Epidemiology & Pathogenicity Notes

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Principles of Disease and Epidemiology

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Learning Objective	Check Your Understanding
14-1 Define pathology , etiology , infection , and disease .	What are the objectives of pathology?
14-2 Define normal microbiota and transient microbiota .	How do normal microbiota differ from transient microbiota?
14-3 Compare commensalism, mutualism, and parasitism, and give an example of each.	Give several examples of microbial antagonism.
14-4 Contrast normal microbiota and transient microbiota with opportunistic microorganisms.	How can opportunistic pathogens cause infections?
14-5 List Koch’s postulates.	Explain some exceptions to Koch’s postulates.
14-6 Differentiate a communicable from a noncommunicable disease.	Does Clostridium perfringens (page 652) cause a communicable disease?
14-7 Categorize diseases according to frequency of occurrence.	Distinguish the incidence from the prevalence of a disease.
14-8 Categorize diseases according to severity.	List two examples of acute and chronic diseases.
14-9 Define herd immunity .	How does herd immunity develop?
14-10 Identify four predisposing factors for disease.	What is a predisposing factor?
14-11 Put the following in proper sequence according to the pattern of disease: period of decline, period of convalescence, period of illness, prodromal period, incubation period.	The incubation period for a cold is 3 days, and the period of disease is usually 5 days. If the person next to you has a cold, when will you know whether you contracted it?
14-12 Define reservoir of infection.	Why are carriers important reservoirs of infection?
14-13 Contrast human, animal, and nonliving reservoirs, and give one example of each.	How are zoonoses transmitted to humans?
14-14 Explain three methods of disease transmission.	Give an example of contact transmission, vehicle transmission, mechanical transmission, and biological transmission.
14-15 Define healthcare-associated infections and explain their importance.	What interacting factors result in nosocomial infections?
14-16 Define compromised host .	What is a compromised host?
14-17 List several methods of disease transmission in hospitals.	How are nosocomial infections primarily transmitted, and how can they be prevented?
14-18 Explain how healthcare-associated infections can be prevented.
14-19 List several probable reasons for emerging infectious diseases, and name one example for each reason.	Give several examples of emerging infectious diseases.
14-20 Define epidemiology , and describe three types of epidemiologic investigations.	After learning that 40 hospital employees developed nausea and vomiting, the hospital infection control officer determined that 39 ill people ate green beans in the hospital cafeteria, compared to 34 healthy people who ate in the cafeteria the same day but did not eat green beans in the hospital cafeteria. What type of epidemiology is this?
14-21 Identify the function of the CDC.	What is the CDC’s function?
14-22 Define the following terms: morbidity , mortality , and notifiable infectious diseases.	In 2003, the morbidity of hemolytic uremic syndrome was 176, and the mortality was 29. The morbidity of listeriosis was 696; the mortality was 33. Which disease is more likely to be fatal?

Chapter Summary

Introduction (p. 389)

Disease-causing microorganisms are called pathogens.
Pathogenic microorganisms have special properties that allow them to invade the human body or produce toxins.
When a microorganism overcomes the body’s defenses, a state of disease results.

Pathology, Infection, and Disease (p. 390)

Pathology is the scientific study of disease.
Pathology is concerned with the etiology (cause), pathogenesis (development), and effects of disease.
Infection is the invasion and growth of pathogens in the body.
A host is an organism that shelters and supports the growth of pathogens.
Disease is an abnormal state in which part or all of the body is not properly adjusted or is incapable of performing normal functions.

Normal Microbiota (pp. 390–394)

ASM 5.4: Microorganisms, cellular and viral, can interact with both human and non-human hosts in beneficial, neutral, or detrimental ways.

Animals, including humans, are usually germ-free in utero.
Microorganisms begin colonization in and on the surface of the body soon after birth.
Microorganisms that establish permanent colonies inside or on the body without producing disease make up the normal microbiota.
Transient microbiota are microbes that are present for various periods and then disappear.

Relationships Between the Normal Microbiota and the Host (pp. 391–393)

The normal microbiota can prevent pathogens from causing an infection; this phenomenon is known as microbial antagonism.
Normal microbiota and the host exist in symbiosis (living together).
The three types of symbiosis are commensalism (one organism benefits, and the other is unaffected), mutualism (both organisms benefit), and parasitism (one organism benefits, and one is harmed).

Opportunistic Microorganisms (p. 393)

Opportunistic pathogens do not cause disease under normal conditions but cause disease under special conditions.

Cooperation among Microorganisms (pp. 393–394)

In some situations, one microorganism makes it possible for another to cause a disease or produce more severe symptoms.

The Etiology of Infectious Diseases (pp. 394–395)

Koch’s Postulates (p. 394)

Koch’s postulates are criteria for establishing that specific microbes cause specific diseases.
Koch’s postulates have the following requirements: (1) the same pathogen must be present in every case of the disease; (2) the pathogen must be isolated in pure culture; (3) the pathogen isolated from pure culture must cause the same disease in a healthy, susceptible laboratory animal; and (4) the pathogen must be re-isolated from the inoculated laboratory animal.

Exceptions to Koch’s Postulates (pp. 394–395)

Koch’s postulates are modified to establish etiologies of diseases caused by viruses and some bacteria, which cannot be grown on artificial media.
Some diseases, such as tetanus, have unequivocal signs and symptoms.
Some diseases, such as pneumonia and nephritis, may be caused by a variety of microbes.
Some pathogens, such as S. pyogenes, cause several different diseases.
Certain pathogens, such as HIV, cause disease in humans only.

Classifying Infectious Diseases (pp. 395–397)

A patient may exhibit symptoms (subjective changes in body functions) and signs (measurable changes), which a physician uses to make a diagnosis (identification of the disease).
A specific group of symptoms or signs that always accompanies a specific disease is called a syndrome.
Communicable diseases are transmitted directly or indirectly from one host to another.
A contagious disease is one that is easily spread from one person to another.
Noncommunicable diseases are caused by microorganisms that normally grow outside the human body and are not transmitted from one host to another.

Occurrence of a Disease (p. 396)

Disease occurrence is reported by incidence (number of people contracting the disease) and prevalence (number of cases at a particular time).
Diseases are classified by frequency of occurrence: sporadic, endemic, epidemic, and pandemic.

Severity or Duration of a Disease (pp. 396–397)

The scope of a disease can be defined as acute, chronic, subacute, or latent.
Herd immunity is the presence of immunity to a disease in most of the population.

Extent of Host Involvement (p. 397)

A local infection affects a small area of the body; a systemic infection is spread throughout the body via the circulatory system.
A primary infection is an acute infection that causes the initial illness.
A secondary infection can occur after the host is weakened from a primary infection.
An inapparent, or subclinical, infection does not cause any signs of disease in the host.

Patterns of Disease (pp. 397–398)

Predisposing Factors (pp. 397–398)

A predisposing factor is one that makes the body more susceptible to disease or alters the course of a disease.
Examples include gender, climate, age, fatigue, and inadequate nutrition.

Development of Disease (p. 398)

The incubation period is the interval between the initial infection and the first appearance of signs and symptoms.
The prodromal period is characterized by the appearance of the first mild signs and symptoms.
During the period of illness, the disease is at its height, and all disease signs and symptoms are apparent.
During the period of decline, the signs and symptoms subside.
During the period of convalescence, the body returns to its prediseased state, and health is restored.

The Spread of Infection (pp. 398–402)

Reservoirs of Infection (pp. 398–399)

A continual source of infection is called a reservoir of infection.
People who have a disease or are carriers of pathogenic microorganisms are human reservoirs of infection.
Zoonoses are diseases that affect wild and domestic animals and can be transmitted to humans.
Some pathogenic microorganisms grow in nonliving reservoirs, such as soil and water.

Transmission of Disease (pp. 399–402)

Transmission by direct contact involves close physical contact between the source of the disease and a susceptible host.
Transmission by fomites (inanimate objects) constitutes indirect contact.
Transmission via saliva or mucus in coughing or sneezing is called droplet transmission.
Transmission by a medium such as water, food, or air is called vehicle transmission.
Airborne transmission refers to pathogens carried on water droplets or dust for a distance greater than 1 meter.
Arthropod vectors carry pathogens from one host to another by both mechanical and biological transmission.

Healthcare-Associated Infections (HAIs) (pp. 402–404)

Healthcare-associated infections include those acquired in settings such as hospitals, nursing homes, surgical centers, and healthcare clinics.
About 5–15% of all hospitalized patients acquire HAIs in the treatment environment.

Microorganisms in the Hospital (pp. 402–405)

Certain normal microbiota are often responsible for HAIs when they are introduced into the body through such medical procedures as surgery and catheterization.
Opportunistic bacteria are the most frequent causes of HAIs.

Compromised Host (p. 404)

Patients with burns, surgical wounds, and suppressed immune systems are the most susceptible to HAIs.

Chain of Transmission (pp. 404–405)

HAIs are transmitted by direct contact between staff members and patients and between patients.
Fomites such as catheters, syringes, and respiratory devices can transmit HAIs.

Control of Healthcare-Associated Infections (p. 405)

Aseptic techniques can prevent HAIs.
Hospital infection control staff members are responsible for overseeing the proper cleaning, storage, and handling of equipment and supplies.

Emerging Infectious Diseases (pp. 405–407)

ASM 1.3: Human impact on the environment influences the evolution of microorganisms (e.g., emerging diseases and the selection of antibiotic resistance).

New diseases and diseases with increasing incidences are called emerging infectious diseases (EIDs).
EIDs can result from the use of antibiotics and pesticides, climatic changes, travel, the lack of vaccinations, and improved case reporting.
The CDC, NIH, and WHO are responsible for surveillance and responses to emerging infectious diseases.

Epidemiology (pp. 407–412)

The science of epidemiology is the study of the transmission, incidence, and frequency of disease.
Modern epidemiology began in the mid-1800s with the works of Snow, Semmelweis, and Nightingale.
In descriptive epidemiology, data about infected people are collected and analyzed.
In analytical epidemiology, a group of infected people is compared with an uninfected group.
In experimental epidemiology, controlled experiments designed to test hypotheses are performed.
Case reporting provides data on incidence and prevalence to local, state, and national health officials.
The Centers for Disease Control and Prevention (CDC) is the main source of epidemiological information in the United States.
The CDC publishes the Morbidity and Mortality Weekly Report to provide information on morbidity (incidence) and mortality (deaths).

Microbial Mechanisms of Pathogenicity

Learning Objective	Check Your Understanding
15-1 Identify the principal portals of entry.	List three portals of entry, and describe how microorganisms gain access through each.
15-2 Define ID ₅₀ and LD ₅₀ .	The LD₅₀of botulinum toxin is 0.03 ng/kg; the LD₅₀ of Salmonella toxin is 12 mg/kg. Which is the more potent toxin?
15-3 Using examples, explain how microbes adhere to host cells.	How would a drug that binds mannose on human cells affect a pathogenic bacterium?
15-4 Explain how capsules and cell wall components contribute to pathogenicity.	What function do capsules and M proteins have in common?
15-5 Compare the effects of coagulases, kinases, hyaluronidase, and collagenase.	Would you expect a bacterium to make coagulase and kinase simultaneously?
15-6 Define and give an example of antigenic variation.	Many vaccines provide years of protection against a disease. Why doesn’t the influenza vaccine offer more than a few months of protection?
15-7 Describe how bacteria use the host cell’s cytoskeleton to enter the cell.	How does E. coli cause membrane ruffling?
15-8 Describe the function of siderophores.	Of what value are siderophores?
15-9 Provide an example of direct damage, and compare this to toxin production.	How does toxigenicity differ from direct damage?
15-10 Contrast the nature and effects of exotoxins and endotoxins.	Differentiate an exotoxin from an endotoxin.
15-11 Outline the mechanisms of action of A-B toxins, membrane-disrupting toxins, and superantigens.	Food poisoning can be divided into two categories: food infection and food intoxication. On the basis of toxin production by bacteria, explain the difference between these two categories.
15-12 Identify the importance of the LAL assay.	Wash water containing Pseudomonas was sterilized and used to wash cardiac catheters. Three patients developed fever, chills, and hypotension following cardiac catheterization. The water and catheters were sterile. Why did the patients show these reactions? How should the water have been tested?
15-13 Using examples, describe the roles of plasmids and lysogeny in pathogenicity.	How can lysogeny turn the normally harmless E. coli into a pathogen?
15-14 List nine cytopathic effects of viral infections.	Define cytopathic effects , and give five examples.
15-15 Discuss the causes of symptoms in fungal, protozoan, helminthic, and algal diseases.	Identify one virulence factor that contributes to the pathogenicity of each of the following: fungi, protozoa, helminths, and algae.
15-16 Differentiate portal of entry and portal of exit.	Which are the most often used portals of exit?

Chapter Summary

Introduction (p. 417)

ASM 2.3: Bacteria and Archaea have specialized structures (e.g., flagella, endospores, and pili) that often confer critical capabilities.

ASM 5.4: Microorganisms, cellular and viral, can interact with both human and non-human hosts in beneficial, neutral, or detrimental ways.

Pathogenicity is the ability of a pathogen to produce a disease by overcoming the defenses of the host.
Virulence is the degree of pathogenicity.

How Microorganisms Enter a Host (pp. 418–421)

The specific route by which a particular pathogen gains access to the body is called its portal of entry.

Portals of Entry (pp. 418–419)

Many microorganisms can penetrate mucous membranes of the conjunctiva and the respiratory, gastrointestinal, and genitourinary tracts.
Most microorganisms cannot penetrate intact skin; they enter hair follicles and sweat ducts.
Some microorganisms can gain access to tissues by inoculation through the skin and mucous membranes in bites, injections, and other wounds. This route of penetration is called the parenteral route.

The Preferred Portal of Entry (p. 419)

Many microorganisms can cause infections only when they gain access through their specific portal of entry.

Numbers of Invading Microbes (p. 420)

Virulence can be expressed as LD₅₀ (lethal dose for 50% of the inoculated hosts) or ID₅₀ (infectious dose for 50% of the inoculated hosts).

Adherence (pp. 420–421)

Surface projections on a pathogen called adhesins (ligands) adhere to complementary receptors on the host cells.
Adhesins can be glycoproteins or lipoproteins and are frequently associated with fimbriae.
Mannose is the most common receptor.
Biofilms provide attachment and resistance to antimicrobial agents.

How Bacterial Pathogens Penetrate Host Defenses (pp. 421–423)

Capsules (p. 421)

Some pathogens have capsules that prevent them from being phagocytized.

Cell Wall Components (p. 421)

Proteins in the cell wall can facilitate adherence or prevent a pathogen from being phagocytized.

Enzymes (pp. 421–423)

Local infections can be protected in a fibrin clot caused by the bacterial enzyme coagulase.
Bacteria can spread from a focal infection by means of kinases (which destroy blood clots), hyaluronidase (which destroys a mucopolysaccharide that holds cells together), and collagenase (which hydrolyzes connective tissue collagen).
IgA proteases destroy IgA antibodies.

Antigenic Variation (p. 423)

Some microbes vary expression of antigens, thus avoiding the host’s antibodies.

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Penetration into the Host Cell Cytoskeleton (p. 423)

Bacteria may produce proteins that alter the actin of the host cell’s cytoskeleton, allowing bacteria into the cell.

How Bacterial Pathogens Damage Host Cells (pp. 424–430)

Using the Host’s Nutrients: Siderophores (p. 424)

Bacteria get iron from the host using siderophores.

Direct Damage (p. 424)

Host cells can be destroyed when pathogens metabolize and multiply inside the host cells.

The Production of Toxins (pp. 424–429)

Poisonous substances produced by microorganisms are called toxins; toxemia refers to the presence of toxins in the blood. The ability to produce toxins is called toxigenicity.
Exotoxins are produced by bacteria and released into the surrounding medium. Exotoxins, not the bacteria, produce the disease symptoms.
Antibodies produced against exotoxins are called antitoxins.
A-B toxins consist of an active component that inhibits a cellular process and a binding component that attaches the two portions to the target cell; e.g., diphtheria toxin.
Membrane-disrupting toxins cause cell lysis; e.g., hemolysins.
Superantigens cause release of cytokines, which cause fever, nausea, and other symptoms; e.g., toxic shock syndrome toxin.
Endotoxins are lipopolysaccharides (LPS), the lipid A component of the cell wall of gram-negative bacteria.
Bacterial cell death, antibiotics, and antibodies may cause the release of endotoxins.
Endotoxins cause fever (by inducing the release of interleukin-1) and shock (because of a TNF-induced decrease in blood pressure).
Endotoxins allow bacteria to cross the blood–brain barrier.
The Limulus amobocyte lysate (LAL) assay is used to detect endotoxins in drugs and on medical devices.

Plasmids, Lysogeny, and Pathogenicity (p. 430)

Plasmids may carry genes for antibiotic resistance, toxins, capsules, and fimbriae.
Lysogenic conversion can result in bacteria with virulence factors, such as toxins or capsules.

Pathogenic Properties of Viruses (pp. 430–432)

Viruses avoid the host’s immune response by growing inside cells.
Viruses gain access to host cells because they have attachment sites for receptors on the host cell.
Visible signs of viral infections are called cytopathic effects (CPE).
Some viruses cause cytocidal effects (cell death), and others cause noncytocidal effects (damage but not death).
Cytopathic effects include stopping mitosis, lysis, formation of inclusion bodies, cell fusion, antigenic changes, chromosomal changes, and transformation.

Pathogenic Properties of Fungi, Protozoa, Helminths, and Algae (pp. 432–433)

Symptoms of fungal infections can be caused by capsules, toxins, and allergic responses.
Symptoms of protozoan and helminthic diseases can be caused by damage to host tissue or by the metabolic waste products of the parasite.
Some protozoa change their surface antigens while growing in a host, thus avoiding destruction by the host’s antibodies.
Some algae produce neurotoxins that cause paralysis when ingested by humans.

Portals of Exit (pp. 433–435)

Pathogens have definite portals of exit.
Three common portals of exit are the respiratory tract via coughing or sneezing, the gastrointestinal tract via saliva or feces, and the genitourinary tract via secretions from the vagina or penis.
Arthropods and syringes provide a portal of exit for microbes in blood.

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