Dark Banquet - Bill Schutt [77]
Initially, the bacterium Orientia tsutsugamushi is inoculated into the skin of a host through a chigger bite or contact with the chigger’s feces. It then spreads through the host’s bloodstream where it invades the endothelium, the flattened layer of cells that compose the inner lining of vertebrate blood vessels. Orientia (a close relative of Rickettsia rickettsii, the bacterium responsible for Rocky Mountain spotted fever) gains access to the endothelial cells’ interior in a rather dodgy way, and in doing so, it pulls off a microscopic version of the famous Trojan horse trick. Phagocytosed by the host cells, Orientia is packaged inside enzyme-filled death baggies called phagosomes. But instead of waiting around to be lysed (or “sliced up,” for those of you who skipped the blood chapter), the bacterium thwarts the host’s defenses by escaping its membrane-bound prison to take up residence in the cells’ gel-like cytoplasm. There, Orientia multiplies rapidly by a form of asexual reproduction called binary fission.*116 Soon the bacteria-packed host cells burst, sending millions of new pathogens to infect new endothelial cells downstream.
During World War II, Allied forces in Southeast Asia and the South Pacific were ravaged by a number of chigger-and tick-borne diseases. Of these, scrub typhus became the most common as well as the most deadly. Sometimes described as mite-borne rickettsia (the rod-shaped bacterium was formerly known as Rickettsia tsutsugamushi), scrub typhus is characterized by high fever, muscle pain, painfully swollen lymph nodes, delirium, and a severe rash. If left untreated or treated too late, scrub typhus can cause encephalitis, circulatory failure, and even death.
In a pattern that’s become familiar to those studying arthropod-transmitted diseases, rodents and not humans were the preferred host of the pathogen-carrying chigger. In the Pacific theater of World War II, rat, vole, and field mouse populations exploded owing to the massive influx of troops, the garbage they produced, and the filthy conditions they endured. As a result, human chigger bites became more and more frequent, until scrub typhus reached epidemic levels. With no specific treatment available during the early 1940s, the disease killed more soldiers in the Burma-India-China theater of operations than any other infectious disease.*117 So serious was the scrub typhus problem that in some of the scientific literature from the 1950s, the chigger responsible for transmitting the disease was described in terms usually reserved for human enemies:
All along the Papuan coast and adjacent islands Akamushi continued its ambush tactics against American troops. Invariably combat troops in most of the engagements of the island-hopping road to Tokyo sought the ever-present cover afforded by the tall kunai grass where Akamushi waited in hiding.
(Emory C. Cushing, History of Entomology in World War II, 80–81)
Not surprisingly, the death toll from scrub typhus generated increased concern about the parasite causing the disease, and this concern led to an intense period of research that ushered in the modern science of acarology (i.e., the study of chiggers, mites, and ticks). Eventually, antibiotics like tetracycline, doxycycline, and chloramphenicol became effective treatments for scrub typhus and other acarid-transmitted diseases.
As with other bacterial pathogens, antibiotic resistance is becoming more of a problem. In parts of northern Thailand, for example, doxycycline-resistant and chloramphenicol-resistant strains of Orientia tsutsugamushi have evolved, and as a result, 15 percent of patients who contract scrub typhus die from the disease. This type of antibacterial resistance can be attributed to several factors: the tremendous rate at which bacteria multiply, the high rate of bacterial mutation, and the misuse of antibiotics.
In that regard, one of the most common ways that antibiotics are misused occurs when a prescribed antibiotic regimen is abandoned,