Posts filed under ‘Micobacterias’

Pulmonary Infections with Nontuberculous Mycobacteria, Catalonia, Spain, 1994–2014

Emerging Infectious Diseases June 2018 V.24 N.6

Santin et al.

Bellvitge University Hospital-IDIBELL, L’Hospitalet de Llobregat, Spain (M. Santin, P. Malchair, L. Gonzalez-Luquero, M.D. Grijota-Camino, J. Dorca, F. Alcaide); University of Barcelona, Barcelona, Spain (M. Santin, J. Dorca, F. Alcaide); Agency of Public Health of Catalonia, Barcelona (I. Barrabeig); Consorci del Laboratory Intercomarcal de l’Alt Penedès, l’Anoia i el Garraf, Vilafranca del Penedès, Spain (M.A. Benitez); Hospital Moisés Broggi, Sant Joan Despí, Spain (J. Sabria, C. Cañete); Hospital de Viladecans, Viladecans, Spain (M. Palau-Benavent, J.A. Lloret-Queraltó)

In Spain, systematic reporting of pulmonary infections with nontuberculous mycobacteria is not mandatory. Therefore, to determine trends, we retrospectively identified cases for January 1994–December 2014 in Catalonia. Over the 21 years, prevalence increased and was associated with being male. Mycobacterium avium complex and M. abscessus prevalence increased; M. kansasii prevalence decreased.

En España, la notificación sistemática de infecciones pulmonares por micobacterias no tuberculosas no es obligatoria. Por lo tanto, para determinar las tendencias, identificamos casos de enero de 1994 a diciembre de 2014 de forma retrospectiva en Cataluña. Durante los 21 años, la prevalencia aumentó y se asoció con ser hombre. El complejo Mycobacterium avium y la prevalencia de M. abscessus aumentaron; La prevalencia de M. kansasii disminuyó.




May 22, 2018 at 7:40 am

Wound healing: Natural history and risk factors for delay in Australian patients treated with antibiotics for Mycobacterium ulcerans disease.

PLoS Negl Trop Dis. 2018 Mar 19;12(3):e0006357.

O’Brien DP1,2,3, Friedman ND1, McDonald A4, Callan P4, Hughes A1, Walton A1, Athan E1.

Author information

1 Department of Infectious Diseases, Barwon Health, Geelong, Australia.

2 Department of Medicine and Infectious Diseases, Royal Melbourne Hospital, University of Melbourne, Melbourne, Australia.

3 Manson Unit, Médecins Sans Frontières, London, United Kingdom.

4 Department of Plastic Surgery, Barwon Health, Geelong, Australia.



Healing times following treatment with antibiotics, and factors that influence healing, have not been reported in Australian patients with Mycobacterium ulcerans.


Healing times were determined for all M. ulcerans cases treated by a single physician with antibiotics at Barwon Health, Victoria, from 1/1/13-31/12/16. Lesions were categorised by induration size: category A ≤ 400mm2, Category B 401-1600mm2 and Category C ≥1601mm2. A logistic regression analysis was performed to determine risk factors for prolonged wound healing (>150 days from antibiotic commencement). 163 patients were included; 92 (56.4%) were male and median age was 58 years (IQR 39-73 years). Baseline lesion size [available in 145 (89.0%) patients] was categorised as A in 46 (31.7%), B in 67 (46.2%) and C in 32 (22.1%) patients. Fifty (30.7%) patients had surgery. In those treated with antibiotics alone, 83.0% experienced a reduction in induration size after 2 weeks, then 70.9% experienced an increase in induration size from the lowest point, and 71.7% experienced an increase in ulceration size. A linear relationship existed between the time induration resolved and wound healing began. Median time to heal was 91 days (IQR 70-148 days) for category A lesions; significantly shorter than for category B lesions (128 days, IQR 91-181 days, p = 0.05) and category C lesions (169 days, IQR 159-214 days, p<0.001). Fifty-seven (35.0%) patients experienced a paradoxical reaction. Of those treated with antibiotics alone, lesions experiencing a paradoxical reaction had longer healing times [median time to heal 177 days (IQR 154-224 days) compared to 107 days (IQR 79-153 days), p<0.001]. On multivariable logistic regression, lesion size at baseline (p<0.001) and paradoxical reactions (p<0.001) were independently associated with prolonged healing times. For category A and B lesions, healing time was significantly shorter with antibiotics plus excision and direct closure compared with antibiotics alone [Category A lesions median 55 days (IQR 21-63 days) compared with 91 days (IQR 70-148 days), p<0.001; Category B lesions median 74 days (IQR 21-121 days) compared to 128 days (IQR 97-181 days), p<0.001].


In Australian patients treated with antibiotics M. ulcerans lesions usually initially improve, then clinically deteriorate with increased induration and ulceration, before healing after the inflammation associated with lesions resolves. The time to complete healing of lesions is generally long, and is further prolonged in those with larger initial lesion size or who develop paradoxical reactions. For small lesions (<4cm2), excisional surgery may reduce healing times.


April 23, 2018 at 7:22 pm

The incubation period of Buruli ulcer (Mycobacterium ulcerans infection) in Victoria, Australia – Remains similar despite changing geographic distribution of disease

PLoS Negl Trop Dis. 2018 Mar 19;12(3):e0006323.

Loftus MJ1,2, Trubiano JA1,3, Tay EL2, Lavender CJ4, Globan M4, Fyfe JAM4, Johnson PDR1,3.

Author information

1 Department of Infectious Diseases, Austin Health, Heidelberg, Victoria, Australia.

2 Victorian Department of Health and Human Services, Melbourne, Victoria, Australia.

3 Department of Medicine, Melbourne University, Parkville, Victoria, Australia.

4 Victorian Infectious Diseases Reference Laboratory, North Melbourne, Victoria, Australia.



Buruli ulcer (BU) is a geographically-restricted infection caused by Mycobacterium ulcerans; contact with an endemic region is the primary risk factor for disease acquisition. Globally, efforts to estimate the incubation period of BU are often hindered as most patients reside permanently in endemic areas. However, in the south-eastern Australian state of Victoria, a significant proportion of people who acquire BU are visitors to endemic regions. During a sustained outbreak of BU on the Bellarine peninsula we estimated a mean incubation period of 4.5 months. Since then cases on the Bellarine peninsula have declined but a new endemic area has developed centred on the Mornington peninsula.


Retrospective review of 443 cases of BU notified in Victoria between 2013 and 2016. Telephone interviews were performed to identify all cases with a single visit to an endemic region, or multiple visits within a one month period. The incubation period was defined as the time between exposure to an endemic region and symptom onset. Data were subsequently combined with those from our earlier study incorporating cases from 2002 to 2012.


Among the 20 new cases identified in short-term visitors, the mean incubation period was 143 days (4.8 months), very similar to the previous estimate of 135 days (4.5 months). This was despite the predominant exposure location shifting from the Bellarine peninsula to the Mornington peninsula. We found no association between incubation period and age, sex, location of exposure, duration of exposure to an endemic region or location of BU lesion.


Our study confirms the mean incubation period of BU in Victoria to be between 4 and 5 months. This knowledge can guide clinicians and suggests that the mode of transmission of BU is similar in different geographic regions in Victoria.



April 23, 2018 at 7:21 pm

Risk factors for Mycobacterium ulcerans infection (Buruli Ulcer) in Togo ─ a case-control study in Zio and Yoto districts of the maritime region.

BMC Infect Dis. 2018 Jan 19;18(1):48.

Maman I1,2, Tchacondo T3, Kere AB4, Piten E5, Beissner M6, Kobara Y7, Kossi K4, Badziklou K4, Wiedemann FX8, Amekuse K8, Bretzel G6, Karou DS3.

Author information

1 Institut National d’Hygiène (INH), National Reference Laboratory for Buruli ulcer disease in Togo, 26 QAD Rue Nangbeto, 1BP, 1396, Lomé, Togo.

2 Ecole Supérieure des Techniques Biologiques et Alimentaires (ESTBA), Laboratoire des Sciences Biologiques et des Substances Bioactives, Université de Lomé, Lomé, Togo.

3 Ecole Supérieure des Techniques Biologiques et Alimentaires (ESTBA), Laboratoire des Sciences Biologiques et des Substances Bioactives, Université de Lomé, Lomé, Togo.

4 Institut National d’Hygiène (INH), National Reference Laboratory for Buruli ulcer disease in Togo, 26 QAD Rue Nangbeto, 1BP, 1396, Lomé, Togo.

5 Centre National de Référence pour le Traitement de l’Ulcère de Buruli (CNRT-UB), Centre Hospitalier Régional (CHR) de Tsévié, Lomé, Togo.

6 Department for Infectious Diseases and Tropical Medicine (DITM), Medical Center of the University of Munich (LMU), Munich, Germany.

7 Programme National de Lutte Contre l’Ulcère de Buruli, la Lèpre et le Pian (PNLUB-LP), Lomé, Togo.

8 German Leprosy and Tuberculosis Relief Association (DAHW-T), Togo office, Lomé, Togo.



Buruli ulcer (BU) is a neglected mycobacterial skin infection caused by Mycobacterium ulcerans. This disease mostly affects poor rural populations, especially in areas with low hygiene standards and sanitation coverage. The objective of this study was to identify these risk factors in the districts of Zio and Yoto of the Maritime Region in Togo.


We conducted a case-control study in Zio and Yoto, two districts proved BU endemic from November 2014 to May 2015. BU cases were diagnosed according to the WHO clinical case definition at the Centre Hospitalier Régional de Tsévié (CHR Tsévié) and confirmed by Ziehl-Neelsen (ZN) microscopy and IS2404 polymerase chain reaction (PCR). For each case, up to two controls matched by sex and place of residence were recruited. Socio-demographic, environmental or behavioral data were collected and conditional logistic regression analysis was used to identify and compare risk factors between BU cases and controls.


A total of 83 cases and 128 controls were enrolled. The median age was 15 years (range 3-65 years). Multivariate conditional logistic regression analysis after adjustment for potential confounders identified age (< 10 years (OR =11.48, 95% CI = 3.72-35.43) and 10-14 years (OR = 3.63, 95% CI = 1.22-10.83)), receiving insect bites near a river (OR = 7.8, 95% CI = 1.48-41.21) and bathing with water from open borehole (OR = 5.77, (1.11-29.27)) as independent predictors of acquiring BU infection.


This study identified age, bathing with water from open borehole and receiving insect bites near a river as potential risk of acquiring BU infection in Zio and Yoto districts of the Maritime Region in south Togo.


April 23, 2018 at 7:20 pm

Mycobacterium ulcerans DNA in Bandicoot Excreta in Buruli Ulcer-Endemic Area, Northern Queensland, Australia.

Emerg Infect Dis. 2017 Dec;23(12):2042-2045.

Röltgen K, Pluschke G, Johnson PDR, Fyfe J.


To identify potential reservoirs/vectors of Mycobacterium ulcerans in northern Queensland, Australia, we analyzed environmental samples collected from the Daintree River catchment area, to which Buruli ulcer is endemic, and adjacent coastal lowlands by species-specific PCR. We detected M. ulcerans DNA in soil, mosquitoes, and excreta of bandicoots, which are small terrestrial marsupials.



April 23, 2018 at 7:19 pm

Increased Severity and Spread of Mycobacterium ulcerans, Southeastern Australia.

Emerg Infect Dis. 2018 Jan;24(1).

Tai AYC, Athan E, Friedman ND, Hughes A, Walton A, O’Brien DP.


Reported cases of Mycobacterium ulcerans disease (Buruli ulcer) have been increasing in southeastern Australia and spreading into new geographic areas. We analyzed 426 cases of M. ulcerans disease during January 1998-May 2017 in the established disease-endemic region of the Bellarine Peninsula and the emerging endemic region of the Mornington Peninsula. A total of 20.4% of cases-patients had severe disease. Over time, there has been an increase in the number of cases managed per year and the proportion associated with severe disease. Risk factors associated with severe disease included age, time period (range of years of diagnosis), and location of lesions over a joint. We highlight the changing epidemiology and pathogenicity of M. ulcerans disease in Australia. Further research, including genomic studies of emergent strains with increased pathogenicity, are urgently needed to improve the understanding of disease to facilitate implementation of effective public health measures to halt its spread.



April 23, 2018 at 7:18 pm

Treatment guidelines and outcomes of hospital-acquired and ventilator-associated pneumonia.

Clin Infect Dis. 2010 Aug 1;51 Suppl 1:S48-53.

Torres A1, Ferrer M, Badia JR.

Author information

1 Pneumology Department, Clinic Institute of Thorax, Hospital Clinic of Barcelona, Institut d’Investigacions Biomèdiques August Pi i Sunyer, University of Barcelona, Ciber de Enfermedades Respiratorias, Barcelona, Spain.

Erratum in

Clin Infect Dis. 2010 Nov 1;51(9):1114.


Hospital-acquired pneumonia is the second most frequent nosocomial infection and the first in terms of morbidity, mortality, and cost. In recent years, international societies and, most recently, the American Thoracic Society jointly with the Infectious Disease Society of America, have developed guidelines for the management of hospital-acquired pneumonia, health care-associated pneumonia, and ventilator-associated pneumonia. These guidelines include recommendations for risk stratification, initial and definitive antibiotic treatment, and prevention. The validation of these guidelines is important because it confirms that they can be used in clinical practice, as quality indicators, and as a standard of care. Several processes can be validated and are included in the guidelines, such as the accuracy of the prediction of microorganisms according to stratification criteria and the impact of guidelines on outcomes, including length of hospital and intensive care unit stay, duration of mechanical ventilation, complications, and in-hospital and 30-day mortality. Clinical studies have shown that the accuracy of predicting microorganisms according to risk stratification is reliable ( approximately 80% and approximately 90%). Three studies suggest that the implementation of guidelines, with a special emphasis on antibiotic treatment, improves several parameters of outcome. Only one study, using a before-and-after design, showed a decrease in 14-day mortality after guidelines implementation. A key issue for these studies is to modify recommendations according to local patterns of microbiology and drug resistance. In summary, implementation of guidelines for the management of hospital-acquired pneumonia and ventilator-associated pneumonia decreases the rate of initial inappropriate antibiotic treatment and decreased 14-day mortality in a study. More clinical studies to validate the influence of guidelines on outcome are warranted.


PDF (hacer clic en PDF) FREE

March 24, 2018 at 11:00 am

Older Posts


July 2018
« Jun    

Posts by Month

Posts by Category