Contagium

Infecciones alrededor del mundo en 36 horas o menos. Infecciones, epidemiología e historia. Around the world with infectious diseases in 36 hours or less.

[PleuralPOCUS | Dr. Jaime Sánchez @PleuralPOCUS]

En 1949 un médico inglés publicó 700 palabras en The Lancet que deberían leerse en voz alta cada vez que entra una generación nueva a un hospital.

Casi nadie las lee.

Los siete pecados de la medicina. 🧵

[Jerome Adams @JeromeAdamsMD]

If you thought CDC morale was in the toilet after literally getting shot at last year, then watching 25% of the workforce get axed while the rest were told to "do more with less" in emergencies... just wait until you tell them they're being shipped to a 50%+ fatality Ebola hot zone halfway around the world, with a rumored 3 days of training, and zero promise of medevac home for real U.S. standard-of-care treatment if they get infected.

Imagine telling troops heading to Iran: "Go fight for America, but if you get blown up, you're staying in the desert. Don't worry though - we're building an 'Alligator Alley' field hospital. You'll be fine!"

This isn’t sound health policy (for reasons detailed below by @ashishkjha). This is the American Hunger Games - except the tributes wear hazmat suits and the Capitol won’t even fly the losers home.

[Jeremy Konyndyk @JeremyKonyndyk]

Over 1000 cases barely a week past detection.

Soon to be the 2nd largest Ebola outbreak ever, and echoing the 2014 mega-outbreak in all the worst ways.

A thread outlining the huge challenge that looms, and some thoughts on what must be done:

https://t.co/Ig3tjEZsDW

[Craig Spencer MD MPH @Craig_A_Spencer]

I’ve read a lot of reporting on Ebola. But this by @jwgale is excellent and essential reading.

Very few pieces pull together so many threads all at once, while giving clarity on what’s happening, and what comes next.

Read and share this @business gift link below:

https://t.co/Aw0z1x8f0v

[Céline Gounder, MD, ScM, FIDSA 🇺🇦 @celinegounder]

CDC Used Title 42 to Ban Travelers Over Ebola. Its Own Order Explains Why That Won’t Work.
Title 42 sat unused for decades, then became an immigration tool during COVID. Now the CDC has invoked it for Ebola, a disease the order itself says can’t be transmitted by asymptomatic cases.
Read & subscribe (for free!) https://t.co/sIWsHVfVAB

[Marion Koopmans, publications: https://pure.eur.nl @MarionKoopmans]

Impressive! Genome sequence of the virus causing the outbreak in DRC/Uganda shared. That will allow checking which types of assays can be used
https://t.co/SSEnfXHsDN?

[Peter Daszak @PeterDaszak]

Dr. Stone nails it, as usual. The irony for richer countries is that most emerging diseases originate in poorer developing countries (high biodiversity, high population density, enhanced envtl. change), but once they start to spread via air/sea, they gravitate to countries w/ highest travel/trade - i.e. the North.

[Krutika Kuppalli, MD FIDSA @KrutikaKuppalli]

One of the most encouraging things to see in this #Ebola outbreak response is how quickly #Uganda and partners have shared genomic sequence data publicly through @pathoplexus

Rapid, transparent data sharing is critical for diagnostics, surveillance, research, and accelerating development of medical countermeasures especially for a rare #Bundibugyo ebolavirus outbreak where approved vaccines and therapeutics are lacking.

This is exactly the kind of global scientific collaboration we need during emerging infectious disease threats.

https://t.co/vdyWUpNHVs

[Krutika Kuppalli, MD FIDSA @KrutikaKuppalli]

Great article by @HelenBranswell

As someone who has worked on Ebola outbreaks and was once admitted myself to rule out Ebola — I can say this is an incredibly frightening situation for these Americans in DRC.

They stepped forward to help during a dangerous situation and deserve support, compassion, and every effort from the U.S. government to safely bring them home. to receive advanced care if needed.

https://t.co/XOHIeFchif

[Helen Branswell 🇨🇦 @HelenBranswell]

1. #WHO has declared the #Ebola #Bundibugyo outbreak in NE DRC a public health emergency of international concern, aka a PHEIC. Yet another sign this is likely to be a very challenging outbreak.
So far there've been 8 confirmed cases, 246 suspected cases & 80 suspected deaths.

[Dr Steven Quay @quay_dr]

The first genome sequences from the current Ebola Bundibugyo outbreak is not released as far as I can tell, but it will absolutely matter.

The 2012 DRC Bundibugyo strain is shown here against the GenBank reference sequence. When the new outbreak sequences are released, I’ll be looking for three things:

Are they closest to the 2007 Uganda lineage, the 2012 DRC lineage, or something more divergent?

Do the glycoprotein changes affect diagnostic sensitivity or antibody binding?

Does the sequence pattern support one spillover followed by spread, or multiple introductions?

This is not just academic.

We have licensed monoclonal antibody treatments for Zaire ebolavirus, including Inmazeb and Ebanga, but not for Bundibugyo virus.

The reason is biology: Ebola is not one virus.

These are different ebolavirus species, and the surface glycoprotein, the main antibody target, differs enough that a Zaire-directed product cannot simply be assumed to work against Bundibugyo.

Until the sequences are public, public health is flying with partial instruments.

Once they are released, the genomes will tell us whether this outbreak is old fire, new fire, or something in between.

[Krutika Kuppalli, MD FIDSA @KrutikaKuppalli]

This picture from the new #Ebola outbreak is deeply concerning.

You can see multiple individuals surrounding a suspected patient with little to no visible PPE.

In an outbreak setting, especially with Ebola, these kinds of exposures place healthcare workers, caregivers, and communities at enormous risk.

It is a stark reminder that outbreak response is also about ensuring frontline workers have the basic protection and resources they need to stay safe.

https://t.co/pADi1pSEWF

[Dr. Saskia Popescu @SaskiaPopescu]

Epidemic of Ebola Disease caused by Bundibugyo virus in the Democratic Republic of the Congo and Uganda determined a public health emergency of international concern https://t.co/DJFRmaGY4Q

[Fernando de la Calle @Fre_CP]

. Pasajeros de avión en la misma fila y dos filas alrededor en vuelos de más de 6 h (ver imágenes). Tripulación del transporte. Quienes manipularon ropa, lencería👙, residuos médicos o fluidos sin protección. Dejo el enlace:https://t.co/o764hi7V8c

[Dr. Tom Frieden @DrTomFrieden]

Disease detectives are usually invisible. Their work is patient, quiet, and methodical, and it saves more lives than almost any other profession.

The Hondius outbreak will end sooner because dozens of them did this work well. https://t.co/r9pCgb87P8

[Rafael Sirera @ProfSirera]

This is the second instalment explaining the pathology associated with #hantavirusandes infection.

And today, the focus is endothelial dysfunction.

The lungs fill with fluid. Blood pressure collapses. Renal filtration becomes abnormal. Yet histologically, endothelial cells often remain structurally intact.

How can a vascular system fail without massive vascular destruction?
The answer lies in the biology of the endothelium itself. The vascular endothelium is not merely a passive lining. It is a dynamic signalling interface continuously deciding what remains inside the vessel, what enters tissues, and how inflammation is spatially controlled.

Under physiological conditions, endothelial permeability is tightly constrained through adherens junctions, tight junctions, cytoskeletal tension, and receptor-mediated signalling. A central component of this architecture is VE-cadherin.
VE-cadherin molecules form adhesive complexes that mechanically “zip” neighbouring endothelial cells together, preserving vascular integrity despite constant haemodynamic stress.

Hantaviruses fundamentally disturb this regulatory system.
After entering endothelial cells through β3 integrins and related receptors, the virus replicates with remarkably limited direct cytopathic effect.

This is biologically important.
If endothelial cells simply died, thrombosis and necrosis would dominate the pathology. Instead, vessels become functionally porous while remaining anatomically intact.

The disease therefore reflects signalling dysregulation far more than mechanical destruction.
One of the central mechanisms involves abnormal sensitisation to vascular endothelial growth factor (VEGF). Under normal conditions, VEGF transiently increases permeability during wound healing, angiogenesis, hypoxia, or inflammation. Endothelial cells regulate this carefully through reversible cytoskeletal contraction and controlled phosphorylation of junctional proteins.

Hantavirus infection amplifies this response disproportionately.
Infected endothelial cells become hypersensitive to VEGF signalling through VEGFR2-dependent pathways. This induces the internalisation of VE-cadherin, actin stress fibre formation, and ultimately intercellular gap formation.

Mechanistically, the endothelial barrier begins losing lateral tension.
Instead of behaving as a continuous sealed surface, microscopic paracellular openings emerge between neighbouring endothelial cells. Fluid then escapes into tissues following hydrostatic gradients.

In the lung, this becomes catastrophic.
The alveolar-capillary membrane is physiologically designed to be extraordinarily thin in order to optimise oxygen diffusion. But the same structural property that maximises gas exchange also makes the pulmonary microvasculature uniquely vulnerable to permeability dysregulation.

The alveolus effectively becomes a fluid trap.

This explains one of the defining paradoxes of hantavirus pathology:
Permeability increases dramatically even in the absence of widespread endothelial death.
The barrier fails because the cells progressively pull apart from one another.

Evidence also suggests amplification through bradykinin pathways. Bradykinin increases nitric oxide production, vasodilation, and endothelial permeability, potentially reinforcing the vascular leakage state.

In severe disease, VEGF, TNF-α, bradykinin, and nitric oxide may converge on the same endothelial phenotype: loss of barrier integrity.

And importantly, vascular leakage is not uniform across organs.
The pulmonary circulation is particularly susceptible because it contains an enormous endothelial surface area, experiences constant haemodynamic flow, and relies on exceptionally delicate gas-exchange interfaces.

Hantavirus endothelial pathology is not a disease of vascular destruction.
It is a disease in which the endothelial barrier progressively stops behaving like a barrier.

[Rafael Sirera @ProfSirera]

#Hantavirus biology is particularly interesting because severe disease emerges less from direct cytopathic destruction and more from dysregulated endothelial and immune responses.
This is one of the reasons hantavirus infection behaves so differently from many classical viral diseases.

The lungs fail, vascular leakage becomes profound, shock may develop rapidly — yet the infected tissues often show surprisingly limited structural destruction. The pathology is not primarily driven by massive cell death, but by a progressive loss of physiological regulation.

In many ways, hantavirus disease is a disorder of signalling before it is a disorder of anatomy. And interestingly, that logic is already visible at the very first step of infection: viral entry.

In the next two posts, I will explain how hantaviruses produce disease through:
— endothelial dysfunction
— immune dysregulation
Because the receptors the virus uses are not random. They are deeply connected to the systems that later fail.

Entry is mediated primarily through three receptor systems:
1⃣ β3 integrins (especially αvβ3) → predominantly linked to vascular biology and endothelial barrier regulation.
These integrins are not simple adhesion molecules. They participate in mechanotransduction, cytoskeletal organisation, vascular permeability, and endothelial quiescence. Pathogenic hantaviruses preferentially interact with inactive αvβ3 conformations, potentially perturbing signalling pathways that normally stabilise the endothelial barrier.

2⃣ Decay-accelerating factor (DAF/CD55) → fundamentally linked to immune regulation.
CD55 is a complement regulatory protein that protects host cells from excessive complement activation. Viral interaction with DAF immediately places hantavirus biology at the interface between infection and innate immune control — particularly relevant in a disease where inflammation itself contributes substantially to pathology.

3⃣ Protocadherin-1 (PCDH1) → associated with intercellular architecture.
Especially important for New World hantaviruses, PCDH1 is involved in cell-cell adhesion processes. This is mechanistically fascinating because hantavirus disease is ultimately characterised by loss of endothelial cohesion and barrier integrity.

In other words, the virus initially engages receptors involved in:
- vascular stability,
- immune modulation,
- and intercellular organisation.
The same systems that later become dysregulated during severe disease.
That mechanistic coherence is what makes hantavirus pathogenesis so biologically compelling.

[Jose Gomez Rial @gomez_rial5]

Mucho debate estos días sobre PCR y #HantavirusAndes

Pero para entender cuándo una PCR sirve (y cuándo no), primero hay que entender el ciclo biológico del virus dentro del cuerpo.

Porque una PCR no “detecta enfermedad”: detecta virus en un lugar y en un momento concreto. 🧵

[Krutika Kuppalli, MD FIDSA @KrutikaKuppalli]

One of the most striking parts of the #AndesVirus outbreak linked to the MV Hondius is that we are watching modern outbreak response collide with modern information chaos in real time.

The virus is spreading far slower than the information about it.

And that may be one of the defining public health challenges of our era.

[Jose Ramos Vivas @joseramosvivas]

Muy interesante este paper sobre la transmisión del #hantavirus ANDES entre las personas:
Este estudio (de los primeros) en Chile analizó cómo se propaga en los hogares. Importante para prevención (salud pública)🧵👇
1⃣El Riesgo en Casa: El estudio siguió a 476 contactos estrechos. La probabilidad de desarrollar el síndrome cardiopulmonar fue significativamente mayor en parejas sexuales (17,6%) que en otras personas que convivían juntas (1,2%). 🏠👥
2⃣ El paper documentó transmisión de persona a persona del Virus Andes, clasificada como definitiva, probable o posible en distintos casos, confirmando que no solo se adquiere por exposición a roedores. 🤝🚫
3⃣ Detección Temprana: 🔍 El ARN viral se detectó en sangre entre 5 y 15 días antes del inicio de síntomas o de la seroconversión. Esto refuerza el valor de la vigilancia activa en contactos de alto riesgo. 🩸⏱️
4⃣ El contacto íntimo fue el principal factor de riesgo identificado. Entre los contactos que desarrollaron la enfermedad, la viremia precedió a los síntomas hasta por dos semanas, lo que abre oportunidades para diagnóstico precoz. 🏥✅
#Hantavirus #SaludPública #Chile #VirusAndes #Epidemiología #Ciencia #Medicina #Prevención #Infectología
👇
🔗 https://t.co/QZz5sKXjSK