Sunday, 25 September 2016

Colombia Zika virus report, Epidemiological Week No. 37...

The latest epidemiological report from Colombia, which includes data on Zika virus disease (ZVD; 11SEP2016-17SEP2016), has been produced by the Colombian National Institute for Health team.[1]
NOTE: While these data were reported the past epidemiological week (EW), they may not be from that week. See earlier post about possible reporting lag.

As of this report, 41 (+1 from last EW) live births have been diagnosed with congenital ZIKV syndrome (CZVS; microcephaly/central nervous system disorder), confirmed as being ZIKV positive. That represents 0.70% of all confirmed ZIKV positive mothers-the 8th consecutive EW in which this proportion has risen.

Some back of napkin calculations looking at these numbers suggest that there are 7 deliveries for every 1,000 ZIKV-positive pregnant women that result in a ZIKV infected baby with microcephaly

This assumes each neonate has been tested for ZIKV as [2] suggests. This figure has no clear understanding of the number of aborted or miscarried foetuses that are also occurring from ZIKV-positive pregnant women. Abortions and miscarriages will need a local baseline to understand the scope of this component of the impact of ZIKV infection.

246 other microcephaly diagnoses (up from 216 last week) are now under investigation - this value had also been rising very quickly until a recent dip and plateau. Its rise once again might suggest suspicious CZVS cases in Colombia are accruing faster than the pace of complete investigation can keep up with. 

The graph below focuses on just the ZIKV-positive cases and those that remain under investigation, highlighting how the investigatory total has changed each week.

The change in confirmed ZIKV infection numbers when detected in
association with a microcephaly diagnosis, compared to the
preceding week's total (yellow bars, left-hand axis). Data are from [1].
Click on graph to enlarge.

It has now been 344 days, or 11 months 8 days, since ZIKV was first confirmed in Colombia on 16th October 2015.[2] Keep in mind that when talking about microcephaly - we have to think back in time to what insult or infection might have occurred during pregnancy. The counts of virus occurring this week will have zero impact on what happened back then. Also keep in mind that Colombia may be reporting things differently from Brazil.[3]

Brazil first reported positive (but unconfirmed) laboratory tests for Zika virus disease on 29th April 2015. Brazil then started to report a rise in foetal anomalies (an initial 141), in the form of microcephaly on 30th October 2015. This was 184 days - or about 6 months later.[4] However, the genetic analyses suggest Zika virus was in Brazil from around 2013. It had a lot longer to get extan;shed. Perhaps this is the difference between Brazil and Colombia.

But whatever the difference, there is a rise in microcephaly in Colombia compared to Brazil as we can see from the data in this Pan American Health Organization (PAHO) report...

401 cases counted up to EW 33 (now at EW 37) is 2.9X higher than the usual microcephaly figure per year for Colombia.
From PAHO report.[4]
References...

  1. http://www.ins.gov.co/boletin-epidemiologico/Boletn%20Epidemiolgico/2016%20Boletin%20epidemiologico%20semana%2037.pdf
  2. Zika Virus Disease in Colombia — Preliminary Report
    http://www.nejm.org/doi/full/10.1056/NEJMoa1604037#t=article
  3. http://virologydownunder.blogspot.com.au/2016/06/the-elephant-squeaked.html
  4. PAHO Zika-Epidemiological Report | Colombia
    http://www.paho.org/hq/index.php?option=com_docman&task=doc_view&gid=35139&Itemid=270&lang=en

Wednesday, 21 September 2016

The reach of Aedes aegypti in Queensland, Australia...

I made this, based on the State of Queensland,(Queensland Health) map from the 2015-2020 Queensland Dengue Management plan.[1] 

Feel free to use this image but please abide by the copyright 
notice found within the 2015-2020 Queensland Dengue management plan.[1]
Click on map to enlarge.
The map may be a useful accompaniment to the recent paper confirming Aedes aegypti is the most likely mosquito vector of Zika virus (ZIKV) in Australia.[2]

While Australia does have these mozzies, it does not have local ZIKV transmission and Dengue is not endemic in Queensland. 

Annual local outbreaks of Dengue do occur in Queensland but these result from imported cases and are confined to north Queensland.[1]

I've added in some other map-related information to the reference section as well.[3,4,5,6]

References...

  1. 2015-2020 Queensland Dengue management plan, Queensland Government.
    https://www.health.qld.gov.au/publications/clinical-practice/guidelines-procedures/diseases-infection/governance/dengue-mgt-plan.pdf
  2. Assessment of Local Mosquito Species Incriminates Aedes aegypti as the Potential Vector of Zika Virus in Australia
    http://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0004959
  3. Dengue and climate change in Australia: predictions for the future should incorporate knowledge from the past
    https://www.mja.com.au/journal/2009/190/5/dengue-and-climate-change-australia-predictions-future-should-incorporate?0=ip_login_no_cache%3D20128744c69e384fe459a669360e8b29
  4. “Dengue” mosquitoes detected in Melbourne: What does it mean?
    https://cameronwebb.wordpress.com/2014/03/16/dengue-mosquitoes-detected-in-melbourne-what-does-it-mean/
  5. The Extinction of Dengue through Natural Vulnerability of Its Vectors
    http://journals.plos.org/plosntds/article/asset?id=10.1371/journal.pntd.0000922.PDF

Saturday, 17 September 2016

MERS is a disease we spread...

There is little doubt now that Middle East respiratory syndrome  (MERS) disease outbreaks are triggered by sporadic zoonotic transmission of the MERS coronavirus (MERS-CoV) from an infected camel to a susceptible human. 

Little doubt to anyone who has followed the story of MERS at all, anyway.

But that's just the tip of the iceberg. 

The majority of human cases that have contributed to those steep rises in the cumulative MERS-CoV detection graph below are there because humans have infected other humans while in or associated with a healthcare facility. A telling picture when you consider that MERS-CoV is not a great transmitter. We've done much to make something from what should have been nothing.

Can we vaccinate against lapses in infection prevention and control?


Thursday, 15 September 2016

Middle East respiratory syndrome coronavirus (MERS-CoV) hotzone map gets a paint job..

A slightly updated MERS-CoV map adding in some camel detection sites in Africa and changing up the colours.

27 countries have been visited - 13 have had local transmission.

And there have been 2 humans in Kenya found to harbour antibodies to MERS-CoV. This helps address the question of why we hadn't seen human MERS cases in Africa despite countries harbouring MERS-CoV infected dromedary camels. The answer of course is, we hadn't looked.

Click on image to enlarge

Wednesday, 7 September 2016

MERS-CoV: alpacapalooza...

In the search for the animals that may be another reservoir for, or just support infection by, Middle East respiratory syndrome coronavirus (MERS-CoV), a few studies have looked at furry little alpacas (Vicugna pacos). 

We already know from Eckerle and colleagues' work that cells derived from alpacas have the required receptor molecule that MERS-COV uses (DPP4) and can support replication of MERS-CoV in the lab,[1] But are cells in flasks different from furry animals in the wild?

Three articles came out in the June 2016 issue of Emerging Infectious Diseases looking at alpacas and MERS-CoV. There's no way to tell who submitted when in this journal.


Colorado State University team sought an easier - but still relevant - animal model than camels to work with.[2] They infected 3 (A1-A3) alpacas with 107 plaque forming units (PFU; a cell-specific measure of the amount of infectious virus in a diluted sample) of the HCoV-EMC/2012 variant of MERS-CoV via 3ml of diluted virus per nostril then housed 3 more uninfected alpacas (A4-A6) with them, 3 days later.  

After 70 days, A1-A6 were infected again ("challenged"), the same way. Three other alpacas were infected the same way but euthanized 5 days after infection and their tissues collected for analysis. Nasal swabs were collected before infection and then daily from all animals for 5 days post-infection and on day 10. A4-A6 were also swabbed 3 times per week to day 19. This could all have been a bit more clearly demonstrated using a timeline by the way.

None of the infected animals had a fever or observable nasal discharge and their appetites and activity remained constant. Infectious MERS-CoV was shed by A1-A3 to day 5 and transmission occurred to the A4-A6 arrivals; A4 was found to shed virus for 1 day, A5 shed no virus and A6 shed across 8 days. Lots of variation even in a controlled environment like this.

When A1-A6 were challenged with a fresh infection. A1-A3 had developed antibodies which protected them from infection as no virus was shed. A4-A6 shed a little infectious virus for at most 2 days. A4-A6 also developed neutralizing antibodies but took longer to do so. 

A wild transmission (from inoculated A1-A3 to naive A4-A6) of MERS-CoV which was of a lower dose than the original inoculum, seemed to elicit a milder antibody response as well. 

Virus was found in the nose, larynx and trachea of A7-A9 but not the lungs.


The Australian/Singapore team also sought an animal model with a better temperament and more manageable size than the camel.[3] 

Under biosafety level 3 conditions, they used a camel MERS-CoV variant (Al-Hasa_KFU-HKU13/2013) and exposed each animal to 106 50% tissue culture infectious doses (TCID50; another cell-specific measure of infectious virus quantity), monitored for 21 days then challenged. Blood as well as nasal, oral, rectal and urogenital swabs were collected over time and tested by sensitive RT-PCR, culture and for the presence of neutralizing antibodies.

The animals once again did not develop a fever (animal No.2 had a raised temperature though) or respiratory illness. 

Infectious virus was isolated from oral upper and deep nasal swabs but not from urogenital or rectal swabs. RNA detection by RT-PCR followed this pattern but after challenge and in the presence of antibodies which had appeared from day 10-12, viral RNA could not be detected anywhere in any animal. 

Neutralizing antibody did not appear until 21 days in animal No. 1, 10 days in No. 2 and still hadn't appeared at day 35 in No. 3. It was apparently unnecessary though, for protection from reinfection in this study of alpacas.  

These 2 studies used 106-107 cell-specific quantities of MERS-CoV to infect the alpacas, but, when sought, less was produced - except in one of the Australian/Singapore animals where the peak of 106 TCID50 detected equalled the input dose. This finding suggests the inoculum may not be relatable to real-world amounts of virus produced from an infected animal source. It may however, just be how much is needed to get an model system infected.

The authors all agreed that alpacas could be a good model for MERS-CoV in camels and that animal infections supported the finding of the initial alpaca cell culture work. But that culture link is quite not so straightforward. 

Deliberately HCoV-EMC/2012 variant infected goats, sheep and horses - also animals whose cells had supported MERS-CoV in the laboratory - showed little or no sign of viral replication and the animals mostly remained healthy (some nasal discharge was seen from 2 of 4 horses).[5] Despite some signs of neutralizing antibody developing in goats and a sheep, the same Colorado team were not convinced that any of these animals would be likely hosts for MERS-CoV in the wild. Cells in a flask are not always the most realistic model for animal transmission I guess.



The final alpaca article was from a Qatar/Netherlands team who tested alpacas in a region of Qatar where MERS-CoV is found to be enzootic among camels.[4] 

Hobby alpaca and camel herds were the subjects of this study. They had been kept about 200m apart in the same farm and cared for by the same animal workers. Blood samples were tested from 15 alpacas and 10 dromedary camels; nasal swabs were collected from the 10 camels but nasal, rectal and oral samples were only collected from a subset of the alpacas for antibody testing and sensitive RT-PCR. 

MERS-CoV neutralizing antibody was present in 15 of 15 alpacas and 9 of the 10 camels according to a 90% plaque-reduction neutralization test. This indicated past natural infections had occurred. Antibodies were also detected that suggested past infection by dromedary betacoronaviruses and camelid alphacoronaviruses but this was not unusual or unexpected. No swabs were positive by RT-PCR so no animals were acutely infected. The authors did not know when, how or how often MERS-CoV may have naturally infected the alpacas.

So we can add alpacas to camels on the short list of animals that can host MERS-CoV infection.

References...
  1. Replicative Capacity of MERS Coronavirus in Livestock Cell Lines
    https://wwwnc.cdc.gov/eid/article/20/2/pdfs/13-1182.pdf
  2. Infection, Replication, and Transmission of Middle East Respiratory Syndrome Coronavirus in Alpacas
    http://wwwnc.cdc.gov/eid/article/22/6/pdfs/16-0192.pdf
  3. Experimental Infection and Response to Rechallenge of Alpacas with Middle East Respiratory Syndrome Coronavirus
    http://wwwnc.cdc.gov/eid/article/22/6/pdfs/16-0007.pdf
  4. MERS-CoV Infection of Alpaca in a Region Where MERS-CoV is Endemic
    http://wwwnc.cdc.gov/eid/article/22/6/pdfs/15-2113.pdf
  5. Inoculation of Goats, Sheep, and Horses with MERS-CoV Does Not Result in Productive Viral Shedding
    http://www.mdpi.com/1999-4915/8/8/230

Sunday, 4 September 2016

There (might be) something in the air tonight... [UPDATE]

UPDATE No.1 06SEPT2016
One of the early pieces of science-based news to come out of the May-2015 Middle East respiratory syndrome coronavirus (MERS-CoV) outbreak in South Korea was a June-2015 piece asking whether air conditioning may have played one (of many?) key role in facilitating the spread of virus from infectious patients, within healthcare facilities.[1]

In a publication that came out in April 2016 (yes, the literature did not see much detail on the South Korean outbreak for quite some time), authors described a study to collect and test air and swabs from surfaces in and outside patient's rooms, and their restrooms, in 2 hospitals that housed 3 male cases of MERS pneumonia.

Whenever RT-PCR is used for this sort of work, it brings with it the question of whether infectious virus-containing droplets were captured, or only bits of non-infectious RNA viral genome was detected. This group, like those in the last post (who did not collect air samples), attempted to grow infectious virus. They could confirm that it was infectious virus by observing cell changes in infected laboratory cultures which were also RT-PCR positive. Also the same approach as that described by the South Korean study reviewed in the last post.[3] Additionally, the infected cell cultures also reacted to an anti-Spike protein antibody in a fluorescent test and they even saw some actual virus from swab cultures (not captured air samples?) using electron microscopy.

Some interesting findings from the use of these test on air and swabs samples included:

  • All airs samples from both hospitals were RT-PCR positive and these included the detection of MERS-CoV of RNA in room, restroom and common corridor air. Infectious virus was grown in cells from from 4 of 7 (57%) samples.
  • 42 of 68 (62%) surface swab samples tested positive for MERS-CoV RNA by RT-PCR and included elevator button and rails, doorknobs and handrails inside and outside a patient's room, telephone button, toilet seat, call button, patient pillow, nasal prong, toilet seat, TV, keyboard, stethoscope and air exhaust dampers. Infectious MERS-CoV was isolated from 15 swabs of some of these items including an elevator button, nasal prong, patient pillow, TV, bed handrail, keyboard, stethoscope, toilet seat and an air exhaust damper

This study really addresses three big issues. 

Firstly MERS-CoV from very ill patients late in their disease course, thoroughly contaminates a hospital room and its surrounds - not just with detectable genetic material, but with infectious, viable MERS-CoV virus. 

Secondly, surface contamination was detected from swabs collected 3-7 hours after daily room cleaning suggesting either that cleaning was insufficient or that new virus was quickly laid down on cleaned surfaces (with no lasting anti-viral effect from the cleaning solution). 

Thirdly, the capture of infectious virus from the air implies that the virus maybe present in droplets or droplet nuclei with implications for the level of personal protective equipment required for healthcare workers and visitors to an infected person bedside. It also pertains to the distance away from a case that is considered "safe" for an uninfected person to be. Six feet may not be nearly enough distance, at least if that is a prolonged period in a room.

More data to explain how MERS-CoV is associated with hospital outbreaks. Why it has been allowed to get away with this is a matter for infection prevention and control specialists in each and every healthcare facility to address.

UPDATE.

After this was published, Van Kerkhove and colleagues wrote a letter to the editor to make some points about the study noting:

  • an absence of negative control sampling from areas where MERS-CoV patients were not housed.
    Absolutely. I'd even suggest a few different sites in very distant hospital areas from where MERS patients were housed, given the possible human-spread of virus around a facility during and the possibility of silent or subclinical infection in patients admitted to hospitals for other reasons during times of outbreak. This will explore whether false positive laboratory results are occurring.
  • other studies have reported surface contamination that did not yield viable virus. Van Kerkhove note that these negative findings need to be published to balance the literature. Always.
    However, it's well known that virus culture is insensitive compared to RT-PCR methods so it
    may fail to detect infectious virus which may be enough to infect a human . It may also be that infectious virus capable of infecting another person who comes into contact with it is not always present in the air or on surfaces. It may be that the surfaces often simply have non-infectious "bits" of virus detected by RT-PCR -these cannot cause a new infection. But in this study infectious virus was able to be isolated from air and surfaces...unless Van Kerkhove and colleagues are implying contamination of the cultures in some way.
  • the need to replicate these findings in other studies.
    Always.
    But as is often the case, let's not wait on those findings to recognise that infectious droplets and contaminated surfaces now have some more data to support them and that they fit nicely into a picture of hospital transmission. Precautionary principle.
A second letter was also written by Myoung-don Oh,[7] noting:

  • few infected cells in the cultures / slow growth.
    This isn't too surprising, it may just reflect that there was a low amount of virus in the air, added to the cell cultures compared to that used from the control virus (cell adapted?) stock.
    This may mean that the risk from airborne transmission in these rooms is low. However, since we don't know what amount of MERS-CoV is required to start a new human infection, this is a moot point.
  • the sequences of the room samples were too different from each other.
    This is a bit surprising since within an outbreak, MERS-CoV doesn't usually vary much at all. I'll have a look at how much South Korea's MERS-CoV Spike gene sequences varied and come back to this point.

Both letters were replied to.[8]

References...



  1. Did poor ventilation lead to MERS 'superspread' in Korea?
    http://www.sciencemag.org/news/2015/06/did-poor-ventilation-lead-mers-superspread-korea
  2. Extensive Viable Middle East Respiratory Syndrome (MERS) Coronavirus Contamination in Air and Surrounding Environment in MERS Isolation Wards
    http://cid.oxfordjournals.org/content/early/2016/06/08/cid.ciw239.abstract
  3. Korea contamination: Middle East respiratory syndrome coronavirus in the room..
    http://virologydownunder.blogspot.com.au/2016/09/korea-contamination-middle-east.html
  4. Interpreting Results From Environmental Contamination Studies of Middle East Respiratory Syndrome Coronavirus
    http://cid.oxfordjournals.org/content/early/2016/08/09/cid.ciw478.full.pdf
  5. STABILITY OF MIDDLE EAST RESPIRATORY SYNDROME CORONAVIRUS (MERS-COV) UNDER DIFFERENT ENVIRONMENTAL CONDITIONS
    http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=20590
  6. Transmissibility of Middle East Respiratory Syndrome by the Airborne Route
    http://cid.oxfordjournals.org/content/early/2016/08/09/cid.ciw479.full.pdf
  7. Interpreting Results From Environmental Contamination Studies of Middle East Respiratory Syndrome Coronavirus
    http://cid.oxfordjournals.org/content/early/2016/08/09/cid.ciw478.full.pdf
  8. Reply to Kerkhove et al and Oh
    http://cid.oxfordjournals.org/content/early/2016/08/09/cid.ciw480.extract
Update...
  1. Added in detail on letter by Van Kerkhove and colleagues [4], and rebuttal authors [5]

Friday, 2 September 2016

Korea contamination: Middle East respiratory syndrome coronavirus in the room..

Remember that MERS-CoV outbreak in South Korea from May 2015? 

It was the biggest outbreak of MERS-CoV to occur outside the Arabian peninsula, killing 20% of those known to be infected. As with all the noticeable MERS-CoV transmission events, it occurred within, and was undoubtedly facilitated by, a hospital setting. 

Back in March 2016, a paper came out looking at routes of infection within in 2 South Korean hospitals (Chungbuk National University Hospital, Hallym University Kangnam Sacred Heart Hospital) among 4 female patients (3 with prior underlying diseases, 1 of whom died) who had developed pneumonia.[1]

Some interesting findings from this study included:
  • Infectious virus could be grown from 3 patients up to 18-22 days after symptom onset (RNA to the 25th day in 1 patient's sputum, suggesting a good correlation between RNA positivity and risk of infection in this small study). The 4th patient shed viral RNA to day 23 after onset but no infectious virus could be isolated. This case also had no underlying diseases so perhaps viral loads were just lower.
  • MERS-CoV RNA could be detected by RT-PCR in hospital rooms 2-5 days after the occupant had died or last tested positive. Anteroom floor and desk samples and medical equipment like X-Ray machines and thermometers were also found to be RNA positive.
    Some of these locations were not directly accessible to the patients and so were likley to have been contaminated via droplets or by healthcare workers.
  • A swabbed air inlet ventilation duct tested positive for MERS-CoV RNA hinting at airborne viral movement
  • Infectious MERS-CoV virus was able to be grown from some items and surfaces including bed sheet, bed rails, intravenous fluid hangers and a table.

All in all, this study highlights how effectively an environmentally stable respiratory virus can deposit itself around the room of a productively shedding patient. 

When you add in:
  • poor or inconsistent infection control
  • room overcrowding
  • family members given some responsibility for care [3]
  • that MERS-CoV is not very good at passing from human-to-human in the community 


...you have a clear explanation for why MERS outbreaks occur entirely in relation to healthcare settings. These settings are where you find close and prolonged contact between infected cases and health care workers and family and friends. You also find those cases contained in multi-bed, flat-surface filled boxes (rooms), ready-made to be contaminated by virus-laden droplets.

While the finding of virus everywhere is not a surprise, it is important to have thorough studies like this that can be referenced in protocols which aim to improve infection control and prevention processes.

Common sense alone is not evidence.

References...
  1. Persistent Environmental Contamination and Prolonged Viral Shedding in MERS Patients During MERS-CoV Outbreak in South Korea
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4946541/pdf/ofv130.11.pdf
  2. Middle East respiratory syndrome coronavirus: how tough is it?
    http://virologydownunder.blogspot.com.au/2013/10/middle-east-respiratory-syndrome.html
  3. 2015 MERS outbreak in Korea: hospital-to-hospital transmission
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4533026/pdf/epih-37-e2015033.pdf

Monday, 29 August 2016

A pile of TWADALs...

During my few days chatting with a gaggle of hardcore vaccine denialists, I developed a term and acronym...TWADAL

The term stands for "Those Who Are Decided Against Learning", because those I engaged with were not "vaccine hesitant" in any sense. 

They were mostly dedicated to pushing an agenda of anti-science, anti-logic, anti-politeness underpinned by memes and quote-cards highlighting every rare bad outcome from a vaccine, every side (well known and mostly minor) adverse event and never once mentioning all the lives that vaccines have saved and protected yesterday, today and in the future. 

By all means describe this as name calling - but go spend some time engaging with TWADALs first - some quality time. Prove to me that they are open to learning anything new. Show me that after they drop into your social media neighbourhood unannounced and spew unsolicited, unverifiable out-of-context untruths about vaccines killing people, collect a few others to pile on, call you a shill for big pharma...that they will then concede any of their points when you try to engage them in a calm discussion. 


Sunday, 28 August 2016

Colombia Zika virus report, Epidemiological Week No. 33...

UPDATE No.1: 29AUG2016
The latest epidemiological report from Colombia, which includes data on Zika virus disease (ZVD; 14AUG2016-20AUG2016), has been produced by the Colombian National Institute for Health team.[1]
NOTE: While these data were reported the past epidemiological week, they may not be from that week. See earlier post about possible reporting lag.

Graph No.1. The cumulative curve of confirmed ZVD cases
(green circles, left-hand axis) and the change in confirmed ZVD case
numbers when compared to the preceding week's total
(green bars, right-hand axis). Data from [1].
Click on graph to enlarge.
Graph No. 1 shows that 0 new laboratory confirmed cases of ZVD were reported this week; the 6th week of this. The total sits at 8,826 or 9% of all clinically suspected Zika virus (ZIKV) detections.

Graph No.2. The cumulative curve of suspected ZVD cases
(pink circles, left-hand axis) and the change in suspected ZVD case
numbers when compared to the preceding week's total
(red bars, right-hand axis). Data from [1].
Click on graph to enlarge.
Graph No. 2 shows the change in suspected cases. These are not laboratory confirmed. The suspected ZVD cases continue to rise but have been slowing for weeks, adding 270 this week to total 93,551.

Graph No.3. The cumulative curve of clinically suspect (lilac triangles, left-hand axis) and confirmed ZIKV infections (lilac circles, left-hand axis) and the change in
confirmed ZIKV infection numbers when compared to the preceding week's total
(purple bars, right-hand axis). Now added the reported number of microcephaly cases
confirmed as ZIKV infected (yellow bars, right-hand axis). Data from [1].
Click on graph to enlarge.
Graph No. 3 shows that to epidemiological week (EW) No. 33, 11,752 suspected (+30 compared to last week) and 6,054 confirmed ZIKV infections (-2) have been identified in pregnant women.

As of this report, 34 (+5 from last EW) live births have been diagnosed with congenital ZIKV syndrome (CZVS; microcephaly/central nervous system disorder), confirmed as being ZIKV positive. That represents 0.53% of all confirmed ZIKV positive mothers-the 4th consecutive EW in which this proportion has risen.

Some back of napkin calculations looking at these numbers suggest that there are 5-6 deliveries for every 1,000 ZIKV-positive pregnant women that result in a ZIKV infected baby with microcephaly. This assumes each neonate has been tested for ZIKV as [6] suggests. This figure has no clear understanding of the number of aborted or miscarried foetuses that are also occurring from ZIKV-positive pregnant women. Abortions and miscarriages will need a local baseline to understand the scope of this component of the impact of ZIKV infection.

209 other microcephaly diagnoses (down from 254 last week) are now under investigation - this value has also been rising very quickly and suggests suspicious CZVS cases in Colombia are accruing faster than the pace of complete investigation can keep up with. 

It now seems very likely that we can expect those bars to keep rising steeply in the coming weeks. The line is well and truly crossed.

Graph No. 4 below focuses on just the ZIKV-positive cases and those that remain under investigation, highlighting how the investigatory total has changed each week and been trending upwards since Epidemiological Week No. 14 and rising by +5 for 2 weeks in a row.

Graph No.4. The change in confirmed ZIKV infection numbers
when detected in association with a microcephaly diagnosis, compared
to the preceding week's total (yellow bars, left-hand axis). Data are from [1].
Click on graph to enlarge.
It has now been 317 days, or 10 months 12 days, since ZIKV was first confirmed in Colombia on 16th October 2015.[2] Colombia is currently carrying the next biggest load of suspected ZVD cases [8] (although more confirmed in Puerto Rico. NB: not all of the "Casos confirmados" are lab confirmed, but I'm told most are).[3] Keep in mind that when talking about microcephaly - we have to think back in time to what insult or infection might have occurred in the first or second trimester (probably-still not definitive). The counts of virus occurring this week will have zero impact on what happened back then. Also keep in mind that Colombia may be reporting things differently from Brazil.[5,7]

Brazil first reported positive (but unconfirmed) laboratory tests for Zika virus disease on 29th April 2015. Brazil then started to report a rise in foetal anomalies (an initial 141), in the form of microcephaly on 30th October 2015. This was 184 days - or about 6 months later.[4]


References...

  1. http://www.ins.gov.co/boletin-epidemiologico/Boletn%20Epidemiolgico/2016%20Boletin%20epidemiologico%20semana%2033.pdf
  2. http://www.who.int/bulletin/online_first/16-171082/en/
  3. http://www.nature.com/news/first-zika-linked-birth-defects-detected-in-colombia-1.19502
  4. http://who.int/bulletin/online_first/16-171082/en/
  5. http://virologydownunder.blogspot.com.au/2016/06/the-elephant-squeaked.html
  6. Zika Virus Disease in Colombia — Preliminary Reporthttp://www.nejm.org/doi/full/10.1056/NEJMoa1604037#t=article
  7. https://www.statnews.com/2016/06/22/zika-abortion-latin-america/
  8. http://www.salud.gov.pr/Estadisticas-Registros-y-Publicaciones/Pages/Informe-Arboviral.aspx
Updates...
  1. Clarified Puerto Rico has more confirmed cases than Colombia but fewer suspected