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| − | <big><big><center>[[WikiBlood|'''BACK TO WikiBlood''']]</center></big></big>
| + | ===Introduction=== |
| − | <br>
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| − | <big><center>[[Immunology - WikiBlood|'''BACK TO IMMUNOLOGY''']]</center></big>
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| − | ----
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| − | =Introduction= | |
| − | [[Image:Routes of Infection.jpg|thumb|right|150px|Routes of Infection - B. Catchpole, RVC 2008]]
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| − | Infection is a primary cause of disease. Four pathways of infection are identified: bacterial, viral, fungal, and parasitic, comprising protozoa and worms (helminths). In all cases, microorganisms can display similar characteristics. They can manifest as '''primary (obligate) pathogens''' or '''secondary (opportunistic) pathogens''', the former of which always corresponds to disease, and the latter of which depends on prerequisites being fulfilled before causing disease. As such, secondary pathogens can be found in healthy animals, but they lie in wait until a primary cause compromises the immune system and then manifest symptoms. Secondary pathogens can even masquerade as '''commensal''' organisms, or those which operate in harmony with the animal, until they become pathogenic.
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| − | Microorganisms can enter the body by three routes: '''contact''' (typically dermatological infection), '''aerosol''' (typically respiratory infection), or '''orofecal''' (typically enteric infection). Infection can be either '''exogenous''' (via entry to epithelial surfaces) or '''endogenous''' (intracellular, extracellular, or vesicular).
| + | One of the main causes of disease is infection by microorganisms, with four types so far identified: |
| | + | *[[Viruses]] |
| | + | *[[Bacteria]] |
| | + | *[[Fungi]] |
| | + | *[[Parasites]]- comprising [[protozoa]] and [[helminths]] |
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| − | =[[Viruses - WikiBlood|Viruses]]=
| + | 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 /> |
| − | [[Image:Virus structure.jpg|thumb|right|150px|Virus Structure - B. Catchpole, RVC 2008]]
| + | <br /> |
| − | ==Structure==
| + | All exist as either: |
| − | 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:
| + | *Primary pathogens ('''obligate'''): presence always corresponds with disease |
| − | *Genetic material, which consists solely of viral RNA
| + | *Secondary ('''opportunistic'''): prerequisites must be fulfilled before disease occurs |
| − | *Capsid proteins surrounding the RNA
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| − | *A lipid envelope | |
| − | *Envelope glycoproteins (or spike proteins) | |
| − | 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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| | + | Microorganisms can enter the body by three routes: |
| | + | *'''Contact''': typically seen in dermatological infections |
| | + | *'''Aerosol''': typically respiratory infections |
| | + | *'''Orofecal''':typically enteric infections |
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| − | ==Replication== | + | {{Learning |
| − | [[Image:Viral replication.jpg|thumb|right|150px|Viral Replication - B. Catchpole, RVC 2008]] | + | |flashcards = [[Host Invasion by Microorganisms Flashcards|Host Invasion Flashcards]] |
| − | Viral lifespans have three distinct phases:
| + | }} |
| − | *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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| | + | ===References=== |
| | + | *<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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| | + | *http://www.cellsalive.com |
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| − | ==Prevention and control==
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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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| − | *Viral evasion of immunity
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| − | **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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| − |
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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
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| − | **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:
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| − | ***'''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
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| − | ***'''Cytotoxic (CD8+) T cells''' target infected cells, which present any number of danger signals
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| − | | + | {{review}} |
| − | *[[Vaccines - WikiBlood|Vaccines]]
| + | <br><br> |
| − | 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'''.
| + | {{Jim Bee 2007}} |
| − | | + | [[Category:Immunology]] |
| − | =[[Bacteria - WikiBlood|Bacteria]]=
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| − | | |
| − | ==Structure==
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| − | [[Image:Bacterial structure.png|thumb|right|150px|Bacteria Structure - Wikimedia Commons 2008]]
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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''', in the form of an '''abscess'''
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| − | *'''Systemic''', in the form of '''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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| − | ==Prevention and control==
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| − | =[[Parasites - WikiBlood|Parasites]]=
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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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