Symbiosis, Infection, and Immunity: A Comprehensive Guide

Posted on Aug 6, 2024 in Biology

Symbiosis: Types and Examples

Symbiosis refers to the close and long-term interaction between two different species. There are four main types of symbiosis:

• Mutualism: Both species benefit from the interaction. Example: Bacteria in the human colon provide nutrients to the host, while the host provides a protective environment for the bacteria.
• Commensalism: One species benefits without significantly affecting the other. Example: Microscopic animals called hair follicle mites live on human skin without causing harm.
• Amensalism: One species is harmed by the other, while the other is neither harmed nor helped. Example: The fungus Penicillium produces penicillin, which inhibits nearby bacteria.
• Parasitism: A parasite derives benefit from its host while harming it. Example: Tuberculosis bacteria in human lungs.

Parasites: Types and Characteristics

Parasites are organisms that live on or within another organism (the host) and derive nutrients at the host’s expense. Parasites can be categorized into:

• Endoparasites: Live inside the host (e.g., tapeworms in animal intestines).
• Ectoparasites: Live on the host’s surface (e.g., lice on mammal skin).

Microbiota: Resident and Transient

Resident microbiota are permanent members of the microbiome found on the skin and mucous membranes of the digestive tract, upper respiratory tract, urethra, and vagina. Most are commensal, feeding on excreted cellular waste. Examples: Fusobacterium (urinary tract), Actinomyces (upper digestive tract), Bacteroides (lower digestive tract).

Transient microbiota are temporary residents that come and go. They may include potential pathogens or benign microorganisms. Factors influencing transient microbiota include diet, hygiene, and exposure to different environments.

Conditions for Normal Microbiota to Cause Disease

Three conditions can create opportunities for normal microbiota to cause disease:

• Immunosuppression
• Disruption of normal flora
• Changes in environment

Reservoirs of Infection in Humans

There are three main types of reservoirs of infection in humans:

• Human reservoirs: Infected individuals who may or may not show symptoms can serve as reservoirs for pathogens.
• Animal reservoirs (zoonoses): Animals can harbor pathogens that can be transmitted to humans. Examples: Rabies from dogs, Hantavirus from rodents, avian influenza from birds.
• Environmental reservoirs: Certain pathogens can survive in non-living environments such as soil, water, or surfaces. Example: Clostridium tetani, the causative agent of tetanus, can persist in soil.

Portals of Pathogen Invasion

Pathogens can invade the body through various portals:

• Skin: Intact skin is a formidable barrier, but pathogens can enter through cuts, abrasions, or insect bites.
• Mucous membranes: Found in the respiratory, gastrointestinal, and urogenital tracts. Pathogens can enter the body via inhalation, ingestion, etc.
• Placenta: Certain pathogens can cross the placental barrier from mother to fetus, potentially causing congenital infections.
• Parenteral route: Pathogens can be introduced directly into tissues through punctures or injections, bypassing usual barriers.

Adhesion Factors and Their Role in Infection

Adhesion factors play a crucial role in infection. They enable pathogens to attach to host cells, which is a critical step in colonization and infection establishment.

• Viruses and bacteria use surface lipoproteins or glycoproteins, called ligands, to bind to complementary receptors on host cells.
• In bacteria, these ligands are known as adhesins, found on fimbriae, flagella, and glycocalyces.
• Host cell receptors are typically glycoproteins, such as mannose or galactose.
• Blocking or altering ligands or receptors can prevent infection.
• Bacteria and viruses that lose the ability to produce ligands become avirulent (harmless).

Biofilms: Facilitating Contamination and Infection

A biofilm is a structured community of microorganisms encapsulated in a self-produced extracellular matrix. They facilitate contamination and infection by:

• Providing a protective environment: The extracellular matrix shields microbes from antibiotics and the immune system.
• Enabling communication: Microorganisms within a biofilm can communicate through quorum sensing.
• Promoting persistent infections: Biofilms can harbor persistent cells that are resistant to treatment, leading to chronic infections.

Infection vs. Disease

Infection refers to the invasion of a pathogen. Infection does not always lead to disease. Disease results only if the pathogen multiplies sufficiently to adversely affect the body.

Morbidity, Pathogenicity, Virulence

• Morbidity: State of being diseased, any change from a state of health.
• Pathogenicity: The ability of a microorganism to cause disease. It indicates whether an organism can produce disease.
• Virulence: The degree of pathogenicity, or the severity of the disease caused by a pathogen.

Symptoms vs. Signs vs. Syndromes

• Symptoms: Subjective characteristics of a disease that can be felt by the patient alone (e.g., pain).
• Signs: Objective manifestations of disease that can be observed or measured by others.
• Syndromes: A collection of signs and symptoms that occur together and characterize a specific disease or condition.

Etiology and Koch’s Postulates

Etiology is the study of the cause or origin of a disease. It involves identifying the factors and mechanisms that lead to the development of a disease.

Koch’s Postulates are a set of criteria established by Robert Koch to identify the causative agent of a disease:

1. The microorganism must be present in all cases of the disease and absent in healthy individuals.
2. It must be isolated and grown in pure culture.
3. The cultured microorganism should cause disease in a healthy, susceptible host.
4. The microorganism must be re-isolated from the experimentally infected host and identified as the same as the original causative agent.

Microbial Extracellular Enzymes and Virulence

Microbial extracellular enzymes play a significant role in virulence by:

• Breaking down host tissues, facilitating invasion and spread of pathogens (e.g., hyaluronidase, collagenase).
• Producing toxins: Exotoxins are secreted, while endotoxins are components of the bacterial cell wall released upon lysis.
• Enabling adhesion: Adhesion factors allow pathogens to attach to host cells.
• Providing antiphagocytic factors: Help pathogens evade phagocytosis by immune cells (e.g., capsules that inhibit engulfment).

Stages of Infectious Diseases

. 1. Incubation Period: The time between exposure to the pathogen and the onset of symptoms. 2. Prodromal Period: The onset of mild, non-specific symptoms 3. Illness: symptoms are most severe. 4. Decline: symptoms begin to subside 5. Convalescence: recovery phase Contrast; Contact Transmission: Involves direct physical contact, indirect contact via fomites (objects or surfaces), or droplet transmission (coughing, sneezing).Vehicle Transmission: spread of pathogens through a medium such as water, food, or air.Vector Transmission: transfer of pathogens via a living organism (vector). Vectors can be mechanical (e.g., flies carrying pathogens on their bodies) or biological (e.g., mosquitoes transmitting malaria). Contrast: Droplet Transmission: spread of pathogens via large respiratory droplets expelled during coughing, sneezing, or talking. Airborne Transmission: spread of pathogens via smaller respiratory droplets or dust particles

Contrast Mechanical Vectors: transmit pathogens by carrying them on their body parts, without being infected themselves. Biological Vectors: transmit pathogens by being infected and playing a role in the pathogen’s life cycle. EX:mosquitoes are biological vectors for the malaria parasite.Classification schemes of infectious diseases: By Etiological Agent, By Body System Affected,By Mode of Transmission, By Duration. (Distinguish):Acute Diseases: rapid onset and a short duration, such as influenza.Subacute Diseases: less rapid onset than acute diseases not as prolonged as chronic diseases, such as subacute bacterial endocarditis.Chronic Diseases: slow onset and long duration, such as tuberculosis or hepatitis.Latent Diseases: pathogen remains dormant in the body and can reactivate, such as herpes.Distinguish: Communicable Diseases: transmitted from one individual to another, either directly or indirectly.Contagious Diseases: A subset of communicable diseases that are easily spread from person to person, through direct contact or respiratory droplets.Noncommunicable Diseases: not transmitted between individuals, often resulting from environmental factors Define: Epidemiology is the study of the distribution, determinants, and control of diseases and health-related events in populations. It aims to understand the patterns and causes of diseases to develop prevention and control strategies.ContrastIncidence: The number of new cases of a disease occurring in a specific population within a defined time period. It measures the risk of developing the disease.Prevalence: The total number of cases of a disease, both new and existing, in a specific population at a given point in time. Endemic: A disease that is consistently present in a specific geographic area or population.Sporadic: A disease that occurs infrequently and irregularly in a population.Epidemic: A sudden increase in the number of cases of a disease above what is normally expected in a specific area or population.Pandemic: An epidemic that spreads across multiple countries or continents, affecting a large number of people.Study diseases in populations.Descriptive Epidemiology: Involves collecting data on the time, place, and individuals affected by a disease to identify patterns and trends.Analytical Epidemiology: Focuses on identifying the causes and risk factors of diseases through observational studies, such as cohort or case-control studies.Experimental Epidemiology: Involves conducting controlled experiments to test hypotheses about the causes and prevention of diseases, often through clinical trials.

– Phagocytes of the epidermis are called: Dendritic cells

–The complement system involves: serum proteins involved in nonspecific defense

-The alternative complement activation pathway involves: factors B, D, and P

-Which of the complement fragments is inflammatory?: C3A, C4A, C5A

– The type of interferon present late in an infection is: gamma interferon.

– Antibodies function to: Mark invading organisms for destruction

–MHC class II molecules bind to exogenous antigens  and trigger helper T cells

– Rejection of a foreign skin graft is an example of: Cell mediated immune response

– Among the key molecules that control cell-mediated cytotoxicity are: Cytokines

– Which of the following lymphocytes predominates in blood? T CELLS 

-The major class of immunoglobulin found on the surfaces of the walls of the intestines and airways is secretory: IgA

– Which cells express MHC class I molecules in a patient? All nucleated cells

– Interferons : they do not protect the cell that secretes them, they stimulate the activity of macrophages AND they cause muscle aches, chills, and fever

– Which of the following is not targeted by a Toll-like receptor? a. lipid A b. eukaryotic flagellar protein c. single-stranded RNA d. lipoteichoic acid

– Toll-like receptors (TLRs) act to bind microbial proteins and polysaccharides. 

– Which of the following binds iron? a. lactoferrin b. siderophores c. transferrin d. all of the above

The first two lines of defense comprise innate immunity. A third line of defense is adaptive immunity

– The first line of defense includes the skin, composed of an outer epidermis and a deeper dermis. Dendritic cells of the epidermis devour pathogens. Competitive inhibition: the competition between the microbiome and potential pathogens, also contributes to the body’s first line of defense. Antimicrobial peptides (defensins) act against pathogens on the skin and mucous membranes and in neutrophils.

-The second line of defense includes cells (especially phagocytes), antimicrobial chemicals (Toll-like receptors, NOD proteins, interferons, complement, lysozyme, and antimicrobial peptides), and processes (phagocytosis, inflammation, and fever). Macrophages, neutrophils, and dendritic cells are phagocytic cells of the second line of defense.

– Opsonization, the coating of pathogens by proteins called opsonins, makes those pathogens more vulnerable to phagocytes. A phagocyte’s pseudopods then surround the microbe to form a sac called a phagosome, which fuses with a lysosome to form a phagolysosome, in which the pathogen is killed.

– Leukocytes can distinguish the body’s normal cells from foreign cells with receptor cells 

– Eosinophils and natural killer lymphocytes (NK cells) attack nonphagocytically, especially in the case of helminth infections and cancerous cells

– Microbial molecules called pathogen-associated molecular patterns (PAMPs) bind to Toll-like receptors (TLRs) on host cells’ membranes or to NOD proteins inside cells, triggering innate immune responses.

– Interferons (IFNs) are protein molecules that inhibit the spread of viral infections. Alpha interferons and beta interferons, which are released within hours of infection, trigger antiviral proteins (AVPs) to prevent viral reproduction in neighboring cells. Gamma interferons produced days after initial infection, activate macrophages and neutrophils.

– Complement system: set of proteins that act as chemotactic attractants, trigger inflammation and fever, and can effect the destruction of foreign cells via the formation of membrane attack complexes (MACs), which result in multiple, fatal holes in pathogens’ membranes. 

– The process of blood clotting triggers formation of bradykinin—a potent mediator of inflammation.

– Macrophages with Toll-like receptors or NOD proteins release prostaglandins and leukotrienes, which increase permeability of blood vessels. 

– Mast cells, basophils, and platelets release histamine when exposed to peptides from the complement system. 

– Fever results when chemicals called pyrogens, affect the hypothalamus in a way that causes it to reset body temperature

– Activated Tc cells reproduce to form memory T cells and more Tc progeny in a process called clonal expansion.

– Cytotoxic T cells destroy their target cells via two pathways: the perforin-granzyme pathway, which kills the affected cells by secreting perforins and granzymes; or the CD95 pathway, in which CD95L binds to CD95 on the target cell, triggering target cell apoptosis. Cytotoxic T cells may also form memory T cells, which function in memory responses.

– Innate immunity: Almost all multicellular eukaryotes, (host cells do not contain PAMPS) . Adaptive immunity: Only in vertebrates (lymphocytes only) Five attributes of adaptive immunity • Specificity • Inducibility • Clonality • Unresponsiveness to self • Memory Two main types of lymphocytes • B lymphocytes (B cells): Mature in the bone marrow • T lymphocytes (T cells) : Mature in the thymus

–Two types of adaptive immune responses: Cell-mediated immune responses and Antibody immune responses

-An epitope (or antigenic determinant) is the three-dimensional shape of a region of an antigen that is recognized by the immune system

Exogenous antigens—include toxins and other components of microbial cell walls, membranes, flagella, and pili • Endogenous antigens—produced by microbes that reproduce inside a body’s cells • Autoantigens—derived from normal cellular processes

Antigens bind in the antigen-binding groove of MHC molecules :Two classes of MHC proteins • MHC class I : Present on all cells except red blood cells  MHC class II • Present on antigen-presenting cells (APCs) • Include macrophages and dendritic cells