Babesiosis as a cause of acute respiratory distress syndrome: a series of eight cases.
The characteristics of patients with Acute Respiratory Distress Syndrome (ARDS) as a complication of Babesia microti infection have not been systematically described.
Adult patients admitted to the medical intensive care unit (MICU) of a tertiary care hospital in the Lower Hudson Valley of New York from 1/1/2008 to 8/1/2016 were evaluated for ARDS complicating babesiosis.
Of 22 patients with babesiosis in the MICU, eight (36.4%; 95% CI: 19.7-57.0%) had ARDS. Six patients (75%) developed ARDS following initiation of anti-babesia drug therapy; however, the mean duration of symptoms in these patients exceeded that of patients who developed ARDS prior to initiation of treatment (7.50 ± 3.83d vs. 4.50 ± 0.71d, p = 0.34). Three patients (37.5%; 95% CI: 13.7-69.4%) expired without recovery from ARDS. In comparison, the mortality rate for the 14 MICU babesiosis patients without ARDS was 14.3% (p = 0.31). There was a trend toward younger age in survivors relative to non-survivors (mean age 54.6 ± 13.8y vs. 74.0 ± 6.24y, p = 0.07). Three of the five survivors did not require mechanical ventilation. The mean sequential organ failure assessment score of non-survivors was significantly higher than that of survivors (12.3 ± 1.15 vs. 6.0 ± 1.4, p = 0.0006).
Among 22 critically ill adult patients with B. microti infection, ARDS developed in eight (35.4%), and three (37.5%) expired without resolution of the ARDS. ARDS often followed the initiation of anti-babesia drug therapy, raising the question of whether the death of the parasite per se contributed to its development. However, this observation was confounded by the longer duration of symptoms preceding initiation of drug therapy.
More on Babesia: https://madisonarealymesupportgroup.com/2016/01/16/babesia-treatment/ According to Dr. Horowitz ARDS is often worsened in hospitalized patients who were given steroids (which suppress the immune system) which can cause death.
The number of symptoms and duration of illness in patients with concurrent Lyme disease and babesiosis are greater than in patients with either infection alone: http://www.lymepa.org/c07%20Lyme%20disease%20and%20Babesiosis%20coinfection.pdf
This finding implies the presence of living spirochetes, because spirochete DNA in blood is amplifiable only when these pathogens remain viable. It also suggests a synergistic inflammatory response to both a parasitemia and an increased spirochetemia. In addition, babesial infection enhances Lyme disease myocarditis in mice, which suggests that coinfection might also synergize spirochete-induced lesions in human joints, heart, and nerves.
The same was found in animals: https://www.sciencedirect.com/science/article/abs/pii/S0020751918302406
Similar to humans, B. microti coinfection appears to enhance the severity of Lyme disease-like symptoms in mice. Coinfected mice have lower peak B. microti parasitaemia compared to mice infected with B. microti alone, which may reflect attenuation of babesiosis symptoms reported in some human coinfections. These findings suggest that B. burgdorferi coinfection attenuates parasite growth while B. microti presence exacerbates Lyme disease-like symptoms in mice.
https://www.sciencedirect.com/science/article/pii/S1877959X18302978 Our findings suggest that Babesia infections may indeed be quite common among individuals who have been exposed to tick bites.
Authorities and mainstream doctors to this day are not considering Lyme/MSIDS a polymicrobial illness, but it usually is: https://madisonarealymesupportgroup.com/2018/10/30/study-shows-lyme-msids-patients-infected-with-many-pathogens-and-explains-why-we-are-so-sick/