Infectious Diseases Quiz

Host-Pathogen Relationships

• Host-pathogen relationships involve the interaction between a host and a pathogen.
• Commensalism: one benefits, the other is unaffected. An example is Corynebacterium in the eyes.
• Mutualism: both benefit. An example is E. coli in the gut.
• Parasitism: one benefits, the other is harmed. An example is any pathogen.
• Pathogenicity depends on host susceptibility and pathogen virulence.

Chapter Overview

• Infectious diseases require basic concepts.
• Host-pathogen relationships determine portals of entry and virulence factors.
• Virulence factors facilitate disease establishment and maintenance.

Definitions

• Pathology: study of disease.
• Etiology: the cause of a disease.
• Pathogenesis: the development of a disease.
• Infection: colonization of a microbe.
• Disease: illness.
• Virulence: degree of pathogenicity.
• Bacteremia: presence of bacteria in the blood.
• Sepsis/Septicemia: body's inflammatory response to an infection.

Infection and Disease

• Infection: invasion by parasitic microbes. Infection doesn't always cause disease.
• HIV infection can lead to AIDS.
• Disease is a change in health, damage to the host.

Phases of Disease

• Incubation: the time between pathogen introduction and symptom onset (variable).
• Illness: experience of disease signs and symptoms.
• Convalescence: recovery period, potentially with pathogen spread.

Types of Disease

• Acute: organism disappears after illness, generally with immunity.
• Chronic: illness persists or recurs.
• Latent: illness may recur, if immunity weakens, after a period of no symptoms.

Sepsis

• Sepsis is a severe systemic inflammatory response to microbial invasion.
• The host response is as important as the pathogen's virulence.
• Bacteremia is critical for diagnosis, however the host's response is the key driver of outcome.

Microbiome

• Microbiome: the community of microorganisms routinely found on a healthy individual.
• Humans have more microbes than stars.
• Most of the microbiome is located in the GI tract.
• The microbiome has significant influence on health and disease.

Opportunistic Pathogens

• Opportunistic pathogens usually do not cause disease.
• However, in certain circumstances, normal flora can cause disease. (In the wrong environment, such as a compromised immune system).
• E. coli in the urinary tract is an example.
• Weakened immunity, such as in AIDS, or conditions like pneumonia can cause opportunistic infections.

Pathogenic Microorganisms

• For disease to occur, a microbe must gain access and evade defenses.
• Possible entry points are mucous membranes, skin, and parenteral(punctures etc).
• The pathogen must then damage tissues.

Portals of Entry

• Respiratory tract: Microbes enter via inhaled moisture or dust particles, causing common cold, flu, tuberculosis, and whooping cough.
• Gastrointestinal tract: Microbes enter via contaminated food or water, causing salmonellosis, shigellosis, botulism, and cholera.
• Genitourinary tract: Sexually transmitted diseases (STDs) like gonorrhea, syphilis, chlamydia, and HIV.
• Conjunctiva: Common diseases include chlamydia and herpes ocularis.
• Skin: Some microbes enter through skin openings or damage, causing staphylococcal infections and mycosis.
• Parenteral: microbes enter through punctures, injections, bites, scratches, or surgery, causing diseases like hepatitis and HIV.

Factors That Determine Disease Establishment

• Pathogen entry does not always result in disease.
• Preferred portal of entry is important.
• Virulence factors (like toxins, or capsule) are essential considerations.

Steps for Pathogen Infection

• Step 1: Adherence: pathogens use pili or other structures to attach to host cells.
• Step 2: Invasion/Colonization: Pathogens multiply, gain nutrients, and evade host defenses (especially the immune system).
• Step 3: Cause Damage: Pathogens destroy tissues through toxins (such as exotoxins and endotoxins) and enzymes.

Virulence Factors

• Virulence factors are substances that promote and maintain disease.
• Types include adhesion factors, evasion of immune responses, degradative enzymes, and toxins.

Adhesion Factors

• Pili (fimbriae) are short, rigid, numerous protrusions.
• Adhesins bind to host receptors on tissues.

Evading Immune Response

• Encapsulation: prevents phagocytosis (by macrophages etc).
• Antigenic mimicry: pathogens resemble host cells.
• Antigenic shift: change in pathogen proteins (antigens) that causes antibody ineffectiveness.
• Inhibition of phagolysosome fusion: inhibits the pathogen from being destroyed.
• Immunoglobulin protease production
• Destruction of phagocyte
• Inhibition of chemotaxis
• Resistance to lysosomal enzymes
• Intracellular replication

Degradative Enzymes

• Leukocidins: kill white blood cells, preventing phagocytosis, (and preventing the host's defense mechanisms from functioning appropriately).
• Hemolysins: cause lysis (breakdown) of red blood cells.
• Coagulase: causes blood clotting, protecting bacteria from phagocytes.
• Kinases: dissolve blood clots, enabling pathogen spread.
• Hyaluronidase: breaks down hyaluronic acid, enabling pathogen spread through tissues.
• Collagenase: breaks down collagen, enabling pathogen spread through tissues.
• Necrotizing factors: cause tissue death.

Toxins

• Toxins are poisonous substances.
• Exotoxins are secreted, heat labile, and may or may not be able to produce an antitoxin.
• Endotoxins (part of cell wall) are similar among species, cause similar symptoms, and are difficult to neutralize.
• Toxemia: toxins in the blood stream causing disease.

Classification of Exotoxins

• Leukotoxins: target white blood cells.
• Cytotoxins: damage host cells (eg., kill).
• Neurotoxins: target nervous system.
• Enterotoxins: target the digestive system.
• Hepatotoxins: target the liver.
• Cardiotoxins: target the heart.

Leukotoxins: Superantigens

• Invoke very strong immune responses.
• Affect T cells, causing severe symptoms

Cytotoxins: Membrane Disrupting Toxins

• Disrupt host plasma membranes (via impacting phospholipids or protein structures).
• Examples include toxins that target RBCs or phagocytes.

Neurotoxins: A-B Toxins

• Toxins of Clostridium botulinum and Clostridium tetani affect neuromuscular transmission; including blocking/stimulating nerve activity.

###Endotoxins

• Component of the outer membrane of Gram-negative bacteria.
• Cause similar symptoms in various species.
• Not easily deactivated.
• Induce excessive/destructive host immune responses.
• Induce TNF release from macrophages.

Endotoxin Symptoms

• Pyrogenic (fever) response: Interleukin-1 prompts prostaglandin release from the hypothalamus.
• Leukopenia followed by leukocytosis – white blood cell abnormalities
• Activation of complement: complement proteins are involved in host immune defenses.
• Thrombocytopenia: abnormal decrease in platelets.
• Disseminated Intravascular Coagulation (DIC): widespread clotting.
• Shock and death.

Host Susceptibility/Resistance

• Factors influencing the host's susceptibility/resistance to infection include age, pre-existing conditions, diet, hygiene, and behavior.
• Stress factors such as weather, can also affect the susceptibility to pathogens.