What are the structural components of bacteria
Cell Wall - Prevents osmotic lysis of CM & has important antigens on surface
- Layer of Peptidoglycan (Much more in gram+) surrounds cm, made of linear chains of N-acetylglucosamine & N-acetylmuramic
- Gram negative cells have outer membrane with LPS
- LPS has lipid A region, causes fever by IL-1 & O-side chain which make surface hydrophilic making it more virulent
Capsule
- Helps evade phagocytosis
- Bacillus anthracis has polyamino acid in capsule, allowing it survice in body
Flagellae
- Facillitate movement by rotating movement
- energy derived from protein motive force
Fibrae
- Surface appendages only on gram negative
- adhere to surfaces
- vaccines can bind to these
Spores
- Only produced by Baccilus and Clostridium
- Can tolerate heat, desicattion, radiation and cold
- Contains DNA, CM, peptidoglycan and external cortex of loose peptidoglycan that dehydrate spore.
- Can remain for years, reactivate in favourible conditions. Re synthesis metabolic enzymes
What are the 3 ways in which bacteria transfer genes
- Conjugation - Plasmid transfer via pili
- Transduction - Accidental packaging of DNA into bacteriophage. It then becomes non infective but can still infect other bacterium
- Transformation - uptake of exogenous DNA. Some do it natuurally others only when treated. Important in genetic engineering
What are transposable elements
Genetic elements capable of transfering a copy of themselfes from one genetic element to another (chromosome to plasmid)
Can be prevented by endonuclease enzymes within receiptent bacterium.
How does autoclaving work
Heated with saturated steam at 121 degress at 15lbs of pressure per inch. time must be allowed for whole object to reach 121 and steam must have access to all surfaces
What is PGE, what is the primary pathogen, & what are the clinical signs and two types
Parasitic Gastro-Enteritis
Ostertagia Ostertagi
Clinical signs:
- Diarrhoea/weight loss
- poor weight gain
- seasonal apperance
- Hypoalbuminaemia
Type 1
- L3 ingested in first grazing system and pass to abomasum
- Develop in gastic glands to L4 and emerge in 3 weeks
- causes epithelial hyperplasia and increased permeability to pepsinogen and albumin
Type 2
- An accumulation of L4 as they arrest
- re emurge at once causing acute case, can cause sudden death (feb-may)
- usually occurs when calves first grazing is at october to december
Disease less likely in beef because calves go out to pasture with dams (mum). cows are immune and therefore dont release alot of eggs onto pasture. Also in spring theres a high mortality of L3 so exposure is less. and grazing in autumn is dominated by cows so no alot of calfs on pasture. whereas dairy cows are weaned.
Control
- Clean pasture
- delay turnout untill after spring mortalitly of L3
- repeated anthelminthic treatment (can lead to resistance)
How are Pathogens detected
- Patter recognition receptors (PRRs) detect foreign structural components known as pathogen associated molecular patterns (PAMPS), e.g peptidoglycan or LPS) These receptors are found on white blood cells
- Some virus infected cells alter the MHC covering the surface of the cell. This is recognised by natural killer cells which destroy these cells
Describe lymphocyte development
B-cells - produced in Bone marrow
- Located in the follicles of Lymph nodes. When theres infection begin to proliferate in germinal centres.
T-cells - Also produced in bone marrow
- Travel to thymus to mature
- Proliferate and pass through to the medulla
- Here they generate antigen receptors which detect antigenic epitopes & decide their phenotype
- Receptors are made through random juggling of variable genes, therefore some receptors fail to engage with MHC and some even are autoreactive, these are destroyed.
What is clonal expansion and what are memory cells?
- Only a few lymphocytes in circulation will have a specific antigen receptor for a specific pathogen
- For an adequate response, once a lymphocyte binds to a pathogen, it must proliferate to have desired response. (clonal expansion)
- occurs in Lymph nodes
- Some clones remain quiescent, and become memory cells. These last years and circulate blood allowing for rapid response if theres re-infection of the same pathogen. This is known as immunity
What are the cells types of the immune system
- Neutrophil - important in inflammatory response and phagocytosisof bacteria
- Eosinophil - Major role in inflammatory response. Is also recruited to tissues when theres a parasitic infection. Degranulates releasing Biologically active molecules onto its surface.
- Basophil (mast cell) - prominant on epithelial surfaces. Contains granules which are inflammatory mediators, including histamine. Degranulation results in potent inflammatory response.
- Monocyte - made in BM and circulate blood. form macrophages and dendritic cells
- Dendritic cells - pick up antigens and bring them to lymph nodes to alert Tcells of infection
What is primary lymphoid tissue
- Bone marrow - produces WBC’s and RBC’s
- Thymus - T-cell maturation. Selectively eliminating T-cells with defective Antigen receptors.
What are secondary lympod tissue
- Spleen - Acts as a large lymph node within the white pulp. No afferent/efferent lymphatics only veins/arteries therefore filters the blood
- Mucosal-associate lymphoid tissue (MALT) - Found in bronchials and gut. M cells deliver pathogens here, high concentration of DC’s, macrophages and t&bcells
- Bursa of fabricus - Organ in birds where B-cells mature
- Lymph nodes - Blood vessels run through forming High endothelial venuels (HEV) allowing lymphocytes to leave blood and enter LN.
Why are type 1 interferons made and what do they do
- Made in response to viral infection. Detected by the presence of double stranded RNA in nucleated cells
- Increases degradation of nucleated cells
- Inhibition of viral protein synthesis
- increased antigen presentation to adaptive immune system
Can be used clinically to treat persistant viral infections
What are acute phase proteins and what are their affects
Proteins that respond to inflammatory cytokines. produced in the liver and act as opsonins (enhance phagocytosis) and stimulate compliment
What is Compliment?
- Part of the innate immune system
- series of pro-enzyme reactions, allowing an initial small signal to be amplified into a massive response
- End result is polymerisation of C9 monomers ina a polymer known as membrane attack complex (MAC)
- MAC creates holes in bacteria and causes lysis
- inactive C3 protein dissociates into C3a & C3b in the blood.
- C3a binds to mast cells, causing degranulation and inflammatory response.
- C3b acts as an opsonin and enzyme for the formation of MAC.
Describe the differences between the MHC complexes
Major histocompatability complex
- MHC class I - protein antigen in cytoplasm digested and transported to ER. then brung to cell surface by MHC. Recognition by CD8+T cells. All nucleated cells express these
- MHC class II - protein antigen in tissue fluid phagocytosed. Fragments then loaded onto MHC at golgi and brung to cell surface. Recognition by CD4+T cells. Expressed on macrophages, B-cells and DC’s
What are the different types of T cells
- CD+8 - destroys virus infected cells. Destroys pathogen in cytoplasm. Releases perforin & granzymes, apoptosis by fas ligand and Cytotoxic cytokines
- CD+4 th-1 - Help macrophages kill bacteria. Pathogens in vesicles. Releases interferon gamma. causes increased prodcution and fusion of lysosomes & also respiratory burst to kill pathogen
- CD+4 th-2 - Helps Bcells make anti bodies. Pathogens in tissue fluid. release IL-4
How to Bcells and Tcells interact to destroy pathogens?
- B-cells binds to MHC class II via IgM on its surface.
- Presents to MHC-antigen complex to TH-2 cells
- They release cytokines that stimulate class switching of IgM to IgG, which is a potent virus neutraliser, opsonin and activates compliment
- IgA - binds to pathogens stoping them causing harm to epithelial cells. also found in colosturm*
- IgE - Absorbed onto mast cells allowing them to bind to parasites more efficively. causing degranulation. abnormal production of IgE leads to allergic reactions*
Whats the difference between DNA-dependant RNA polymerase and RNA dependant RNA polymerase ?
- DNA-dependant RNA polymerase forms single stranded RNA from DNA
- RNA-dependant RNA polymerase catalyses the replication of RNA from a RNA template
RNA-dependant RNA polymerase Can not proof read RNA strands that are made, making it prone to error. therefore increasing the likelyhood of mutation. Also RNA of viruses are segmented, making it easier for reassortment
What are the 3 different capsid structures and what makes enveloped viruses different to non enveloped
- Icosahedral - 20 triangular sides, confering stability and allowing virus to survive in environment for months
- Helical - Protein subunits form a helix around the nucleic acid material. Usually enveloped viruses
- Complex - Larger viruses
- Enveloped viruses are susceptible to damage from environment (heat,cold,ph,radiation e.t.c). But they dont have to lyse sell to replicate.
Explain Virus replication stages
- Attachment - Viral surface proteins bind to cell surface
- Entry - Endocytosis, once inside the cell PH change causes virus release from endosome, Enveloped virus can fuse directly to plasma membrane
- Uncoating - Viral nucleic acids released from capsid
- Polymerases - Viral nucleic acids expressed. DNA viruses must travel to nucleus to gain access to DNA polymerase, whereas positive sense RNA can translate in cytoplasm.)
- Assembley - Packaging of new genomes/viral proteins
- Budding - Exocytosis & obtains envelope. If naked then cell lysed.
What are the stages of viral infection
- Entry - Enter via skin (orf), Respiratory (influenze), alimentary orr transplacenta.
- Replication :
- Local - acute, replication at the site of infection e.g influenza/orf
- Systemic - replication followed by dissemination to distant sites via blood/lymph. More severe pathology
- Shedding - Virus reahes highest titre in orggan/tissue then sheds
What are cytopathic effects of viruses
- Inclusion bodies
- Cell membrane abnormalities
- syncitia formation
- lysosomal damage
- cell lysis
- Re entering of cell cycle
Types Of viral infection
- Acute - Short inoculation, quicker onset of disease
- chronic
- Recover but still infectous microbe. intermittent shedding
- recovery i followed by growth at privilidged site ( antigen can be introduced with no inflammatory response)
- slow continous growth
