AssessmentsCoxiella burnetii (Q fever)
Coxiella burnetii (Q fever)
Coxiella burnetti infection causes a (positive/negative) Weil-Felix reaction.
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A 36-year-old male cattle farm worker comes to the clinic with a chief complaint of several days of flu-like symptoms including fever, malaise, headache, unusual sweating, fatigue, shortness of breath, and dry cough. The patient also reports intermittent right upper quadrant abdominal pain and nausea. The patient's blood pressure is 130/75 mm Hg, pulse is 80 bpm, respiration rate is 22/min. Physical exam is notable for fever, crackles auscultated over the right lung base, and mild hepatomegaly. Rest of the exam is unremarkable. Liver biopsy is performed, and the findings include multiple foci of granulomatous inflammation. Which of the following organisms most likely caused this patient's symptoms?
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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.
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.