Age & Sex: 48 years old; Male Medical History: Long history of alcoholism Alcoholic hepatitis Hallucinosis Description(s): Admitted to the ICU Hypotension and GI bleeding Treatment(s) Intubated, IV fluids, RBC transfusion Remained intubated and ventilator dependent for several weeks Fevers, and treated with wide-spectrum antibiotics Specimen(s) By tracheal aspirate – Staphylococcus aureus Given further antibiotic therapy Gram staining result(s) from trachea Polymorphonuclear leukocytes (PMNs) Gram-negative rod
Description(s): Chest radiograph result(s) Infiltrate and changes consistent with multiple small abscesses Specimen(s) Obtain the sample by tracheal aspirate Sheep blood agar (Fig. 2A) MacConkey agar plate (Fig. 2B) Disk susceptibility plate (Fig. 3) Fig. 2A Sheep blood agar Mucoid, smooth colonies Fig. 2B MacConkey agar Colorless, shinny, non-lactose fermenter
Figure 3 Disk susceptibility plate Green pigment produced on the surface Susceptible Resistant
Isolated by eosin-methylthionine blue agar Fruity odor Pigment production – blue-green color (pyocyanin) Able to grow at 42°C Catalase: Positive Oxidase: Positive Lipase: Positve TSI: K/K, No gas, No H 2 S H and O Antigens
Agent of infection Pseudomonas aeruginosa. Classification: Family: Pseudomonadaceae Genus: Pseudomonas Species: aeruginosa Common cause of nosocomial infections Pneumonia Urinary tract infections Surgical wounds Sepsis Immunocompromised individual Patients with Cystic Fibrosis (CF) Cancer Burn wounds Bone marrow transplantation Multidrug-resistant P. aeruginosa was discovered in 1979 in Robert Fass in vitro studies
This organism produces exotoxin A that is similar to diphteria toxin produced by Corynebacterium diphtheriae Top: P. aeruginosa Exotoxin A Bottom: C. diphtheriae toxin (DT) 3 functional domains: Activity (ADP-R) Translocation (T) Receptor (R/B) Both inhibit ADP-Ribosylate Elongation Factor 2 Functional domains are organized in reverse order (Deng & Barbieri, Annu. Rev. Microbiol., 2008)
A Toxin Nascent protein Host receptor Exotoxin A Golgi Apparatus Endoplasmic Reticulum mRNA ADP-ribosylate EF-2
Patients with CF are highly susceptible to P. aeruginosa infections Abnormal secretion of viscous mucus in the lungs Decreased airway fluid, resulting in reduced ciliary clearance of aspirated microbes It leads to colonization of the organism P. aeruginosa resists to host immune responses – embedded in biofilms in the lungs of CF patients Thus, plays a critical role in preventing effective opsonization and phagocytosis of P. aeruginosa cells. Other mechanism in successful pathogenesis (i) Elastolytic and (ii) non- elastolytic proteases P. aeruginosa disseminates in to the body with the use of elastolytic proteases. Elastin, which can be found in lung tissue and blood vessels, is broken down by this protease. The breakdown of this compound causes an inflammatory reaction that aids in the dissemination of the organism. Inactivate complement, cleave IgG & IgA antibodies, inactivate interferon (INF), tumor necrosis factor (TNF) and some other cytokines
This organism was isolated after the patient received a prolonged course of broad-spectrum antibiotics. This therapy predispose the patient to infection with this organism Hospitalization The patient is highly susceptible to infections with this organism. Background Alcoholic Alcoholic hepatitis P. aeruginosa frequently cause hospital-acquired infections, particularly in immuno- compromised or critically ill patients This organism able to survive in the presence of antimicrobial agents Broad range of antibiotic treatment Treatment to the primary staphylococcal infection allowed the organism to undergo outer membrane changes resulting in resistance to a wide range of antibiotics.
Neutropenic patients are at increased risk for bacteremia with this organism Steps could be taken to minimize the risk Treatment with one active beta-lactam antibiotic or combination of aminoglycoside and β-lactam agent to achieve synergistic effects Increase awareness in managing equipments Careful cleaning and monitoring of respirators, catheters, and other instruments Administer effective antibiotic to the patients
Patients infected with mucoid P. aeruginosa had poorer survival than patients who had non-mucoid phenotype Acquisition of mucoid P. aeruginosa was associated with an accelerated rate of decline in pulmonary function. Immunocomprimised and CF patients are prone to P. aeruginosa infection Frequently resistant to many commonly used antibiotics Common antibiotics: Gentamicin Tobramycin, Colistin Fluoroquinolins Triple antimicrobial therapy was suggested – ceftazidime, amikacin and sulbactam 8
Leung, C. H., et. al., 2008, Antimicrobial therapy and control of multidrug-resistant Pseudomonas aeruginosa bacteremia in a teaching hospital in Taiwan. Journal Microbiology, Immunology, and Infection, 41: 491-498 Purpose Investigate the source of an outbreak of multi-drug resistant (MDR) P. aeruginosa Role of combination therapy Methods Isolate MDR P. aeruginosa from MacKay Memorial Hospital, Taipei, Taiwan Perform antibiotic susceptibility tests Genetic analysis by pulsed-field gel electrophoresis from bacteremia patients Results Combination of ceftazidime, amikacin and sulbactam showed significant results Found the major source of MDR P. aeruginosa and stringent infection control
Leung, C. H., et. al., 2008, Antimicrobial therapy and control of multidrug-resistant Pseudomonas aeruginosa bacteremia in a teaching hospital in Taiwan. Journal Microbiology, Immunology, and Infection, 41: 491-498 Results Conclusion Triple antibiotics could be used as an alternative treatment for MDR P. aeruginosa infection
Urinary tract infections, respiratory system infections, dermatitis, soft tissue infections, bacteremia, bone and joint infections, GI infections, Typical symptoms: Fever, chills and production of purulent matter in infected wounds Pathogen is Pseudomonas aeruginosa Antibiotic therapy: Gentamicin, tobramycin, colistin, and/or fluoroquinolins Prognosis: Patients with CF infected by mucoid P. aeruginosa has poorer survival rate compared with non-mucoid P. aeruginosa Prevention: Aseptic technique, and careful cleaning and monitoring of respirators, catheters, and other instruments Transmission: In health care units – disinfectants, respiratory equipment, food, sinks, taps, toilets, showers and mops By visitors and patients to other facilities, patient to patient, direct contact of contaminated reservoirs and by ingestion of contaminated foods and water Threat is occurring in debilitated patients with diminished resistance resulting from other disease or therapy
1. Chuang, H. L., et. al., 2009, Influence of Age on Susceptibility to Pseudomonas aeruginosa Exotoxin A-induced Hepatotoxicity in Long-Evans Rats. The Journal of Veterinary Medical Science, 71: 163-169. 2. Deng, Q., et. al., 2008, Molecular mechanisms of the cytotoxicity of ADP-ribosylating toxins. Annual Review of Microbiology, 62: 271-288. 3. Dunn, M., et. al., 1995, Ventilator-associated pneumonia caused by Pseudomonas infection. Clinics In Chest Medicine, 16: 95-109. 4. Döring, G., et. al., 2008, Vaccines and immunotherapy against Pseudomonas aeruginosa. Vaccine, 26: 1011-1024. 5. Forestier, C., et. al., 2008, Oral probiotic and prevention of Pseudomonas aeruginosa infections: a randomized, double-blind, placebo-controlled pilot study in intensive care unit patients. Critical Care, 12: R69. 6. Govan, J. R., et. al., 1996, Microbial pathogenesis in cystic fibrosis: mucoid Pseudomonas aeruginosa and Burkolderia cepacia. Microbiology and Molecular Biology Reviews, 60: 539-574. 7. Kwakman, P. H., et. al., 2008, Medical-grade honey kills antibiotic-resistant bacteria in vitro and eradicates skin colonization. Clinical Infectious Diseases, 46: 1677-1682. 8. Leung, C. H., et. al., 2008, Antimicrobial therapy and control of multidrug-resistant Pseudomonas aeruginosa bacteremia in a teaching hospital in Taiwan. Journal Microbiology, Immunology, and Infection, 41: 491-498. 9. Liang, H., et. al., 2009, Identification of a novel regulator of the quorum-sensing in Pseudomonas aeruginosa. FEMS Microbiology Letters, Published online March 2, 2009. 10. Moser, C., et. al., 2009, Novel experimental Pseudomonas aeruginosa lung infection model mimicking long-term host-pathogen interactions in cystic fibrosis. Acta Pathologica, Microbiologica, et Immunologica Scandinavica, 117: 95-107. 11. Mukhopadhyay, C., et. al., 2008, Ventilator-associated pneumonia with Col-S strans: a successful comeback of colistin! The Brazilian Journal of Infectious Diseases, 12: 444-446. 12. Sagel, S. D., et. al., 2009, Impact of Pseudomonas and Staphylococcus infection on inflammation and clinical status in young children with cystic fibrosis. The Journal of Pediatrics, 154: 183-188. 13. Wolf, P., et. al., 2009, Pseudomonas exotoxin A: from virulence factor to anti-cancer agent. International Journal of Medical Microbiology, 299: 161-176.
Your consent to our cookies if you continue to use this website.