15 Microbial Mechanisms of Pathogenicity: Study Notes

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Microbial Mechanisms of Pathogenicity

Introduction

This chapter explores how microorganisms cause disease, focusing on the mechanisms by which pathogens enter, survive, and damage their hosts. Understanding these processes is essential for microbiology students to grasp the basis of infectious diseases and host-pathogen interactions.

How Microorganisms Enter a Host

Portals of Entry

Pathogens must enter the host through specific portals to initiate infection. The main portals of entry include:

Mucous membranes: Entry via respiratory, gastrointestinal, and genitourinary tracts. The respiratory tract is the most common portal (e.g., influenza, pneumonia).
Skin: Although unbroken skin is a strong barrier, some microbes enter through hair follicles or sweat gland ducts (e.g., trachoma, conjunctivitis).
Parenteral route: Microbes are deposited directly into tissues beneath the skin or mucous membranes via bites, cuts, or injections (e.g., tetanus, hepatitis viruses).

Illustration of a dog bite as a parenteral route of entry Diagram of skin layers showing microbial entry through hair follicles and sweat glands

ID50 and LD50

The virulence of a microbe is often measured by:

ID50 (Infectious Dose 50): The number of pathogen cells or virions required to cause infection in 50% of a test population.
LD50 (Lethal Dose 50): The amount of toxin required to kill 50% of a test population.

Lower ID50 or LD50 values indicate higher virulence or toxicity.

Poison bottle representing LD50 concept

Adherence to Host Tissues

Most pathogens must adhere to host tissues to establish infection. This process involves:

Adhesins (ligands): Surface molecules on pathogens that bind specifically to complementary receptors on host cells. Adhesins are often located on the glycocalyx or fimbriae.
If adherence is blocked, infection can often be prevented.

Diagram of pathogen adhesin binding to host cell receptor Diagram of bacterial cell with labeled fimbriae and glycocalyx

Biofilms

Microbes can form biofilms, which are communities of microorganisms attached to a surface and encased in a self-produced matrix. Biofilms enhance adherence and protect microbes from host defenses.

Examples: Dental plaque, algae on swimming pool walls.

Stages of biofilm formation: attachment, growth, dispersal

How Pathogens Penetrate Host Defenses

Capsules and Cell Wall Components

Some bacteria evade host defenses using:

Capsules: Glycocalyx layers that impair phagocytosis (e.g., Streptococcus pneumoniae).
Cell wall components:
- M protein: Resists phagocytosis (Streptococcus pyogenes).
- Opa protein: Aids attachment (Neisseria gonorrhoeae).
- Mycolic acid: Waxy lipid resists digestion (Mycobacterium tuberculosis).

Enzymes as Virulence Factors

Bacteria may secrete enzymes that facilitate invasion and damage:

Coagulases: Clot fibrinogen in blood.
Kinases: Digest fibrin clots.
Hyaluronidase: Digests polysaccharides holding cells together.
Collagenase: Breaks down collagen in connective tissue.
IgA proteases: Destroy IgA antibodies.

Diagram of bacterial enzymes acting on host tissues

Antigenic Variation

Some pathogens evade the immune system by altering their surface antigens, rendering antibodies ineffective. This process is called antigenic variation.

Diagram showing antigenic variation with new surface antigens

Penetration into Host Cells

Bacteria can invade host cells by manipulating the host cytoskeleton:

Invasins: Surface proteins that rearrange actin filaments, causing membrane ruffling (e.g., Salmonella entry).
Some bacteria use actin to move between cells (e.g., Shigella, Listeria).

SEM of Salmonella entering host cell via membrane ruffling Diagram of bacterial movement inside and between host cells using actin

Biofilms and Evasion of Phagocytosis

Biofilms protect bacteria from phagocytosis by shielding antigens and sometimes killing phagocytes with their extracellular polymeric substance (EPS).

Diagram of biofilm formation and EPS matrix

How Bacterial Pathogens Damage Host Cells

Mechanisms of Host Cell Damage

Pathogens damage host cells by:

Using host nutrients (e.g., iron via siderophores)
Direct damage (disrupting cell function, producing waste, causing cell rupture)
Producing toxins (exotoxins and endotoxins)
Inducing hypersensitive reactions

Siderophores

Siderophores are proteins secreted by pathogens to scavenge iron from the host, which is essential for bacterial growth.

Structure of enterobactin, a bacterial siderophore Diagram of siderophores binding iron and returning to bacterium

Toxins

Toxins are poisonous substances produced by microbes that can cause fever, shock, diarrhea, and other symptoms. The ability to produce toxins is called toxigenicity, and the presence of toxins in blood is toxemia.

Exotoxins

Exotoxins are proteins secreted by bacteria (mainly Gram-positive) that are highly potent and specific in their action. Genes for exotoxins are often carried on plasmids.

Diagram and SEM of exotoxin production and release

Antitoxins: Antibodies that neutralize exotoxins.
Toxoids: Inactivated exotoxins used in vaccines.

Tetanus antitoxin vaccine

Types of Exotoxins

A-B toxins: Consist of an active (A) and binding (B) component. Example: diphtheria toxin.
Membrane-disrupting toxins: Cause cell lysis by disrupting plasma membranes (e.g., hemolysins, leukocidins).
Superantigens: Trigger excessive immune responses, leading to fever, shock, and sometimes death.

Diagram of A-B toxin mechanism

Table: Diseases Caused by Exotoxins

Disease	Bacterium	Type of Exotoxin	Mechanism
Botulism	Clostridium botulinum	A-B	Neurotoxin prevents nerve impulse transmission; flaccid paralysis.
Tetanus	Clostridium tetani	A-B	Blocks muscle relaxation pathway; uncontrollable contractions.
Diphtheria	Corynebacterium diphtheriae	A-B	Inhibits protein synthesis in nerve, heart, kidney cells.
Toxic shock syndrome	Staphylococcus aureus	Superantigen	Causes fluid loss, low blood pressure.
Traveler’s diarrhea	E. coli, Shigella spp.	A-B	Enterotoxin causes diarrhea.

Endotoxins

Endotoxins are lipid components (Lipid A) of the outer membrane of Gram-negative bacteria. They are released when bacteria die and can cause fever, shock, and other systemic effects.

All endotoxins produce similar symptoms regardless of bacterial species.
Endotoxins are heat-stable and not easily neutralized by antitoxins.

Diagram of Gram-negative cell wall with endotoxin location Diagram of endotoxin-induced fever (pyrogenic response)

Table: Comparison of Exotoxins and Endotoxins

Property	Exotoxins	Endotoxins
Chemistry	Proteins (A-B structure)	Lipid A (LPS)
Source	Gram-positive & Gram-negative	Gram-negative only
Heat Stability	Unstable (destroyed at 60–80°C)	Stable (withstands 121°C)
Toxicity	High	Low
Fever-producing	No	Yes
Immunology	Can be neutralized by antitoxin	Not easily neutralized
Lethal Dose	Small	Large

Plasmids, Lysogeny, and Pathogenicity

Plasmids may carry genes for toxins, antibiotic resistance, and enzymes. Lysogenic conversion (integration of a prophage) can turn non-pathogenic bacteria into pathogens by introducing new virulence factors.

Pathogenic Properties of Viruses, Fungi, Protozoa, Helminths, and Algae

Pathogenic Properties of Viruses

Viruses cause disease through cytopathic effects (CPE), which are visible changes in host cells due to viral infection. Examples include:

Stopping cell synthesis
Causing lysosome release
Forming inclusion bodies
Fusing cells to form syncytia
Inducing chromosomal changes
Loss of contact inhibition (leading to cancer)

Micrograph of viral cytopathic effects: inclusion bodies and cytoplasmic mass

Alpha and beta interferons produced by infected cells protect neighboring cells by inhibiting viral protein synthesis and inducing apoptosis in infected cells.

Pathogenic Properties of Fungi

Fungi may cause disease by:

Producing toxic metabolic products (e.g., trichothecene toxins)
Provoking allergic responses
Producing proteases that modify host membranes
Forming capsules to evade phagocytosis
Producing mycotoxins (e.g., aflatoxin, ergot alkaloids, phalloidin, amanitin)

Diagram of fungal toxins and their effects

Pathogenic Properties of Protozoa

Protozoa cause symptoms by:

Digesting host cells and tissues
Growing inside phagocytes
Undergoing antigenic variation

Diagram of protozoa and their effects on host cells

Pathogenic Properties of Helminths

Helminths (parasitic worms) cause disease by:

Using host tissues for growth
Producing large masses that cause cellular damage
Releasing waste products that provoke symptoms

Image of lymphatic filariasis (elephantiasis) caused by nematode infection

Pathogenic Properties of Algae

Some algae produce neurotoxins, such as saxitoxin, which can cause paralytic shellfish poisoning (PSP). These toxins are heat-stable and not destroyed by cooking.

Diagram of shellfish poisoning due to algal toxins

Portals of Exit

Major Portals of Exit

Pathogens leave the host through specific portals, which often mirror the portals of entry:

Respiratory tract: Coughing and sneezing
Gastrointestinal tract: Feces and saliva
Genitourinary tract: Urine and genital secretions
Skin
Blood: Via arthropod bites or contaminated needles

Illustration of respiratory, gastrointestinal, and blood portals of exit

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