Lawrence, can you run us through a case?

I'm happy to.

A 42-year-old male agricultural worker from rural West Africa presents to a district health care center with a six-week history of intermittent fever, severe frontal headaches, generalized muscle weakness, joint pains, and progressive weight loss.

Initially, assuming he had malaria, he took a full course of antimetallomephrine, but his symptoms persisted and gradually worsened.

Over the past two weeks, his family noticed striking behavioral changes.

He has become unusually forgetful, irritable, and emotionally withdrawn.

He experiences profound daytime sleepiness, frequently falling asleep mid-conversation, yet suffers from severe nocturnal insomnia.

When a clinician encounters a patient with this constellation of prolonged fever, winter bottom sign, behavioral changes, and sleep-wake reversal in sub-Saharan Africa, what should immediately come to mind?

Dr. Lawrence, can you walk us through the pathophysiology of CCHF?

I would be happy to.

The primary route of infection is the bite of an infected tick, particularly of the genus Hyaloma, which is the principal vector.

When the tick bites, it releases the virus into the skin, then spreads it via the bloodstream to multiple organs.

It infects endothelial cells, lining blood vessels, as well as macrophages, dendritic cells, and hepatocytes.

The skin entry is usually aided by this GT glycoprotein, which will bind to the low-density lipoprotein receptor on the host cell.

Thick saliva itself enhances viral entry and spread via saliva-assisted transmission, suppressing the local immune response and shortening the incubation period.

Dr. Lawrence, can you touch on infection prevention and control? Oh, absolutely, Alfred.