Most humans mount significant Immunoglobulin E (IgE) responses only as a defense against parasitic infections. However, some individuals mount an IgE response against common environmental antigens. This hereditory predisposition is called atopy. In atopic individuals, non-parasitic antigens stimulate inappropriate IgE production, leading to type I hypersensitivity. Sensitivities vary from one person to another and it is possible to be allergic to an extraordinary range of substances.
Types of allergies
Dust mite excretion, pollen and pet dander are all common allergens, but it is possible to be allergic to anything from chlorine to perfume. Food allergies are not as common as food sensitivity, but some foods such as peanuts (really a legume), nuts, seafood and shellfish are the cause of serious allergies in many people.
Officially, the Food and Drug Administration does recognize 8 foods as being common for allergic reactions in a large segment of the sensitive population, which includes, peanuts, tree nuts, eggs, milk, shellfish, fish, wheat and their derivatives, soy and their derivatives, and sulphites (chemical based, often found in flavors and colors in foods) at 10ppm and over. See the FDA website for complete details. It should be noted that other countries, due to differences in genetic profiles of its citizens and different levels of exposure to different foods, the "official" allergen list will change. Canada recognizes all eight of the allergens recognized by the US, and also recognizes sesame seeds.
A few people have been recorded to be allergic to certain chemicals found in almost all water, and even water itself (see Aquagenic pruritus).
Another type of allergen is urushiol, a resin produced by poison ivy and poison oak. It causes the skin rash condition known as urushiol-induced contact dermatitis by changing a skin cell's configuration so that it is no longer recognized by the immune system as part of the body. A little over half of North Americans are known to be allergic to urushiol and repeated exposure can increase one's sensitivity to the allergen.
An allergic reaction can be caused by any form of direct contact with the allergen—eating or drinking a food you are sensitive to (ingestion), breathing in pollen, perfume or pet dander (inhalation), or brushing your body against an allergy-causing plant (direct contact, generally resulting in hives). Other common causes of serious allergy are wasp, fire ant and bee stings, penicillin, and latex. An extremely serious form of an allergic reaction, which can kill in mere minutes, is called anaphylaxis. One form of treatment is the administration of sterile epinephrine (via "Epi-Pen") to the person experiencing anaphylaxis, which suppresses the body's overreaction to the food ingested, and allows for time to be transported to a medical facility (it does not "cure" the allergic reaction).
Tuesday, March 31, 2009
Avian influenza
* Influenza
* Virus
* Avian influenza
* Flu season
* Research
* Vaccine
* Treatment
* Genome project
* H5N1 strain
For the H5N1 subtype of Avian influenza see H5N1.
Avian influenza, sometimes Avian flu, and commonly Bird flu, refers to "influenza caused by viruses adapted to birds."
"Bird flu" is a phrase similar to "Swine flu", "Dog flu", "Horse flu", or "Human flu" in that it refers to an illness caused by any of many different strains of influenza viruses that have adapted to a specific host. All known viruses that cause influenza in birds belong to the species: Influenza A virus. All subtypes (but not all strains of all subtypes) of Influenza A virus are adapted to birds, which is why for many purposes avian flu virus is the Influenza A virus (note that the "A" does not stand for "avian").
Adaptation is non-exclusive. Being adapted towards a particular species does not preclude adaptations, or partial adaptations, towards infecting different species. In this way strains of influenza viruses are adapted to multiple species, though may be preferential towards a particular host. For example, viruses responsible for influenza pandemics are adapted to both humans and birds. Recent influenza research into the genes of the Spanish Flu virus shows it to have genes adapted to both birds and humans; with more of its genes from birds than less deadly later pandemic strains.
Genetics
Genetic factors in distinguishing between "human flu viruses" and "avian flu viruses" include:
PB2: (RNA polymerase): Amino acid (or residue) position 627 in the PB2 protein encoded by the PB2 RNA gene. Until H5N1, all known avian influenza viruses had a Glu at position 627, while all human influenza viruses had a lysine.
HA: (hemagglutinin): Avian influenza HA bind alpha 2-3 sialic acid receptors while human influenza HA bind alpha 2-6 sialic acid receptors. Swine influenza viruses have the ability to bind both types of sialic acid receptors. Hemagglutinin is the major antigen of the virus against which neutralizing antibodies are produced and influenza virus epidemics are associated with changes in its antigenic structure.
Influenza pandemic
Pandemic flu viruses have some avian flu virus genes and usually some human flu virus genes. Both the H2N2 and H3N2 pandemic strains contained genes from avian influenza viruses. The new subtypes arose in pigs coinfected with avian and human viruses and were soon transferred to humans. Swine were considered the original "intermediate host" for influenza, because they supported reassortment of divergent subtypes. However, other hosts appear capable of similar coinfection (e.g., many poultry species), and direct transmission of avian viruses to humans is possible. The Spanish flu virus strain may have been transmitted directly from birds to humans.
In spite of their pandemic connection, avian influenza viruses are noninfectious for most species. When they are infectious they are usually asymptomatic, so the carrier does not have any disease from it. Thus while infected with an avian flu virus, the animal doesn't have a "flu". Typically, when illness (called "flu") from an avian flu virus does occur, it is the result of an avian flu virus strain adapted to one species spreading to another species (usually from one bird species to another bird species). So far as is known, the most common result of this is an illness so minor as to be not worth noticing (and thus little studied). But with the domestication of chickens and turkeys, humans have created species subtypes (domesticated poultry) that can catch an avian flu virus adapted to waterfowl and have it rapidly mutate into a form that kills in days over 90% of an entire flock and spread to other flocks and kill 90% of them and can only be stopped by killing every domestic bird in the area. Until H5N1 infected humans in the 1990s, this was the only reason avian flu was considered important. Since then, avian flu viruses have been intensively studied; resulting in changes in what is believed about flu pandemics, changes in poultry farming, changes in flu vaccination research, and changes in flu pandemic planning.
H5N1 has evolved into a flu virus strain that infects more species than any previously known flu virus strain, is deadlier than any previously known flu virus strain, and continues to evolve becoming both more widespread and more deadly causing Robert Webster, a leading expert on avian flu, to publish an article titled "The world is teetering on the edge of a pandemic that could kill a large fraction of the human population" in American Scientist. He called for adequate resources to fight what he sees as a major world threat to possibly billions of lives. Since the article was written, the world community has spent billions of dollars fighting this threat with limited success.
* Virus
* Avian influenza
* Flu season
* Research
* Vaccine
* Treatment
* Genome project
* H5N1 strain
For the H5N1 subtype of Avian influenza see H5N1.
Avian influenza, sometimes Avian flu, and commonly Bird flu, refers to "influenza caused by viruses adapted to birds."
"Bird flu" is a phrase similar to "Swine flu", "Dog flu", "Horse flu", or "Human flu" in that it refers to an illness caused by any of many different strains of influenza viruses that have adapted to a specific host. All known viruses that cause influenza in birds belong to the species: Influenza A virus. All subtypes (but not all strains of all subtypes) of Influenza A virus are adapted to birds, which is why for many purposes avian flu virus is the Influenza A virus (note that the "A" does not stand for "avian").
Adaptation is non-exclusive. Being adapted towards a particular species does not preclude adaptations, or partial adaptations, towards infecting different species. In this way strains of influenza viruses are adapted to multiple species, though may be preferential towards a particular host. For example, viruses responsible for influenza pandemics are adapted to both humans and birds. Recent influenza research into the genes of the Spanish Flu virus shows it to have genes adapted to both birds and humans; with more of its genes from birds than less deadly later pandemic strains.
Genetics
Genetic factors in distinguishing between "human flu viruses" and "avian flu viruses" include:
PB2: (RNA polymerase): Amino acid (or residue) position 627 in the PB2 protein encoded by the PB2 RNA gene. Until H5N1, all known avian influenza viruses had a Glu at position 627, while all human influenza viruses had a lysine.
HA: (hemagglutinin): Avian influenza HA bind alpha 2-3 sialic acid receptors while human influenza HA bind alpha 2-6 sialic acid receptors. Swine influenza viruses have the ability to bind both types of sialic acid receptors. Hemagglutinin is the major antigen of the virus against which neutralizing antibodies are produced and influenza virus epidemics are associated with changes in its antigenic structure.
Influenza pandemic
Pandemic flu viruses have some avian flu virus genes and usually some human flu virus genes. Both the H2N2 and H3N2 pandemic strains contained genes from avian influenza viruses. The new subtypes arose in pigs coinfected with avian and human viruses and were soon transferred to humans. Swine were considered the original "intermediate host" for influenza, because they supported reassortment of divergent subtypes. However, other hosts appear capable of similar coinfection (e.g., many poultry species), and direct transmission of avian viruses to humans is possible. The Spanish flu virus strain may have been transmitted directly from birds to humans.
In spite of their pandemic connection, avian influenza viruses are noninfectious for most species. When they are infectious they are usually asymptomatic, so the carrier does not have any disease from it. Thus while infected with an avian flu virus, the animal doesn't have a "flu". Typically, when illness (called "flu") from an avian flu virus does occur, it is the result of an avian flu virus strain adapted to one species spreading to another species (usually from one bird species to another bird species). So far as is known, the most common result of this is an illness so minor as to be not worth noticing (and thus little studied). But with the domestication of chickens and turkeys, humans have created species subtypes (domesticated poultry) that can catch an avian flu virus adapted to waterfowl and have it rapidly mutate into a form that kills in days over 90% of an entire flock and spread to other flocks and kill 90% of them and can only be stopped by killing every domestic bird in the area. Until H5N1 infected humans in the 1990s, this was the only reason avian flu was considered important. Since then, avian flu viruses have been intensively studied; resulting in changes in what is believed about flu pandemics, changes in poultry farming, changes in flu vaccination research, and changes in flu pandemic planning.
H5N1 has evolved into a flu virus strain that infects more species than any previously known flu virus strain, is deadlier than any previously known flu virus strain, and continues to evolve becoming both more widespread and more deadly causing Robert Webster, a leading expert on avian flu, to publish an article titled "The world is teetering on the edge of a pandemic that could kill a large fraction of the human population" in American Scientist. He called for adequate resources to fight what he sees as a major world threat to possibly billions of lives. Since the article was written, the world community has spent billions of dollars fighting this threat with limited success.
Antibiotic resistance
Antibiotic resistance is the ability of a microorganism to withstand the effects of antibiotics. It is a specific type of drug resistance. Antibiotic resistance evolves via natural selection acting upon random mutation, but it can also be engineered by applying an evolutionary stress on a population. Once such a gene is generated, bacteria can then transfer the genetic information in a horizontal fashion (between individuals) by plasmid exchange. If a bacterium carries several resistance genes, it is called multiresistant or, informally, a superbug. The term antimicrobial resistance is sometimes used to explicitly encompass organisms other than bacteria.
Antibiotic resistance can also be introduced artificially into a microorganism through transformation protocols. This can aid in implanting artificial genes into the microorganism. If the resistance gene is linked with the gene to be implanted, the antibiotic can be used to kill off organisms that lack the new gene.
Causes and risk factors
Schematic representation of how antibiotic resistance evolves via natural selection. The top section represents a population of bacteria before exposure to an antibiotic. The middle section shows the population directly after exposure, the phase in which selection took place. The last section shows the distribution of resistance in a new generation of bacteria. The legend indicates the resistance levels of individuals.
Antibiotic resistance can be a result of horizontal gene transfer, and also of unlinked point mutations in the pathogen genome and a rate of about 1 in 108 per chromosomal replication. The antibiotic action against the pathogen can be seen as an environmental pressure; those bacteria which have a mutation allowing them to survive will live on to reproduce. They will then pass this trait to their offspring, which will result in a fully resistant colony.
Several studies have demonstrated that patterns of antibiotic usage greatly affect the number of resistant organisms which develop. Overuse of broad-spectrum antibiotics, such as second- and third-generation cephalosporins, greatly hastens the development of methicillin resistance. Other factors contributing towards resistance include incorrect diagnosis, unnecessary prescriptions, improper use of antibiotics by patients, the impregnation of household items and children's toys with low levels of antibiotics, and the administration of antibiotics by mouth in livestock for growth promotion.
Researchers have recently demonstrated the bacterial protein LexA may play a key role in the acquisition of bacterial mutations.
Mechanisms
The four main mechanisms by which microorganisms exhibit resistance to antimicrobials are:
1. Drug inactivation or modification: e.g. enzymatic deactivation of Penicillin G in some penicillin-resistant bacteria through the production of β-lactamases.
2. Alteration of target site: e.g. alteration of PBP—the binding target site of penicillins—in MRSA and other penicillin-resistant bacteria.
3. Alteration of metabolic pathway: e.g. some sulfonamide-resistant bacteria do not require para-aminobenzoic acid (PABA), an important precursor for the synthesis of folic acid and nucleic acids in bacteria inhibited by sulfonamides. Instead, like mammalian cells, they turn to utilizing preformed folic acid.
4. Reduced drug accumulation: by decreasing drug permeability and/or increasing active efflux (pumping out) of the drugs across the cell surface.
Resistant pathogens
Staphylococcus aureus
Staphylococcus aureus (colloquially known as "Staph aureus" or a Staph infection) is one of the major resistant pathogens. Found on the mucous membranes and the skin of around a third of the population, it is extremely adaptable to antibiotic pressure. It was the first bacterium in which penicillin resistance was found—in 1947, just four years after the drug started being mass-produced. Methicillin was then the antibiotic of choice, but has since been replaced by oxacillin due to significant kidney toxicity. MRSA (methicillin-resistant Staphylococcus aureus) was first detected in Britain in 1961 and is now "quite common" in hospitals. MRSA was responsible for 37% of fatal cases of blood poisoning in the UK in 1999, up from 4% in 1991. Half of all S. aureus infections in the US are resistant to penicillin, methicillin, tetracycline and erythromycin.
This left vancomycin as the only effective agent available at the time. However, strains with intermediate (4-8 ug/ml) levels of resistance, termed GISA (glycopeptide intermediate Staphylococcus aureus) or VISA (vancomycin intermediate Staphylococcus aureus), began appearing in the late 1990s. The first identified case was in Japan in 1996, and strains have since been found in hospitals in England, France and the US. The first documented strain with complete (>16ug/ml) resistance to vancomycin, termed VRSA (Vancomycin-resistant Staphylococcus aureus) appeared in the United States in 2002.
A new class of antibiotics, oxazolidinones, became available in the 1990s, and the first commercially available oxazolidinone, linezolid, is comparable to vancomycin in effectiveness against MRSA. Linezolid-resistance in Staphylococcus aureus was reported in 2003.
CA-MRSA (Community-acquired MRSA) has now emerged as an epidemic that is responsible for rapidly progressive, fatal diseases including necrotizing pneumonia, severe sepsis and necrotizing fasciitis. Methicillin-resistant Staphylococcus aureus (MRSA) is the most frequently identified antimicrobial drug-resistant pathogen in US hospitals. The epidemiology of infections caused by MRSA is rapidly changing. In the past 10 years, infections caused by this organism have emerged in the community. The 2 MRSA clones in the United States most closely associated with community outbreaks, USA400 (MW2 strain, ST1 lineage) and USA300, often contain Panton-Valentine leukocidin (PVL) genes and, more frequently, have been associated with skin and soft tissue infections. Outbreaks of community-associated (CA)-MRSA infections have been reported in correctional facilities, among athletic teams, among military recruits, in newborn nurseries, and among active homosexual men. CA-MRSA infections now appear to be endemic in many urban regions and cause most CA-S. aureus infections.
Streptococcus and Enterococcus
Streptococcus pyogenes (Group A Streptococcus: GAS) infections can usually be treated with many different antibiotics. Early treatment may reduce the risk of death from invasive group A streptococcal disease. However, even the best medical care does not prevent death in every case. For those with very severe illness, supportive care in an intensive care unit may be needed. For persons with necrotizing fasciitis, surgery often is needed to remove damaged tissue. Strains of S. pyogenes resistant to macrolide antibiotics have emerged, however all strains remain uniformly sensitive to penicillin.
Resistance of Streptococcus pneumoniae to penicillin and other beta-lactams is increasing worldwide. The major mechanism of resistance involves the introduction of mutations in genes encoding penicillin-binding proteins. Selective pressure is thought to play an important role, and use of beta-lactam antibiotics has been implicated as a risk factor for infection and colonization. Streptococcus pneumoniae is responsible for pneumonia, bacteremia, otitis media, meningitis, sinusitis, peritonitis and arthritis.
Penicillin-resistant pneumonia caused by Streptococcus pneumoniae (commonly known as pneumococcus), was first detected in 1967, as was penicillin-resistant gonorrhea. Resistance to penicillin substitutes is also known as beyond S. aureus. By 1993 Escherichia coli was resistant to five fluoroquinolone variants. Mycobacterium tuberculosis is commonly resistant to isoniazid and rifampin and sometimes universally resistant to the common treatments. Other pathogens showing some resistance include Salmonella, Campylobacter, and Streptococci.
Pseudomonas aeruginosa
Pseudomonas aeruginosa is a highly prelevant opportunistic pathogen. One of the most worrisome characteristics of P. aeruginosa consists in its low antibiotic susceptibility. This low susceptibility is attributable to a concerted action of multidrug efflux pumps with chromosomally-encoded antibiotic resistance genes and the low permeability of the bacterial cellular envelopes. Besides intrinsic resistance, P. aeruginosa easily develop acquired resistance either by mutation in chromosomally-encoded genes, or by the horizontal gene transfer of antibiotic resistance determinants. Development of multidrug resistance by P. aeruginosa isolates requires several different genetic events that include acquisition of different mutations and/or horizontal transfer of antibiotic resistance genes. Hypermutation favours the selection of mutation-driven antibiotic resistance in P. aeruginosa strains producing chronic infections, whereas the clustering of several different antibiotic resistance genes in integrons favours the concerted acquisition of antibiotic resistance determinants. Some recent studies have shown that phenotypic resistance associated to biofilm formation or to the emergence of small-colony-variants may be important in the response of P. aeruginosa populations to antibiotics treatment.
Clostridium difficile
Clostridium difficile is a nosocomial pathogen that causes diarrheal disease in hospitals world wide. Clindamycin-resistant C. difficile was reported as the causative agent of large outbreaks of diarrheal disease in hospitals in New York, Arizona, Florida and Massachusetts between 1989 and 1992. Geographically dispersed outbreaks of C. difficile strains resistant to fluoroquinolone antibiotics, such as Cipro (ciprofloxacin) and Levaquin (levofloxacin), were also reported in North America in 2005.
Acinetobacter baumannii
On the 5th November 2004 , the Centers for Disease Control and Prevention (CDC) reported an increasing number of Acinetobacter baumannii bloodstream infections in patients at military medical facilities in which service members injured in the Iraq/Kuwait region during Operation Iraqi Freedom and in Afghanistan during Operation Enduring Freedom were treated. Most of these showed multidrug resistance (MRAB), with a few isolates resistant to all drugs tested.
Antibiotic resistance can also be introduced artificially into a microorganism through transformation protocols. This can aid in implanting artificial genes into the microorganism. If the resistance gene is linked with the gene to be implanted, the antibiotic can be used to kill off organisms that lack the new gene.
Causes and risk factors
Schematic representation of how antibiotic resistance evolves via natural selection. The top section represents a population of bacteria before exposure to an antibiotic. The middle section shows the population directly after exposure, the phase in which selection took place. The last section shows the distribution of resistance in a new generation of bacteria. The legend indicates the resistance levels of individuals.
Antibiotic resistance can be a result of horizontal gene transfer, and also of unlinked point mutations in the pathogen genome and a rate of about 1 in 108 per chromosomal replication. The antibiotic action against the pathogen can be seen as an environmental pressure; those bacteria which have a mutation allowing them to survive will live on to reproduce. They will then pass this trait to their offspring, which will result in a fully resistant colony.
Several studies have demonstrated that patterns of antibiotic usage greatly affect the number of resistant organisms which develop. Overuse of broad-spectrum antibiotics, such as second- and third-generation cephalosporins, greatly hastens the development of methicillin resistance. Other factors contributing towards resistance include incorrect diagnosis, unnecessary prescriptions, improper use of antibiotics by patients, the impregnation of household items and children's toys with low levels of antibiotics, and the administration of antibiotics by mouth in livestock for growth promotion.
Researchers have recently demonstrated the bacterial protein LexA may play a key role in the acquisition of bacterial mutations.
Mechanisms
The four main mechanisms by which microorganisms exhibit resistance to antimicrobials are:
1. Drug inactivation or modification: e.g. enzymatic deactivation of Penicillin G in some penicillin-resistant bacteria through the production of β-lactamases.
2. Alteration of target site: e.g. alteration of PBP—the binding target site of penicillins—in MRSA and other penicillin-resistant bacteria.
3. Alteration of metabolic pathway: e.g. some sulfonamide-resistant bacteria do not require para-aminobenzoic acid (PABA), an important precursor for the synthesis of folic acid and nucleic acids in bacteria inhibited by sulfonamides. Instead, like mammalian cells, they turn to utilizing preformed folic acid.
4. Reduced drug accumulation: by decreasing drug permeability and/or increasing active efflux (pumping out) of the drugs across the cell surface.
Resistant pathogens
Staphylococcus aureus
Staphylococcus aureus (colloquially known as "Staph aureus" or a Staph infection) is one of the major resistant pathogens. Found on the mucous membranes and the skin of around a third of the population, it is extremely adaptable to antibiotic pressure. It was the first bacterium in which penicillin resistance was found—in 1947, just four years after the drug started being mass-produced. Methicillin was then the antibiotic of choice, but has since been replaced by oxacillin due to significant kidney toxicity. MRSA (methicillin-resistant Staphylococcus aureus) was first detected in Britain in 1961 and is now "quite common" in hospitals. MRSA was responsible for 37% of fatal cases of blood poisoning in the UK in 1999, up from 4% in 1991. Half of all S. aureus infections in the US are resistant to penicillin, methicillin, tetracycline and erythromycin.
This left vancomycin as the only effective agent available at the time. However, strains with intermediate (4-8 ug/ml) levels of resistance, termed GISA (glycopeptide intermediate Staphylococcus aureus) or VISA (vancomycin intermediate Staphylococcus aureus), began appearing in the late 1990s. The first identified case was in Japan in 1996, and strains have since been found in hospitals in England, France and the US. The first documented strain with complete (>16ug/ml) resistance to vancomycin, termed VRSA (Vancomycin-resistant Staphylococcus aureus) appeared in the United States in 2002.
A new class of antibiotics, oxazolidinones, became available in the 1990s, and the first commercially available oxazolidinone, linezolid, is comparable to vancomycin in effectiveness against MRSA. Linezolid-resistance in Staphylococcus aureus was reported in 2003.
CA-MRSA (Community-acquired MRSA) has now emerged as an epidemic that is responsible for rapidly progressive, fatal diseases including necrotizing pneumonia, severe sepsis and necrotizing fasciitis. Methicillin-resistant Staphylococcus aureus (MRSA) is the most frequently identified antimicrobial drug-resistant pathogen in US hospitals. The epidemiology of infections caused by MRSA is rapidly changing. In the past 10 years, infections caused by this organism have emerged in the community. The 2 MRSA clones in the United States most closely associated with community outbreaks, USA400 (MW2 strain, ST1 lineage) and USA300, often contain Panton-Valentine leukocidin (PVL) genes and, more frequently, have been associated with skin and soft tissue infections. Outbreaks of community-associated (CA)-MRSA infections have been reported in correctional facilities, among athletic teams, among military recruits, in newborn nurseries, and among active homosexual men. CA-MRSA infections now appear to be endemic in many urban regions and cause most CA-S. aureus infections.
Streptococcus and Enterococcus
Streptococcus pyogenes (Group A Streptococcus: GAS) infections can usually be treated with many different antibiotics. Early treatment may reduce the risk of death from invasive group A streptococcal disease. However, even the best medical care does not prevent death in every case. For those with very severe illness, supportive care in an intensive care unit may be needed. For persons with necrotizing fasciitis, surgery often is needed to remove damaged tissue. Strains of S. pyogenes resistant to macrolide antibiotics have emerged, however all strains remain uniformly sensitive to penicillin.
Resistance of Streptococcus pneumoniae to penicillin and other beta-lactams is increasing worldwide. The major mechanism of resistance involves the introduction of mutations in genes encoding penicillin-binding proteins. Selective pressure is thought to play an important role, and use of beta-lactam antibiotics has been implicated as a risk factor for infection and colonization. Streptococcus pneumoniae is responsible for pneumonia, bacteremia, otitis media, meningitis, sinusitis, peritonitis and arthritis.
Penicillin-resistant pneumonia caused by Streptococcus pneumoniae (commonly known as pneumococcus), was first detected in 1967, as was penicillin-resistant gonorrhea. Resistance to penicillin substitutes is also known as beyond S. aureus. By 1993 Escherichia coli was resistant to five fluoroquinolone variants. Mycobacterium tuberculosis is commonly resistant to isoniazid and rifampin and sometimes universally resistant to the common treatments. Other pathogens showing some resistance include Salmonella, Campylobacter, and Streptococci.
Pseudomonas aeruginosa
Pseudomonas aeruginosa is a highly prelevant opportunistic pathogen. One of the most worrisome characteristics of P. aeruginosa consists in its low antibiotic susceptibility. This low susceptibility is attributable to a concerted action of multidrug efflux pumps with chromosomally-encoded antibiotic resistance genes and the low permeability of the bacterial cellular envelopes. Besides intrinsic resistance, P. aeruginosa easily develop acquired resistance either by mutation in chromosomally-encoded genes, or by the horizontal gene transfer of antibiotic resistance determinants. Development of multidrug resistance by P. aeruginosa isolates requires several different genetic events that include acquisition of different mutations and/or horizontal transfer of antibiotic resistance genes. Hypermutation favours the selection of mutation-driven antibiotic resistance in P. aeruginosa strains producing chronic infections, whereas the clustering of several different antibiotic resistance genes in integrons favours the concerted acquisition of antibiotic resistance determinants. Some recent studies have shown that phenotypic resistance associated to biofilm formation or to the emergence of small-colony-variants may be important in the response of P. aeruginosa populations to antibiotics treatment.
Clostridium difficile
Clostridium difficile is a nosocomial pathogen that causes diarrheal disease in hospitals world wide. Clindamycin-resistant C. difficile was reported as the causative agent of large outbreaks of diarrheal disease in hospitals in New York, Arizona, Florida and Massachusetts between 1989 and 1992. Geographically dispersed outbreaks of C. difficile strains resistant to fluoroquinolone antibiotics, such as Cipro (ciprofloxacin) and Levaquin (levofloxacin), were also reported in North America in 2005.
Acinetobacter baumannii
On the 5th November 2004 , the Centers for Disease Control and Prevention (CDC) reported an increasing number of Acinetobacter baumannii bloodstream infections in patients at military medical facilities in which service members injured in the Iraq/Kuwait region during Operation Iraqi Freedom and in Afghanistan during Operation Enduring Freedom were treated. Most of these showed multidrug resistance (MRAB), with a few isolates resistant to all drugs tested.
Leachate
Leachate is the liquid that drains or 'leaches' from a landfill; it varies widely in composition regarding the age of the landfill and the type of waste that it contains. It can usually contain both dissolved and suspended material.
Generation of leachate
The generation of leachate is caused principally by precipitation percolating through waste deposited in a landfill. Once in contact with decomposing solid waste, the percolating water becomes contaminated and if it then flows out of the waste material it is termed leachate. Additional leachate volume is produced during this decomposition of carbonaceous material producing a wide range of other materials including methane, carbon dioxide and a complex mixture of organic acids, aldehydes, alcohols and simple sugars.
The risks of leachate generation can be mitigated by properly designed and engineered landfill sites, such as sites that are constructed on geologically impermeable materials or sites that use impermeable liners made of geotextiles or engineered clay. The use of linings is now mandatory within both the United States and the European Union except where the waste is deemed inert. In addition, most toxic and difficult materials are now specifically excluded from landfilling. However despite much stricter statutory controls leachates from modern sites are found to contain a range of contaminants that may either be associated with some level of illegal activity or may reflect the ubiquitous use of a range of difficult materials in household and domestic products which enter the waste stream legally.
Composition of leachate
When water percolates through the waste, it promotes and assists process of decomposition by bacteria and fungi. These processes in turn release by-products of decomposition and rapidly use up any available oxygen creating an anoxic environment. In actively decomposing waste the temperature rises and the pH falls rapidly and many metal ions which are relatively insoluble at neutral pH can become dissolved in the developing leachate. The decomposition processes themselves release further water which adds to the volume of leachate. Leachate also reacts with materials that are not themselves prone to decomposition such as fire ash and cement based building materials changing the chemical composition. In sites with large volumes of building waste, especially those containing gypsum plaster, the reaction of leachate with the gypsum can generate large volumes of hydrogen sulfide which may be released in the leachate and may also form a large component of the landfill gas.
In a landfill that receives a mixture of municipal, commercial, and mixed industrial waste, but excludes significant amounts of concentrated specific chemical waste, landfill leachate may be characterized as a water-based solution of four groups of contaminants ; dissolved organic matter (alcohols, acids, aldehydes, short chain sugars etc.), inorganic macro components (common cations and anions including sulfate, chloride, Iron, aluminium, zinc and ammonia), heavy metals (Pb, Ni, Cu, Hg, , and xenobiotic organic compounds such as halogenated organics, (PCBs, dioxins etc.).
The physical appearance of leachate when it emerges from a typical landfill site is a strongly-odoured yellow- or orange-coloured cloudy liquid. The smell is acidic and offensive and may be very pervasive because of hydrogen, nitrogen and sulfur rich organic species such as mercaptans.
Leachate management
In older landfills and those with no membrane between the waste and the underlying geology, leachate is free to egress the waste directly into the groundwater. In such cases high concentrations of leachate are often found in nearby springs and flushes. As leachate first emerges it can be black in colour, anoxic and may be effervescent with dissolved and entrained gases. As it becomes oxygenated it tends to turn brown or yellow because of the presence of Iron salts in solution and in suspension. It also quickly develops a bacterial flora often comprising substantial growths of Sphaerotilus.
Membrane and collection for treatment
More modern landfills in the developed world have some form of membrane separating the waste from the surrounding ground and in such sites there is often a leachate collection series of pipes laid on the membrane to convey the leachate to a collection or treatment location. For an example of a treatment system with only minor membrane use, see Nantmel Landfill Site.
All membranes are porous to some limited extent so that over time low volumes of leachate will cross the membrane. The design of landfill membranes is at such low volumes that they should never have a measurable adverse impact on the quality of the receiving groundwater. A more significant risk may be the failure or abandonment of the leachate collection system. Such systems are prone to internal failure as landfills suffer large internal movements as waste decomposes unevenly and thus buckles and distorts pipes. If a leachate collection system fails, leachate levels will slowly build in a site and may even over-top the containing membrane and flow out into the environment. Rising leachate levels can also wet waste masses that have previously been dry triggering off a new way of active decomposition and leachate generation. Thus what appears to be a stabilised and inactive site can become re-activated and restart significant gas production and exhibit significant changes in finished ground levels.
Re-injection into landfill
One method of leachate management that was more common in uncontained sites was leachate re-circulation in which leachate was collected and re-injected into the waste mass. This process greatly accelerated decomposition and therefore gas production and had the impact of converting some leachate volume into landfill gas and reducing the overall volume of leachate for disposal. However it also tended to increase substantially the concentrations of contaminant materials making it a more difficult waste to treat.
Removal to sewer system
In some older landfills, leachate was directed to the sewers, but this can cause a number of problems. Toxic metals from leachate passing through the sewage treatment plant concentrate in the sewage sludge making it difficult or dangerous to dispose of to land without incurring a risk to the environment. In Europe regulations and control have improved in recent decades and toxic wastes are now no longer permitted to be disposed of to the Municipal Solid Waste landfills, and in most developed countries the metals problem has diminished. Paradoxically, however, as sewage treatment works discharges are being improved throughout Europe and many other countries, the sewage treatment works operators are finding that leachates are difficult waste streams to treat because they contain very high ammoniacal nitrogen concentrations, they are usually very acidic , they are often anoxic and, if received in large volumes relative to the incoming sewage flow, the lack of Phosphorus in particular can result in nutrient starvation for the biological communities that perform the sewage treatment processes making leachate a difficult to treat waste stream. However, within aging municipal solid waste landfills this may not be a problem as the pH returns close to neutral after the initial stage of acidogenic leachate decomposition. Many sewer undertakers limit maximum ammonical nitrogen concentration in their sewers to 250 mg/l to protect sewer maintenance workers, as the WHO's maximum occupational safety limit would be exceeded at above pH 9 to 10, which is often the highest permitted pH of permitted sewer discharges.
Many older leachate streams also contained a variety of synthetic organic species and their decomposition products, some of which had the potential to be acutely damaging to the environment.
Environmental impact
The risks from waste leachate are due to its high organic contaminant concentrations and high ammoniacal nitrogen. Pathogenic microorganisms and toxic substances that might be present in it are often cited as the most important, but pathogenic organism counts reduce rapidly with time in the landfill, so this only applies to the most fresh leachate.
Most landfills containing organic material will produce methane, some of which dissolves in the leachate. This could in theory be released in weakly ventilated areas in the treatment plant. All plants in Europe must now be assessed under the EU ATEX Directive and zoned where explosion risks are identified to prevent future accidents. The most important requirement is the prevention of discharge of dissolved methane from untreated leachate when it is discharged into public sewers, and most sewage treatment authorities limit the permissible discharge concentration of dissolved methane to 0.14 mg/l, or 1/10th of the lower explosive limit. This entails methane stripping from the leachate.
The greatest environmental risks occur in the discharges from older sites constructed before modern engineering standards became mandatory and also from sites in the developing world where modern standards have not been applied. There are also substantial risks from illegal sites and ad-hoc sites used by criminal gangs to dispose of waste materials. Leachate streams running directly into the aquatic environment have both an acute and chronic impact on the environment which may be very severe and can severely diminish bio-diversity and greatly reduce populations of sensitive species. Where toxic metals and organics are present this can lead to chronic toxin accumulation in both local and far distant populations. Rivers impacted by leachate are often yellow in appearance and often support severe overgrowths of sewage fungus
Other types of leachate
Leachate can also be produced from land that was contaminated by chemicals or toxic materials used in industrial activities such as factories, mines or storage sites. Composting sites in high rainfall also produce leachate.
Generation of leachate
The generation of leachate is caused principally by precipitation percolating through waste deposited in a landfill. Once in contact with decomposing solid waste, the percolating water becomes contaminated and if it then flows out of the waste material it is termed leachate. Additional leachate volume is produced during this decomposition of carbonaceous material producing a wide range of other materials including methane, carbon dioxide and a complex mixture of organic acids, aldehydes, alcohols and simple sugars.
The risks of leachate generation can be mitigated by properly designed and engineered landfill sites, such as sites that are constructed on geologically impermeable materials or sites that use impermeable liners made of geotextiles or engineered clay. The use of linings is now mandatory within both the United States and the European Union except where the waste is deemed inert. In addition, most toxic and difficult materials are now specifically excluded from landfilling. However despite much stricter statutory controls leachates from modern sites are found to contain a range of contaminants that may either be associated with some level of illegal activity or may reflect the ubiquitous use of a range of difficult materials in household and domestic products which enter the waste stream legally.
Composition of leachate
When water percolates through the waste, it promotes and assists process of decomposition by bacteria and fungi. These processes in turn release by-products of decomposition and rapidly use up any available oxygen creating an anoxic environment. In actively decomposing waste the temperature rises and the pH falls rapidly and many metal ions which are relatively insoluble at neutral pH can become dissolved in the developing leachate. The decomposition processes themselves release further water which adds to the volume of leachate. Leachate also reacts with materials that are not themselves prone to decomposition such as fire ash and cement based building materials changing the chemical composition. In sites with large volumes of building waste, especially those containing gypsum plaster, the reaction of leachate with the gypsum can generate large volumes of hydrogen sulfide which may be released in the leachate and may also form a large component of the landfill gas.
In a landfill that receives a mixture of municipal, commercial, and mixed industrial waste, but excludes significant amounts of concentrated specific chemical waste, landfill leachate may be characterized as a water-based solution of four groups of contaminants ; dissolved organic matter (alcohols, acids, aldehydes, short chain sugars etc.), inorganic macro components (common cations and anions including sulfate, chloride, Iron, aluminium, zinc and ammonia), heavy metals (Pb, Ni, Cu, Hg, , and xenobiotic organic compounds such as halogenated organics, (PCBs, dioxins etc.).
The physical appearance of leachate when it emerges from a typical landfill site is a strongly-odoured yellow- or orange-coloured cloudy liquid. The smell is acidic and offensive and may be very pervasive because of hydrogen, nitrogen and sulfur rich organic species such as mercaptans.
Leachate management
In older landfills and those with no membrane between the waste and the underlying geology, leachate is free to egress the waste directly into the groundwater. In such cases high concentrations of leachate are often found in nearby springs and flushes. As leachate first emerges it can be black in colour, anoxic and may be effervescent with dissolved and entrained gases. As it becomes oxygenated it tends to turn brown or yellow because of the presence of Iron salts in solution and in suspension. It also quickly develops a bacterial flora often comprising substantial growths of Sphaerotilus.
Membrane and collection for treatment
More modern landfills in the developed world have some form of membrane separating the waste from the surrounding ground and in such sites there is often a leachate collection series of pipes laid on the membrane to convey the leachate to a collection or treatment location. For an example of a treatment system with only minor membrane use, see Nantmel Landfill Site.
All membranes are porous to some limited extent so that over time low volumes of leachate will cross the membrane. The design of landfill membranes is at such low volumes that they should never have a measurable adverse impact on the quality of the receiving groundwater. A more significant risk may be the failure or abandonment of the leachate collection system. Such systems are prone to internal failure as landfills suffer large internal movements as waste decomposes unevenly and thus buckles and distorts pipes. If a leachate collection system fails, leachate levels will slowly build in a site and may even over-top the containing membrane and flow out into the environment. Rising leachate levels can also wet waste masses that have previously been dry triggering off a new way of active decomposition and leachate generation. Thus what appears to be a stabilised and inactive site can become re-activated and restart significant gas production and exhibit significant changes in finished ground levels.
Re-injection into landfill
One method of leachate management that was more common in uncontained sites was leachate re-circulation in which leachate was collected and re-injected into the waste mass. This process greatly accelerated decomposition and therefore gas production and had the impact of converting some leachate volume into landfill gas and reducing the overall volume of leachate for disposal. However it also tended to increase substantially the concentrations of contaminant materials making it a more difficult waste to treat.
Removal to sewer system
In some older landfills, leachate was directed to the sewers, but this can cause a number of problems. Toxic metals from leachate passing through the sewage treatment plant concentrate in the sewage sludge making it difficult or dangerous to dispose of to land without incurring a risk to the environment. In Europe regulations and control have improved in recent decades and toxic wastes are now no longer permitted to be disposed of to the Municipal Solid Waste landfills, and in most developed countries the metals problem has diminished. Paradoxically, however, as sewage treatment works discharges are being improved throughout Europe and many other countries, the sewage treatment works operators are finding that leachates are difficult waste streams to treat because they contain very high ammoniacal nitrogen concentrations, they are usually very acidic , they are often anoxic and, if received in large volumes relative to the incoming sewage flow, the lack of Phosphorus in particular can result in nutrient starvation for the biological communities that perform the sewage treatment processes making leachate a difficult to treat waste stream. However, within aging municipal solid waste landfills this may not be a problem as the pH returns close to neutral after the initial stage of acidogenic leachate decomposition. Many sewer undertakers limit maximum ammonical nitrogen concentration in their sewers to 250 mg/l to protect sewer maintenance workers, as the WHO's maximum occupational safety limit would be exceeded at above pH 9 to 10, which is often the highest permitted pH of permitted sewer discharges.
Many older leachate streams also contained a variety of synthetic organic species and their decomposition products, some of which had the potential to be acutely damaging to the environment.
Environmental impact
The risks from waste leachate are due to its high organic contaminant concentrations and high ammoniacal nitrogen. Pathogenic microorganisms and toxic substances that might be present in it are often cited as the most important, but pathogenic organism counts reduce rapidly with time in the landfill, so this only applies to the most fresh leachate.
Most landfills containing organic material will produce methane, some of which dissolves in the leachate. This could in theory be released in weakly ventilated areas in the treatment plant. All plants in Europe must now be assessed under the EU ATEX Directive and zoned where explosion risks are identified to prevent future accidents. The most important requirement is the prevention of discharge of dissolved methane from untreated leachate when it is discharged into public sewers, and most sewage treatment authorities limit the permissible discharge concentration of dissolved methane to 0.14 mg/l, or 1/10th of the lower explosive limit. This entails methane stripping from the leachate.
The greatest environmental risks occur in the discharges from older sites constructed before modern engineering standards became mandatory and also from sites in the developing world where modern standards have not been applied. There are also substantial risks from illegal sites and ad-hoc sites used by criminal gangs to dispose of waste materials. Leachate streams running directly into the aquatic environment have both an acute and chronic impact on the environment which may be very severe and can severely diminish bio-diversity and greatly reduce populations of sensitive species. Where toxic metals and organics are present this can lead to chronic toxin accumulation in both local and far distant populations. Rivers impacted by leachate are often yellow in appearance and often support severe overgrowths of sewage fungus
Other types of leachate
Leachate can also be produced from land that was contaminated by chemicals or toxic materials used in industrial activities such as factories, mines or storage sites. Composting sites in high rainfall also produce leachate.
Arbovirus infection
Arbovirus is a shortened name given to viruses that are transmitted by arthropods, or arthropod-borne viruses .
Some Arboviruses are able to cause emergent disease. Arthropods are able to transmit the virus upon biting allowing the virus to enter the bloodstream which can cause viraemia.
The majority of the Arboviruses are spherical in shape although a few are rod shaped. They are 17-150 nm in diameter and most have an RNA genome (the single exception is African Swine Fever virus, which has a DNA genome). These viruses do not normally infect humans but if they do, they usually cause a mild infection such as a fever or a rash. Others however are epidemic and can cause serious infections such as meningitis and encephalitis that can be fatal.
There are ways of preventing these infections from occurring such as using mosquito repellents and getting rid of the breeding grounds that mosquitoes use. Insecticides can also be used. People can also reduce the risk of getting bitten by the mosquito by wearing protective clothing.
The immune system plays a role in defense against the infections. Arboviruses usually stimulate interferon. Antibodies are made and these can prevent viraemia from occurring. The cell mediated immunity is also important.
Arbovirus infections can be diagnosed by carrying out ELISA and PCR techniques. Complement fixation can also be used.
Some Arboviruses are able to cause emergent disease. Arthropods are able to transmit the virus upon biting allowing the virus to enter the bloodstream which can cause viraemia.
The majority of the Arboviruses are spherical in shape although a few are rod shaped. They are 17-150 nm in diameter and most have an RNA genome (the single exception is African Swine Fever virus, which has a DNA genome). These viruses do not normally infect humans but if they do, they usually cause a mild infection such as a fever or a rash. Others however are epidemic and can cause serious infections such as meningitis and encephalitis that can be fatal.
There are ways of preventing these infections from occurring such as using mosquito repellents and getting rid of the breeding grounds that mosquitoes use. Insecticides can also be used. People can also reduce the risk of getting bitten by the mosquito by wearing protective clothing.
The immune system plays a role in defense against the infections. Arboviruses usually stimulate interferon. Antibodies are made and these can prevent viraemia from occurring. The cell mediated immunity is also important.
Arbovirus infections can be diagnosed by carrying out ELISA and PCR techniques. Complement fixation can also be used.
Visual pollution
Visual pollution is the term given to unattractive or unnatural (human-made) visual elements of a vista, a landscape, or any other thing that a person might not want to look at. Visual pollution is an aesthetic issue, referring to the impacts of pollution that impair one's ability to enjoy a vista or view. The term is used broadly to cover visibility, limits on the ability to view distant objects, as well as the more subjective issue of visual clutter, structures that intrude upon otherwise "pretty" scenes. Commonly cited examples are advertisements, billboards, landfills, houses, automobiles, traffic signs, roadsigns, highways, roadways, litter, graffiti, overhead powerlines, utility poles, contrails, skywriting, buildings and weeds.
Quicksand
Quicksand is a colloid hydrogel consisting of fine granular matter (such as sand or silt), clay, and salt water. In the name, as in that of quicksilver (mercury), "quick" does not mean "fast," but "living" (cf. the expression the quick and the dead).
Water circulation underground can focus in an area with just the right mixture of fine sands and other materials such as clay. The water moves up and then down slowly in a convection-like manner throughout a column of sand under optimal conditions, and the sand remains a generally solid mass. This lubricates the sand particles and renders them unable to support any significant weight, since they move around with very little friction, behaving more like a liquid when exposed to stress. Since the water does not usually go all the way up through the sand, the sand above does not appear to move at all, and can support leaves and other small debris, making quicksand difficult to distinguish from the surrounding environment.
Properties
Quicksand is a non-Newtonian fluid: when undisturbed it often appears to be solid ("gel" form), but a minor (less than 1%) change in the stress on the quicksand will cause a sudden decrease in its viscosity ("sol" form). After an initial disturbance—such as a person attempting to walk on it—the water and sand in the quicksand separate and dense regions of sand sediment form; it is because of the formation of these high volume fraction regions that the viscosity of the quicksand seems to increase suddenly. Someone stepping in it will start to sink. In order to move within the quicksand, a person or object must apply sufficient pressure on the compacted sand to re-introduce enough water to liquefy it. The forces required to do this are quite large: to remove a foot from quicksand at a speed of one centimeter per second would require the same amount of force as "that needed to lift a medium-sized car."
Recent research findings
It was commonly believed that the behavior of quicksand was due solely to saturated or supersaturated suspensions of granules in water. Pressure from underground sources of water would separate and suspend the granular particles, reducing the friction between them. As of September 2005, it has been shown that it is the presence of salt that is largely responsible The stability of the colloidal quicksand is compromised by the presence of salt, increasing the likelihood of sand flocculation and the formation of the high viscosity regions of sediment responsible for quicksand's "trapping" power.
Prevalence
Quicksand may be found inland (on riverbanks, near lakes, or in marshes), or near the coast.
One region notorious for its quicksands is Morecambe Bay, England. As the bay is very broad and shallow, a person trapped by the quicksand would be exposed to the danger of the returning tide, which can come in rapidly.
Water circulation underground can focus in an area with just the right mixture of fine sands and other materials such as clay. The water moves up and then down slowly in a convection-like manner throughout a column of sand under optimal conditions, and the sand remains a generally solid mass. This lubricates the sand particles and renders them unable to support any significant weight, since they move around with very little friction, behaving more like a liquid when exposed to stress. Since the water does not usually go all the way up through the sand, the sand above does not appear to move at all, and can support leaves and other small debris, making quicksand difficult to distinguish from the surrounding environment.
Properties
Quicksand is a non-Newtonian fluid: when undisturbed it often appears to be solid ("gel" form), but a minor (less than 1%) change in the stress on the quicksand will cause a sudden decrease in its viscosity ("sol" form). After an initial disturbance—such as a person attempting to walk on it—the water and sand in the quicksand separate and dense regions of sand sediment form; it is because of the formation of these high volume fraction regions that the viscosity of the quicksand seems to increase suddenly. Someone stepping in it will start to sink. In order to move within the quicksand, a person or object must apply sufficient pressure on the compacted sand to re-introduce enough water to liquefy it. The forces required to do this are quite large: to remove a foot from quicksand at a speed of one centimeter per second would require the same amount of force as "that needed to lift a medium-sized car."
Recent research findings
It was commonly believed that the behavior of quicksand was due solely to saturated or supersaturated suspensions of granules in water. Pressure from underground sources of water would separate and suspend the granular particles, reducing the friction between them. As of September 2005, it has been shown that it is the presence of salt that is largely responsible The stability of the colloidal quicksand is compromised by the presence of salt, increasing the likelihood of sand flocculation and the formation of the high viscosity regions of sediment responsible for quicksand's "trapping" power.
Prevalence
Quicksand may be found inland (on riverbanks, near lakes, or in marshes), or near the coast.
One region notorious for its quicksands is Morecambe Bay, England. As the bay is very broad and shallow, a person trapped by the quicksand would be exposed to the danger of the returning tide, which can come in rapidly.
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