly not influence the development of septicaemia. PMID: 19884335 [PubMed - as supplied by publisher]
Human platelets recognize a novel surface protein PadA on Streptococcus gordonii through a unique interaction involving fibrinogen receptor GPIIbIIIa.
Petersen HJ, Keane C, Jenkinson HF, Vickerman MM, Jesionowski A, Waterhouse JC, Cox D, Kerrigan SW Human platelets recognize a novel surface protein PadA on Streptococcus gordonii through a unique interaction involving fibrinogen receptor GPIIbIIIa. Infect Immun. 2009 Nov 2; Authors: Petersen HJ, Keane C, Jenkinson HF, Vickerman MM, Jesionowski A, Waterhouse JC, Cox D, Kerrigan SW The concept of an infectious agent playing a role in cardiovascular disease is slowly gaining attention. Among several pathogens identified, the oral bacterium Streptococcus gordonii has been implicated as a plausible agent. Platelet adhesion and subsequent aggregation are critical events in the pathogenesis and dissemination of the infective process. Here we describe the identification and characterization of a novel cell wall anchored surface protein PadA (397 kDa) of S. gordonii DL1 that binds to the platelet fibrinogen receptor GPIIbIIIa. Wild-type S. gordonii cells induced platelet aggregation and supported platelet adhesion in a GPIIbIIIa-dependent manner. Deletion of the padA gene had no effect on platelet aggregation by S. gordonii but significantly reduced (>75%) platelet adhesion to S. gordonii. Purified N-terminal PadA recombinant polypeptide adhered to platelets. The padA mutant was unaffected in production of other platelet-interactive surface proteins Hsa, SspA and SspB, and adherence levels of the mutant to fetuin or platelet receptor GPIb were unaffected. Wild-type S. gordonii, but not the padA mutant, bound to Chinese Hamster Ovary cells stably transfected with GPIIbIIIa, and this interaction was ablated by addition of GPIIbIIIa inhibitor Abciximab. These results highlight the growing complexity of interactions between S. gordonii and platelets and demonstrate a new mechanism by which the bacterium could contribute to unwanted thrombosis. PMID: 19884334 [PubMed - as supplied by publisher]

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