Welcome to the Microbiology Information

On the morning during August, several students from Northern Lehigh High School showed symptoms of staphylococcus infections or possibly respiratory “walking pneumonia.”

Later in the day, Principal Aileen Yadush wrote a letter to parents and had it posted on the school district’s Web site under a bold red link reading, “Alert!: Staphylococcus Infection Letter.”

The letter mentions the source of the infections was unclear but they narrowed it down to the school’s field house weight room.

The field house was closed and a professional cleaning crew was hired to scrub every surface and every piece of equipment.

The letter explained what type of bacteria it is – staphylococcus aureus, how to look for symptoms and what to do in case something unusual is found on students’ bodies.

The letter also assured parents and students “we will take every possible precaution in maintaining their safety and health.” which is a bold statement.

In a recent environmental survey conducted by University of Arizona researchers, surfaces in teachers’ classrooms came in as the Number 1 workplace for germs which is nearly 20 times higher than those found in lawyers’ offices, and seven times higher than doctors’ offices.

With over 2,000 parents questioned in the survey, 14 percent said they send their children to school despite running a fever higher than 100 degrees.

Educating children on proper hand washing and taking basic sanitation measures could hold down the germ level.

Bethlehem Health Bureau Director Judy Maloney says the bureau and local schools work clean-hand in clean-hand using a program called Germ City: Clean Hands, Healthy People.

The bureau also mailed a letter to principals at elementary and middle schools.

That letter urges schools to contact parents and let them know how important it is to keep sick children home.

Dr. Bonnie Coyle, director of St. Luke’s Hospital’s Community Health Department in Fountain Hill, says direct education programs are recommended by the Centers for Disease Control and Prevention to corral germs.

“If there is a child that has a disease that is a community health threat,” she says, “we get involved.”

In New Jersey, Mary Van Horn, supervisor of the Warren County Board of Health in Washington, says, “My department focuses on flu and pneumonia immunization, but good hand washing is so important.”

Coyle ventures one reason why.

“I think we’re seeing more emerging infectious disease threats,” Coyle says. “As the world becomes smaller through international travel, we’re seeing more drug-resistant tuberculosis. Then there are the things that have always been there (flu, staphylococcus, meningitis and other infectious diseases.)”

Coyle also says that since the 9/11 terrorism attacks, bioterrorism is becoming an issue.

“It’s certainly not a crisis,” she soothes, “but it’s something schools need to keep in mind.”

Source

A team of scientist have developed a specially tailored viruses could eradicate chronic bacterial infections. When certain bacteria multiply, they produce exo-polysaccharides which lead to biofilms which are nearly impossible to eradicate using conventional antibiotics. Biofilms can be found on medical devices such as catheters.

Boston University biomedical engineers have designed a new, highly effective means of dispersing and killing the bacteria living in biofilms. Led by synthetic biologist James Collins, the team has engineered viruses that attack biofilms on two fronts: by killing the bacteria that live in them, and by dissolving the carbohydrates that hold them together. If such bacteria attacking viruses are proved safe for industrial and clinical use, says Collins, researchers could develop stocks of different kinds of viruses, each tailored to attack a different kind of biofilm.

Collins has designed a virus that can disperse more than 99 percent of the E. coli in a model biofilm. Helen Blackwell a chemist at the University of Wisconsin-Madison, believes that this is an “enormous” achievement: “I haven’t seen anything as effective as this approach.” Collins’s engineered virus is described online in the journal Proceedings of the National Academy of Sciences.

Bacteria living communally in biofilms are one thousand times more resistant to antibiotics than free-swimming bacteria are, says Collins. They are protected by a sticky carbohydrate scaffold called a matrix. The matrix blocks antibiotics and cells from the human immune system, and even provides something like a primitive circulatory system for the bacteria.

In a few cases, including some chronic ear infections in children and chronic lung infections in cystic-fibrosis patients, the tissue harboring a biofilm must simply be cut out. Large doses of antibiotics can usually eradicate these infections, says Blackwell.

But she notes that there is some worry that drug-resistant biofilm infections are becoming more common, and that the use of antibiotics seems to induce biofilm formation.

“One thing I like about Collins’s approach is that it is two-pronged, says Philip Stewart, director of the Center for Biofilm Engineering at Montana State University. “The viruses kill the bacteria, but they also target the biofilm matrix.” Collins’s approach is to select a virus that already targets the bacteria of interest, such as E. coli or Staphylococcus. Then he introduces into the virus a gene for an enzyme that dissolves the main carbohydrate component of the biofilm matrix protecting the bacteria.

There are viruses specialized to infect every bacterial species. These viruses replicate inside bacterial cells, then burst them open, killing the bacteria, and spread to other bacterial cells. But they do not harm animal cells or bacteria other than the kind to which they are targeted.

Naturally occurring viruses can attack biofilms. But Collins showed that giving a virus a gene for dissolving the matrix increased the virus’s effectiveness by 4.5 orders of magnitude.

Collins’s proof-of-concept virus is tailored to a particular type of E. coli biofilm. “There are many species and strains of bacteria out there,” he says, and a single biofilm might support multiple bacterial species and strains. To a lesser degree, there is also some diversity in the components of the biofilm matrix. However, Collins says that because of the increasing speed and falling price of DNA-sequencing and synthesis technologies, it would not be difficult to develop a virus tailored to each kind of biofilm.

Collins’s viral technique appears to overcome some of the problems with chemical techniques. Blackwell, who is designing small molecules to disrupt the bacterial signaling pathways that maintain biofilms, says that delivery of biofilm-disrupting chemicals such as enzymes has been a major hurdle.

The risks of such viruses are unclear, but there is some concern that they might provoke a dangerous immune response. One reason they might not have been widely studied for their potential to treat infection, says Collins, is that antibiotics have been sufficient so far. But with the emergence of multi-drug resistant bacterial strains in hospitals, “a number of companies are looking to viruses,” he says.

For industrial applications where you’re not putting them in someone’s body, these viruses could have a huge impact”. Finding and farming bacteria could change the way we live.

Following an inquest into the deaths of 3 people from the Legionella bacteria, it may now become compulsory for results of cooling towers to be made available to health officials.

According to Canterbury’s medical officer of health, Alistair Humphrey who told an inquest looking into three deaths from legionella in winter 2005 says that New Zealand should adopt a compulsory regime on testing and reporting of legionnaire’s disease.

All 3 deaths were part of an outbreak of 19 cases clustered in the southwest of Christchurch, Dr Humphrey told Southland-Central Otago coroner Trevor Savage at the inquest, which is likely to last two days.

“It is appropriate that New Zealand moves to adopt a compulsory regime,” Dr Humphrey said. “It will in my view minimise the risk of another outbreak and will be likely to save lives.”

Attention has centred on the cooling tower at the Ravensdown plant in the suburb of Hornby as a possible source, and the company had lawyer Robert Osborne at today’s hearing.

He asked about gaps in the testing of cooling towers, and reporting of results under the present voluntary regime, and Dr Humphrey agreed it was possible that none of the cases came from the Ravensdown cooling tower.

But Dr Humphrey also said: “Our view is that there is no way you can say none of them came from that point source. Everything pointed to a cluster in the southwest of Christchurch around the plant we are talking about, with what we found to be genetically identical species of legionella.”

He agreed with Mr Osborne that the strain was the ubiquitous Christchurch type of the disease.

Inquiries by health officials during the outbreak turned up 141 cooling towers. Some of the owners or those leasing the buildings had not co-operated by testing and providing results and had to be visited by officials.

It meant there were gaps in the knowledge of what was happening during the April to August outbreak. When tests were done it was not known how many had already used biocide to kill organisms in the cooling systems — a call made by health officials to contain the outbreak.

The inquest is hearing evidence on the deaths of Ross Hern 56, Peter Jones, 48, and Valmai Finlayson, 87, who died of legionnaire’s disease at Christchurch Hospital.

Legionella species are widely found in lakes, rivers, groundwater and soil. The hearing was told it was “generally benign” until it was turned into a mist and spread. This could be through hot water systems, air cooling systems, cooling towers, water spraying devices, water sprinklers, demisters, and spa pools. An Auckland outbreak had been traced to a high pressure hose used in a boat washing operation.

When Ravensdown tested its tower in April, it was found to have a high level of 2400 colony-forming units of legionella. Biocide was used and a later test showed the level was down to 260 units.

Ravensdown provided its results to the health authorities.

Dr Humphrey suggested four changes were needed to tighten testing and reporting procedures for legionella, consistent with requirements in New South Wales, Victoria, and now being considered by South Australia.

He wants local bodies to maintain a register of cooling towers, evaporation condensers, and scrubbing towers. In the 2005 outbreak it took health officials about two weeks to gather information on all these installations from Christchurch City Council records.

He also wants compulsory testing by owners and operators, and compulsory disclosure of the results to local authorities and medical authorities.

He also wants a consistent testing regime between commercial and industrial properties.

Giving evidence this afternoon, a senior technical adviser to the Department of Building and Housing, Bruce Trevor Klein, told the coroner that since 2004 all new buildings with water cooling towers required a building compliance certificate.

Owners were required to test their systems regularly for bacterial organisms.

Cooling towers under the 2004 Act had to be sited away from building air conditioning intake systems.

Building owners must furnish annual documents showing the cooling towers had been tested monthly for legionella bacteria.

Legislation required owners or operators of cooling towers showing a level of legionella bacteria exceeding 1000 colony-forming units (cfus) should notify a medical officer of health within 48 hours.

Test results had to be retained for two years.

Questioned by Mr Savage, Mr Klein said his department would need to investigate whether it would support the mandatory reporting of all water cooler test results to health authorities.

He cautioned against Canterbury Medical Officer of Health Alister Humphrey’s earlier assertion that New Zealand should adopt Australia’s reporting system.

Mr Klein said he understood the Ministry of Health was investigating adopting a system that would require the mandatory reporting of high legionella bacterial counts.

As the law stood now, building owners, cooling tower operators and laboratories had no onus to make such reports available despite having to test regularly and retain results.

Questioned by Donna Blandford, niece of the late Mr Hern, Mr Klein said under the Building Act, cooling tower owners or operators faced fines of up to $200,000 for non-compliance.

He was unaware of any prosecutions.

Source

The first detailed images of an elusive drug that targets the outer wall of bacteria may provide scientists with enough new information to aid design of novel antibiotics. The drugs are much needed to treat deadly infections initiated by Staphylococcus aureus and other bacterial pathogens.

The research team, led by Natalie Strynadka, a Howard Hughes Medical Institute (HHMI) international research scholar at the University of British Columbia in Vancouver, Canada, published its findings in the March 9, 2007, issue of the journal Science.

“This enzyme is an awesome target for antibiotics. We have a totally new understanding of how the enzyme works and how a very good animal antibiotic inhibits the enzyme”, Dr Strynadka said.

Penicillin and many newer antibiotics work by blocking a piece of the machinery bacteria use to construct their durable outer walls. Without these tough, protective coatings, bacteria die. The enzymatic machinery (known as PBP2) studied by Strynadka’s group has two main parts: One end assembles long sugar fibers; the other end stitches them together with bits of protein to form a sturdy inter-locking mesh shell.

Strynadka’s team has provided a long-awaited look at the portion of the enzyme used in the first step of the biochemical pathway that initiates assembly of the sugar coating. The second step is targeted by penicillin and has been well studied.

Although scientists have spent many years identifying bacterial components whose structural features might have weaknesses that can be exploited by antibiotics, progress in turning up bona fide drug targets has been slow. The cell wall enzymes in particular have tantalized scientists, Strynadka said. “The cell wall has all the hallmarks of a great drug target,” she explained. “It is essential to the survival of all bacteria. The enzymes that create the cell wall are unique to bacteria. And it is accessible; you don’t have to get the
antibiotics into the cell.”

In their structural studies, the researchers focused on Staphylococcus aureus, a notorious human pathogen. An epidemic strain of the bacteria known as methicillin-resistant Staphylococcus aureus is resistant to several common antibiotics, including penicillin and amoxicillin, and is a great cause for concern among hospital infectious disease staff.

Postdoctoral fellow Andrew Lovering, who is first author on the paper, hopes the group’s three-dimensional pictures of the sugar-building enzyme from S. aureus will accelerate the search for an effective weapon against the infamous super bug.

The images produced by Strynadka’s team show the enzyme frozen in place by a powerful antibiotic called moenomycin. Moenomycin has been used for decades in animal feed to promote livestock growth. Bacteria have shown very little evidence of resistance to this antibiotic so far, and scientists think related compounds may be promising candidates for use in humans.

“This enzyme is an awesome target for antibiotics,” said Strynadka. “We have a totally new understanding of how the enzyme works and how a very good animal antibiotic inhibits the enzyme.” Although moenomycin is poorly absorbed by the human body, the new understanding of exactly how it
interferes with bacterial enzyme function should help scientists design modified versions that are more suitable for use in people.

Understanding the structure of this enzyme should also speed up screening and design of new antibiotics, which are in constant demand as microbes continually evolve new ways to evade the drugs that researchers design to thwart them.

The time it takes for bacteria to develop resistance to new antibiotics has been as short as one year for penicillin V and as long as 30 years for vancomycin.

Researchers attempting to solve the structure of this enzyme have struggled to recreate its cellular environment in the laboratory. But after much tinkering with different combinations of detergent, ions, and chemical additives, Strynadka’s team was able to crystallize the enzyme so that it would diffract x-rays into a pattern that would ultimately reveal its natural structure. They then were able to repeat the feat to reveal the crystal structure of the enzyme combined with the animal antibiotic.

Their findings help reveal how the enzyme prepares to assemble the bacteria’s sugar-coating by plucking sugars from a fat-sugar package known as lipid II. The antibiotic, which is another kind of sugar-lipid, probably mimics the lipid II molecule by tucking into a fold in the enzyme and taking up the space needed to bind to lipid II, the researchers believe. “We would like to see the enzyme in a complex with its natural substrates as well as with inhibitors,” Lovering said.

In the meantime, scientists now have the details of its shape and key contact points between enzyme and
antibiotic. The enzyme structure is the first ever solved of a member of a family of enzymes that remove sugars from lipids and attach them to other sugars. This process is used in a wide range of biochemical reactions, including allergic responses and cell signaling in cancer.

Researchers from the University of Sheffield have received joint funding from the Engineering and Physical Science Research Council (EPSRC) and the Ministry of Defence (MoD) to develop an innovative sensor to detect bacteria. The new method will use a polymer which will give a fluorescent signal when it encounters bacteria, allowing scientists to easily identify infected wounds much earlier than using conventional methodologies.

The new technology will be of immediate benefit to healthcare industries in general, as well as those involved in detecting infection in battlefield conditions and bacterial contamination, whether accidental or deliberate.

Currently identifying bacterial infection takes several days and requires swabbing and culturing of bacterial swabs as well as the use of specialist bacteriology laboratory facilities.

By combining polymers, which change shape when they encounter bacteria, and developing a light signal through fluorescence non radiative energy transfer (NRET), the researchers will be able to detect early stages of bacterial contamination.

Being developed by a multi-disciplinary team of researchers from the University’s Departments of Chemistry, Engineering Materials and the Dental School, the sensor will have widespread applications beyond the initial project.

Dr Steve Rimmer from the University’s Department of Chemistry, said: “The project is a great example of progress that can be achieved at the life sciences/physical sciences interface and we hope the project will deliver technology of real importance.”

The multi-disciplinary team will be led by Dr Steve Rimmer of the Department of Chemistry and consists of Dr Linda Swanson (Chemistry) Professor Sheila MacNeil (Engineering Materials) and Dr Ian Douglas (Clinical Dentistry).

The project received £670,000 funding jointly from the Engineering and Physical Science Research Council and the Defence Science and Technology Laboratory – an agency of the Ministry of Defence over three years and started in December 2006.

Now here is an interesting study where the aim of this double-blind, randomised cross-over study was to compare the antibacterial effect and the substantivity of two toothpaste formulations containing amine fluoride (AmF) or zinc chloride (ZnCl2).

After a professional tooth cleaning, 20 volunteers refrained from all oral mechanical hygiene measures for the subsequent 24 hours (day 0). Subsequently, a plaque sample was taken from three teeth and analysed for vitality of the plaque bacteria by means of the vital fluorescence technique (VF0; in %). After assessment of this baseline value the subjects had to brush their teeth for 2 minutes with 1.2 ml of the allocated toothpaste containing (a) 0.66% AmF or (b) 0.2% ZnCl2. For the following 8 hours no oral hygiene measures were allowed. After 4 and after 8 hours further plaque samples were analysed for biofilm vitality (VF4, VF8). During the following 3 days the volunteers had to brush twice daily for 2 minutes with the allocated toothpaste. On day 4, plaque index was assessed using the criteria of Quigley and Hein (Turesky modification). After a washout time of 9 days the next test cycle with the other toothpaste was started.

The results from both toothpastes reduced the biofilm vitality significantly at VF4 and VF8 compared with VF0 (p < or =0.001). While after 8 hours the vitality values for the ZnCl2-toothpaste obtained significantly higher reductions (53%) than for the AmF-toothpaste (44%), results for plaque index were not significantly different (0.98 and 1.04 respectively).

Finally both toothpastes showed a significant and prolonged anti-bacterial effect up to 8 hours with a benefit in favour of the ZnCl2 toothpaste.

Oral Health Prev Dent. 2007;5(1):25-32.
Auschill TM, Deimling D, Hellwig E, Arweiler NB
Department of Operative Dentistry and Periodontology, Albert-Ludwigs-University, Freiburg, Germany. thorsten.auschill@uniklinik-freiburg.de

Over the past twenty years, the rapid emergence and increased prevalence of opportunistic Gram-negative bacilli demonstrating resistance to the β-lactam class of antibiotics has become a major health care crisis.

The production of β-lactamases, the innate capabilities of these organisms to genetically adapt structural and regulatory genes and the ease with which resistance genes are transferred via plasmids, transposons and integrons between different species, have broadened the ability of Gram-negative bacteria to inactivate the β-lactam antibiotics. This diminishes the clinical utility of these key anti-microbial agents making them resistant.

Extended spectrum β-lactamases (ESβLs) hydrolyse the penicillins, first-, second- and third-generation cephalosporins, especially cefotaxime, ceftriaxone, ceftazidime and cefpodoxime, and the oxyimino-monobactam, aztreonam.

ESβLs are inhibited by β-lactamase inhibitors, such as clavulanic acid, and are susceptible to the carbapenems (imipenem, meropenem and ertapenem) and the cephamycins (cefoxitin and cefotetan), though there have been a number of reports stating that ESβL-producing organisms can become resistant to the cephamycins due to the loss of an outer membrane porin protein (Martinéz-Martinéz et al 1996).

Since their discovery following the clinical introduction of the third-generation oxyimino-cephalosporins in 1981, there are now approximately 160 Temoneira (TEM), 100 sulfhydryl-variable (SHV), 64 cefotaxime-hydrolysing (CTX-M) and 102 oxacillinase (OXA) variant enzymes, along with a number of minor ESβL variants (Jacoby and Bush 2007).

Extensive laboratory and clinical experience exists regarding the detection and treatment of ESβL-producing Gram-negative bacilli. This suggest that the knowledge of their existence via means of antibiotic selective pressure, adaption and dissemination, may have an impact on therapeutic choices and the health and well-being of patients via targeted pragmatic antimicrobial selection and infection control practices.

It is unclear; however, if ESβL-producing organisms are being accurately detected 100% of the time. Furthermore, with the recent emergence of metallo β-lactamase-producing Gram-negative bacilli, it is also unclear whether the same mandate exists for the accurate detection, treatment and control of metallo β-lactamases. Metallo β-lactamases (MβLs) are a therapeutic disaster.

These enzymes hydrolyse all β-lactam antibiotics (except the monobactams), including the “drugs of last resort” the carbapenems (imipenem and meropenem), thus requiring the use of alternative, potentially more toxic classes of antibiotics to circumvent the hydrolytic actions of these β-lactamases.

Metallo β-lactamases, which are found in organisms such as Pseudomonas aeruginosa, Acinetobacter specie and members of the Enterobactericeae group such as salmonella and especially Escherichia coli and Klebsiella pneumoniae. They all utilise metal ions (usually zinc) to coordinate water molecules that serve as nucleophiles and hydrolyse the amide bond of the β-lactam ring, rendering the β-lactam antibiotic inactive.

These enzymes are divided into four genetically mobile variants: the older imipenem-hydrolysing (IMP) and Verona integron-encoded metallo β-lactamase (VIM) enzymes; and the more recently described Sao Paolo metallo β-lactamase (SPM) and GIM types (Poirel et al 2004).

Gram-negative bacteria that produce extended-spectrum and metallo β-lactamases are being discovered and isolated at a significant rate worldwide, while the development of new synthetic and natural antimicrobial agents to combat and elude the hydrolytic actions of these β-lactamases has significantly decreased in recent years (Valenzuela et al 2004).

Clinicians prescribing antibiotics need to know, understand and appreciate the short and long term outcomes of the inappropriate use of antibiotics for their patients, which, if not controlled and decreased, will inevitably reduce or eliminate the therapeutic options available in the future.

References

Franklin, C., Liolios, L., Peleg, A.Y. (2006). Phenotypic detection of carbapenem-susceptible metallo β-lactamase-producing Gram-negative bacilli in the clinical laboratory. Journal of Clinical Microbiology, 44: 3139-3144.

Martinéz-Martinéz, L., Hernández-Allés, S., Albertí, S., Tomás, J., Benedi, V., Jacoby,G.A. (1996). In vivo selection of porin-deficient mutants of Klebsiella pneumoniae with increased resistance to cefoxitin and expanded-spectrum cephalosporins. Antimicrobial Agents and Chemotherapy, 40, pp. 342-348.

Poirel, L., Heritier, C., Spicq, C., Nordmann, P. (2004). In vivo acquisition of high-level resistance to imipenem in Escherichia coli. Journal of Clinical Microbiology, 42 (8), pp. 3831-3833.

Valenzuela, J., Thomas, L., Iredell, J. for Australian Society of Microbiology (ASM). (2004). Beta-lactam resistance in Gram-negative bacteria. Antimicrobial Susceptibility Testing: Methods and Practices with an Australian Perspective, 5, pp. 127-157.

Mycobacterium tuberculosis has thrived in South Asia for over 100 years, but until now no one had studied the diversity of the strains present. To do this, Niyaz Ahmed and his colleagues from the University of Hyderabad, India, analysed 91 samples of tuberculosis taken from all over the country, studying the number and type of short, repetitive DNA sequences within three key genes.

They discovered that the ancestral strain is widespread, suggesting that India is the ancient reservoir for tuberculosis, from which more recent strains evolved and spread to other countries.

This may have enabled the immune systems of people living there to adapt to it, providing some degree of protection. However, that might be about to change, because the Indian population is far less well adapted to a recent strain of tuberculosis known as Beijing strain, found in India only since 2002. This highly infectious strain is threatening to replace the ancestral one, says Ahmed, who presented his results at a conference in Bangkok, Thailand, last month. Coinciding with a surge in HIV cases, this could spell disaster for the 5.7 million Indians infected with the virus.

Source: 10 January 2007 From New Scientist Print Edition issue 2585, page 15

The New Zealand Food Safety Authority’s (NZFSA) strategy to tackle New Zealand’s unacceptably high levels of human campylobacteriosis is progressing well with several areas of research and monitoring work already underway.

NZFSA has adopted a whole-of-food-chain approach to fighting the disease. All of the processes and procedures in place at each stage between rearing and eating poultry are under close scrutiny, with assistance from industry.

“We want to produce the greatest reductions in bacteria numbers as early as possible in the food chain (that is, as close to the farm as is practical and effective), and make further reductions at as many other points as practical and effective,” says Executive Director Andrew McKenzie.

“Working with the poultry industry, we have now established a data collection process that helps monitor the prevalence of Campylobacter in flocks and on carcasses.
“The data will help identify seasonal, geographic and demographic factors that may impact on flock prevalence; poor performing sheds and farms; opportunities for continuous improvement (i.e.: reduction) in flock prevalence and in the number of birds in a flock that may be infected.

“We are also working with Massey University and Mid Central Health to determine the actual (rather than suspected) source of human cases of infection to enhance surveillance. This work, centered in Manawatu, involves an intensive analysis of cases as soon as possible after diagnosis.

“The analysis will aid in-depth investigation of the precise circumstances that led to the cause of the food borne illness, such as cross-contamination or under-cooking.”

NZFSA is also working on:

Labelling is one of the key options being considered.

Our strategy is in line with what’s being done internationally to address Campylobacter in poultry. It is also pragmatic and recognizes that, because Campylobacter is a natural part of the gut bacteria of poultry it is unlikely to be completely eliminated. For this reason, consumer information will always be a key element of poultry food safety, just as it is with many other foods.

Industry-led trials of Campylobacter decontamination processes in a poultry processing premises have been delayed until later in the year because of a fire at the original site.

“We are now talking to various poultry companies to look at other intervention options being trialed and have called for data to be submitted for consideration,” says Dr McKenzie. “We are also seeking alternative ways of getting valid data should further delays eventuate.”

Campylobacter in Poultry Risk Management Strategy 2006-2009 can be downloaded here

Source

There have been increasing numbers of applications using oral fluids, saliva in particular, as the target substrate for performing clinical diagnostic tests. These have focused primarily on point of care (POC) testing.

These POC testing approaches range from, for example, currently available, highly specialized screening tests for the presence of antibodies recognizing HIV to the potential development of “lab-on-a-chip” platforms. Broad claims have been made that the latter will revolutionize clinical laboratory testing.

From the perspective of large centralized clinical laboratories, multiple issues must be considered before implementing individual tests using saliva as the target fluid in a POC format or using saliva as a universal test fluid for measuring multiple analytes in a centralized laboratory format.

The current scope of laboratory testing is large and comprehensive, involving both POC and centralized testing. Current academic laboratory programs have the ability to qualitatively identify and/or quantitatively measure several thousand analytes in various target matrices including blood, plasma, serum, urine, joint fluid, pleural fluid, peritoneal fluid, cerebrospinal fluid, and tissue. These tests fall into multiple clinical pathology disciplines, including clinical chemistry, hematology, coagulation, transfusion medicine, microbiology, cytogenetics, molecular diagnosis, and immunology.

In addition, before implementing a given test, multiple issues need to be evaluated to ensure the validity of the reported result; these include considerations involving the three major phases of testing: pre-analytical (e.g., patient identification and specimen collection, stability, and transport), analytical (e.g., sensitivity, specificity, accuracy, and precision), and post-analytical (e.g., reporting results, quality improvement, and turn-around-time).

Ann N Y Acad Sci. 2007 Mar;1098:192-9. Pesce MA, Spitalnik SL
Department of Pathology, College of Physicians