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Coxiella burnetii (Q fever)

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Coxiella burnetii (Q fever)

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Coxiella burnetii (Q fever)

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A 55-year-old woman presents to the primary care physician with a 2-month history of worsening   weakness, fatigue, and cough. The patient reports the cough is non-productive and notes some shortness of breath on exertion. Medical history is notable for rheumatic heart disease when she was 7 years old. A screening colonoscopy performed at age 50 showed no polyps or abnormalities. She currently works as a cattle rancher at a nearby farm. Temperature is 37.6°C (99.7°F) , pulse is 92/min, respirations are 18/min, blood pressure is 122/63 mmHg, and oxygen saturation is 93% on room air. Cardiopulmonary examination is notable for holosystolic murmur appreciated at the cardiac apex as well as bibasilar rales. Nail examination is notable for small ecchymotic lesions of the upper nail beds bilaterally. Follow-up blood cultures are negative. Which of the following is the most likely organism implicated in this patient’s disease process?  

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Content Reviewers:

Viviana Popa, MD

Coxiella Burnetii, is a short, gram-negative rod that causes a disease called Q fever.

This bacteria is highly resistant to environmental stressors including high temperatures and ultraviolet light, and spreads to humans from mammals like cows, so Q fever is considered a zoonotic infection.

Now, Coxiella Burnetii is gram negative, meaning that its cell wall has a thin peptidoglycan layer so it cannot retain a stain called crystal violet stain.

Instead, it stains pink with Safranin dye used during Gram staining.

So it looks like a little pink rod under the microscope.

C. Burnetii is also non-motile, and it can undergo endosporulation when it feels threatened by the environment, like when the temperature becomes too high or too low, in case of extreme dryness, or when there’s harmful radiation around.

Endosporulation means that the bacteria starts by replicating its DNA, and then it forms a wall inside the cell, isolating a portion from the rest of the cell - let’s call it the mother cell.

Next, the plasma membrane of the cell surrounds the mother cell and then pinches it off, forming a separate body known as a forespore.

The forespore then invaginates into the mother cell and gets completely engulfed by it.

Inside the dying mother cell, the forespore loses water and accumulates calcium, and at the same time gets wrapped in a super tough cortex from the dying mother cell.

At this point, the endospore is able to resist heat, harsh chemicals, digestive enzymes, and even antibiotics.

Finally, as the mother cell dies off, the endospore is released outside.

Surprisingly, an endospore can last over a thousand years out, waiting for favorable conditions to come, and then germinate into the bacterial, or vegetative form, which can then grow, divide and infect organisms.

Coxiella Burnetii is also an obligate intracellular organism, because it can’t make its own energy in the form of ATP.

So it can only replicate inside other cells, like our macrophages.

The bacteria does not routinely grow on standard agar plates but can be grown using animal inoculation or can be cultivated in embryonated eggs or cell culture.

Now, the primary disease that Coxiella Burnetii causes is called Q fever, an atypical pneumonia.

This disease results when people inhale the coxiella spores.

This usually happens when spores are blown downwind from animal farms or when they come into close contact with livestock that are harboring the bacteria.

So people at high risk for infections include people in contact with farm animals, particularly cattle or the amniotic fluid of cattle, and slaughterhouse workers.

In terms of pathogenesis, Coxiella Burnetii is transmitted through aerosolized spores; however, the exact mechanism of disease is poorly understood.

What is known is that C. Burnetti has a capsule that expresses proteins called phase I and phase II antigens that allow it to infect cells and replicate. .

When C. burnetii expresses a protein called phase I antigen it is highly infectious and a single bacterium can be enough to cause acute disease in humans.

Phase I antigen binds to receptors on phagocytes like macrophages in the lung,

Normally, phagocytes destroy invading bacteria via endocytosis, which is when bacteria is engulfed by the phagocyte, wrapped in a vesicles called a phagosome.

The phagosomes would normally merge with another intracellular organelle called a lysosomes, forming a phagolysosome.

Lysosomes release hydrolytic enzymes inside the phagolysosome, which normally destroy the invading bacteria.

However, C. burnetii can escape the immune recognition by using type IV secretion system, or T4SS for short, which is a collection of proteins that can dampen the immune response.

So macrophages don’t gobble up C. burnetii like they should.