Saturday, August 26, 2006


Bacterial infection transmitted by human tissue allograft transplantation.

Bacterial infection transmitted by human tissue allograft transplantation.

Cell Tissue Bank - July 2006

Eastlund T.
Department of Laboratory Medicine and Pathology, University of Minnesota Medical School, Box MMC 198 420, Delaware Street S.E., Minneapolis, Minnesota, USA.

Bacterial contamination of tissue allografts obtained from cadaveric donors has been a serious cause of morbidity and mortality in recipients. Recent cases of fatal and nonfatal bacterial infections in recipients of contaminated articular cartilage (distal femur) and tendon allografts have called attention to the importance of avoiding tissue donors suspected of carrying infectious disease, of not processing donated tissue carrying virulent bacteria, the occurrence of falsely negative final sterility tests, and the need to sterilize tissues.

These cases demonstrated that contamination can arise from an infected donor, during tissue removal from cadaveric donors, from the processing environment, and from contaminated supplies and reagents used during processing. Final sterility testing can be unreliable, especially when antibiotics remain on tissues.

There is an increasing need for control of microbial contamination in tissue banks, and sterilization of tissue allografts should be recommended whenever possible.

PMID: 16933037 [PubMed - in process]

See Also:

Clostridium infections associated with musculoskeletal-tissue allografts.

Invasive Streptococcus pyogenes after allograft implantation--Colorado, 2003.

Update: Allograft-Associated Bacterial Infections --- United States

Sunday, August 20, 2006


MRSA - Reported Cases Continue to Rise - News Updates

MRSA - leading cause for skin infections

Gunika Khurana - August 19, 2006
MRSA or Methicillin-resistant Staphylococcus aureus, a rare germ, that seldom affected people a decade back, is now the major cause for skin infections in most American cities.

On average, Methicillin-resistant Staphylococcus aureus (MRSA) accounts for 59 percent of skin infections in the ER, the study found.

MRSA is resistant to many standard antibiotics that have been used for years, but it can still be effectively treated with one of several antibiotics, experts said .

"MRSA is now the most common cause of skin infections in most of the big U.S. cities," said researcher Dr. Gregory Moran, a professor of medicine at the University of California, Los Angeles, David Geffen School of Medicine.

"When doctors are deciding if a patient needs antibiotics, they should be given antibiotics that cover MRSA. That's a change from things we've been doing for a decade. This has changed. A different type of bacteria is now the most common cause of infections," Dr. Moran noted.

Patients with MRSA skin infections, which can cause painful lesions or sores, often mistakenly blame the infection on a spider bite, the researchers found. They advise doctors to "consider the possibility of MRSA infection in patients who report spider bites."


MRSA and bedbugs are found in hospital

By Nigel Gould18 August 2006 - Belfast Telegraph An Ulster hospital is tackling an outbreak of MRSA - and an infestation of bedbugs.

Doctors and nurses had to be moved from the Enniskillen-based Erne Hospital's residential block because of the bedbugs.

The Trust said there was no risk to any patients or visitors to the hospital.

Meanwhile, 11 patients in an elderly ward are believed to have contracted feared superbug, MRSA.
In a statement, Dr Richard Smithson, consultant in communicable disease control, said: "MRSA control is a challenge for all hospitals across NI and has become an increasing problem in the community.

"Overall the Erne Hospital has no greater a problem with this bug than any other hospital in Northern Ireland.
"Fortunately none of the patients found to be carriers of this bug has indicated any infection or has become unwell as a result of it.

"The MRSA problem in general has arisen chiefly because of the overuse of antibiotics.
"With regard to the bedbugs in the residential block, the expert opinion is that it is no indication of housekeeping standards or lack of cleanliness.

"Bedbugs are transported into environments. Once introduced into environments specialist measures are required to eradicate them.

"It is not a matter of cleaning the area."

Last month, the Belfast Telegraph revealed that MRSA-related deaths in Northern Ireland had quadrupled in just four years.

Figures show the antibiotic-resistant superbug played a part in the deaths of 69 people throughout the province during 2005. That compares to just 17 in 2001.

Overall between 2001 and 2005 there were no fewer than 186 MRSA-connected deaths.
Places of death include hospitals, nursing homes or the patient's residence.

In each case, MRSA was mentioned on the patient's death certificate - although it is not clear whether the bug was the primary cause of death or where the infection was initially picked up.

Bedbugs are small nocturnal insects of the family Cimicidae that feed on the blood of humans and other warm-blooded hosts.

They live in bedclothes, mattresses, bedsprings and frames, soft furnishing, cracks and crevices and under wallpaper.

Females lay between 200-500 eggs in batches of 10-50, on rough surfaces such as wood or paper.
Eggs are white, sticky and about 1/3 inch long. They are laid in cracks or crevices, never on people.
A bedbug's entire life cycle can take between five weeks to four months, depending upon the temperature and availability of food.

Meanwhile, this time last year the Belfast Telegraph revealed that doctors were forced out of their flat inside the complex of Craigavon Hospital - by an army of ants.


Rise in community MRSA
[Posted: Fri 18/08/2006]

Antibiotic-resistant infections account for more than half of the skin infections treated in A&E units in US hospitals, it has been found.

A new study sponsored by the Centers for Disease Control and Prevention analysed all skin infections among adults who visited hospital emergency departments in 11 US cities in August 2004.

The researchers, reporting in the New England Journal of Medicine, found that 249 out of the 422 cases , or 59%, were caused by MRSA. In some of the hospitals, MRSA infections accounted for between 15 and 74% of the total skin infections encountered in hospital A&Es.

The study provides evidence of the continuing prevalence of drug resistant infections such as MRSA in the community as well as in hospitals.

A study earlier this year found that 17% of drug-resistant staphylococcal infections were acquired in communities rather than from hospitals.


Monday, August 14, 2006


A Case of Cutaneous T Cell Pseudolymphoma in a Patient with Helicobacter pylori Infection.

A Case of Cutaneous T Cell Pseudolymphoma in a Patient with Helicobacter pylori Infection.
Mitani N, Nagatani T, Ikezawa Z, Kakemizu N, Yamakawa Y, Aihara M, Nozawa A, Tomita N,
Tanaka K.

Department of Environmental Immuno-Dermatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Cutaneous pseudolymphomas (CPL) are benign cutaneous lymphoproliferative infiltrations of various origin, including among others bacterial infections, viral infections and drugs . Helicobacter pylori has been frequently founded in the stomach of patients with MALT lymphoma. In January 2001, a 43-year-old man was referred to our department because of a 1-month history of itchy erythematous patches, plaques and flat tumors on his body.

Histological examination revealed nodular infiltrations composed of lymphocytes, plasma cells and histiocytes with exocytosis of lymphocytes within the epidermis. Molecular analysis of rearrangement of T cell receptor and immunoglobulin heavy-chain genes did not reveal monoclonality. Based on these clinical, laboratory and histopathological data, a diagnosis of cutaneous T cell pseudolymphoma (CTPL) was made.

The patient was anti-H. pylori antibody-positive, and was treated with anti-H. pylori combination with the result that all of the tumors had disappeared by January 2002. The patient has maintained complete response up to the last follow-up visit in December 2005. Copyright (c) 2006 S. Karger AG, Basel.

PMID: 16902296 [PubMed - in process]

Thursday, August 10, 2006


Invasive group A streptococcal infections

Invasive group A streptococcal infections

Erica Weir* and Cheryl Main
*Public Health Physician, York Region, Infectious Diseases and Medical Microbiology, Hamilton Health Sciences, Hamilton, Ont.

Background and epidemiology:

Streptococcus pyogenes is a ubiquitous bacterial organism that gives rise to a wide variety of cutaneous and systemic infections (Fig. 1). It is an important cause of acute pharyngitis and can lead to the development of scarlet fever and nonsuppurative sequelae such as rheumatic heart disease and glomerularnephritis.1 S. pyogenes primarily comes to the attention of public health officials when it manifests as invasive group A streptococci (GAS) infection. This occurs when GAS are isolated either from a normally sterile site or from a nonsterile site and there is evidence of clinical severity: toxic shock syndrome, necrotizing fasciitis ("flesh-eating disease") or meningitis.

In 2000, Health Canada added invasive GAS infection to the list of reportable diseases. The estimated incidence of these infections for that year was 1.95/100 000 — still relatively rare, although the incidence appeared to be increasing.

Susceptibility to invasive GAS infection appears to depend on a combination of agent and host factors (Box 1). The bacteria produces a number of exotoxins and proteins, including M protein, an important virulence determinant. Strains rich in M protein are resistant to phagocytosis, multiply rapidly in human blood and are capable of initiating disease. GAS may be divided into serotypes according to antigenic differences in the M protein and, more recently, into genotypes on the basis of nucleotide differences in the emm gene encoding the molecule. More than 150 different M-protein gene sequences types (emm types) have been documented, rendering the emm type an important surveillance tool in investigations of the dynamics of GAS disease.2

Clinical management:

Necrotizing fasciitis is an infection of the subcutaneous tissues and fascia characterized by extensive and rapidly spreading necrosis. It may start innocently and should be suspected when the patient's pain is out of proportion to the clinical findings. The area of cellulitis often progresses rapidly and may look necrotic. Management requires prompt recognition, surgical débridement, high-dose intravenous penicillin, and clindamycin to reduce toxin (protein) synthesis by the organism.1

Toxic shock syndrome is diagnosed when hypotension coexists with signs of 2 or more of adult respiratory distress syndrome, coagulopathy, liver dysfunction, a generalized maculopapular rash, renal impairment and soft-tissue necrosis. Treatment amounts to penicillin, clindamycin and immune globulin (all delivered intravenously) with intensive supportive care.1


No vaccine currently exists that will prevent GAS infections. Patients admitted to hospital should undergo droplet precautions for the first 24 hours of antibiotic therapy.

Although such patients' close contacts are conventionally administered prophylactic antibiotics, a recent review of evidence3 suggests that this convention may be based more on tradition than evidence. We recommend instead that prophylaxis be administered to contacts with risk factors for sporadic disease (Box 1) and their household members. Patient contacts without risk factors should, instead of receiving antibiotics automatically, be educated about the clinical manifestations of GAS infections and maintain a heightened index of suspicion for 30 days after the diagnosis of the index case.

Oral penicillin is the prophylactic antibiotic of choice. Azithromycin is indicated for patients who are allergic to penicillin, provided that the bacterial strain isolated in the index case demonstrates susceptibility to it.3


Bisno A, Stevens D. Streptococcus pyogenes. In: Mandell G, Bennett J, Dolin R, editors. Principles and practice of infections diseases, vol. 2. 6th ed. New York: Churchill Livingstone; 2005. p. 2362-79.
Ekelund K, Darenberg J, Norrby-Teglund A, et al. Variations in emm type among group A streptococcal isolates causing invasive or non-invasive infections in a nationwide survey. J Clin Microbiol2005;43:3101-9.
[Abstract/Free Full Text]
Smith A, Lamagni T, Oliver I, et al. Invasive group A streptococcal disease: Should close contacts routinely receive antibiotic prophylaxis? Lancet Infect Dis 2005;5:494-500.

Canadian Medical Association Journal

Sunday, August 06, 2006




Gamma Proteobacteria
AcinetobacterBrisou & Prévot 1954

Acinetobacter is a genus of Proteobacteria. It is Gram-negative, non-motile, oxidase-negative, and occurs in pairs under magnification.


Using FLN, or Fluorescence-Lactose-Denitrification medium, to find the amount of acid produced by metabolism of glucose, different species of bacteria under this genus can be identified.

Species of the genus Acinetobacter, except some of the A. lwoffii strain, grow very well on MacConkey agar. Most Acinetobacters are infectious, and the strain A.baumannii is the most common nosocomial infection in health care centers and military medical facilities. A. baumannii can cause infections including skin and wound infections and pneumonia. It also causes meningitis, but A. lwoffi is mostly responsible for that. A. baumannii can live on human skin or dry surfaces for weeks.

Since the start of the Iraq War, over 300 cases of A. baumannii had infected U.S. soldiers in the Middle East. At least five have died.

Ethanol has been found to stimulate the virulence of A. baumannii. Tests on infected nematode worms that were dosed with ethanol found that the worms laid fewer eggs and their life spans were only 80% of worms infected with a version of A. baumannii that didn't respond to ethanol. This study suggests that the common misconception that drinking alcohol kills infections is false and drinking alcohol may actually help the infection to grow. (Smith & Snyder, 2005)


Since bacteria have evolved, most are immune to their first enemy, penicillin, and Acinetobacters are one of these bacteria. Also, they are immune to chloramphenicol, another common antibiotic. Therefore, the most potent treatment against this genus of bacteria is a combination of aminoglycoside and ticarcillin. A dramatic increase in antibiotic resistance in Acinetobacter strains has been reported by the Centers for Disease Control and Prevention (CDC).

In November, 2004, the CDC reported an increasing number of A. baumannii bloodstream infections in patients at military medical facilities in which service members injured in the Iraq/Kuwait region during Operation Iraqi Freedom (OIF) and in Afghanistan during Operation Enduring Freedom (OEF) were treated. Most of these were multidrug-resistant. Among one set of isolates from Walter Reed Army Medical Center, 13 (35%) were susceptible to imipenem only, and two (4%) were resistant to all drugs tested. One antimicrobial agent, colistin (polymyxin E), has been used to treat infections with multidrug-resistant A. baumannii; however, antimicrobial susceptibility testing for colistin was not performed on isolates described in this report. Because A. baumannii can survive on surfaces for up to 20 days, they pose a high risk of spread and contamination in hospitals, potentially putting immune-compromised and other patients at risk for drug resistant infections that are often fatal and generally expensive to treat.


CDC Morbidity and Mortality Report, November 19, 2004
Alliance for the Prudent Use of Antibiotics
Smith, M.G., and M. Snyder (2005). "
Ethanol-induced virulence of Acinetobacter baumannii". American Society for Microbiology meeting, Atlanta.

* * * *

The Acinetobacter Working Group


Bacteria of the genus Acinetobacter are widespread in nature, and can be recovered from water, soil and living organisms. They are non-motile, coccobacillary, strictly aerobic and Gram-negative; they can use a variety of carbon sources for growth, and can be cultured on relatively simple media, including trypticase soya agar or nutrient agar. Extensive reviews of the genus have been written by Juni (15) and by Bergogne-Bérézin & Towner (1). Strains of A. baumannii, and the unnamed groups 3 and 13 TU are recovered predominantly from clinical specimens, with A. baumannii being notorious for its capacity to colonise and infect severely ill, hospitalised patients. Strains of this genomic species can persist in hospitals and give rise to outbreaks; they are usually highly resistant to antibiotics, which makes them difficult to eradicate.

Two recently described species, A. ursingii ('phenon 1') and A. schindlerii ('phenon 2') (17, 18) are also associated with patients; thus A. ursingii was cultured from the blood of severely ill hospitalised patients, and A. schindlerii from non-sterile body sites of outpatients. Most other (genomic) species of Acinetobacter have been found in different environments, e.g. strains of A. calcoaceticus are isolated predominantly from soil and A. johnsonii from activated sludge and frozen food, although representatives of these and other species have also been recovered occasionally from human specimens. Strains of A. venetianus, including the emulsan-producing strain RAG-1, have been found in seawater and oil-degrading consortia (7, 22). Overall, the natural habitats of most Acinetobacter (genomic) species have not been well-studied.

Within the context of ENEMTI, the Acinetobacter Working Group will seek to develop two different protocols that can be used for the development of an interactive database for the exchange of microbial typing database:-

(i) a high-resolution typing method suitable for use in reference laboratories: AFLP protocol

(ii) a simpler rapid typing method for use in routine hospital laboratories: RAPD method

The ENEMTI initiative aims to harmonise typing methods so that the fingerprints generated can be used to set up electronic databanks by which the geographic spread of particular strains can be depicted and monitored.
ENEMTI participants have also collaborated with members of the EU ARPAC Concerted Action ('Antibiotic Resistance Prevention and Control') to develop an Acinetobacter database based on pulsed-field gel electrophoresis (PFGE) fingerprint profiles. Click
here to enter the Acinetobacter PFGE database.
More information on the genus Acinetobacter, a heterogeneous group of organisms.


Currently, the genus Acinetobacter comprises at least 23 genomic species (DNA-DNA hybridisation groups; DNA groups), 10 of which have been given species names; other DNA groups are designated by numbers (for Table 1, see the original Word document). The numbers 13-15 have been given to sets of strains in two independent studies (6, 20); DNA group 13 of Bouvet & Jeanjean (BJ) has been found to correspond to group 14 of Tjernberg & Ursing (TU), whereas no correlation was found for the two other groups. Strains of A. calcoaceticus, A. baumannii, and the unnamed groups 3 and 13TU are genetically closely related and difficult to separate phenotypically, and are therefore sometimes unified in the so-called A. calcoaceticus – A. baumannii (Acb) complex (10). Apart from the known genomic species, additional strains have been found, some of which are closely related to the Acb complex (12), while the taxonomic status of others has not yet been resolved.

Genus identification

Bacteria can be identified to the genus Acinetobacter by the phenotypic criteria listed in Table 2 (see the original Word document). A simple test for identification to the genus Acinetobacter is based on the finding that DNA of organisms belonging to the genus can be used to transform an auxotrophic Acinetobacter strain (BD413 trpE27) to prototrophy (14).

(Genomic) species identification

DNA-DNA hybridisation is the gold standard for identification of Acinetobacter strains, but this method is not applicable in most laboratories. A phenotypic identification scheme, including enzymatic and nutritional tests and growth at different temperatures, was devised by Bouvet & Grimont (4, 5). Several studies have shown that some genomic species are difficult to identify by phenotypic tests (10, 16). Similarly, commercial phenotypic identification systems, such as API 20NE and Biolog, show only moderate performance (2, 3). In particular, A. baumannii, DNA groups 3 and 13TU are difficult to differentiate by these systems.
Several genotypic methods have been proposed for identifying acinetobacters to the genomic species level, including ribotyping (11), tDNA fingerprinting (9), amplified ribosomal DNA restriction analysis (ARDRA) (8, 21), and AFLP (13). An overview of ARDRA patterns for species identification can be found

Despite the progress made in subdividing the genus Acinetobacter and the efforts to develop easy identification methods, identification to the genomic species level can still be problematic. This may be overcome by using a combination of methods, which results in a so-called 'consensus identification' (17).

Typing of Acinetobacter strains

Virtually all currently available typing methods have been used for discrimination of acinetobacters below the species level. Phenotypic methods, including biotyping, cell envelope protein electrophoresis, and quantitative antibiogram typing were applied successfully in the 1980s and 1990s. More recently, genotypic methods including plasmid typing (now rarely used), ribotyping, pulsed-field gel electrophoresis (PFGE), PCR fingerprinting and AFLP analysis have been used in numerous studies. In general, a combination of typing methods is recommended for unambiguous strain identification in local situations.


Bergogne-Bérézin E & Towner KJ (1996). Acinetobacter spp. as nosocomial pathogens: microbiological, clinical, and epidemiological features. Clin Microbiol Rev 9, 148-165.
Bernards AT, Dijkshoorn L, van der Toorn J, Bochner BR & van Boven CPA (1995). Phenotypic characterization of Acinetobacter strains of 13 DNA-DNA hybridization groups by means of the Biolog system. J Med Microbiol 42, 113-119.
Bernards AT, van der Toorn J, van Boven CPA. & Dijkshoorn L (1996). Evaluation of the ability of the API 20NE system to identify Acinetobacter genomic species. Eur J Clin Microbiol Infect Dis 15, 303-308.
Bouvet PJM & Grimont PAD (1986). Taxonomy of the genus Acinetobacter with the recognition of Acinetobacter baumannii sp. nov., Acinetobacter haemolyticus sp. nov., Acinetobacter johnsonii sp. nov., and Acinetobacter junii sp. nov., and emended descriptions of Acinetobacter calcoaceticus and Acinetobacter lwoffii. Int J Syst Bacteriol 36, 228-240.
Bouvet PJM & Grimont PAD (1987). Identification and biotyping of clinical isolates of Acinetobacter. Ann Inst Pasteur/Microbiol 138, 569-578.
Bouvet PJM & Jeanjean S (1989). Delineation of new proteolytic genomic species in the genus Acinetobacter. Res Microbiol 140, 291-299.
DiCello F, Pepi M, Baldi F & Fani R (1997). Molecular characterization of an n-alkane-degrading bacterial community and identification of a new species, Acinetobacter venetianus. Res Microbiol 148, 237-249.
Dijkshoorn L, van Harsselaar B, Tjernberg I, Bouvet PJM & Vaneechoutte M (1998). Evaluation of amplified ribosomal DNA restriction analysis for identification of Acinetobacter genomic species. Syst Appl Microbiol 21, 33-39.
Ehrenstein B, Bernards AT, Dijkshoorn L, Gerner-Smidt P, Towner KJ, Bouvet PJ, Daschner FD & Grundmann H (1996). Acinetobacter species identification by using tRNA spacer fingerprinting.J Clin Microbiol 34, 2414-2420.
Gerner-Smidt P, Tjernberg I & Ursing J (1991). Reliability of phenotypic tests for identification of Acinetobacter species. J Clin Microbiol 29, 277-282.
Gerner-Smidt P (1992). Ribotyping of the Acinetobacter calcoaceticus-Acinetobacter baumannii complex. J Clin Microbiol 30, 2680-2685
Gerner-Smidt P & Tjernberg I (1993). Acinetobacter in Denmark: II. Molecular studies of the Acinetobacter calcoaceticus- Acinetobacter baumannii complex. APMIS 101, 826-832.
Janssen P, Maquelin K, Coopman R, Tjernberg I, Bouvet P, Kersters K & Dijkshoorn L (1997). Discrimination of Acinetobacter genomic species by AFLP fingerprinting. Int J Syst Bacteriol 47, 1179-1187.
Juni E (1972). Interspecies transformation of Acinetobacter: Genetic evidence for a ubiquitous genus. J Bacteriol 112, 917-931.
Juni E (1984). Genus III Acinetobacter Brisou and Prévot 1954, 727 AL. In: Bergey’s Manual of Systematic Bacteriology vol. 1, Krieg, N.R. (ed). Williams and Wilkins, Baltimore, pp 303-307.
Kämpfer P, Tjernberg I & Ursing J (1993). Numerical classification and identification of Acinetobacter genomic species. J Appl Bacteriol 75, 259-268.
Nemec A, Dijkshoorn L & Ješek P (2000). Recognition of two novel phenons of the genus Acinetobacter among glucose non-acidifying isolates from human specimens. J Clin Microbiol 38, 3937-3941.
Nemec A, De Baere T, Tjernberg I, Vaneechoutte M, van der Reijden TJK & Dijkshoorn L (2001). Acinetobacter ursingii sp.nov. and Acinetobacter schindleri sp. nov., isolated from human clinical specimens. Int J Syst Evol Microbiol, in press.
Nishimura Y, Ino T & Iizuka H (1988). Acinetobacter radioresistens sp. nov. isolated from cotton and soil. Int J Syst Bacteriol 38, 209-211.
Tjernberg I & Ursing J (1989). Clinical strains of Acinetobacter classified by DNA-DNA hybridization. APMIS 97, 595-605.
Vaneechoutte M, Dijkshoorn L, Tjernberg I, Elaichouni A, de Vos P, Claeys G & Verschraegen G (1995). Identification of Acinetobacter genomic species by amplified ribosomal DNA restriction analysis. J Clin Microbiol 33, 11-15.
Vaneechoutte M, Tjernberg I, Baldi F, Pepi M, Fani R, Sullivan ER, van der Toorn J & Dijkshoorn L (1999). Oil-degrading Acinetobacter strain RAG-1 and strains described as 'Acinetobacter venetianus' sp. nov. belong to the same genomic species. Res Microbiol 150, 69-73.


* * * * *

Overview of Drug Resistant Acinetobacter Infections in Healthcare Settings

Released: September 24, 2004

What is Acinetobacter?

Acinetobacter (ass in ée toe back ter) is a group of bacteria commonly found in soil and water. It can also be found on the skin of healthy people, especially healthcare personnel. While there are many types or “species” of Acinetobacter and all can cause human disease, Acinetobacter baumannii accounts for about 80% of reported infections.

Outbreaks of Acinetobacter infections typically occur in intensive care units and healthcare settings housing very ill patients. Acinetobacter infections rarely occur outside of healthcare settings.

What are the symptoms of Acinetobacter infection?

Acinetobacter causes a variety of diseases, ranging from pneumonia to serious blood or wound infections and the symptoms vary depending on the disease. Typical symptoms of pneumonia could include fever, chills, or cough. Acinetobacter may also “colonize” or live in a patient without causing infection or symptoms, especially in tracheostomy sites or open wounds.

How do people get Acinetobacter infection?

Acinetobacter poses very little risk to healthy people. However, people who have weakened immune systems, chronic lung disease, or diabetes may be more susceptible to infections with Acinetobacter.Hospitalized patients, especially very ill patients on a ventilator, those with a prolonged hospital stay, or those who have open wounds, are also at greater risk for Acinetobacter infection. Acinetobactercan be spread to susceptible persons by person-to-person contact, contact with contaminated surfaces, or exposure in the environment.

How is Acinetobacter infection treated?

Acinetobacter is often resistant to many commonly prescribed antibiotics. Decisions on treatment of infections with Acinetobacter should be made on a case-by-case basis by a healthcare provider. Acinetobacter infection typically occurs in very ill patients and can either cause or contribute to death in these patients.

What should I do to prevent the spread of Acinetobacter infection to others?

Acinetobacter can live on the skin and may survive in the environment for several days. Careful attention to infection control procedures such as hand hygiene and environmental cleaning can reduce the risk of transmission.

For more information on infection control practices and hand hygiene, see Hand Hygiene in Healthcare Settings and Guideline for Isolation Precautions in Hospitals.

Date last modified: September 24, 2004Content source: Division of Healthcare Quality Promotion (DHQP)



New lethal superbacteria found in Scottish hospitals

New lethal superbacteria found in Scottish hospitals



A VIRTUALLY untreatable new superbug has been found in Scotland for the first time after causing death and panic in hospitals in the US and England.

Eleven patients have tested positive for the presence of multi-antibiotic-resistant Acinetobacter, which - unlike MRSA - can only be treated with one medicine.

Health chiefs believe the new superbug is now present throughout Scotland and it is only a matter of time before it mutates into a particularly deadly form which does not respond to any known antibiotic.
That form of Acinetobacter has wreaked havoc in the health service south of the Border over the past two years, killing 39 people at one London hospital alone.

Scotland appears to be fighting a losing battle against hospital-acquired infection. Scotland on Sunday recently revealed that cases of MRSA had soared despite a multi-million pound campaign to cut cases of infection.

The revelation that an even more dangerous superbug has been discovered in Scotland will add to the pressure on ministers to take action to reduce the toll of 1,000 Scots infected annually by MRSA alone.
Tests carried out by NHS Tayside found that 11 patients were carrying Acinetobacter over the past year, although none were infected by it. All were immediately isolated.

The bacteria can only be treated with "last-resort" antibiotics called carbapenems. Doctors are keen to use these as sparingly as possible because over-use allows the bacteria to develop resistance.
Microbiologist Dr Ian Gould, from Aberdeen University, said it was likely the bacteria would be present in other Scottish hospitals.

And he called for health boards to step up their surveillance of the bug, warning that it was only a matter of time before carbapenem-resistant Acinetobacter reached Scotland.

He said: "Unfortunately these bacteria will grow increasingly resistant to antibiotics as they evolve. What is causing major concern is the strains that are resistant to carbapenems. Acinetobacter are particularly good at producing enzymes that destroy these antibiotics.

"One would expect them to percolate north of the Border from transfer patients who move between hospitals. Sooner or later carbapenems-resistant Acinetobacter is going to arrive here."

Acinetobacter is commonly found in water and soil but normally causes no problems unless it infects critically ill, elderly or vulnerable patients.

Throughout Scotland, during the first three months of 2006, there were 20 cases of patients being infected with "treatable" strains of Acinetobacter.

Doctors in England are now being forced to resort to outdated antibiotics that were abandoned 50 years ago for being highly toxic to patients in order to defeat the deadliest versions of the bug. At St Mary's Hospital in Paddington, West London, 39 people died after catching Acinetobacter.

The Health Protection Agency in England has issued guidelines on tackling the bug and NHS Trusts have been ordered to monitor drug-resistant strains of the bacterium.

But in Scotland health boards only monitor Acinetobacter on a voluntary basis. The discovery of multi-resistant strains north of the Border has now led to calls for increased surveillance. Gould said: "I think there are so many other pressures that in the current state of alert, it is hard to convince health boards to screen for that particular bacteria as it is not particularly easy to do."

Professor Curtis Gemmell, a microbiologist at Glasgow University, said it was impossible to determine if the bacteria was spreading unless it was monitored more closely.

He said: "Without knowing if this bacteria has become established on hospital wards it could be an isolated case or something more serious that will spread from hospital to hospital.

"At the moment we have not had any infections in patients. Only when that happens do we need to start worrying."

Shona Robison, SNP shadow health minister, said: "The threat this bacteria poses is very concerning and highlights the need for hygiene and cleanliness to be the best it possibly can be.
A spokeswoman for the Scottish Executive said it was attempting to standardise diagnosis and detection of antibiotic resistance for a range of organisms.

She added: "This infection does not present a significant problem in Scotland but we remain vigilant in tackling all sorts of healthcare-associated infections." News

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