The infection connection pg. 3
“We do not think it’s the cause of MS,” Sriram says. “We think it’s a cofactor—a secondary mediator, or possibly one of the polymicrobial infectious agents in the disease process.”
Sriram and his colleagues recently completed a pilot study, which suggested that a six-month course of antibiotics might stabilize the brain lesions and brain atrophy characteristic of MS. The researchers are planning a larger, longer-term study, which will be necessary to prove a pathogenic basis for MS.
“In my studies with MS, the problem in finding a link is that we have very little tissue of patients with MS in early stages. MS is not a fatal disease, and so we obtain postmortem brain tissue from people who’ve had the disease for 40 to 50 years,” Sriram said.
“It is impossible to identify what factors caused these lesions to develop 30 to 40 years ago. What we see is the result of something having happened—‘the aftermath of a battle’.”
To address this problem, the Mid South Chapter of the National MS Society is setting up a donor program to collect brain tissue from MS patients who die of causes unrelated to the disease. This tissue will allow scientists to examine the initial events that cause MS.
As in the H. pylori story, the disease process likely depends on an interaction between the germs and the host’s response to them. In general, Sriram agrees with Ewald’s theory of infectious agents causing chronic diseases but adds, “we can’t blame it all on the pathogen. The host bears some responsibility in the ultimate outcome.”
Premature labor, the leading cause of perinatal morbidity and mortality worldwide, also appears to have an inflammatory origin. According to Roberto Romero, M.D., chief of the Perinatology Research Branch at the National Institute of Child Health and Human Development, “one of every four premature babies are born to women with subclinical infections of the amniotic cavity.”
Romero’s studies have shown that chronic, often silent infections within the amniotic cavity incite inflammation of the membranes and the fetus. The most frequent offenders are the normal bacterial residents of the vagina—Ureaplasma urealyticum, Mycoplasma hominis, and Fusobacterium species.
“For unclear reasons, bacteria from the lower genital tract cross the cervix, get into the uterus, and cross intact fetal membranes to gain access to the amniotic cavity. Microorganisms within the amniotic cavity may infiltrate the fetus when it breathes in infected amniotic fluid, through the ear or even through the skin,” Romero says. This prompts the fetus to mount an exaggerated inflammatory response, known as Fetal Inflammatory Response Syndrome.
Inflammatory cytokines produced by intrauterine tissues and the fetus are believed to mediate the key aspects of normal labor and delivery: uterine contractions, cervical dilation, and rupture of the membranes. However, if the fetus has a systemic inflammatory response due to intra-amniotic infection, this response may trigger premature birth.
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