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Chapter: Medical Microbiology: An Introduction to Infectious Diseases: Overview

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Infectious Disease

Of the thousands of species of viruses, bacteria, fungi, and parasites, only a tiny por- tion are involved in disease of any kind. These are called pathogens.


Of the thousands of species of viruses, bacteria, fungi, and parasites, only a tiny por- tion are involved in disease of any kind. These are called pathogens. There are plant pathogens, animal pathogens, fish pathogens, as well as the subject of this book, hu- man  pathogens.  Among  pathogens,  there  are  degrees  of  potency  called  virulence, which sometimes makes the dividing line between benign and virulent microorganisms difficult to draw. Many bacteria and some fungi are part of a normal flora that colo- nizes the skin and mucosal surfaces of the body, where most of the time they appear to do no harm. In extreme circumstances, a few of these organisms are associated with mild disease, making them low-virulence pathogens at best. Other pathogens are virtu- ally always associated with disease of varying severity. Yersinia pestis, the cause of plague, causes fulminant disease and death in 50 to 75% of individuals who come in contact with it. It is highly virulent. Understanding the basis of these differences in vir- ulence is a fundamental goal of this book. The better students of medicine understand how a pathogen causes disease, the better they will be prepared to intervene and help their patients.

For any pathogen the basic aspects of how it interacts with the host to produce disease can be expressed in terms of its epidemiology, pathogenesis, and immunity. Usually our knowledge of one or more of these topics is incomplete. It is the task of the physician to relate these topics to the clinical aspects of disease and be prepared for new developments which clarify, or in some cases, alter them. We do not know everything, and not all of what we believe we know is correct.


Epidemiology is the “who, what, when, and where” of infectious diseases. The power of the science of epidemiology was first demonstrated by Semmelweis, who by careful data analy-sis alone determined how streptococcal puerperal fever was transmitted. He even devised a means to prevent it decades before the organism itself was discovered. Since then each organism has built its own profile of vital statistics. Some agents are trans-mitted by the air, others by food, others by insects, and some spread by the person-to-person route. Some agents occur worldwide, and others only in certain geographic locations or ecologic circumstances. Knowing how an organism gains access to its victim and spreads are crucial to understanding the disease. It is also essential to discovering the emergence of “new” diseases, whether they are truly new (AIDS) or just undiscovered (Legionnaires’ disease). Solving mysterious outbreaks or recognizing new epidemiologic patterns have usually pointed the way to the isolation of new agents.

Epidemic spread and disease are facilitated by malnutrition, poor socioeconomic conditions, natural disasters, and hygienic inadequacy. In previous centuries, epidemics, sometimes caused by the introduction of new organisms of unusual virulence, often resulted in high morbidity and mortality. The possibility of recurrence of old pandemic infections remains, and, in the case of AIDS, we are currently witnessing a new and extended pandemic infection. Modern times and technology have introduced new wrinkles to epidemiologic spread. Intercontinental air travel has allowed diseases to leap continents even when they have very short incubation periods (cholera). The effi-ciency of the food industry has sometimes backfired when the distributed products are contaminated with infectious agents. The well-publicized outbreaks of hamburger-associated Escherichia coli O157:H7 infection are an example. The nature of massive meatpacking facilities allowed organisms from infected cattle on isolated farms to be mixed with other meat and distributed rapidly and widely. By the time outbreaks are recognized, cases of disease are widespread, and tons of meat must be recalled. In simpler times, local outbreaks from the same source would have been detected and con-tained more quickly.

Of course, the most ominous and uncertain epidemiologic threat of these times is not amplification of natural transmission but the specter of unnatural, deliberate spread. Anthrax is a disease uncommonly transmitted by direct contact of animals or animal products with humans. Under natural conditions, it produces a nasty but usually not life-threatening ulcer. The inhalation of human-produced aerosols of anthrax spores could produce a lethal pneumonia on a massive scale. Smallpox is the only disease officially eradicated from the world. It took place so long ago that most of the population has never been exposed or immunized and are thus vulnerable to its reintroduction. We do not know if infectious bioterrorism will work on the scale contemplated by its perpetrators, but in the case of anthrax we do know that sophisticated systems have been designed to attempt it. We hope that we will never learn whether bioterrorism will work on a large scale


Once a potential pathogen reaches its host, features of the organism determine whether or ot disease ensues. The primary reason pathogens are so few in relation to the microbial world is that being a successful pathogen is very complicated. Multiple features, called virulence factors, are required to persist, cause disease, and escape to repeat the cycle.

The variations are many, but the mechanisms used by many pathogens are now being dissected at the molecular level.

The first step for any pathogen is to attach and persist at whatever site it gains access. This usually involves specialized surface molecules or structures that correspond to re-ceptors on human cells. Because human cells were not designed to receive the microor-ganisms, they are usually exploiting some molecule important for essential functions of the cell. For some toxin-producing pathogens, this attachment is all they need to produce disease. For most pathogens, it just allows them to persist long enough to proceed to the next stage, invasion into or beyond the mucosal cells. For viruses, invasion of cells is es-sential, because they cannot replicate on their own. Invading pathogens must also be able to adapt to a new milieu. For example, the nutrients and ionic environment of the cell sur-face differs from that inside the cell or in the submucosa.

Persistence and even invasion do not necessarily translate immediately to disease. The invading organisms must disrupt function in some way. For some, the inflammatory response they stimulate is enough. For example, a lung alveolus filled with neutrophils responding to the presence ofStreptococcus pneumoniae loses its ability to exchange gases. The longer a pathogen can survive in the face of the host response, the greater the compromise in host function. Most pathogens do more than this. Destruction of host cells through the production of digestive enzymes, toxins, or intracellular multiplication is among the more common mechanisms. Other pathogens operate by altering the function of a cell without injury. Cholera is caused by a bacterial toxin, which causes intestinal cells to hypersecrete water and electrolytes leading to diarrhea. Some viruses cause the insertion of molecules in the host cell membrane, which cause other host cells to attack it. The variations are diverse and fascinating.


Although the science of immunology is beyond the scope of this book, understanding the immune response to infection  is an important part of appreciating patho-genic mechanisms. In fact, one of the most important virulence attributes any pathogen can have is an ability to evade the immune response. Some pathogens attack the immune effector cells, and others undergo changes that confound the immune response. The old observation that there seems to be no immunity to gonorrhea turns out to be an example of the latter mechanism. Neisseria gonorrhoeae, the causative agent of gonorrhea, under-goes antigenic variation of important surface structures so rapidly that antibodies directed against the bacteria become irrelevant.

For each pathogen, the primary interest is whether there is natural immunity and, if so, whether it is based on humoral (antibody) or cell-mediated immunity (CMI). Humoral and CMI responses are broadly stimulated with most infections, but the specific response to a particular molecular structure is usually dominant in mediating immunity to reinfec-tion. For example, the repeated nature of strep throat (group A streptococcus) in child-hood is not due to antigenic variation as described above for gonorrhea. The antigen against which protective antibodies are directed (M protein) is stable but naturally exists in over 80 types. Each requires its own specific antibody. Knowing the molecule against which the protective immune response is directed is particularly important for devising preventive vaccines.

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