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| − | {{toplink
| + | ===Introduction=== |
| − | |backcolour = FFE4E1
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| − | |linkpage =WikiBlood
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| − | |linktext =WIKIBLOOD
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| − | |maplink = Haematopoiesis and Blood Cells (Concept Map) - WikiBlood
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| − | |tablelink = Haematopoiesis and Blood Cells (Table) - WikiBlood
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| − | |sublink1 =Immunology - WikiBlood
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| − | |subtext1 =IMMUNOLOGY
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| − | |pagetype =Blood
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| − | }}
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| − | | |
| − | =Introduction=
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| | | | |
| | One of the main causes of disease is infection by microorganisms, with four types so far identified: | | One of the main causes of disease is infection by microorganisms, with four types so far identified: |
| − | *Viruses | + | *[[Viruses]] |
| − | *Bacteria | + | *[[Bacteria]] |
| − | *Fungi | + | *[[Fungi]] |
| − | *Parasites- comprising protozoa and helminths | + | *[[Parasites]]- comprising [[protozoa]] and [[helminths]] |
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| | + | A fifth controversial type are Pirons, which are infectious proteins that are believed to be the cause of bovine spongiform encephalopathy (BSE) and the human variant Creutzfeldt–Jakob disease (vCJD).<br /> |
| | + | <br /> |
| | All exist as either: | | All exist as either: |
| | *Primary pathogens ('''obligate'''): presence always corresponds with disease | | *Primary pathogens ('''obligate'''): presence always corresponds with disease |
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| | *'''Orofecal''':typically enteric infections | | *'''Orofecal''':typically enteric infections |
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| | + | {{Learning |
| | + | |flashcards = [[Host Invasion by Microorganisms Flashcards|Host Invasion Flashcards]] |
| | + | }} |
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| − | =[[Viruses - WikiBlood|Viruses]]= | + | ===References=== |
| − | [[Image:Virus structure.jpg|thumb|right|150px|Virus Structure - B. Catchpole, RVC 2008]]
| + | *<div id="Janeway">{{citation|initiallast = Murphy|initialfirst = K|2last = Travers|2first = P|finallast = Walport|finalfirst = M|year = 2008|title = Janeway's Immunobiology|ed = 7th |city = New York|pub = Garland Science Publishing}}</div> |
| − | [[Image:Viral replication.jpg|thumb|right|150px|Viral Replication - B. Catchpole, RVC 2008]]
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| − | [[Image:B Cell viral response.jpg|thumb|right|150px|B Cell Immunity to Viruses - B. Catchpole, RVC 2008]]
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| − | [[Image:T Cell viral response.jpg|thumb|right|150px|T Cell Immunity to Viruses - B. Catchpole, RVC 2008]]
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| − | ==Structure== | |
| − | Viruses are very simple structures that do not carry any cellular machinery of their own. They depend on host cells to replicate and flourish. As such, their structure is streamlined, containing only:
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| − | *Genetic material, which consists solely of viral RNA | |
| − | *Capsid proteins surrounding the RNA
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| − | *A lipid envelope
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| − | *Envelope glycoproteins (or spike proteins)
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| − | All of these elements can be recognized by the host as foreign material, and will provoke an immune response. Viruses have an advantage if they are able to penetrate host cell walls in that they are then capable of masquerading as host cells. The immune system must then counter by killing off host cells it recognizes as infected.
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| − | | |
| − | ==Pathogenesis== | |
| − | | |
| − | ==Replication== | |
| − | Viral lifespans have three distinct phases:
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| − | *Infectious (extracellular): as they seek out a host target
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| − | *Replicative (intracellular): as they overtake the host cell's utilities to multiply
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| − | *Dissemination (extracellular): as they leave the host cell and migrate to those surrounding
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| | | | |
| − | ==Immunity to Viruses==
| + | *http://www.cellsalive.com |
| − | *Viral evasion of immunity | |
| − | **Latency: Viruses can "hide" in host cells until the immune system is suppressed
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| − | **Transformation: the virus incorporates into the host genome, activating an '''oncogene''', which causes cells to become neoplastic
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| | | | |
| − | *[[The innate immune system - WikiBlood#Innate Immunity to Viruses|Innate Immunity to Viruses]]
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| − | *Adaptive Immunity to Viruses
| + | {{review}} |
| − | **The adaptive immune system has two main ways of dealing with viral infection: the first targets viruses in its initial extracellular phase, the second targets infected host cells:
| + | <br><br> |
| − | ***'''B-lymphocytes''' are capable of producing Antibody to neutralize the spike proteins of the viral lipid envelope, preventing the virus from attaching to host cells
| + | {{Jim Bee 2007}} |
| − | ***'''Cytotoxic (CD8+) T cells''' target infected cells, which present any number of danger signals
| + | [[Category:Immunology]] |
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| − | ==Prevention and control==
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| − | *[[Vaccines - WikiBlood|Vaccines]]
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| − | Antibiotics cannot treat viral infection. While anti-viral therapies do exist, they are costly and often ineffective. The alternatives, therefore, include '''vaccination''' (priming the immune response to create memory lymphocytes for a particular virus) or '''eradication'''.
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| − | | |
| − | =[[Bacteria - WikiBlood|Bacteria]]=
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| − | [[Image:Bacterial structure.png|thumb|right|150px|Bacteria Structure - Wikimedia Commons 2008]]
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| − | ==Structure==
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| − | Bacteria offer the immune system a greater range of foreign components with which to be recognized, including:
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| − | *Flagellum
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| − | *Pili
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| − | *Capsule
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| − | *Cellular components: membrane, cell sap containing enzymes, genetic material, cell wall
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| − | | |
| − | ==Pathogenesis==
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| − | Bacterial invasion can be either:
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| − | *'''Localized''', such as an '''abscess'''
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| − | *'''Systemic''', such as '''septicemia'''
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| − | | |
| − | Some bacteria also produce toxins:
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| − | *'''Endotoxogenic''': cell wall degradation products (lipopolysaccharide) released into the blood stream, causing toxic shock
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| − | *'''Exotoxogenic''': bacteria produce and secrete toxin (such as tetanus and botulism)
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| − | | |
| − | ==Replication==
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| − | The lifespan of bacteria differs from that of viruses in that it includes a '''colonization''' phase, which occurs on epithelial surfaces. As bacteria are capable of self-replication (i.e. they don't require host cellular machinery), this colonization phase allows them to develop a highly skilled and lethal army before invading the body. Once invasion occurs, spread can occur via the vascular or lymphatic systems. The pathogenesis of a particular strain of bacteria very much depends upon its location in the body: "''Streptococcus pneumoniae'' in the lung causes pneumonia...whereas in the blood it causes a rapidly fatal systemic illness, pneumoncoccal sepsis." (Murphy, et al, 43)
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| − | | |
| − | ==Immunity to Bacteria==
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| − | *Bacterial evasion of immunity
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| − | **Bacterial capsules can avoid phagocytosis and complement activation
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| − | **Some bacteria are able to survive phagocytosis and evade digestion (such as mycobacterium and ''Leptospira'')
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| − | | |
| − | *[[Innate Immune System - WikiBlood#Innate Immunity to Bacteria|Innate Immunity to Bacteria]]
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| − | *Adaptive Immunity to Bacteria:
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| − | Phagocytosis and digestion are the primary tools of the Immune System to conquering bacterial infection. These are enhanced by the production of [[Immunoglobulin G - WikiBlood|IgG]] and CD8+ Tcells, as well as by [[Complement - WikiBlood|complement]] activation.
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| − | | |
| − | ==Prevention and control==
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| − | '''Antibiotics''' can be used to prevent and control bacterial invasion, replication, and dissemination.
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| − | | |
| − | =[[Parasites - WikiBlood|Parasites]]=
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| − | | |
| − | ==Types==
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| − | Parasites broadly include:
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| − | *Helminths (worms)
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| − | *Arthropods (insects)
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| − | *Protozoa (single-celled eukaryotes)
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| − | | |
| − | ==Immunity to Parasites==
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| − | The immune system relies on granulocytes ([[Mast Cells - WikiBlood|mast cells]] and [[Eosinophils - WikiBlood|eosinophils]]) and the production of [[Immunoglobulin E - WikiBlood|IgE]] antibody to combat parasitic infection. Once produced in response to danger signals, IgE attaches to circulating granulocytes. IgE then binds to the parasite, signals mast cell and eosinophil degranulation, and causes enzymatic digestion of the intruder.
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| − | | |
| − | =References=
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| − | *<div id="Janeway">{{citation|initiallast = Murphy|initialfirst = K|2last = Travers|2first = P|finallast = Walport|finalfirst = M|year = 2008|title = Janeway's Immunobiology|ed = 7th |city = New York|pub = Garland Science Publishing}}</div>
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