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1

Niels, Høiby, Hrsg. Pseudomonas aeruginosa infection. Basel: Karger, 1989.

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2

Hauser, Alan R., und Jordi Rello, Hrsg. Severe Infections Caused by Pseudomonas Aeruginosa. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0433-7.

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3

name, No. Severe infections caused by Pseudomonas aeruginosa. Boston, MA: Kluwer Academic Publishers, 2003.

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4

G, Döring, Holder Ian Alan und Botzenhart K, Hrsg. Basic research and clinical aspects of Pseudomonas aeruginosa. Basel: Karger, 1987.

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5

Y, Homma J., Hrsg. Pseudomonas aeruginosa in human diseases. Basel: Karger, 1991.

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6

1926-, Baltch Aldona L., und Smith Raymond P. 1946-, Hrsg. Pseudomonas aeruginosa: Infections and treatment. New York: M. Dekker, 1994.

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7

Mario, Campa, Bendinelli Mauro und Friedman Herman 1931-, Hrsg. Pseudomonas aeruginosa as an opportunistic pathogen. New York: Plenum Press, 1993.

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8

Pseudomonas aeruginosa as an Opportunistic Pathogen. Springer, 2011.

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9

Friedman, Herman, Mauro Bendinelli und Mario Campa. Pseudomonas aeruginosa as an Opportunistic Pathogen. Springer, 2012.

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10

Rello, Jordi, und Alan R. Hauser. Severe Infections Caused by Pseudomonas Aeruginosa. Springer, 2012.

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11

1959-, Hauser Alan R., und Rello Jordi, Hrsg. Severe infections caused by Pseudomonas aeruginosa. Boston: Kluwer Academic Publishers, 2003.

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12

B, Fick Robert, Hrsg. Pseudomonas aeruginosa, the opportunist: Pathogenesis and disease. Boca Raton: CRC Press, 1993.

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13

Baltch. Pseudomonas Aeruginosa Infections and Treatment (Infectious Disease and Therapy). Informa Healthcare, 1994.

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14

Pseudomonas aeruginosa - Biofilm Formation, Infections and Treatments [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.87468.

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15

P, Gacesa, und Russell Nicholas J, Hrsg. Pseudomonas infection and alginates: Biochemistry, genetics, and pathology. London: Chapman and Hall, 1990.

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16

(Editor), Alan R. Hauser, und Jordi Rello (Editor), Hrsg. Severe Infections Caused by Pseudomonas aeruginosa (Perspectives on Critical Care Infectious Diseases). Springer, 2003.

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17

Labiris, Nancy Renee. Inhaled aminoglycosides for the treatment of chronic respiratory Pseudomonas aeruginosa infections in cystic fibrosis. 2002.

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18

Govan, John, und Andrew Jones. Microbiology of CF lung disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0003.

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This chapter presents the microbiology of CF and describes the classical bacterial pathogens including Staphylococcus aureus, Haemophilus influenza, Pseudomonas aeruginosa and organisms of the Burkholderia cepacia complex. The dominant of these is P. aeruginosa. Infections with other opportunistic pathogens including non-tuberculous mycobacteria, Stenotrophomonas maltophila, and Achromobacter (Alcaligenes) xylosoxidans are also encountered. This chapter details measures to prevent the onset of chronic infection with these organisms include regular screening of respiratory tract samples for bacterial pathogens and the use of aggressive antibiotic therapy to eradicate initial infection before the pathogen can adapt to the environment of the CF lung. Patient-to-patient spread of transmissible strains of bacterial pathogens has led to the implementation of strict infection control measures at CF centres, including patient segregation. In addition to bacterial pathogens, the contribution of fungal infection in CF lung disease is increasingly recognized.
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19

Wilson, A. P. R. Microbiological surveillance in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0281.

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Patients in the ICU are at high risk of acquiring multiresistant pathogens. Surveillance quickly identifies outbreaks and promotes antimicrobial stewardship. Catheter-related bacteraemia is often used as a performance measure and intervention using a package of preventative measures can be very successful. Ventilator-associated pneumonia in contrast can be difficult to define accurately. Water sources should be monitored. Pseudomonas aeruginosa may become established in taps and cause invasive infections especially in neonates. Screening of nasal swabs for MRSA followed by topical suppression has been effective in reducing spread during ICU admission. With rising prevalence of multiresistant Gram-negative species, screening of faeces or rectal swabs may become necessary. Acinetobacter is very disruptive if it causes an outbreak and it can be difficult to control. Screening is one method of limiting its’ spread. National surveillance networks are increasing and may be mandatory as they appear to be successful in controlling nosocomial infection.
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20

Cuttle, Lisa. Dermatologic Manifestations of Infectious Disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0044.

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Toxic infectious exfoliative conditions include staphylococcal toxic shock syndrome (TSS), streptococcal toxic shock syndrome (STSS), and staphylococcal scalded skin syndrome (SSSS). All three are mediated by bacterial toxin production and are considerations in the differential diagnosis of a febrile, hypotensive patient with a rash. Meningococcemia is potentially fatal and extremely contagious with a short incubation period. Disseminated gonococcal infection (DGI) presents with tenosynovitis, dermatitis, and polyarthralgias without purulent arthritis or with purulent arthritis but without skin lesions. Ecthyma gangrenosum (EG) is a cutaneous manifestation of Pseudomonas aeruginosa infection. Rocky Mountain Spotted Fever (RMSF) is caused by Rickettsia rickettsii, most commonly transmitted by the American dog tick. Patients present with nonspecific symptoms, such as fever, headache, myalgias, arthralgias, nausea, vomiting, and abdominal pain. Finally, vibrio vulnificus is a gram-negative bacterium that causes serious wound infections, sepsis, and diarrhea in patients exposed to shellfish or marine water.
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21

Gilchrist, Francis J., und Alex Horsley. Management of respiratory exacerbations. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0005.

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Cystic fibrosis lung disease is characterized by chronic infection, inflammation and a progressive loss of lung function. Patients are also affected by recurrent episodes of increased respiratory symptoms, called exacerbations which have a detrimental effect on quality of life, the rate of lung function decline, and mortality. Early diagnosis and treatment is vital. Diagnosis relies on a combination of symptoms, examination findings, the results of laboratory tests, and lung function. Antibiotics are the mainstay of treatment but airway clearance, nutrition, and glucose homeostasis must also be optimized. Mild exacerbations are usually treated with oral antibiotics and more severe exacerbations with intravenous antibiotics. The choice of antibiotic is guided by the patient’s chronic pulmonary infections, the in-vitro antibiotic sensitivities, known antibiotic allergies, and the previous response to treatment. In patients with chronic Pseudomonas aeruginosa infection, antibiotic monotherapy is thought to increase the risk of resistance and treatment with 2 antibiotics is therefore suggested (usually a β‎-lactam and an aminoglycoside). Although there is a lack of evidence on the duration of treatment, most patients receive around 14 days. This can be altered according to the time taken for symptoms and lung function to return to pre-exacerbation levels. If patients are carefully selected and receive appropriate monitoring, home intravenous antibiotics can be as effective as in-patient treatment. They are also associated with decreased disruption to patients / family life, decreased risk of cross infection and decreased costs.
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