Archive for January 5, 2014

A comparative analysis of community acquired and hospital acquired methicillin resistant Staphylococcus aureus.

J Clin Diagn Res. 2013 Jul;7(7):1339-42.

P R V, M J.


Tutor, Department of Microbiology, Chettinad Hospital and Research Institute, Chettinad University, India.



Staphylococcus aureus has developed resistance against most of the therapeutic agents. The most notable example of this phenomenon was the emergence of Methicillin resistant Staphylococcus aureus (MRSA).

We are reporting the prevalence and the antibiotic susceptibility pattern of the MRSA isolates from a tertiary care hospital.


A total of 450 Staphylococcus aureus isolates from clinical samples were taken up for the study and they were screened for MRSA by using standard microbiological methods. An antibiotic assay was done for the confirmed MRSA isolates. The differentiation of the isolates into community acquired MRSA (CAMRSA) and hospital acquired MRSA (HAMRSA) was done according to the prescribed criteria. The double disc diffusion test was performed for both the groups, to identify the inducible clindamycin resistance. The HAMRSA and the CAMRSA isolates were subjected to a molecular analysis by PCR, to detect the presence of the Mec A gene and the PVL gene respectively.


Out of the 450 Staphylococcus aureus isolates, 121 were Methicillin Resistant Staphylococcus aureus (MRSA, 27%) and 329 were Methicillin Sensitive Staphylococcus aureus (MSSA, 73%). 91 MRSA isolates were grouped into HAMRSA and 30 were grouped into CAMRSA, with a prevalence of 20% and 7% respectively. All the MRSA strains were resistant to Penicillin (100%), Cefoxitin (100%) and Oxacillin (100%). 53.7% of the HAMRSA isolates showed inducible clindamycin resistance against that of 44.4% among the CAMRSA isolates. All the isolates were susceptible to Vancomycin and Linezolid. 64% of the HAMRSA isolates showed the presence of the Mec A gene and 48% of the CAMRSA isolates showed the presence of the PVL genes.


The prevalence of the HAMRSA was higher than that of the CAMRSA and they showed a higher drug resistance.


January 5, 2014 at 6:33 pm

A retrospective observational study on the efficacy of colistin by inhalation as compared to parenteral administration for the treatment of nosocomial pneumonia associated with multidrug-resistant Pseudomonas aeruginosa.

BMC Infect Dis. 2011 Nov 15;11:317.

Naesens R, Vlieghe E, Verbrugghe W, Jorens P, Ieven M.



Colistin is used as last treatment option for pneumonia associated with multidrug-resistant (MDR) Pseudomonas spp.. Literature about the best administration mode (inhalation versus parenteral treatment) is lacking.


A retrospective study of 20 intensive care patients with a pneumonia associated with MDR P. aeruginosa receiving colistin sulphomethate sodium (Colistineb®) between 2007 and 2009 was performed. A strain was considered multidrug-resistant if it was resistant to at least 6 of the following antibiotics: piperacillin-tazobactam, ceftazidime, cefepime, meropenem, aztreonam, ciprofloxacin, and amikacin. The administration mode, predicted mortality based on the SAPS3 score, SOFA score at onset of the colistin treatment, clinical and microbiological response, and mortality during the episode of the infection were analysed. The non parametric Kruskal-Wallis and Fisher’s Exact test were used for statistical analysis of respectively the predicted mortality/SOFA score and mortality rate.


Six patients received colistin by inhalation only, 5 were treated only parenterally, and 9 by a combination of both administration modes. All patients received concomitant beta-lactam therapy. The mean predicted mortalities were respectively 72%, 68%, and 69% (p = 0.91). SOFA scores at the onset of the treatment were also comparable (p = 0.87). Clinical response was favorable in all patients receiving colistin by inhalation (6/6) and in 40% (2/5) of the patients receiving colistin parenterally (p = 0.06). In the patients with colistin administered both via inhalation and parenterally, clinical response was favorable in 78% of the patients (7/9) (p = 0.27 as compared to the treatment group receiving colistin only parenterally). When all patients with inhalation therapy were compared to the group without inhalation therapy, a favorable clinical response was present in respectively 87% and 40% (p = 0.06). In none of the patients, the Pseudomonas spp. was eradicated from the follow-up cultures.All patients in the parenterally treated group died. None of the patients receiving colistin by inhalation, and 3 of 9 patients of the combination group eventually died (p = 0.002 and p = 0.03 respectively as compared to the group receiving colistin only parenterally).


Aerosolized colistin could be beneficial as adjunctive treatment for the management of pneumonia due to MDR P. aeruginosa.


January 5, 2014 at 6:28 pm

Chronic Pseudomonas aeruginosa infection in COPD.

Clin Infect Dis. 2008 Dec 15;47(12):1526-33.

Martínez-Solano L, Macia MD, Fajardo A, Oliver A, Martinez JL.



Pseudomonas aeruginosa infections are increasingly associated with acute exacerbations in chronic obstructive pulmonary disease (COPD). We aimed to determine whether an underlying chronic infection might be behind this process and to determine the epidemiological characteristics of the isolates involved, to implement useful protocols for preventing and treating these infections.


P. aeruginosa isolates obtained from respiratory samples of 13 patients with COPD and from blood samples of 10 patients in intensive care units were investigated. In 8 patients with COPD, isolates were obtained during sequential exacerbation episodes. Five patients presented a single infection episode. Production of virulence determinants and genetic relationships were analyzed in all isolates.


Patients with COPD were usually infected with 1 P. aeruginosa clone that remained in the lung for years, without evidence of interpatient transmission. During chronic infection, each clone diversified, which led to the coexistence of isolates with different morphotypes and antibiotic susceptibility. Overall, P. aeruginosa evolved toward an increased mutation rate, increased antibiotic resistance, and reduced production of proteases. Isolates from samples of infected lungs tend to be less cytotoxic and motile and to produce more biofilm, compared with isolates from blood samples.


These results provide the first evidence supporting the hypothesis that P. aeruginosa causes chronic infections in COPD, with patterns of infection and evolution that resemble those observed in cystic fibrosis. Experience gained from treating cystic fibrosis might be useful for implementing new procedures for the prevention, diagnosis, and treatment of infection due to P. aeruginosa in COPD.


January 5, 2014 at 6:25 pm

West nile virus in the United States – a historical perspective.

Viruses. 2013 Dec 10;5(12):3088-108.

Roehrig JT.


Prior to 1999, West Nile virus (WNV) was a bit player in the screenplay of global vector-borne viral diseases. First discovered in the West Nile District of Uganda in 1937, this Culex sp.-transmitted virus was known for causing small human febrile outbreaks in Africa and the Middle East.

Prior to 1995, the last major human WNV outbreak was in the 1950s in Israel. The epidemiology and ecology of WNV began to change in the mid-1990s when an epidemic of human encephalitis occurred in Romania.

The introduction of WNV into Eastern Europe was readily explained by bird migration between Africa and Europe. The movement of WNV from Africa to Europe could not, however, predict its surprising jump across the Atlantic Ocean to New York City and the surrounding areas of the United States (U.S.).

This movement of WNV from the Eastern to Western Hemisphere in 1999, and its subsequent dissemination throughout two continents in less than ten years is widely recognized as one of the most significant events in arbovirology during the last two centuries.

This paper documents the early events of the introduction into and the spread of WNV in the Western Hemisphere.

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January 5, 2014 at 6:22 pm


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