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29 Symbiotic Associations: Parasitism, Pathogenicity, and Resistance

 

CHAPTER OVERVIEW

This chapter continues the discussion of symbiosis and focuses on parasitism. One of the possible consequences of parasitismCpathogenicityCis also discussed. Most higher animals, including man, possess various defense mechanisms that are employed against parasitic, pathogenic organisms. Some of these are general, nonspecific mechanisms for resistance and are discussed in this chapter. Other more specific mechanisms associated with the immune system are discussed in subsequent chapters.

 

CHAPTER OBJECTIVES

After reading this chapter you should be able to:

! discuss the general characteristics of parasitic symbiosis

! discuss the concepts of pathogens, disease, and infection

! describe the stages which pathogens must go throughCtransmission, colonization, multiplication, and interferenceCin order to cause disease

! discuss the general, physical, chemical, and biological barriers that organisms have for defending themselves against continual parasitic invasion

 

CHAPTER OUTLINE

I. Introduction

A. Parasitism has evolved in nearly all groups of microorganisms

B. There are more parasitic organisms than nonparasitic organisms

II. Host-Parasite Relationships (Parasitism)

A. ParasitismCa relationship in which a symbiont harms or lives at the expense of a host

B. HostCthe body of the animal in which the parasite lives; it provides the microenvironment that shelters and supports the growth and multiplication of the parasitic organism

C. ParasiteCusually the smaller of the two organisms; it is metabolically dependent on the host

D. EctoparasiteClives on the surface of the host

E. EndoparasiteClives within the host

F. Final hostCthe host on (or in) which the parasite either gains sexual maturity or reproduces

G. Intermediate hostCa host that serves as a temporary but essential environment for parasite development

H. Transfer hostCa host that is not necessary for development but that serves as a vehicle for reaching the final host

I. Reservoir hostCan organism (other than a human) that is infected with a parasite that can also infect humans

J. InfectionCthe state occurring when a parasite is growing and multiplying on or within a host

K. Infectious diseaseCa change from a state of health as a result of an infection by a parasitic organism

L. PathogenCany parasitic organism that produces an infectious disease

M. PathogenicityCthe ability of a parasitic organism to cause a disease

N. VirulenceCthe degree or intensity of pathogenicity of an organism; it is determined by three characteristics of the pathogen:

1. InvasivenessCthe ability of the organism to spread to adjacent tissues

2. InfectivityCthe ability of the organism to establish a focal point of infection

3. Pathogenic potentialCthe degree to which the pathogen can cause morbid symptoms (e.g., toxigenicity)

O. The final outcome of most host-parasite relationships is dependent on three main factors:

1. The number of pathogenic organisms present

2. The virulence of the organism

3. The host=s defenses or degree of resistance

P. Endogenous diseaseCa disease caused by the host=s own microbiota because the host=s resistance has dropped

III. Determinants of Infectious Diseases

A. Transmissibility of the pathogenCinvolves initial transport to the host

1. Direct contactCcoughing, sneezing, body contact

2. Indirect contactCsoil, water, food

3. VectorsCliving organisms that transmit a pathogen

4. FomitesCinanimate objects contaminated with a pathogen that spread the pathogen

B. Attachment and colonization (multiplication) by the pathogen

1. Pathogen must be able to adhere to and colonize host cells and tissue; this is mediated by special molecules or structures called adhesins

2. Pathogen must compete with normal microbiota for essential nutrients

C. Invasion of the pathogen

1. Penetration of the host=s epithelial cells or tissues

a. Pathogen-associated mechanisms involve the production of lytic substances that may:

(1) Attack the ground substance and basement membranes of integuments and intestinal linings

(2) Depolymerize carbohydrate-protein complexes between cells or on cell surfaces

(3) Disrupt cell surfaces

b. Passive mechanisms of entry involve:

(1) Breaks, lesions, or ulcers in the mucous membranes

(2) Wounds, abrasions, or burns on the skin surface

(3) Arthropod vectors that penetrate when feeding

(4) Tissue damage caused by other organisms

(5) Endocytosis by host cells

2. Gaining of access to deeper tissues

3. Penetration into the circulatory system

D. Growth and multiplication of the pathogenCpathogen must find an appropriate environment

E. ToxigenicityCthe capacity of an organism to produce a toxin

1. IntoxicationsCdiseases that result from the entry of a specific toxin into the host

2. ToxinCa specific substance, often a metabolic product of the organism, that damages the host in some specified manner

3. ToxemiaCsymptoms caused by toxins in the blood of the host

4. ExotoxinsCsoluble, heat-labile proteins produced by and released from an organism; may damage the host at some remote site

a. Neurotoxins damage nervous tissue

b. Enterotoxins damage the small intestine

c. Cytotoxins do general tissue damage

5. EndotoxinsCmolecules that are part of the cell wall of the pathogen

a. Released only when the microorganism, whose cell wall contains it, lyses or during bacterial multiplication

b. One of the best characterized is lipopolysaccharide (LPS), which is part of the cell wall of gram-negative bacteria

c. Usually capable of producing fever, shock, blood coagulation, weakness, diarrhea, inflammation, intestinal hemorrhage, and/or fibrinolysis

d. Stimulates fever directly by acting as an exogenous pyrogen; also may stimulate fever indirectly by causing macrophages to release interleukin-1, an endogenous pyrogen

e. May affect macrophages and monocytes by binding to special LPS-binding proteins in the plasma that, in turn, bind to receptors on the macrophages and monocytes triggering cytokine release that produces endotoxin effects

6. LeukocidinsCextracellular enzymes that kill phagocytic leukocytes

7. HemolysinsCextracellular enzymes that kill erythrocytes

IV. General or Nonspecific Host Immune Defense MechanismsCmechanisms designed to prevent infection; can be general, physical, chemical, or biological

A. General barriers

1. NutritionCthe more malnourished the host, the greater the susceptibility to infection

2. Acute-phase reactantsCduring an acute infection by one organism, qualitative and quantitative changes in the host=s blood can increase or decrease the virulence of another organism or the defense capabilities of the host

3. FeverCelevated body temperature; usually induced by exogenous or endogenous pyrogens

a. Stimulates leukocytes into action

b. Enhances microbiostasis (growth inhibition) by decreasing availability of iron

c. Enhances specific activity of the immune system

4. AgeCthe very young and the very old are more susceptible

5. Genetic factorsCinclude host temperature; metabolic, physiologic, and anatomic differences; and food procurement abilities

B. Physical barriers

1. Skin and mucous membranes

a. SkinCreasonably effective mechanical barrier

b. Mucous membranesCmucus secretions form a protective covering that contains antibacterial substances, such as lysozyme

2. Respiratory systemCaerodynamic filtration deposits organisms onto mucosal surfaces, and mucociliary blanket transports them away from the lungs

3. Gastrointestinal tract and enzymes

a. StomachCgastric acid

b. Small intestineCpancreatic enzymes, bile, intestinal enzymes, and secretory IgA

c. Peristalsis and loss of columnar epithelial cells help eliminate pathogens

d. Large intestineCnormal microbiota may create unfavorable environment for colonization

4. Genitourinary tract

a. Unfavorable environment (e.g., acid pH in the vagina)

b. Flushing action

c. Length of urethra in males constitutes a distance barrier

5. The eyeCflushing action, lysozyme, and other antibacterial substances

C. Chemical barriers

1. Gastric juices, salivary glyco-proteins, lysozyme, oleic acid on the skin, urea (already discussed)

2. FibronectinCglycoprotein that reacts with bacteria to promote clearance, or with host cell receptors to prevent attachment

3. HormonesCaffect inflammatory response and immune system activity; have cyclical effects on vaginal microbiota

4. Beta-lysin and other polypeptidesCmay lyse or otherwise damage specific types of microorganisms

5. InterferonsCrespond to viruses and other inducing agents to reduce the spread of viruses to neighboring cells

6. Tumor necrosis factors (I and J)Creleased from monocytes or macrophages, natural killer cells or various lymphocytes mediate the inflammatory response, enhance phagocytosis, and TNFX is cytotoxic for tumor cells

7. BacteriocinsCplasmid-encoded antibacterial substances produced by the normal microbiota of the body

D. Biological barriers

1. Normal indigenous microbiota may be involved in the following ways:

a. Bacteriocin production

b. Competition for space and nutrients

c. Prevention of pathogen attachment

d. Influence on specific clearing mechanisms

2. Inflammation

a. Response to tissue injury through the release of chemical signals (inflammatory mediators)

b. Interaction of selectins on vascular endothelial surface and integrins on neutrophil surface; promotes neutrophil extravasation

c. Involves neutralization and elimination of the offending pathogen, usually by phagocytosis and fibrin formation, which walls off the inflamed area

d. Characterized by redness, heat, pain, swelling, and altered function

3. Phagocytosis

a. Phagocytic cells arriving at the site of inflammation attach and phagocytize infecting organisms

b. Recognition is mediated through surface receptors that allow them to attach nonspecifically to a variety of organisms

c. May damage the pathogen by respiratory burst (formation of highly reactive, toxic oxygen products, such as superoxides and peroxides)

d. Phagosomes may fuse with lysosomes and thereby hydrolyze the invading organism

e. Neutrophils also release defensins, a family of broad spectrum antimicrobial peptides


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