DRC: Reports Of A Large Monkeypox Outbreak

DRC

# 11,000


Last month, in Monkeypox Outbreak Reported In Central African Republic we looked at what was apparently a small outbreak of the virus - now quashed according to local reports - in the Bangassou district, an area on the north bank of the Mbomou River which serves as a border with the Democratic Republic of Congo (DRC). 

Over the past 24 hours, reports of several outbreaks of Monkeypox have been coming out of the DRC (although their Health Ministry site makes no mention of it), including 51 recent cases in Bas-Uéle (350 km from the CAR outbreak).

While small monkeypox outbreaks are not unusual in central Africa (the DRC reported 20 cases in September 2015), today's report suggests a much larger, and wider spread outbreak. Reportedly nearly 200 cases have emerged in the past few weeks. 


This report from the L'Observateur Nation.

Aketi / Bas Uélé: Reappearance of the outbreak of monkeypox

L'Observateur Nation

The outbreak of monkeypox, a viral disease similar to smallpox surfaced in Aketi territory of the province of Bas-Uélé, where 51 new cases were recorded in the first week of February current. 

Also known as monkey pox, the disease has already killed two people, alerted Tuesday, February 9 aware of the area Medical Officer Aketi, Dr Innocent Akonda. In the process, he says that thirteen cases are diagnosed in the Bombongolo health area, fifteen in that of Aboso and twenty-one other in the twelve other health areas of the territory.

According to several local sources, the situation is alarming and requires immediate intervention. With the new cases, the health area is already 195 cases including 8 deaths, said Dr. Innocent Akonda.

For Dr. Innocent Akonda, this highly contagious disease spread in the Aketi health area because of several difficulties that do not facilitate the fight against the monkeypox virus.

These difficulties became almost a brake for better medical care to the population, he has cited the lack of qualified medical personnel and lack of adequate sanitation.

(Continue . . . )

Credit CDC

Monkeypox is a rare virus, endemic in monkeys and rodents in central Africa, that produces a remarkably `smallpox looking'  illness in humans. although not as deadly. Human monkeypox was first identified in 1970 in the DRC, and since then has sparked small, sporadic outbreaks in the Congo Basin and Western Africa.

The name `monkeypox’  is a bit of a misnomer. It was first detected (in 1958) in laboratory monkeys, but further research has revealed its host to be rodents or possibly squirrels.

Humans can contract it in the wild from an animal bite or direct contact with the infected animal’s blood, body fluids, or lesions, but consumption of undercooked bushmeat is also suspected as an infection risk.

Human-to-human transmission is also possible.  This from the CDC’s Factsheet on Monkeypox:

The disease also can be spread from person to person, but it is much less infectious than smallpox. The virus is thought to be transmitted by large respiratory droplets during direct and prolonged face-to-face contact. In addition, monkeypox can be spread by direct contact with body fluids of an infected person or with virus-contaminated objects, such as bedding or clothing.

According to the CDC there are two distinct genetic groups (clades) of monkeypox virus—Central African and West African. West African monkeypox is associated with milder disease, fewer deaths, and limited human-to-human transmission.

In 1996-97, an unusually large outbreak occurred in the Democratic Republic of Congo (see Eurosurveillance Report), infecting more than 500 in the Katako-Kombe and Lodja regions.  Mortality rates were lower for this outbreak (1.5%) than earlier ones, but this was the biggest, and longest duration outbreak on record.

Somewhat famously, in 2003 the United States saw an outbreak (of the milder, West African clade) that affected 47 confirmed and probable cases across six states—Illinois, Indiana, Kansas, Missouri, Ohio, and Wisconsin - all of whom had contact with infected prairie dogs purchased as pets.

These pets became infected when an animal distributor imported hundreds of small animals from Ghana, which in turn infected prairie dogs that were subsequently sold to the public (see MMWR Update On Monkeypox 2003).

While still considered a geographically limited threat, in 2010 a study that appeared in PNAS warned that the incidence of human monkeypox infection was increasing, and that it posed a potential risk well beyond localized outbreaks in Africa.


Given the size, and quick spread of this latest outbreak, we'll continue to check in on it in the days and weeks ahead.

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How To Really Show Your Love This Valentine's Day

Credit CDC

#10,999




Each year the United States sees – on average – 60 to 80 major disasters (see FEMA list), and thousands of Americans are beset by smaller emergencies each day, and yet most remain woefully unprepared to deal with the unexpected. 

Which is why I promote preparedness gifts for the holidays (see Holiday Preparedness Stocking Stuffers) each year in this blog. 

While maybe not to the exclusion of jewelry or flowers, a first aid kit, a flashlight, a water filter, or a weather radio make wonderful birthday, anniversary, and Valentines gifts, and show you really care. 

For a list of some of the preparedness items I've given over the years, you might wish to revisit #NatlPrep - The Gift Of Preparedness.

To validate your Valentine's theme, the APHA (American Public Health Association) has a growing list of free e-cards that incorporate preparedness advice into the traditional Valentine’s Day message.


I've reprinted a couple I really like, but follow the link below to view, and send, an appropriate card from their much larger selection.

Get ready with one of our free e-cards!
 
If you're a fan of APHA's Get Ready campaign, we know you love to be prepared as much as we do. To help you spread the message, we created some Get Ready e-cards so that you can share the importance of preparedness with your loved ones.

Browse our cards below. When you find one you'd like to send, click on the image. From there, you can share the card with friends and family!

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ECDC EFSA Report: Antimicrobial Resistance On The Rise In The EU

Credit CDC PHIL

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While pandemics and outbreaks of novel diseases like avian flu, MERS, and Zika make the immediate headlines, in terms of long term threats, there is little that can match the potential harm from the rise of antibiotic resistant bacteria around the globe.

It's a threat that has prompted both CDC Director Thomas Frieden and WHO Director General Margaret Chan to warn that the world faces a `post-antibiotic' era.  

Although today's report from the ECDC/EFSA is technically current through the end of 2014, it contains references to the recently discovered MCR-1 Colistin resistance gene (see The Lancet: Dissemination Of The MCR-1 Colistin Resistance Gene and Referral: McKenna On The Latest MCR-1 Finding) which is turning out to already be surprisingly widespread.  

A discovery made all the more concerning because, like the NDM-1 gene, MCR-1 resistance can be transferred laterally via plasmids - tiny snippets  of DNA - that can shuttle from one bacterial strain to another (see MCR-1: The Return Of The Plasmids).

First the press release, then the abstact and link to the full report:

Antimicrobial resistance on the rise in the European Union, ECDC and EFSA warn


11 Feb 2016

​Bacteria in humans, food and animals continue to show resistance to the most widely used antimicrobials, says the latest report on antimicrobial resistance in zoonotic bacteria in Europe. Resistance to ciprofloxacin, an antimicrobial that is critically important for the treatment of human infections, continues to be very high in Campylobacter, thus reducing the options for effective treatment of severe foodborne infections. In addition, multi-drug resistant Salmonella bacteria continue to spread across Europe.

The report also found evidence of resistance to the antimicrobial colistin in Salmonella and E. coli  among poultry in the EU. “This is worrying because it means that this last-resort drug may soon no longer be effective for treating severe human infections with Salmonella” said Mike Catchpole, Chief Scientist for ECDC.

Besides the high levels of resistance shown throughout Europe, there are significant regional differences. The highest levels of antimicrobial resistance are observed in eastern and southern Europe. “In northern Europe, there is lower resistance in bacteria from poultry, particularly in countries with low use of antimicrobials in animals,” said Marta Hugas, Head of EFSA’s Biological Hazards and Contaminants unit.

Turning the tide on antimicrobial resistance is at the top of ECDC’s agenda. In 2015, the eighth European Antibiotic Awareness Day was launched, with more than 40 countries participating. This European health initiative coordinated by ECDC aims to support Member States in their efforts to promote prudent use of antimicrobials. 

(Continue . . . )

At 200+ pages, the following PDF file isn't exactly light reading, but the following report provides a remarkable amount of data on the rise and spread of antimicrobial resistance in the EU.

The European Union summary report on antimicrobial resistance in zoonotic and indicator bacteria from humans, animals and food in 2014 

European Food Safety Authority
European Centre for Disease Prevention and Control
Abstract 
 
The data on antimicrobial resistance in zoonotic and indicator bacteria in 2014, submitted by 28 EU Member States (MSs), were jointly analysed by EFSA and ECDC. Resistance in zoonotic Salmonella and Campylobacter species from humans, animals and food, and resistance in indicator Escherichia coli as well as meticillin-resistant Staphylococcus aureus in animals and food was assessed.

‘Microbiological’ resistance was assessed using epidemiological cut-off (ECOFF) values; for some countries, quantitative data on human isolates were interpreted in a way which corresponds closely to the ECOFF-defined ‘microbiological’ resistance. In Salmonella from humans, high proportions of isolates were resistant to ampicillin, sulfonamides and tetracyclines, whereas resistance to third-generation cephalosporins and to fluoroquinolones remained generally low, although it was markedly higher in some serovars commonly associated with broilers and turkeys.

In Salmonella and Escherichia coli isolates from broilers, fattening turkeys and meat thereof, resistance to ampicillin, (fluoro)quinolones, tetracyclines and sulfonamides was frequently detected, whereas resistance to third-generation cephalosporins was uncommon. For the first time, presumptive extended spectrum beta-lactamase (ESBL)-/AmpC-/carbapenemase production in Salmonella and Escherichia coli was monitored in poultry. The occurrence of ESBL-/AmpC-producers was low, and carbapenemase-producers were not detected. Resistance to colistin was observed at low levels in Salmonella and Escherichia coli from poultry and meat thereof.

In Campylobacter from humans, a high to very high proportion of isolates were resistant to ciprofloxacin and tetracyclines, whereas resistance to erythromycin was low to moderate. Resistance to fluoroquinolones in some MSs was extremely high; in such settings, the effective treatment options for human enteric Campylobacter infection may be significantly reduced. High resistance to ciprofloxacin and tetracyclines was observed in Campylobacter isolates from broilers and broiler meat, whereas much lower levels were recorded for erythromycin.

Co-resistance to critically important antimicrobials in both human and animal isolates was generally uncommon, but very high to extremely high MDR levels were observed in some Salmonella serovars. A minority of Salmonella isolates from animals belonging to a few serovars (notably Kentucky and Infantis) exhibited high-level resistance to ciprofloxacin.

© European Food Safety Authority and European Centre for Disease Prevention and Control, 2016

 

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NEJM: Probable Hospital Cluster of H7N9 - China, 2015

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Despite having been identified in more than 700 patients since 2013 (and suspected to have infected many more), we've seen surprisingly few clusters of H7N9 reported by China's surveillance system.

That isn't to say there have been none. 

We've seen a handful of household clusters over the years (see 2014 WHO H7N9 FAQ   &  EID Journal: H7N9 In Two Travelers Returning From China - Canada, 2015), and last November we looked at a report (see Study: Probable Nosocomial Transmission Of H7N9 In China) describing a small (n=2) cluster in a hospital ward in Zhejiang Province last February.


Today we've a short correspondence, appearing in the NEJM, describing a second nosocomial cluster that occurred in Shantou, Guandong province at roughly the same time. 

In this case, two doctors attending a patient admitted with respiratory symptoms (later determined to be  H7N9) were infected.

The index patient (M,28), who had frequent contact with poultry, was admitted to a Shantou hospital with respiratory symptoms on January 25th. Seven days later his attending physician (Pt #2, M,33) fell ill, followed 4 days later by a second attending physician in the same department (Pt #3, M,35).


All three were confirmed infected with H7N9 by RT-PCR, and while all recovered, the index patient was shown to be still shedding the virus 42 days after his initial onset of symptoms. Sequence and phylogenic analysis showed the three hospital isolates formed an independent clade that carried two unique nucleotide polymorphisms.


Follow the link below to read the full report and supplemental materials. I'll have a short comment when you return. 

Correspondence

Probable Hospital Cluster of H7N9 Influenza Infection

N Engl J Med 2016; 374:596-598

February 11, 2016 DOI: 10.1056/NEJMc1505359

Although no sustained H7N9 transmission has been reported in the community (very few secondary infections detected in contacts of known cases) - since only the `sickest of the sick’ are ever tested - there’s a pretty good chance that a substantial number of mild cases go unnoticed.

One study conducted after the first wave in the spring of 2013 – where just 134 cases were recorded – estimated the real number of cases ran into the thousands (see Lancet: Clinical Severity Of Human H7N9 Infection).

The H7N9 virus continues to evolve and diversify over time (see EID Journal: H7N9’s Evolution During China’s Third Wave – Guangdong Province), and many researchers worry that it may eventually adapt well enough to human physiology to pose a genuine pandemic threat.

It may be entirely coincidental, but the day-to-day reporting of H7N9 out of China virtually stopped in early March of last year – at roughly the same time China was dealing with these two hospital clusters  -  something I blogged about in H7N9: No News Is . . . . Curious on March 19th.   

Although the limited data we've seen suggests this year's outbreak may be lighter than the past two years, this report illustrates that is can sometimes take up to a year for some of the grittier details to filter out of China.

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RESEP SAYUR SOP BAKSO SEDAP DAN GURIH

Resep Sayur Sop Bakso - Masakan berkuah bening dengan cita rasa kuah yang segar dan gurih sudah tentu sangat sedap disantap panas-panas. Cara membuat sup bakso daging sapi bening campur sayur bisa menjadi menu rumahan yang enak dan sederhana sebagai hidangan spesial keluarga dan juga favorit untuk anak.

Memasak sayur sop sering kali menjadi pilihan utama saat ingin menyajikan aneka menu sehat dari sayur mayur, selain mudah dan praktis juga rasanya sangat cocok bagi semua anggota keluarga.

Kita dapat menetukan pilihan bermacam-macam jenis sayur yang diinginkan. Supaya kuah berasa lebih gurih berkaldu maka dikombinasikan dengan ayam, daging, sosis, bakso ikan atau bakso daging dalam resep kali ini.

Persiapan Bahan Bumbu Sayur Sop Bakso

• 150 gram kol dipotong sesuai selera
• 150 gram jamur kancing dibelah 4 bagian
• 150 gram wortel dipotong bulat tipis
• 1 buah kentang besar (200 gram) dikupas lalu potong dadu
• 10 buah bakso sapi dibelah 2, lalu kerat menyilang
• 2 batang daun bawang dipotong sesuai selara
• 2 liter air
• 1 sdt pala bubuk
• 1/2 sdt kaldu bubuk atau penyedap sesuai selera
• 1 sdt lada/merica bubuk
• 1 sdm garam
• 1 sdt gula pasir
• 1 buah tomat belah 4 bagian
• 6 butir bawang merah dihaluskan
• 3 siung bawang putih dihaluskan
• 2 cm jahe dihaluskan
• minyak untuk menumis bumbu
• bawang goreng untuk taburan

Cara Membuat Sayur Sop Bakso

1. Panaskan sedikit minyak, kemudian tumis bawang merah, bawang putih dan jahe halus hingga harum. Tuang air, aduk lalu masak hingga mendidih.
2. Masukkan wortel, kentang dan bakso, serta beri garam, gula, kaldu bubuk, merica dan pala bubuk. Aduk rata lalu masak hingga mendidih kembali, bakso mekar serta wortel dan kentang empuk.
3. Masukkan kol, jamur dan daun bawang, lanjutkan memasak hingga matang. Terakhir masukkan potongan tomat lalu matikan api, angkat dan siap untuk disajikan hangat-hangat dengan taburan bawang goreng.

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MMWR: Evidence Of Zika Infection In Brain & Placental Tissues From Congenital Infections

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Although there are still a lot of unanswered questions, today's Early Release from the MMWR contains some of the strongest evidence to date linking maternal infection with the Zika virus to microcephaly and/or fetal death.

Analysed are four cases from Brazil, two involving fetuses that spontaneously miscarried late in the first trimester, and two babies born with microcephaly at or near full term that died within 20 hours of delivery. 

All four mothers had clinical signs of Zika infection during their first trimester, and subsequent post mortem testing of brain and placental tissues (see details below), showed evidence of Zika infection.
 
 

FEBRUARY 10, 2016
 
A surge in the number of children born with microcephaly has been noted in regions of Brazil with a high prevalence of suspected Zika virus disease. This report describes evidence of a link between Zika virus infection and microcephaly and fetal demise through detection of viral RNA and antigens in brain tissues from infants with microcephaly and placental tissues from early miscarriages.

Notes from the Field: Evidence of Zika Virus Infection in Brain and Placental Tissues from Two Congenitally Infected Newborns and Two Fetal Losses — Brazil, 2015

Early Release / February 10, 2016 / 65(06);1–2

Format:

 

 

Roosecelis Brasil Martines, MD, PhD¹; Julu Bhatnagar, PhD¹; M. Kelly Keating, DVM¹; Luciana Silva-Flannery, PhD¹; Atis Muehlenbachs, MD, PhD¹; Joy Gary, DVM, PhD¹; Cynthia Goldsmith, MS¹; Gillian Hale, MD¹; Jana Ritter, DVM¹; Dominique Rollin, MD¹; Wun-Ju Shieh, MD, PhD¹; Kleber G. Luz, MD, PhD²; Ana Maria de Oliveira Ramos, MD, PhD³; Helaine Pompeia Freire Davi, MD, PhD⁴; Wanderson Kleber de Oliveria, MD⁵; Robert Lanciotti, PhD⁶; Amy Lambert, PhD⁶; Sherif Zaki, MD, PhD¹

Zika virus is a mosquito-borne flavivirus that is related to dengue virus and transmitted primarily by Aedes aegypti mosquitoes, with humans acting as the principal amplifying host during outbreaks. Zika virus was first reported in Brazil in May 2015 (1). By February 9, 2016, local transmission of infection had been reported in 26 countries or territories in the Americas.* Infection is usually asymptomatic, and, when symptoms are present, typically results in mild and self-limited illness with symptoms including fever, rash, arthralgia, and conjunctivitis. However, a surge in the number of children born with microcephaly was noted in regions of Brazil with a high prevalence of suspected Zika virus disease cases. More than 4,700 suspected cases of microcephaly were reported from mid-2015 through January 2016, although additional investigations might eventually result in a revised lower number (2). In response, the Brazil Ministry of Health established a task force to further investigate possible connections between the virus and brain anomalies in infants (3).

Since November 2015, CDC has been developing assays for Zika virus testing in formalin-fixed, paraffin-embedded (FFPE) tissue samples. In December 2015, FFPE tissues samples from two newborns (born at 36 and 38 weeks gestation) with microcephaly who died within 20 hours of birth and two miscarriages (fetal losses at 11 and 13 weeks) were submitted to CDC, from the state of Rio Grande do Norte in Brazil, for histopathologic evaluation and laboratory testing for suspected Zika virus infection. All four mothers had clinical signs of Zika virus infection, including fever and rash, during the first trimester of pregnancy, but did not have clinical signs of active infection at the time of delivery or miscarriage. The mothers were not tested for antibodies to Zika virus. Samples included brain and other autopsy tissues from the two newborns, a placenta from one of the newborns, and products of conception from the two miscarriages.

FFPE tissues were tested by Zika virus reverse transcription-polymerase chain reaction (RT-PCR) targeting the nonstructural protein 5 and envelope genes using general methods for RT-PCR (4), and by immunohistochemistry using a mouse polyclonal anti-Zika virus antibody, using methods previously described (5). Specific specimens from all four cases were positive by RT-PCR, and sequence analysis provided further evidence of Zika virus infection, revealing highest identities with Zika virus strains isolated from Brazil during 2015. In the newborns, only brain tissue was positive by RT-PCR assays. 

Specimens from two of the four cases were positive by immunohistochemistry: viral antigen was noted in mononuclear cells (presumed to be glial cells and neurons within the brain) of one newborn, and within the chorionic villi from one of the miscarriages. Testing for dengue virus was negative by RT-PCR in specimens from all cases.

For both newborns, significant histopathologic changes were limited to the brain, and included parenchymal calcification, microglial nodules, gliosis, and cell degeneration and necrosis. Other autopsy tissues and placenta had no significant findings. Tests for toxoplasmosis, rubella, cytomegalovirus, herpes simplex, and HIV were negative in the two mothers who experienced miscarriages. Placental tissue from one miscarriage showed heterogeneous chorionic villi with calcification, fibrosis, perivillous fibrin deposition, and patchy intervillositis and focal villitis, while tissue from the other miscarriage had sparsely sampled normal-appearing chorionic villi.

This report describes evidence of a link between Zika virus infection and microcephaly and fetal demise through detection of viral RNA and antigens in brain tissues from infants with microcephaly and placental tissues from early miscarriages. Histopathologic findings indicate the presence of Zika virus in fetal tissues. These findings also suggest brain and early gestational placental tissue might be the preferred tissues for postmortem viral diagnosis. Nonfrozen, formalin-fixed specimens or FFPE blocks are the preferred sample type for histopathologic evaluation and immunohistochemistry, and RT-PCR can be performed on either fresh frozen or formalin-fixed specimens. To better understand the pathogenesis of Zika virus infection and associated congenital anomalies and fetal death, it is necessary to evaluate autopsy and placental tissues from additional cases, and to determine the effect of gestational age during maternal illness on fetal outcomes.

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CDC Video: Zika 101

Click to watch On YouTube

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There's been so much hype and misinformation out there about the Zika virus that I'm pleased to see that the CDC's Principal Deputy Director Anne Schuchat, M.D. has been selected to present a 4 minute video explaining the Zika threat. 

Admiral Schuchat was the `voice' of the CDC during the opening months of the 2009 H1N1 pandemic, and her ability to convey rapidly changing and unscripted  information – while acknowledging those things that were still unknown – earned her a lot of fans in the media.

Follow this link, or click the image below, to watch the presentation.

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