Posts filed under ‘FIEBRE en el POST-VIAJE’

Zika-Associated Birth Defects and Neurodevelopmental Abnormalities Possibly Associated with Congenital Zika Virus Infection — U.S. Territories and Freely Associated States, 2018

MMWR August 8, 2018 V.67  Early Release

Marion E. Rice, MPH; Romeo R. Galang, MD; Nicole M. Roth, MPH; et al.


Zika virus infection during pregnancy causes serious birth defects and might be associated with neurodevelopmental abnormalities in children. Early identification of and intervention for neurodevelopmental problems can improve cognitive, social, and behavioral functioning.


Pregnancies with laboratory evidence of confirmed or possible Zika virus infection and infants resulting from these pregnancies are included in the U.S. Zika Pregnancy and Infant Registry (USZPIR) and followed through active surveillance methods. This report includes data on children aged ≥1 year born in U.S. territories and freely associated states. Receipt of reported follow-up care was assessed, and data were reviewed to identify Zika-associated birth defects and neurodevelopmental abnormalities possibly associated with congenital Zika virus infection.


Among 1,450 children of mothers with laboratory evidence of confirmed or possible Zika virus infection during pregnancy and with reported follow-up care, 76% had developmental screening or evaluation, 60% had postnatal neuroimaging, 48% had automated auditory brainstem response-based hearing screen or evaluation, and 36% had an ophthalmologic evaluation. Among evaluated children, 6% had at least one Zika-associated birth defect identified, 9% had at least one neurodevelopmental abnormality possibly associated with congenital Zika virus infection identified, and 1% had both.


One in seven evaluated children had a Zika-associated birth defect, a neurodevelopmental abnormality possibly associated with congenital Zika virus infection, or both reported to the USZPIR. Given that most children did not have evidence of all recommended evaluations, additional anomalies might not have been identified. Careful monitoring and evaluation of children born to mothers with evidence of Zika virus infection during pregnancy is essential for ensuring early detection of possible disabilities and early referral to intervention services.




MMWR August 8, 2018 V.67  Early Release

Interim Guidance for Preconception Counseling and Prevention of Sexual Transmission of Zika Virus for Men with Possible Zika Virus Exposure — United States, August 2018

Kara D. Polen, MPH; Suzanne M. Gilboa, PhD; Susan Hills, MBBS; et al.

Zika virus infection can occur as a result of mosquitoborne or sexual transmission of the virus. Infection during pregnancy is a cause of fetal brain abnormalities and other serious birth defects (1,2). CDC has updated the interim guidance for men with possible Zika virus exposure who 1) are planning to conceive with their partner, or 2) want to prevent sexual transmission of Zika virus at any time (3). CDC now recommends that men with possible Zika virus exposure who are planning to conceive with their partner wait for at least 3 months after symptom onset (if symptomatic) or their last possible Zika virus exposure (if asymptomatic) before engaging in unprotected sex. CDC now also recommends that for couples who are not trying to conceive, men can consider using condoms or abstaining from sex for at least 3 months after symptom onset (if symptomatic) or their last possible Zika virus exposure (if asymptomatic) to minimize their risk for sexual transmission of Zika virus. All other guidance for Zika virus remains unchanged. The definition of possible Zika virus exposure remains unchanged and …



August 8, 2018 at 8:26 am

Zika virus infection: epidemiology, clinical manifestations and diagnosis

Current Opinion in Infectious Diseases: October 2016 – Volume 29 – Issue 5 – p 459–466

Calvet, Guilherme Amaral; Santos, Flavia Barreto dos; Sequeira, Patricia Carvalho

Purpose of review

Zika virus (ZIKV) is an arbovirus previously believed to cause only a mild and self-limiting illness. Recently, it has emerged as a new public health threat that caused a large outbreak in French Polynesia in 2013–2014 and since 2015 an explosive outbreak in Brazil, with an increase in severe congenital malformations (microcephaly) and neurological complications, mainly Guillain–Barré syndrome (GBS). Since then, it has spread through the Americas. On 1 February 2016, the WHO declared the ZIKV epidemic in Brazil a Public Health Emergency of International Concern. We reviewed the epidemiology of ZIKV infection, clinical presentations and diagnosis. We highlighted the clinical features and nonvector borne transmission of the virus.

Recent findings

Association between ZIKV infection and severe foetal outcomes, including microcephaly and other birth defects; increased rate of GBS and other neurological complications due to the ongoing ZIKV outbreak; increased evidence to date of ZIKV being the only arbovirus linked to sexual transmission; the challenge of ZIKV diagnosis; and the need for a specific point-of care test in epidemic scenarios.


The findings illustrate the emergence of a viral disease with the identification of new associated disorders, new modes of transmission, including maternal–foetal and sexual transmission.

FULL TEXT,_clinical.6.aspx?WT.mc_id=HPxADx20100319xMP


June 30, 2018 at 10:51 am

Minireview – Nipah Virus Infection

J. Clin. Microbiol. June 2018 56:10 e01875-17

Brenda S. P. Ang, Tchoyoson C. C. Lim, and Linfa Wang

Nipah virus, a paramyxovirus related to Hendra virus, first emerged in Malaysia in 1998.

Clinical presentation ranges from asymptomatic infection to fatal encephalitis.

Malaysia has had no more cases since 1999, but outbreaks continue to occur in Bangladesh and India.

In the Malaysia-Singapore outbreak, transmission occurred primarily through contact with pigs, whereas in Bangladesh and India, it is associated with ingestion of contaminated date palm sap and human-to-human transmission.

Bats are the main reservoir for this virus, which can cause disease in humans and animals.

There are currently no effective therapeutics, and supportive care and prevention are the mainstays of management.



June 12, 2018 at 7:37 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

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