Pathogens and the host Flashcards
Describe some of the features of viral pathogenesis.
> Cell destruction following virus infection
- Death of T4+ cells by HIV
Virus-induced changes to cellular gene expression
- Cellular transformation by tumour viruses.
Immunopathogenic disease
- Influenza A virus.
- Coxsackievirus-induced myocarditis.
Define the terms pathogen and commensal.
A pathogen is an organism which can cause disease
A commensal is an organism which is part of normal flora e.g. E. coli in the gut, Staph aureus in the nose, axilla
Describe in outline the human defence mechanisms of innate and acquired immunity.
I. Innate Immunity
A. Overview
First line of defense
Non-specific response
Immediate action against pathogens
B. Physical Barriers
Skin
Mucous membranes
Cilia in respiratory tract
C. Chemical Barriers
Antimicrobial peptides
Lysozyme in saliva and tears
Stomach acid
D. Cellular Defenses
Phagocytes a. Neutrophils b. Macrophages
Natural Killer (NK) cells
Dendritic cells
E. Inflammatory Response
Signs of inflammation (redness, heat, swelling, pain)
Release of cytokines and chemokines
Recruitment of immune cells
F. Complement System
Activation pathways (classical, lectin, alternative)
Role in opsonization and lysis of pathogens
II. Acquired Immunity
A. Overview
Specific immune response
Takes time to develop
Memory formation for faster response upon re-exposure
B. Humoral Immunity
B cells a. Activation and differentiation into plasma cells b. Production of antibodies
Antibodies a. Neutralization of pathogens b. Opsonization c. Activation of complement
C. Cell-Mediated Immunity
T cells a. Helper T cells (CD4+)
Role in activating B cells and cytotoxic T cells b. Cytotoxic T cells (CD8+)
Direct killing of infected cells
Memory T cells a. Long-lived response b. Quick activation upon re-exposure
D. Antigen Presentation
Role of Major Histocompatibility Complex (MHC) a. MHC Class I for cytotoxic T cells b. MHC Class II for helper T cells
E. Cytokines and Interferons
Communication between immune cells
Regulation of immune responses
III. Interaction Between Innate and Acquired Immunity
A. Cooperation in Response to Infection
Innate cells presenting antigens to T cells
Activation of adaptive immunity by innate signals
B. Influence of Innate Immunity on Acquired Responses
Innate factors shaping T and B cell responses
Role of cytokines in bridging both systems
Explain the meaning of the terms colonisation, latent or asymptomatic infection and
infection.
- Colonization
Definition: Colonization refers to the establishment of a microbial population within a host without causing disease.
Characteristics:
The microbes (bacteria, fungi, etc.) may reside on surfaces such as skin or mucous membranes.
They may be part of the normal flora (commensal organisms) and do not trigger an immune response.
While they are present, they do not interfere with the host’s normal functions or health. - Latent or Asymptomatic Infection
Definition: A latent infection occurs when a pathogen is present in the body but remains inactive or dormant, causing no symptoms. Asymptomatic infections are those where the individual is infected but does not show clinical symptoms.
Characteristics:
The pathogen can reactivate later, leading to illness (e.g., latent tuberculosis).
The person may still be contagious, depending on the pathogen.
It may involve a period of initial active infection followed by dormancy. - Infection
Definition: Infection is the invasion and multiplication of pathogens in the body, leading to tissue damage and symptoms of disease.
Characteristics:
It can be acute (sudden onset) or chronic (long-lasting).
Symptoms can range from mild to severe, depending on the pathogen and the host’s immune response.
Infections can result from various pathogens, including bacteria, viruses, fungi, and parasites.
Describe the features of clinical infection
- Presence of Pathogens
Infection Agent: Involves bacteria, viruses, fungi, or parasites that invade the host.
Replication: The pathogens multiply and spread within the host’s tissues. - Symptoms and Signs
Manifestation: Clinical infections typically present with identifiable symptoms, such as:
Fever
Pain (localized or systemic)
Swelling
Redness
Fatigue
Cough or respiratory symptoms
Duration: Symptoms can be acute (sudden onset) or chronic (lasting for an extended period). - Immune Response
Host Response: The body’s immune system responds to the infection, which can include:
Inflammation
Activation of immune cells (e.g., leukocytes)
Production of antibodies
Symptoms of Immune Response: Fever and inflammation are common as the body attempts to fight the infection. - Diagnosis
Clinical Evaluation: Diagnosis may involve:
Patient history
Physical examination
Laboratory tests (blood tests, cultures, imaging studies)
Identification of Pathogen: Determining the specific pathogen responsible for the infection. - Transmission
Infectiousness: Many clinical infections can be contagious, meaning they can be spread to others through direct or indirect contact, respiratory droplets, or other means. - Complications
Potential for Severity: Clinical infections can lead to complications, such as:
Sepsis
Organ dysfunction
Secondary infections
Risk Factors: Certain populations (e.g., immunocompromised individuals) may be more susceptible to severe outcomes. - Treatment and Management
Therapeutic Interventions: Clinical infections often require treatment, which may include:
Antibiotics for bacterial infections
Antiviral medications for viral infections
Supportive care (e.g., hydration, pain relief)
Monitoring: Ongoing evaluation of the infection’s progress and response to treatment. - Resolution
Recovery Process: Clinical infections can resolve through:
Successful treatment
Immune clearance
Development of immunity (which may lead to protection against future infections).
Define pathogenicity and describe the concepts of infectivity and virulence
Pathogenicity is the overarching ability of an organism to cause disease, while infectivity and virulence are specific aspects of this capability:
Infectivity focuses on the likelihood of infection establishment.
Virulence addresses the severity and impact of the disease caused by the pathogen.
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Pathogenicity
Definition: Pathogenicity is the ability of an organism, usually a pathogen such as bacteria, viruses, or fungi, to cause disease in a host. It encompasses the mechanisms by which pathogens invade, survive, and damage host tissues, leading to clinical symptoms.
Concepts of Infectivity and Virulence
1. Infectivity
Definition: Infectivity refers to the ability of a pathogen to establish an infection within a host. It is a measure of how readily a pathogen can enter, survive, and multiply in a host.
Key Points:
Transmission: Infectivity is influenced by the mode of transmission (e.g., airborne, vector-borne, direct contact).
Inoculum Size: The number of pathogens required to initiate an infection plays a role; some pathogens need only a few organisms to infect, while others require a larger dose.
Host Factors: The susceptibility of the host, including immune status and genetic factors, also affects infectivity.
2. Virulence
Definition: Virulence is the degree of pathogenicity of a pathogen, specifically its ability to cause severe disease or damage to the host. It reflects the severity of the disease caused by the pathogen.
Key Points:
Quantitative Measure: Virulence can be measured in terms of the severity of disease (e.g., mortality rate, morbidity) or the dose of the pathogen required to cause disease in a susceptible host.
Factors Influencing Virulence:
Toxins: Some pathogens produce toxins that directly damage host cells.
Adhesion Factors: Mechanisms that allow pathogens to adhere to host tissues and evade the immune response.
Immune Evasion: Strategies employed by pathogens to avoid detection or destruction by the host’s immune system (e.g., antigen variation).
Describe the features of pathogenic toxins and their effects
Features of Pathogenic Toxins
Types of Toxins
Exotoxins:
Secreted by bacteria into the surrounding environment.
Typically highly potent and can cause significant damage even in small amounts.
Examples include:
Neurotoxins (e.g., botulinum toxin from Clostridium botulinum)
Enterotoxins (e.g., cholera toxin from Vibrio cholerae)
Cytotoxins (e.g., diphtheria toxin from Corynebacterium diphtheriae)
Endotoxins:
Components of the bacterial cell wall (specifically lipopolysaccharides found in Gram-negative bacteria).
Released upon bacterial lysis and can trigger systemic inflammatory responses.
Generally less potent than exotoxins but can lead to severe effects, such as septic shock.
Mechanism of Action
Cellular Interference: Toxins can disrupt normal cellular functions by:
Inhibiting protein synthesis (e.g., diphtheria toxin).
Altering cell signaling pathways.
Causing cell lysis or death.
Immune System Modulation: Some toxins can suppress or manipulate immune responses, allowing the pathogen to evade detection.
Toxicity and Potency
Lethal Dose (LD50): The amount of toxin required to kill 50% of a test population, indicating the potency of the toxin. Exotoxins typically have a lower LD50 compared to endotoxins.
Variability: The toxicity can vary widely between different pathogens and even different strains of the same pathogen.
Specificity
Target Cells: Some toxins have specific target cells (e.g., neurotoxins target nerve cells), while others may affect a broader range of cell types.
Binding Mechanism: Toxins often bind to specific receptors on host cells, facilitating their entry and action.
Effects of Pathogenic Toxins
Local Effects
Tissue Damage: Toxins can directly destroy host tissues, leading to inflammation, necrosis, and ulceration.
Disruption of Barrier Functions: Toxins may compromise epithelial barriers, facilitating further invasion by pathogens.
Systemic Effects
Fever: Toxins can induce fever by triggering the release of pyrogens.
Shock: Endotoxins can cause septic shock, characterized by widespread inflammation, vasodilation, and hypotension.
Multiple Organ Dysfunction: Severe toxin exposure can lead to failure of multiple organ systems.
Neurological Effects
Neuromuscular Effects: Neurotoxins can cause paralysis, muscle weakness, or spasms (e.g., botulism leading to flaccid paralysis).
Cognitive and Sensory Impairments: Some toxins may affect brain function, leading to confusion, seizures, or loss of consciousness.
Gastrointestinal Effects
Diarrhea and Vomiting: Enterotoxins can disrupt intestinal function, leading to severe gastrointestinal symptoms (e.g., cholera).
Immune System Effects
Immunosuppression: Some toxins can inhibit immune responses, making the host more susceptible to secondary infections.
Describe the sites of viral entry
Conjunctiva, arthropod, capillary, skin, urinogenital tract, alimentary, respiratory
Describe the features of acute viral infections with the use of examples
Localised to specific site of body
Development of viraemia with widespread infection of tissues.
Influenza A virus – respiratory infection
Enterovirus – enteric and neurological infections
The time when you have the most amount of virus in your body is when you are still asymptomatic. Your symptoms only last for a very small time while you are infected.
Describe the features of enterovirus infection with the use of examples
The group of RNA viruses you’re referring to includes enteroviruses. These viruses are known for primarily infecting the gastrointestinal tract but can also spread to other parts of the body, including the central nervous system. Here are some key points about enteroviruses:
Transmission:
Primarily transmitted through the fecal-oral route, often via contaminated food or water.
Can also spread through respiratory droplets and direct contact with infected surfaces.
Symptoms:
Many enterovirus infections are asymptomatic or mild.
When symptoms do occur, they can include fever, sore throat, rash, and gastrointestinal symptoms like diarrhea.
Severe cases can lead to viral meningitis, encephalitis, or paralysis (especially in the case of poliovirus).
Infection Process:
After ingestion, the virus replicates in the gastrointestinal tract and can enter the bloodstream.
From the bloodstream, it can reach the central nervous system or other tissues, causing more severe disease.
Prevention:
Good hygiene practices, such as handwashing and safe food handling, can reduce the risk of infection.
Vaccines are available for some enteroviruses, notably the poliovirus vaccine.
Poliomyelitis (poliovirus)
Aseptic meningitis (many enteroviruses)
Myocarditis (coxsackie B viruses)
Pancreatitis (coxsackie B viruses)
Respiratory infections (many enteroviruses)=
Describe how virus can induce tumours with the use of examples
Virus infects cell.
Virus nucleic acid, as DNA, integrates into cellular genome.
Virus causes changes in cellular gene expression.
Uncontrolled cell multiplication and tumour formation.
For Example:
Papillomaviruses (HPV) – cervical carcinoma
Retroviruses – lymphomas and leukemias
Describe humoral and cell mediated immunity
Summary
Humoral Immunity: Involves B cells and antibody production to neutralize pathogens in body fluids.
Cell-Mediated Immunity: Involves T cells and the direct attack on infected cells, crucial for responding to intracellular pathogens.
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Humoral Immunity
Definition: Humoral immunity involves the production of antibodies by B cells in response to antigens.
Mechanism:
B Cell Activation: When B cells encounter a specific antigen, they can differentiate into plasma cells, which produce antibodies.
Antibodies: These proteins bind to antigens, neutralizing pathogens or marking them for destruction by other immune cells.
Memory B Cells: Some activated B cells become memory cells, providing long-term immunity by remembering the specific antigens for faster responses in future infections.
Role: Primarily effective against extracellular pathogens (e.g., bacteria, viruses in the bloodstream) and toxins.
Cell-Mediated Immunity
Definition: Cell-mediated immunity involves T cells and does not rely on antibodies but rather on the direct action of immune cells.
Mechanism:
T Cell Activation: T cells, particularly CD4+ helper T cells and CD8+ cytotoxic T cells, are activated by recognizing antigens presented on the surface of infected or abnormal cells via Major Histocompatibility Complex (MHC) molecules.
CD4+ T Cells: These helper T cells assist in activating B cells and other immune cells, enhancing the immune response.
CD8+ T Cells: Cytotoxic T cells directly kill infected or cancerous cells.
Memory T Cells: Similar to B cells, some activated T cells become memory cells for quicker responses in subsequent exposures.
Role: Particularly effective against intracellular pathogens (e.g., viruses, some bacteria) and cancer cells.
