A monitor in the intensive care unit at Cook County Hospital in Chicago continuously beeped and flashed alarms as the young woman's pulse rose above 140 beats per minute and her blood pressure fell. Her skin was ashen and clammy, her muscles slack, her lips cracked, her eyes rolled up under limp lids. It was clear she was dying. What wasn't clear was whether she could withstand the extreme measures required to save her.
The patient was in her late twenties and had begun experiencing severe pelvic pain following her last menstrual period two weeks before. By the time her mother brought her to the emergency room, she couldn't stand up straight because of swelling from an anaerobic bacterial infection in her belly. A DNA probe identified the original infection as Neisseria gonorrhoeae, which attaches to cells in the reproductive tract that nourish sperm. Although cervical mucus contains antibacterial compounds, menstrual blood can wash the mucus out, making it easier for Neisseria and other microbes to migrate up the reproductive tract and into the fallopian tubes. Her gynecologists put her on intravenous antibiotics and waited for her to heal. Instead, after four days, her infection had only grown worse.
A century ago, pelvic infections from gonorrhea were a major source of disability and one of the causes of the "female complaint" many patent medicines were marketed to relieve. In that preantibiotic era, many women suffered from lingering infections that could sometimes kill. Even today, about 150 women in the United States die each year from complications of pelvic inflammatory disease. This patient was about to become one of them.
As gonococcal bacteria multiply in the fallopian tubes, components in the bacterial cell walls rouse the immune system defenses. Antibodies bind to the cells, marking them for engulfment and destruction by white blood cells. Substances in the blood called complement proteins punch lethal holes in the bacteria. There is also a structural barrier: Loops of bowel and a membrane called the omentum stick together, shielding the abdominal cavity from bacterial infiltration. But in a few cases, bacteria get through. The fallopian tubes fill with pus, an acidic soup of toxic enzymes and exhausted immune cells. As the pus collects, the body walls it off in a capsule formed of a blood component called fibrin. That pocket, or abscess, contains the infection. An abscess lacks blood vessels, so white blood cells, substances secreted by immune cells, and antibiotics have difficulty reaching the infection. The body tries to make up for the lack of blood flow: Small blood vessels grow leaky to permit immune defenses to seep out into infected tissue. But the leakiness also allows bacterial products into the bloodstream, which can further ignite an inflammatory response. Eventually, the body cannot keep the arteries filled, and blood pressure falls. Heart function falters. Deprived of blood flow, the major organs fail, and the patient dies.
