Acinetobacter: (back)

Acinetobacter infections acquired in the community are very rare and most strains found outside hospitals are sensitive to antibiotics.  While Acinetobacter poses few risks to healthy individuals, a few species, particularly Acinetobacter baumannii, can cause serious infections – mainly in very ill hospital patients.  The most common Acinetobacter infections include pneumonia, bacteraemia (blood stream infection), wound infections, and urinary tract infections.  'Hospital-adapted' strains of Acinetobacter are sometimes resistant to antibiotics and are increasingly difficult to treat.

Ref:  HPA infectious diseases library

FAQs

What is Acinetobacter?

Acinetobacter is a common type of bacteria that can be found in many sources in the environment including water and soil, but are rarely a medical threat to healthy, uninjured people. There are at least 25 different strains of Acinetobacter, and some strains can cause infections.

How can Acinetobacter be acquired?

Acinetobacter can be acquired by person-to-person contact, through contact with contaminated surfaces, or as a result of wounds contaminated with dirt or debris.

If I acquire Acinetobacter does that mean I’m infected?

Not necessarily. You can be colonised or infected with the bacteria:
Acinetobacter colonisation means that the bacteria is simply 'sitting on the skin' (in any site) but is causing no adverse affect to the patient. Many people live with the bacteria on their skin throughout their lives, without it causing any problems or symptoms of illness.  In an Acinetobacter infection, the bacteria are causing clinical signs of infection in the patient.

What infections can Acinetobacter cause?

Sometimes Acinetobacter causes skin or wound infections. In patients who are ill, it can cause lung infection (pneumonia) or infection in the blood.

Who is at risk of infection?

The people most likely to be infected are those who are already ill and who have been admitted to the hospital. Patients, who have compromised immune systems, such as those with HIV/AIDS, transplant patients, those on intensive care units, etc., are at risk for this and other infections.

How is Acinetobacter treated?

Many strains of Acinetobacter that can cause infection are easily treated with common antibiotics, however some of these strains of Acinetobacter are resistant to common antibiotics and this is called multidrug-resistant or MDR-Acinetobacter. This is thought to be due to an increased use of antibiotics in society; some bacteria have evolved to withstand the common antibiotic’s attack.   Therefore, infections with MDR-Acinetobacter are more difficult to treat, but they can be treated using special treatments such as stronger antibiotics.   Not all patients tested with a positive culture of MDR-Acinetobacter will actually be infected. The bacteria can live on skin or in wounds without causing an infection and will not need special treatment.

What will this mean for my hospital care?

All patients who have a positive culture for Multidrug resistant (MDR) Acinetobacter will be placed on isolation precautions. This just means that they will be placed apart from other patients. These precautions are used to prevent the spread of MDR-Acinetobacter among patients. Hospital staff will wear gowns and gloves to care for you. A card will be placed on the door to alert everyone what precautions are needed to enter the room. Visitors should report to the nurses’ station for directions on what to do to enter your room. All of these steps are to keep germs from spreading.  Please remember that hand washing is a key method to prevent the spread of any infection.

What will happen when I go home?

At home, in most cases, you need only to use good hand hygiene. The nursing staff will give you discharge instructions.

 **Acinetobacter does not usually pose a threat to healthy people, hospital staff or to family members or close contacts of an infected patient.

Ref: Addenbrooks Hospital/Cambridge University NHS Trust

N C H I   April 2007

Back to Top

Campylobacter: (back)

Campylobacter’s are mainly spiral-shaped, S-shaped or curved, rod-shaped bacteria. There are 16 species and six subspecies assigned to the genus Campylobacter, of which the most frequently reported in human disease are C. jejuni (subspecies jejuni) and C. coli. C. laridis and C. upsaliensis are also regarded as primary pathogens, but are generally reported far less frequently in cases of human disease. Most species prefer a micro-aerobic (containing 3-10% oxygen) atmosphere for growth. A few species tend to favour an anaerobic environment, although they will grow under micro-aerobic conditions also.

The Disease:

• Campylobacteriosis is the disease caused by the presence of campylobacter’s. The onset of disease symptoms usually occurs two to five days after infection, but can range from one to ten days.
• The most common clinical symptoms of campylobacter infections include diarrhoea (frequently with blood in the faeces), abdominal pain, fever, headache, nausea, and/or vomiting. The symptoms typically last three to six days.
• A fatal outcome is rare and is usually confined to very young or elderly patients, or to those already suffering from another serious disease such as AIDS.
• Complications such as bacteremia, hepatitis, pancreatitis (infections of the blood, liver and pancreas respectively), and abortion have all been reported with various degrees of frequency. Post-infection complications may include reactive arthritis (painful inflammation of the joints which can last for several months) and neurological disorders such as Guillain-Barré syndrome, a polio-like form of paralysis that can result in respiratory and severe neurological dysfunction or death in a small, but significant, number of cases.
• The high incidence of campylobacter diarrhoea, as well as its duration and possible sequelae, makes it highly important from a socio-economic perspective.

Sources and Transmission:

• Campylobacter’s are widely distributed and occur in most warm-blooded domestic, production and wild animals. They are prevalent in food animals such as poultry, cattle, pigs, sheep, ostriches and shellfish; and in pets, including cats and dogs.
• The main route of transmission is generally believed to be food borne, via undercooked meats and meat products, as well as raw or contaminated milk. The ingestion of contaminated water or ice is also a recognized source of infection.
• Campylobacteriosis is considered to be a zoonosis, a disease transmitted to humans from animals or animal products. In animals, campylobacter’s seldom cause disease.
• One of the major gaps in our knowledge at present is the relative contribution of each of the above sources to the overall burden of disease. Since common-source outbreaks account for a rather small proportion of cases, the vast majority of reports are made sporadically, with no easily discernible pattern. Estimation of the importance of all known sources is therefore extremely difficult. In addition, the wide occurrence of campylobacter’s also hinders the development of strategies to control campylobacter’s in the food supply "from farm to fork".

Control and Prevention Methods:

• Treatment is not generally indicated, except electrolyte replacement and rehydration. Antimicrobial treatment (erythromycin, tetracycline, quinolones) is indicated in invasive cases or to eliminate the carrier state.
• The prevention of infection requires control measures at all stages of the food chain, from agricultural production on the farm, to processing, manufacturing and preparation of foods in both commercial establishments and the domestic environment.
• Specific intervention methods on the farm have been shown to reduce the incidence of campylobacter in poultry. Measures include enhanced biosecurity to avoid horizontal transmission of campylobacter from the environment to the flock of birds. This control option is feasible only where birds are kept in closed housing conditions.
• There are no proven intervention methods to reduce campylobacter in cattle farms. Prevention of the contamination of raw milk on the farm is not consistently possible; therefore, consumption of raw milk should be avoided.
• Good hygienic slaughtering practices will reduce contamination of carcasses by faeces, but will not guarantee the absence of campylobacter from meat and meat products. Education in hygienic handling of foods for abattoir workers and those involved in the production of raw meat is essential to keep microbiological contamination to a minimum.
• The only effective method of eliminating campylobacter from contaminated foods is to introduce a bactericidal treatment, such as heating (e.g. cooking or pasteurization) or irradiation.
• Preventive measures for campylobacter infection in the household kitchen are similar to those used against other foodborne bacterial diseases.
• In countries without adequate sewage disposal systems, faeces and articles soiled with faeces may need to be disinfected before disposal.

Recommendations for the Public and Travellers:

• Make sure your food is properly cooked and still hot when served.
• Avoid raw milk and products made from raw milk. Drink only pasteurized or boiled milk.
• Avoid ice unless you are sure it is made from safe water.
• When the safety of drinking water is doubtful, boil it or if this is not possible, disinfect it with a reliable, slow-release disinfectant agent. These are usually available at pharmacies.
• Wash hands thoroughly and frequently using soap, in particular after contact with pets or farm animals, or after having been to the toilet.
• Wash fruits and vegetables carefully, particularly if they are eaten raw. If possible, vegetables and fruits should be peeled.
• WHO's brochure A Guide on Safe Food for Travellers gives practical advice for safeguarding health when travelling*.

Recommendations for Food Handlers:

• Both professional and domestic food handlers should be vigilant during the preparation of food and should observe hygienic rules of food preparation.
• Professional food handlers who suffer from fever, diarrhoea, vomiting or visible infected skin lesions should report to their employer immediately.
• More information for food handlers is given in the WHO Guide on Hygiene in Food Service and Mass Catering Establishments (Document code: WHO/FNU/FOS/94.5).

Ref:  World Health Organisation

NCHI ~ April 2007

Back to Top

Clostridium Difficile: (back)

Q. How do you catch it?

C. difficile can cause illness when certain antibiotics disturb the balance of 'normal' bacteria in the gut. Its effects can range from nothing in some cases to diarrhoea of varying severity, which may resolve once antibiotic treatment is stopped, through to severe inflammation of the bowel which can sometimes be life threatening.

It is possible for the infection to spread from person to person because those suffering from C. difficile -associated disease shed spores in their faeces. Spores can survive for a very long time in the environment and can be transported on the hands of health care personnel who have direct contact with infected patients or with environmental surfaces (floors, bedpans, toilets etc.) contaminated with C. difficile.

Q. What are the symptoms of C. difficile infection?

The effects of C. difficile can vary from nothing to diarrhoea of varying severity and much more unusually to severe inflammation of the bowel.

Other symptoms can include fever, loss of appetite, nausea and abdominal pain or tenderness

Q. How do doctors diagnose C. difficile infection?

It is difficult to diagnose C. difficile infection on the basis of its symptoms alone, therefore the infection is normally diagnosed by carrying out laboratory testing which shows the presence of the C. difficile toxins in the patient's faecal sample.

Q. Who does it affect? Are some people more at risk?

The elderly are most at risk, over 80% of cases are reported in the over 65-age group. Immuno-compromised patients are also at risk. Children under the age of 2 years are not usually affected. Repeated enemas and/or gut surgery increase a person's risk of developing the disease. C. difficile infection occurs when the normal gut flora is altered, allowing C. difficile to flourish and produce a toxin that causes a watery diarrhoea. Antibiotics may also alter the normal gut flora and increase the risk of developing C. difficile diarrhoea.

Q. How can it be treated? 

C. difficile can be treated with specific antibiotics. There is a risk of relapse in 20-30% of patients and other treatments may be tried, including pro-biotic (good bacteria) treatments, with the aim of re-establishing the balance of flora in the gut. Most cases of C.difficile diarrhoea make a full recovery. However, elderly patients with other underlying conditions may have a more severe course. Occasionally, infection in these circumstances may be life threatening.

Q. What should I do to prevent the spread of Clostridium difficile to others?

If you are infected you can spread the disease to others. However, only people that are hospitalized or on antibiotics are likely to become ill. In order to reduce the chance of spreading the infection to others: it is advisable to wash hands with soap and water, especially after using the restroom and before eating; keeping surfaces in bathrooms, kitchens and other areas clean and cleaning these on a regular basis with household detergent/disinfectants.

Q. How can hospitals prevent the spread of C. difficile?

Unfortunately patients with diarrhoea, especially if severe or accompanied by incontinence, may unintentionally spread the infection to other patients, which may lead to outbreaks of C. difficile in hospitals. In addition, the ability of this bacterium to form spores enables it to survive for long periods in the environment (e.g. on floors and around toilets) and disseminate in the air e.g. during bed making. Staff should wear disposable gloves and aprons when caring for infected patients and affected patients may be segregated from others. Rigorous cleaning with warm water and detergent is probably the most effective means of removing spores from the contaminated environment, whilst staff should observe good hand washing practice. Alcohol gels should be used routinely by healthcare staff between treating patients, but only if their hands are not visibly soiled. When hands are visibly soiled, they must always be washed with soap and water first. In an outbreak situation, the Infection Control Team may introduce special measures for staff, patients and visitors to follow.

Q. I have heard that some patients are at increased risk for Clostridium difficile - associated disease. Is that true?

That is true – the risk for disease increases in patients with the following:

Q. Has a new type of C. difficileinfection been detected recently?

The HPA has initiated a sampling scheme to detect new types of C.difficile infection. A new type of C.difficile closely related to one previously found in North America has recently been detected in the UK, including at Stoke Mandeville Hospital.

Q. How common is this strain in the UK?

It is not possible to make an assessment of how prevalent this is in the UK because data have not been collected in sufficient quantities to give us a true picture of the current position.

Q. Is this strain more difficult to treat?

This strain of C.difficile can be treated with antibiotics, in the same way as other types.

Q. Is this hospital infection caused by C. difficile any more difficult to remove from the environment than other hospital infections?

C.difficile are types of bacteria that produce resistant spores that are able to persist in the environment longer than other bacteria. Although they will not be killed by alcohol hand gels, they can be removed with soap and water. Staff, patients and visitors need to wash hands with soap and water in addition to using alcohol hand gels. Disinfectants containing bleach need to be used on surfaces and floors to ensure that the spread of infection is controlled.

Ref: HPA reference library/infectious diseases 2006

Back to Top

ESBL: (back)

Where do these ESBL producing bacteria come from

Its not exactly known but it seems that the genes for ESBL production arose in one particular bacterial strain by natural mutation and then spread to many others, especially E.Coli.  this may have happened first in animals or humans.

How are ESBLs spread

There is some evidence to suggest that they can be found in the faeces of farm animals as well as some humans.  This means that it is possible that contamination of food eg raw meat, by bacteria from animal faeces has led to infections in humans.  It is also possible that these bacteria are passed from person to person on contaminated hands (of healthcare workers or patients) or by poor practise in urinary catheter care.  In addition the genes coding for production of ESBLs can be passed between bacterial species, so it is not just the spread of a single strain of bacterium which matters but the spread of genes between strains as well.  Spread is made easier if the bacteria normally present in the gut (and which help protect against invasion by other strains) are killed by taking antibiotics.  Use of some newer antibiotics appears to predispose patients to infection with ESBL-producing bacteria which may explain why this has now become an issue.

What are Extended-Spectrum Beta-Lactamase (ESBL) producing E.coli

ESBL (Extended-Spectrum Beta-Lactamase) producing E.coli are antibiotic resistant strains of E.coli.  E.coli are very common bacteria that normally live harmlessly in the gut.  ESBL-producing strains are bacteria that produce an enzyme called extended-spectrum beta-lactamase, which makes them more resistant to antibiotics and makes the infections harder to treat.  In many instances, only two oral antibiotics and a very limited group of intravenous antibiotics remain effective.

What illnesses do ESBL-producing E.coli cause

E.coli are one of the most common bacteria causing infections in humans, particularly urinary tract infections (UTIs).  These infections can sometimes progress to cause more serious infections such as blood poisoning which can be life threatening.  ESBL-producing strains are ones more difficult to treat because of their antibiotic resistance.

Are some people more at risk than others

Most of the infections have occurred in people with underlying medical conditions who are already very sick and in elderly people.  Patients who have been taking multiple courses of antibiotics or who have been previously hospitalised are mainly affected.

Is this the type of E.coli that causes severe food poisoning

No.  There is a specific strain of E.coli called E.coli 0157, which causes food poisoning and sometimes kidney failure when people eat undercooked meat.  That is a completely different strain.  The ESBL-producing E.coli are associated with UTIs rather than food poisoning.

How do people contract it

Further research is needed to look at the risk factors associated with different strains of ESBL-producing E.coli and how they are transmitted between patients and also in the community.

Is it treatable

The important factor is quick diagnosis and recognition that the bacteria causing infection are resistant to antibiotics, so that the most appropriate treatment can be prescribed quickly.  There are only two oral antibiotics and a few intravenous antibiotics that are effective against such infections.

Which antibiotics are these infections resistant to

Most ESBL-producing E.coli are resistant to cephalosporins, penicillins, fluoroquinolones, trimethoprim, tetracycline and some other antibiotics leaving only limited options for oral treatment in the community, usually only nitrofurantoin and fosfomycin.

How can the spread be controlled

Robust infection control measures are always important to prevent the spread of infection.  These include interventions, such as, handing washing and patient isolation.  It is also important to ensure that antibiotics are prescribed only when needed, in the right dose, for the right duration, so as to reduce resistance developing bacteria.

Surveillance

Currently there is voluntary national surveillance of blood poisoning caused by E.coli poisoning, but surveillance needs to be extended to look for ESBL-producing E.coli as a cause of blood poisoning and also of UTIs in the community.  The surveillance of E.coli bacteraemias from 1994 to 2004 indicates a year on year increase in the number of these infections.  Total numbers of E.coli bacteraemias have more than doubled in the last decade from 8,640 to 17,416 cases in 1994 and 2004 respectively.

Ref:  HPA reference library/infectious diseases/ESBLs

N C H I

February 2007

Back to Top

GRE: (back)

What illnesses do GRE cause?

GRE commonly cause wound infections, bacteraemia (blood poisoning) and infections of the abdomen and pelvis. GRE may also occasionally cause infections in the bile duct (cholangitis), heart valves (endocarditis) or the urinary tract.

Are some people more at risk than others?

Infections caused by GRE mainly occur in hospital patients, particularly those who are immuno-compromised, those who have had previous treatment with certain other antibiotics (particularly cephalosporins and glycopeptides), those who are on a prolonged hospital stay, or those in specialist units such as intensive care or renal units. However, GRE are sometimes found in the faeces of people who have never been in hospital or have not recently been given antibiotics.

How do people contract it?

There are two routes by which patients tend to contract GRE infections. The first is by cross-infection, which occurs when bacteria causing infection in one patient are passed to another patient, who also becomes infected. The second involves the spread of GRE bacteria that reside harmlessly in a person's gut to other areas of the body where they are not normally found.

Is it treatable?

GRE are not particularly virulent bacteria, but they are difficult to treat because of limitations in the range of antibiotics which are effective against them. Two antibiotics, linezolid and synercid, may be used, while others (daptomycin or tigecycline) have already been launched in the United States and are anticipated in the UK in the near future. Synercid is active against most E. faecium but lacks useful activity against E. faecalis, while linezolid is usually active against both species. GRE resistant to these antibiotics have been isolated from hospital patients, though they are rare.

Which antibiotics are these infections resistant to?

GRE are resistant to vancomycin and commonly (but not invariably) to teicoplanin. Many GRE, especially if they are E. faecium, are resistant to multiple other antibiotics.

Have there been any deaths as a result of this infection?

Enterococci usually cause infections in patients who are already seriously ill with underlying problems that predispose them to infection. This means that if a patient with a GRE infection dies, it is often difficult to know if this was due to the pre-existing illness or as a result of the infection.

How can the spread be controlled?

Prompt recognition of bacteria with unusual resistances and good infection control procedures are needed to prevent spread. Restriction of the use of certain antibiotics, especially vancomycin, teicoplanin and cephalosporins, to those patients who really need them, will help to limit the occurrence of GRE infections.

GRE is most commonly spread via hands, equipment, and sometimes the environment. It is important that healthcare workers and visitors wash their hands before and after visiting a patient. Provided hands are not soiled (when they should be washed with soap and water), rapid acting alcohol and other hand hygiene solutions are now advocated in healthcare; they are easier and faster to use than hand washing. Equipment should also be cleaned after use.

REF:  HPA Reference Library/Infectious Diseases

NCHI ~ April 2007

Back to Top

Hospital – Acquired Pneumonia (HAP)(back)

What is HAP
Pneumonia is a collective term for any infection or inflammation of the lungs. HAP also known as nosocomial pneumonia that is neither present or incubating at the time a patient is admitted to hospital, but which develops a minimum of 48 hours after hospital admission.

What is ventilator-associated pneumonia (VAP)
A large number of HAP cases occur as a consequence of ventilator associated pneumonia (VAP) where infection has arisen following mechanical ventilation

Causes of HAP
HAP is the result of an infection of the lungs which in the main is caused by bacteria.  The infection can be spread from person to person or caused by environmental contamination

Symptoms of HAP
With HAP, symptoms may come on quite suddenly and include pain in the side of the chest that can make breathing and coughing uncomfortable and /or reduced cough reflex, fever, aches and pains, and loss of appetite.

HAP risk factors

Guideline recommendations
Recent American HAP guidelines have encouraged medical professionals to tackle HAP on the basis of prevention, more effective diagnosis and the use of antimicrobial treatment.  The BSAC Hospital-Acquired Pneumonia (HAP) evidence-based guidelines are the first to address these three areas in Europe

Prevention
Prevention centres on the two main causes, person-to-person transmission and transmission from the environment.  The new guidelines highlight that it is essential that staff are educated on appropriate prevention methods and where possible opting for non-invasive (e.g. a face mask that improves oxygenation) rather than invasive assisted ventilation (e.g. a tube that is inserted down the throat) helps to prevent HAP

Diagnosis
Diagnostic testing for HAP has two main purposes: to determine whether a patient does indeed have pneumonia, and to identify the cause of the pneumonia, in particular the type of bacteria.  Though controversies about clinical diagnosis exist, the HAP guidelines clarify that radiological and microbiological tests should not form the basis for diagnosis, but only serve to support clinical diagnosis.

Treatment
When HAP is caused by bacteria, treatment will always be with antibiotics.  However, the inappropriate use of antibiotics has meant that many bacteria have found clever ways of becoming resistant to them and have therefore made some infections more difficult to treat.

Until now there has been no clear and consistent approach in treating suspected HAP cases.  Often, healthcare professions will wait for the results of diagnostic tests before choosing which antibiotic to treat with – yet this process promotes the emergence of antibiotic resistance which therefore increases the patients’ risk of mortality.  The HAP guidelines use the latest evidence to recommend that treating quickly with an empiric broad spectrum antibiotic, effective against most common bacteria in that particular hospital or unit should be used.  In all cases it is recommended that local problem bacteria in any one hospital or unit needs to be taken into account when choosing an antibiotic.
Once the HAP diagnosis has been confirmed the guidelines recommend switching to an antibiotic that targets the specific bacteria causing the infection.  The use of a single antibiotic is recommended as there are no benefits in using combination therapy.

Ref : BSAC guidelines for Hospital-Acquired Pneumona (HAP) published july 2008:
Wyeth has provided an unrestricted educational grant for the development and production of the guidelines.

Summary

Back to Top

Norovirus: (back)

How does Norovirus spread?

The virus is easily transmitted from one person to another. It can be transmitted by contact with an infected person; by consuming contaminated food or water or by contact with contaminated surfaces or objects.

What are the symptoms?

The symptoms of Norovirus infection will begin around 12 to 48 hours after becoming infected. The illness is self-limiting and the symptoms will last for 12 to 60 hours. They will start with the sudden onset of nausea followed by projectile vomiting and watery diarrhoea. Some people may have a raised temperature, headaches and aching limbs. Most people make a full recovery within 1-2 days, however some people (usually the very young or elderly) may become very dehydrated and require hospital treatment.

Why does Norovirus often cause outbreaks?

Norovirus often causes outbreaks because it is easily spread from one person to another and the virus is able to survive in the environment for many days. Because there are many different strains of Norovirus, and immunity is short-lived, outbreaks tend to affect more than 50% of susceptible people. Outbreaks usually tend to affect people who are in semi-closed environments such as hospitals, nursing homes, schools and on cruise ships.

How can these outbreaks be stopped?

Outbreaks can be difficult to control and long-lasting because Norovirus is easily transmitted from one person to another and the virus can survive in the environment. The most effective way to respond to an outbreak is to disinfect contaminated areas, to institute good hygiene measures including hand-washing and to provide advice on food handling. Those who have been infected should be isolated for up to 48 hours after their symptoms have ceased.

How is Norovirus treated?

There is no specific treatment for Norovirus apart from letting the illness run its course. It is important to drink plenty of fluids to prevent dehydration.

If I’m suffering from Norovirus, how can I prevent others from becoming infected?

Good hygiene is important in preventing others from becoming infected – this includes thorough hand washing before and after contact. Food preparation should also be avoided until 3 days after symptoms have gone altogether.

Who is at risk of getting Norovirus?

There is no one specific group who are at risk of contracting Norovirus – it affects people of all ages. The very young and elderly should take extra care if infected, as dehydration is more common in these age groups.  Outbreaks of Norovirus are reported frequently in semi-closed institutions such as hospitals, schools, residential and nursing homes and hotels. Anywhere that large numbers of people congregate for periods of several days provides an ideal environment for the spread of the disease. Healthcare settings tend to be particularly affected by outbreaks of Norovirus. A recent study done by the Agency shows that outbreaks are shortened when control measures at healthcare settings are implemented quickly, such as closing wards to new admissions within 4 days of the beginning of the outbreak and implementing strict hygiene measures.

How common is Norovirus?

Norovirus is not a notifiable disease so reporting is done on a voluntary basis. The HPA only receives reports of outbreaks and we see anywhere between 130 and 250 outbreaks each year. It is estimated that Norovirus affects between 600,000 and a million people in the UK each year.

Are there any long-term effects?

No, there are no long-term effects from Norovirus.

What can be done to prevent infection?

It is impossible to prevent infection; however, taking good hygiene measures (such as frequent hand washing) around someone who is infected is important. Certain measures can be taken in the event of an outbreak, including the implementation of basic hygiene and food handling measures and prompt disinfection of contaminated areas, and the isolation of those infected for 48 hours after their symptoms have ceased.

Ref: HPA Infectious Disease Library

NCHI ~ April 2007

Back to Top

Pseudomonas: (back)

Pseudomonas aeruginosa is a Gram-negative bacterium commonly found in soil and ground water.  It rarely affects healthy people and most community-acquired infections are associated with prolonged contact with contaminated water.                

P. aeruginosa is increasingly important clinically as it is a major cause of both healthcare-associated infections and chronic lung infections in people with cystic fibrosis.                                                                                                                

Although P. aeruginosa is an opportunistic pathogen (i.e. more likely to infect those patients who are already very sick as opposed to healthy patients), it can cause a wide range of infections, particularly among immunocompromised people (HIV or cancer patients) and persons with severe burns, diabetes mellitus or cystic fibrosis.                    

P. aeruginosa is one of the more common causes of healthcare-associated infections and is increasingly resistant to many antibiotics.  In hospitals the organism contaminates moist/wet reservoirs such as respiratory equipment and indwelling catheters and infections can occur in almost every body site but are particularly serious in the bloodstream (bacteraemia).                                                                          

Most infections are susceptible to third generation cephalosporins (ceftazidime), carbapenems (imipenem and meropenem), aminoglycosides (gentamicin and tobramycin) and colistin.  Serious infections are usually treated with ticarcillin or piperacillin (both broad-spectrum penicillins), often in combination with an aminoglycoside.  Experimental vaccines currently undergoing clinical testing may be particularly helpful for patients with cystic fibrosis. 

Fact Sheet:  Ref: HPA Infectious Disease Library

Pseudomonads

Pseudomonads are a ubiquitous group of environmental gram negative bacterial organisms. They comprise a number of true Pseudomonas species as well as many species formerly classified in the genus. Pseudomonas aeruginosa is the type strain of the genus. They are natural residents of soil and water and may cause primary skin infections in the healthy. This is most associated with recreational water activities and is characterised by a self-limiting skin rash or folliculitis. In the immunocompromised infections can occur in almost any body system and may be severe and accompanied by high mortality. The genus Pseudomonas once comprised over 100 species but over the last decade many of these have been reclassified into different genera. There are five main groups of pseudomonads of medical interest. These are the fluorescent or 'true' pseudomonas, P.aeruginosa (formerly known as P. pyocyanea), P. fluorescens and P. putida. The second group are contained within the genus Burkholderia and within this genus, three species B.cepacia, B. pseudomallei and B. mallei, are associated with human and animal infection. lly distinct but phenotypically similar). B. pseudomallei is the aetiological agent of melioidosis, a life threatening septic infection prevalent in SE Asia and Northern Australia and B. mallei causes glanders in horses and other species. The other three generic groups of pseudomonads are Delftia, Brevundimonas and Stenotrophomonas.                                                                   

With the exception of the medically important species (P. aeruginosa, B. cepacia, B. mallei and B. pseudomallei) the organisms within the five groups are best regarded as true opportunists. They are relatively insusceptible to antiseptics, disinfectants and antibiotics compared with the natural surrounding bacterial flora and are usually associated with contaminated water reservoirs in respiratory equipment in hospitals. Instillation, injection or inhalation of these organisms by immunocompromised or post surgical patients may pose a significant threat to health. However their isolation from clinical specimens most often reflects colonization rather than invasive infection owing to their relatively low virulence.                                                             

Pseudomonas and related species are aerobically growing bacteria which are gram negative. They are able to grow over a wide range of temperatures (11C to 44C) but P. fluorescens and P. putida are psychrophylic and are able to multiply at 4C. They occasionally contaminate refrigerated blood products which when transfused into a patient may cause endotoxic shock. P. fluorescens may occasionally be recovered from the sputum of cystic fibrosis (CF) patients. It is also a recognized food spoilage agent, particularly of refrigerated meat, and it may spoil UHT milk if this is stored above 5^oC. They may be recovered from fresh vegetables or plants, and sinks, taps and drains in the hospital environment. Most species are motile and can utilize a range of simple organic compounds as energy sources, and metabolize glucose by an oxidative pathway. Some can reduce nitrate or form ammonia from arginine. Anaerobic growth is possible only in the presence of an alternative electron acceptor such as nitrate or arginine.

Pseudomonas aeruginosa

P. aeruginosas found almost anywhere in the natural habitat in sites ranging from surface waters to vegetation and soil. It can multiply in distilled water but is rarely isolated from sea water except near sewage outfalls and polluted river estuaries. It is not a fish pathogen. The organism is a resident of the soil and rhizosphere and is frequently recovered from fresh vegetables and plants. It is pathogenic for plants such as tobacco, cucumbers and lettuce and is also a well-established pathogen of grasshoppers and insects.                                                                                                

P. aeruginosa has been isolated from a variety of sources including, among others, aviation fuel, cutting oils, cosmetics, plasticizers, photographic materials etc. Hospital and domestic sink traps, taps and drains are invariably colonised by pseudomonads. Faecal carriage rates vary from 25 to 15% and are higher in vegetarians.                    

P. aeruginosa dies rapidly on dry human skin but in conditions of superhydration of the skin, such as divers in long term saturation chambers and military personnel in swampy terrain, the frequency of colonization is markedly increased and infections such as otitis externa in divers and toe web rot in soldiers are common.             

Despite the ubiquity of the organism, community-acquired infections with P.aeruginosa are relatively rare. In hospitals, however, it may account for about 10% of all infections acquired during the patients' stay. It is a frequent cause of pneumonia and urinary tract, surgical wound and blood stream infections are common. The species is particularly frequent as a cause of chronic respiratory infection in CF patients. P. aeruginosa has low intrinsic virulence in man and animals. Thermal injury or neutropenia or the introduction of relatively large inocula direct into tissues are often necessary perquisites for the establishment of infection.                    

Compared to enterobacteria, P. aeruginosa is relatively resistant to many antibiotics but there are a number of antimicrobial agents with good to excellent activity against most isolates of the species. These include ceftazidime, ticarcillin, piperacillin, imipenem, meropenem, gentamicin, tobramycin, amikacin, ciprofloxacin and aztreonam.

As many as 80% of CF patients may be colonised in the lung with P. aeruginosa and once established it is particularly refractory to antibiotic treatment. Many isolates grow as mucoid colonies but mixtures of different colonial forms are frequently found on primary plates. These variants invariably prove to be genetically identical. P. aeruginosa from CF patients are often atypical in growth requirements and may be auxotrophic for specific amino acids, be non motile and a minority may exhibit extreme susceptibility to semi synthetic penicillins.                                                  

For epidemiological studies, isolates of P. aeruginosa can be serotyped by slide agglutination of live cultures. There are 21 internationally accepted O-serotypes but four types account for approximately 50% of clinical and environmental isolates. Further discrimination between serotypes can be achieved by DNA fingerprinting using pulsed-field gel electrophoresis of XbaI restriction endonuclease digests. Other typing systems used include ribotyping and random PCR typing (Grundmann et al. 1995).

Burkholderia

The genus Burkholderia was defined in 1992 by Yabuuchi for Pseudomonas species formerly of rRNA group II. There are at least 20 validly named species in the genus but the medically important species are B. cepacia, B. pseudomallei and B. mallei. The organism formerly known as Pseudomonas pickettii was reassigned by Yabuuchi to Burkholderia but has subsequently been reclassified as Ralstonia pickettii. Occasional clinically significant isolates of B. pickettii are recovered from hospital patients but they are most often isolated from the ward environment and as a contaminant of antiseptic and disinfectant solutions. It is oxidase and nitrate positive and arginine negative.

Burkholderia cepacia

The B. cepacia complex currently comprises nine genomic species or genomovars. Cystic fibrosis patients appear to be susceptible to lung infection with these organisms which can be particularly severe and lead to the death of a minority of patients from a fulminant necrotizing pneumonia. Patients with chronic granulomatous disease may also succumb to B. cepacia infection due to its resistance to opsonophagocytes of patients with this disease. Apart from these conditions, B. cepacia may be acquired by patients in hospitals from contaminated equipment water reservoirs such as nebulizers and contaminated antiseptic irrigation fluids.                                                          

They grow moderately well on nutrient agar and a variety of non-fluorescent pigments may be produced by some strains. They grow slowly at 37^oC and extended incubation for 48 hours is recommended to optimise their recovery from sputum. Cultures often die rapidly on storage on nutrient agar slopes but survive remarkably well suspended in sterile distilled water. Selective media based on their constitutive resistance to colistin and bile salts have been described but other colistin resistant gram negative rods may also be recovered on these media. Members of the complex are not differentiated well by phenotypic tests but PCR assays specific for individual genomovars have been reported (Coeyne et al. 2001).                                                  

B. cepacia has high intrinsic resistance to antimicrobials and is generally resistant to the antibiotics active against P. aeruginosa. It is resistant to aminoglycosides, colistin, ticarcillin, azlocillin and imipenem. Variable susceptibility is shown to temocillin, aztreonam, ciprofloxacin and tetracycline and about two-thirds of strains from CF patients are susceptible to ceftazidime, piperacillin/tazobactam and meropenem.

Burkholderia pseudomallei

This is an important pathogen of humans (melioidosis) and farm animals in tropical and subtropical areas of SE Asia and Northern Australia, where it is endemic in rodents and is found in moist soil, on vegetables and on fruit. A closely related but non-pathogenic species, B. thailandensis, has been described from environmental samples. Cultures should be sent to a reference laboratory for species confirmation. For further information on these organisms and melioidosis, see Dance (1999). Cultures on blood agar and nutrient agar at 37°C give mucoid or corrugated, wrinkled, dry colonies in 1-2 days, and an orange pigment may develop on prolonged incubation. Variation between rough and smooth colonies is frequent. Cells may also exhibit bipolar staining in gram stains. B. pseudomallei is a strict aerobe, it is motile, oxidizes glucose and breaks down arginine. Most isolates are reliably identified by API 20NE microgalleries but must be distinguished from non-pigmented strains of P. aeruginosa, P. stutzeri and B. mallei. It is resistant to colistin and gentamicin but isolates are generally susceptible to imipenem, piperacillin, amoxycillin-clavulanic acid, doxycycline, ceftazidime, aztreonam and chloramphenicol.

Burkholderia mallei

B.mallei is the causative agent of glanders, a rare disease of horses and no isolates of the organism have been recovered in the UK since the last World War.  Both B. pseudomallei and B. mallei must be handled in category 3 containment facilities and their exchange between laboratories is restricted.

Delftia acidovorans

This organism was reclassified from the genus Comamonas. It is found on occasion in clinical specimens and the hospital environment. Isolates grow as non-pigmented colonies overnight at 37^oC but incubation should be extended to 48 hours for slow growing strains. Some isolates exhibit resistance to colistin and gentamicin and may grow on B. cepacia selective media. Antimicrobial susceptibility is variable but most isolates are susceptible to ureidopenicillins, tetracycline, the quinolones and trimethoprim-sulphamethoxazole.

Brevundimonas diminuta and Brevundimonas vesicularis

These are closely related species previously of rRNA homology group IV of Pseudomonas, are rare in clinical specimens and of doubtful clinical significance. They grow slowly on nutrient agar and require 48 hours incubation at 37^oC. B. vesicularis grows as orange pigmented colonies on nutrient agar and gives a weak oxidase reaction. B. diminuta is not pigmented.

Stenotrophomonas maltophilia

This species once a member of the genus Xanthomonas has been isolated from a variety of hospital environmental sources and may be clinically significant in severely immunocompromised patients. The extensive use of imipenem, to which S. maltophilia is resistant, appears to be associated with nosocomial outbreaks. S. maltophilia is increasingly isolated from CF sputum and is often misidentified as B. cepacia as it grows reasonably well on colistin-containing media. Most strains are susceptible to co-trimoxazole, doxycycline and minocycline and third-generation cephalosporins but are resistant to aminoglycosides.  Colonies resemble those of P. aeruginosa but a yellow or brown diffusible pigment may be produced; on blood agar they can  appear as faint lavender. It is usually oxidase negative, does not hydrolyse arginine and does not grow on cetrimide agar. It is the only pseudomonad that gives a positive lysine decarboxylase reaction.

Sphingomonas paucimobilis

S. paucimobilis produces a non-diffusible yellow pigment and is most likely to be confused with flavobacteria. Motility is poor and best seen in cultures incubated at room temperature. It has been found in clinical material and recovered from hospital equipment. Most strains are susceptible to erythromycin, tetracycline, chloramphenicol and aminoglycosides.

Ref:  HPA Reference Library/Infectious Diseases

N C H I  April 2007

Back to Top

PVL-associated Staphylococcus aureus (back)

How common is PVL S. aureus ?

The PVL toxin is carried by less than 2% of S. aureus and can be carried by both MRSA (methicillin resistant Staphylococcus aureus ) and MSSA (methicillin sensitive Staphylococcus aureus ).We are aware of isolated cases in the community across the United Kingdom (UK). Microbiology laboratories across the UK are asked to be vigilant and have been requested to send any suspicious samples to the HPA for further analysis.

What are the symptoms?

Infections caused by PVL strains of S. aureus normally cause cellulitis (inflammation of layers under the skin) and pus-producing skin infections (eg abscesses, boils and carbuncles). However, they can, on very rare occasions, lead to more severe invasive infections, such as septic arthritis, bacteraemia (blood poisoning) or necrotising pneumonia (a severe, life-threatening form of pneumonia).

Why do people get PVL S. aureus infections?

Not all patients with PVL S. aureus will suffer an infection. When these occur they are usually associated with the presence of other risk factors such as overcrowding, skin abrasions resulting from close contact sports such as wrestling or rugby, or using contaminated articles such as sharing towels, razors, poor hand hygiene and damaged skin from other conditions such as eczema.

What should people do to protect themselves?

The risk to the general public of becoming infected with PVL S. aureus is small but it is always good practice to maintain appropriate hygiene measures which include proper cleansing and disinfection of cuts and minor wounds. Wounds should be covered with a bandage until healed and individuals should avoid contact with other peoples' bandages and lesions.  If the infection spreads or recurs go to your GP or Accident and Emergency for further investigation and/or treatment. Such spreading infection should not be ignored. Other simple measures are regular bathing/showering, regular changing of linen and underwear, hand washing, avoiding sharing personal items (eg toothbrushes, face cloths, towels) and keeping wounds covered.

Chances of contracting all types of S. aureus infections are reduced by maintaining good hand hygiene and not sharing personal items. In shared facilities (for instance, in gyms) it is good practice to use liquid soap and disposable towels, to place a towel on the bench before sitting, and to ensure the facilities are cleaned frequently and that there is good ventilation to the locker room and showers.

Is this a new type of MRSA?

No, PVL-producing strains of S. aureus have been seen in the UK before. In the 1950s and 1960s PVL methicillin sensitive S. aureus were common in hospitals, but are not common currently. It is thought that PVL-positive MRSA have evolved from strains such as these. The small numbers of PVL cases reported have usually been in the community rather than a hospital setting.

Can people die from it?

Infection with PVL-producing strains of S. aureus normally causes skin infection, but can occasionally cause more severe infections. The HPA have been notified of seven deaths in England and Wales associated with PVL-positive MRSA over the last two years (this includes the two recently reported at a hospital in the West Midlands  - 2006). Most