Host-Pathogen Interactions Flashcards
Pathogen
Virus which causes diesease
Slow Infection
Prolonged incubation period, lasting months or years. Quantities of infectious virus gradually increase during a very long preclinical phase. Slow progressive lethal disease.
Cytokines
Broad cateogory of small proteins that are important in cell signaling, act as mediators and regulators of immune processes. Also cause inflammation
Viremia
Presence of a virus in the blood. Virus may be free in blood or in a cell
Retrograde Spread
Travel opposite direction of nerve impulse flow. Invade axon terminals and then spread to dendrite or cell body and cross synapse to reach next axon terminal
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Running against the wind
Ulcer
Opening in the skin caused by sloughing of necrotic tissue, extending past the epidermis
Acute Viremia
Viremia following inital virus replication in host. Release of virions from the initail site of replication to the blood stream
Systemic Infection
Number of organisms or tissues become infected
Infectious Dose 50
Dose of virus that will infect 50% of an experimental group of host/animals
Rash
General term applied to any temporary eruption on the skin, usually a shade of red
Incubation period of localized vs systemic infections
Localized - Short
Systemic - Long
Avirulent
Not virulent - not harmful to the host
Effect of viral infection son the hemopoietic system
Damage to the endothelium
Disseminated intravascular coagulation (DIC)
Edema
Infarction
Neural spread of viruse to CNS through olfactory routes
Olfactory Epithelium > Olfactory Nerve > Glomerulus > Olfactory Bulb
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Anterograde
Pantropic Virus
Can replicate in ore than one host organ/tissue
Outcome of a fetus is infected with BVDV during months 5-9 of gestation
Middle - Abortion or Abnormalities
Late - Normal Calves
Neurovirulent Virus
Viruses that cause disease of nervous tissue, manifest by neurological symptoms and often death
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How severe the disease is
Petechiae Hemorrhage
Pin point, small spots of hemorrhage
Shedding is critical for what
Maintenace of infection
Transmission of viruses
What may facillitate viruses reaching subepithelial layers
Inflammatory response and damaged epithelium
Transcytosis
Relationship of ID50 and LD50 in accordance to virulence of pathogens.
Low ID50 and LD50 = More Virulent
Ways that viruses spread in the host
Epithelial Surfaces
Subepithelial Invasion and Lymphatic Spread
Bloodstream
Nerves
Monokines
Cytokines produced by mononuclear phagocytic cells
Lymphokines
Cytokines produced by activated lymphocytes (Th cells)
Types of Viral Infections
Inapparent Infections
Acute Infection
Persistant Infection
Latent Infection
Chronic Infection
Slow Infection
Tropism
Specificity/ affinity of a virus for a particular host tissue
Acute Infection
Short term infection. Short clinical course, rapid clearance from host immune response
Pattern of shedding in acute infections
Usually intensive shedding over short period of time
Secondary Viremia
Virus has replicated in major organs and once more entered the circulation
Pathogenicity
Ability of a virus to cause disease in a host
Wart
Benign skin growth that appear when a virus infects the top layer of skin
Effect of viral infections on the CNS
Lytic infections of neurons leads to encephalitis or encephalomyelitis characterized by neruonal necorosis, phagocytosis of neurons and perivascular infiltrations of inflammatory cells
Immunosuppression occurs when
Immunodeficiency viruses infect and destroy different,but specific cells of the immune system
Inapparent Infection
Clinical signs and symptoms not evident, too few cells may be infected. Possible source of virus spread
Ecchymoses Hemorrhage
Large areas of hemorrhage, ill-defined margins
Virulence
Quantitative or relative measure of the degree of pathogenicity of the infecting virus
Erythema
Redding of the skin, consequence of systemic viral infections, endothelial injury in blood vessels throughout the body, including SQ tissues
Chronic Infection
Acute infection followed by chronic infection in which the virus is continuously shed from or is persistant in infected tissue. Established when host immune system is unable to clear virus from acute infection.
Immunopathology
Tissue injury mediated by host immune response to viral infection
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Price paid by the host to clear viral infection
Viruses get cleared from the bloodstream by
Mononuclear phagocytes in the spleen, liver and bone marrow
Antibody Clearance
Complement- mediated clearance
Steps of Viral Infection
Entry and Primary Replication
Spread, Tropism and Infection of Target Organ
Virus-Cell Interactions and Secondary Replication
Tissue and Organ Injury
Shedding
Pathogenesis
Manner/mechanism of development of a disease
Iceberg Concept of Infection and Disease
Possible outcomes following an interaction with a host and virus
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Exposure with no infection, Subclinical infection, Severe disease, Death, etc
Anterograde Spread
Travel in direction of nerve impulse flow. Virus invades dendrites or cell bodies and then spread to axon terminals, and then cross synaptic contacts to invade dendrite of next neuron
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Run with the wind
Persistant Infection
Infectious virus is demonstratale continuously, whether or not there is ongoing disease. Pathogen is not cleared efficiently by the adaptive immune response
Trojan Horse
Trafficking monocytes to transport viruses
How do viruses spread on epithelial spurfaces
Replicate at the site of entry and infect contigous cells
Pattern of shedding in persistant infections
Shed a low titers for months to years
Centripetal Movement of Virus
Towards the brain or CNS
Lethal Dose 50
Dose of the virus required to cause death in 50% of animals
ID50 : LD50 Ratio
Ratio of the dose of a particular strain of virus that causes infection in 50% animals to the dose that kills 50% of animals
Role of T Cells in Immunopathology
Can directly destroy virus infected cells or release cytokines that damage cell
Cytotoxic cell mediated lysis of infected host cells
Release of cytokines cause inflammation and tissue damage that cause chronic/persistant virus infections
Centrifugal Movement of Virus
From CNS within peripheral nerves to other locations in body
Defenses of the mucous membranes against viral infections
IgA
Virucidal proteins
Defenses of the Skin against viral infection
Dense Keratin Layer
Low pH
Presence of Fatty Acids
Bacterial Flora
Dryness
Innate and Adaptive Immunity
Outcome of a fetus is infected with BVDV during month 1 of gestation
Embryo death
Primary Viremia
Initial entry into the blood after injection
Rabies Virus readily infects the PNS and spreads to the CNS with 100% lethality.
Rabies viruses demonstrates (high/low) neuroinvasiveness and neurovirulence
High Neuroinvasiveness
High Neurovirulence
Defenses of the Respiratory Tract against viral infection
Mucociliary blanket
Alveolar macrophages
NALT
BALT
Temperature gradient
Variables related to the host that affect the virulence of a virus
Species
Immunity
Expression of critical receptors
Physiologic factors
Interferons
Fever
Interleukins
Cytokines that act as mediators between leukocytes
Common clinical manifestations of viral infections
Rash
Vesicle
Ulcer
Nodule
Wart
Papules
Erythema
Neurotropic Virus
Virus that can infect neural cells
Passive Viremia
Direct inoclulation of virus in blood. No initial replication elsewhere in host before
Teratogenesis
Abnormal development or arrest in development of the embryo or fetus
Disseminated Intravascular Coagulation (DIC)
- Widespread activation of clotting cascade results in formation of blood clots
- Clots clog the vessels and cut off blood supply to organs (liver, kidney, brain)
- Lack of blood flow causes damage to organs
- Clotting proteins are consumed/used up causing severe bleeding from various sites
Transcytosis
Vesicular transport of macromolecules from one side of a cell to the other
Secretory IgA is important in (localized/systemic) infections
Localized infections
Nodule
Palpable, solid, elevated mass with distinct borders
Variables related to the virust that can affect it’s virulence
Virus Strain
Portal of Entry into host
Tropism to host organs
Dose infection
Immuno evasion
Mechanism of immunopathology related to toxicity from antibody response
Antibody binds to infected cell and activates compliment causing inflammatory reaction
Engagement of IgG with Fc receptors on inflammatory cells cause inflammatory release
Initiation of complement cascade
Routes of entry of a virus into a host
Skin
GI Tract
Respiratory Tract
Vesicle
Small distinct elevation with fluid
Effect of viral infection on the GI tract
Destruction of enterocytes leading to gastrointestinal disease, malabsorption and hypersecretion
Latent Infection
Infectious virus is not demonstratable except when reactivation occurs. Reactivation is stimulated by immunosuppression and/or by the action of a cytokine or hormone
Viremia occurs in (localized/systemic) infections
Systemic
Effect of viral infection of the embryo or fetus (transplacental infection)
Teratogenesis
Cerebellar Hypoplasia
Arthrogryposis
Bovine Viral Diarrhea
Secondary bacterial infections (increase/decrease) mortality %
Increase, drastically
Herpes Simplex Virus always enters the PNS but rarely enters the CNS. When it does, the consequences are almost always severe, if not fatal.
Herpes Simplex virus has (high/low) neuroinvasiveness and neurovirulence
Low Neuroinvasiveness
High Neurovirulence
Defenses of the GI tract against viral infection
Mucous membrane
Acidity of stomach
Alkalinity of intestine
Layer of mucous
Lipolytic bile
Proteolytic pancreatic encymes
Defensins
IgA
Scavenging macrophages
Duration of immunity of localized vs systemic infections
Localized - variable but short
Systemic - mostly lifelong
Outcome of a fetus is infected with BVDV during months 2-4 of gestation
Persistant Infection Calves (Immunotolerant)
Neural spread of viruses to the CNS through Blood Brain Barrier can occur by what methods
Increased permeability of endothelial cells through the secretion of Tumor Necrosis Factor (TNF)
Breakdown of endothelial cell junctions through Maxtrix Metalloproteinase (MMP)
Trojan Horse
Viruses interact with macrophages in order to
Prolong time in blood or to be passively transferred to adjacent cells
Role of the innate immunity in immunopathology
Invading viruses and their replicative intermediates are recognized by several innate immune receptors
Activation of receptors cause production of pro-inflammatory cytokines and interferons and recruitment of cells involved in inflammation
Free Radicals produced in abundance cause tissue damage
In neural spread of viruses, transport of the virus may occur
Within Axons
In Perineural Lymphatics
In the Endoneural Space
Via infected Schwann cells
Neuroinvasive Virus
Viruses that enter the central nervous system after infection of a peripheral site
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How likely it will get to the CNS
Disseminated Infection
Infection spread beyond the primary site of infection
Virus spread by subepithelial invasion and lymphatics
Virus transverses the epithelium and get access to lymphatics, phagocytes and tissue fluids. Targeted migration and replication occurs.
Viruses can enter tissues from the bloodstream by
Going through fenestrae
Transcytosis
Trojan Horse
Replication in endothelial cells
Site of pathology of Localized vs Systemic infections
Localized - Portal of entry
Systemic - Distant sites
Persistant infections are important because of
Recrudescent episodes of disease
Immunopathology
Survival of virus in host and continuous shedding
Mumps virus infects the CNS but the neurological disease is mild.
Mumps virus causes (high/low) neuroinvasiveness and neuovirulence
High Neuroninvasiveness
Low Neurovirulence
Mechanism by which immune-complex formation causes vasculitis
- Spike proteins bind to antibodies
- Antibodies fail to neutralize the virus
- Antigen-Antibody immune complex formed
- Activates the complement cascade
