A bacterial species normally found in the urinary tract, known as Ureaplasma species, has been discovered to be causing brain damage and death in lung organ transplant patients. Systemic infection with Ureaplasma species causes the development of hyperammonemia, a condition characterized by progressive increases of the amount of the chemical ammonia in the blood. This leads to neurological abnormalities, cerebral oedema (swelling) and death. According to new research, those bacteria are concerned to cause fatal illness and death in a number of lung transplant recipients.
Healthy people have undetectable amounts of those ureaplasma bacteria in their urinary tract. These small amounts of Ureaplasma present in healthy people produce tiny amounts of ammonia which seeps into the bloodstream but the liver of healthy patient is able to break down the ammonia, rendering it harmless. In some organ transplant recipients however, the amount of ammonia in the blood explodes because of the sudden increase in the amount of Ureaplasma species, and they develop hyperammonemia.
Researchers tested tissue from three lung transplant patients who had died from hyperammonemia and from two lung transplant recipients who had hyperammonemia but were still alive. All of the lung samples showed evidence of infection with either Ureaplasma species. In contrast, 20 lung transplant recipients who didn’t develop hyperammonemia were tested and no such Ureaplasma bacteria were found.
Scientists suggest that transmission of Ureaplasma species from the donor is the most conceivable mechanism that causes Ureaplasma infection and hyperammonemia to lung transplant recipients. This is because they found that the lungs of one donor already contained those bacteria before the organs were transplanted into the recipient. So donor organs could deliver the microbes to patients who develop hyperammonemia. The effect is enhanced by the fact that organ transplant recipients have suppressed immune systems, and the bacteria might take advantage of their weakened defences.
The infection of lung transplant patient with Ureaplasma, although devastating, is incredibly rare which hampers the systematic study of the disease etiology and prevents scientists from developing effective therapies. This research demonstrates that administration of Ureaplasma- directed antimicrobials such as, azithromycin and levofloxacin, to patients with hyperammonemia syndrome resulted in biochemical and clinical resolution of the disorder by decreasing ammonia concentrations and recovering patients’ mental status. However this is not a guaranteed therapy as a patient may relapse due to antimicrobial resistance. The microbes are vulnerable to three families of antibiotics, so a combination of drugs would be a better choice to avoid resistance, scientists support.
Yet, these results are inconsistent as only a small group of 25 patients was inspected, and thus further studies are obligatory for determining the source of Ureaplasma dissemination in the host along with the incidence of donor and recipient colonisation.
Screening of patients and donors for Ureaplasma species before or directly after transplantation may help inform future consideration of global or targeted prophylaxis. The thoracic surgeon Ankit Bharat of the Northwestern University Feinberg School of Medicine, proposes the necessity to test for the presence of Ureaplasma in donor organs and offer empiric antimicrobial treatment while awaiting microbiological confirmation.
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