Archive for December, 2009

Immunity to Bacteria

Another article is up on www.jameswatts.co.uk, this one is about how the immune system deals with bacteria – Below is only the introduction, if you would like to read more then remember to check out the above ^^^

Introduction

Bacteria exist naturally on many biological surfaces, for example the skin or the lining of the intestines. Bacteria like these make up the body’s natural flora and have a range of symbiotic relationships; a good example would be the flora of the rumen in cattle which degrade food materials, providing energy for both the cattle and the bacteria. The three main types of symbiotic relationship are:

•Mutualism – Both members of the symbiotic relationship benefit

•Commensalism – No apparent harm/benefit occurs to either member of the relationship

•Parasitism – One member of the relationship is living at the expense of the other resulting in disease

The pathogenicity of a certain bacteria depends on its survival inside the host – how well is it able to resist or evade host defence mechanisms and immune response. The resulting disease/damage caused to tissue is due to either the pathogenicity of the bacteria or the immune response of the host itself.

Bacterium Structure

Prokaryotes vs. Eukaryotes

Bacteria are prokaryotes, they differ from eukaryotic cells (such as those in humans) because the structures within prokaryotic cells are typically not compartmentalised. Prokaryotes also lack nuclear membranes, mitochondria, endoplasmic reticulum, a Golgi body, phagosomes and lysosomes (unlike eukaryotes). Also, prokaryotes only have a single, circular chromosome – unlike the nucleus of a eukaryotic cell.

Gram Staining

Bacteria can be very broadly categorised into two groups, gram negative and gram positive. This describes whether or not the bacterial will stain when using a gram stain. Gram-negative bacteria do not take up the gram stain; this is due to an extra outer membrane. Gram-positive bacteria do not have this extra outer membrane and so will take up the gram stain.

Bacterial Structures

•Plasmids – This is an extra-chromosomal strand of circular DNA, it is able to replicate independently from the main chromosome in the bacteria and the genes which the plasmid codes for aren’t typically essential for survival. The plasmid may be shared between bacteria which may be of concern as the plasmid often codes for pathogenesis and anti-bacterial resistance.

•Cell Envelope – This is the extra outer membrane seen in gram-negative bacteria

•Flagella – A protein organelle (consisting of flagellin) which is used for locomotion

•Pili (Fimbriae) – This is the organelle which allows adhesion to the epithelium of host cells.

•Capsules and ‘slime’ layers – These are layers outside of the cell envelope in some specialised bacteria. This extra layer allows the inhibition of ingestion by phagocytes as they are unable to detect the bacterium. A well-defined layer is known as a capsule, a lesser defined layer is known as a slime layer.

•Endospores – This is a term given to dormant forms of bacteria which are able to survive harsh conditions

Advertisements

Bacterial Immunity

This article can be found in full length at www.jameswatts.co.uk – Only the introduction is shown here

Introduction

Bacteria exist naturally on many biological surfaces, for example the skin or the lining of the intestines. Bacteria like these make up the body’s natural flora and have a range of symbiotic relationships; a good example would be the flora of the rumen in cattle which degrade food materials, providing energy for both the cattle and the bacteria. The three main types of symbiotic relationship are:

  • Mutualism – Both members of the symbiotic relationship benefit
  • Commensalism – No apparent harm/benefit occurs to either member of the relationship
  • Parasitism – One member of the relationship is living at the expense of the other resulting in disease

The pathogenicity of a certain bacteria depends on its survival inside the host – how well is it able to resist or evade host defence mechanisms and immune response. The resulting disease/damage caused to tissue is due to either the pathogenicity of the bacteria or the immune response of the host itself.

Developing Immunity in New-Borns

The start if the article about new-born immunity is below, if you would like to see this in full then please remember to visit www.jameswatts.co.uk where you can also find a multitude of other articles and stories as well!

Introduction

Any new-born animal is born from a sterile environment (e.g. a mother’s womb) into an environment which is filled with microbes and pathogens. Therefore it is important that the newly born animal is able to protect itself in its new, harsh environment. In most species (especially those with longer gestation periods) at birth, the immune system is well on its way to being fully developed but is not yet complete, taking some time (up to several weeks) to become fully functional.

For the immune system to develop, antigenic stimulation must occur, along with the development of antigen sensitive cells. This means that for the first few weeks of a new-borns life they are vulnerable to infection as their immune system is not yet complete. To overcome this, a temporary support system is provided by the mother. The mother is able to pass to her offspring antibodies and T-cells. These are able to temporarily support the animal whilst it builds up its own immune system. This is known as passive immunity.

The Developing Immune System

The development of the immune system in mammals as a foetus follows a consistent pattern. The initial lymphoid organ which develops is the thymus which is then followed by the secondary lymphoid organs (e.g. tonsils, Peyer’s patches, spleen, adenoids, skin etc.). The ability of the foetus to initiate a cell-mediated immune response develops around the same time as antibody production begins.

Vaccination

Here is the start of our most recent article, vaccination… to view/download/print this article head to www.jameswatts.co.uk as a shortcut you are now able to click the download button on the home page to download the most recent article, thus saving you from clicking through to the index.

Introduction

There are two main types of immunisation, either passive or active immunity. Passive immunity being that derived naturally from a mother. A young animal will gain antibodies from its mother either during birth via the placenta or shortly after birth when the animal consumes colostrum from its mother. It is also possible to gain passive immunity by artificial means, this involves injecting an individual with an antisera (containing specific immunoglobulins). There are advantages and disadvantages of this artificial passive immunisation, the main benefit being that the resulting immunisation is immediately effective. The disadvantages include:

  • Temporary effect, lasting only until the Ig proteins are metabolised (a few weeks)
  • Only has an effect with diseases where an antibody response is the principle method of protection (as opposed to cell-mediated responses)
  • There is the possibility that hypersensitivity may arise from use of serums which have been obtained from foreign species
  • Induction of an active acquired immunity is blocked

The other type of immunisation is active immunisation, this is actively acquired immunity derived from either a natural infection or from artificial immunisation (inoculation with a weakened or dead organism).

Cellular Mediated Immunity

Ok so today you are getting a little more than the introduction… arent you lucky! But the premise is still the same, to view/download/print this article, please head to http://www.jameswatts.co.uk! Apart from that, id like to present: Cellular Mediated immunity! (Or at least 1 of the 6 pages)

Introduction

The two major components of the adaptive immune system are known as cellular and humoral immunity. For an effective immune system these two branches of the adaptive immune system must interact. The main effector cells of these two systems are the T and B-lymphocytes.

T and B-lymphocytes both develop from a common progenitor in the bone marrow. T cells then move on to fully develop in the thymus and B cells develop in the bone marrow (in the foetus they develop in the liver). Any T or B cells that are at rest are morphologically indistinguishable.

Both T and C cells are able to recognise and bind an antigen and show a specific memory. B cells recognise antigens with the surface membrane Ig – which determines the specificity of the cell. T cells recognise the antigen with the T cell receptor which has both variable and hypervariable regions similar to yet still distinct from those of the immunoglobulin molecules.

Stimulation of a T cell by a specific antigen leads to the generation of effector T cells, which may directly and specifically kill cells bearing the appropriate antigen (or have other protective effects)

T and B cells can be distinguished by; their surface cells markers or their antigens. Many of these have a functional role e.g. CD8 are T Cytotoxic cells.

The Complement System / Cascade

As ever, below is only the introduction to this article. To review the article in its entirety please visit http://www.jameswatts.co.uk where you will find the full article for this and many similar articles under the “Learn” section. Hope this helps you:

Introduction

The complement system or complement cascade as it is also known is a complex system of multiple proteins involved in inflammation and immunological response. The components of the complement system can be found throughout the body in fluids, providing the body with a systemic means of protection. Antibodies depend on complement for many of their biological activities.

Why is complement important?

  • It opsonises pathogens to promote phagocytosis by phagocytes which display receptors for complement
  • Certain components of complement act as good chemoattractants recruiting and activating phagocytes at the site of infection
  • Complement structures can cause cytolysis or damage to certain bacteria by puncturing their membrane

The important protein components of complement are number C1 to C9 (they are numbered in their order of discovery however and not their order of action as you will see later). Upon activation certain components may split into sub components, usually the small components are named with an ‘a’ e.g. C5a (these are the components which are able to diffuse through tissue readily) and the larger components with a ‘b’ e.g. C5b (these are the components which do not easily diffuse).

The complement system is known as a cascade because of the triggering and amplification of further components of the system. In the cascade once a component has been activated by a proteinase, the molecule itself which was activated becomes a proteinase for the next component of the cascade. The whole complement cascade can be triggered in its entirety in a matter of microseconds. During the activation process the smaller ‘a’ subcomponent peptides which are formed mediate many of the other effects caused by the complement cascade, for example acting as chemoattractants.

There are three types of complement cascade, the classical and alternative pathways and the Mannan-binding lectin pathway. Both provide a path to the cleavage of C3 which is a central event in complement activation.

Chronic Inflammation

For the rest of this article please visit www.jameswatts.co.uk/vetsci/learn were you can download it for free!

Introduction

Chronic inflammation is inflammation which has been of prolonged duration. It is the simultaneous occurrence of active inflammation, tissue destruction and attempts at repair.

Chronic inflammation can either follow on from acute inflammation or it can begin insidiously (a lack of symptoms, the patient is unaware of the onset of the disease with a subtle and cumulative harmfulness) e.g. tuberculosis

Chronic inflammation arises with the following conditions:

  • Persistent infections such as those from mycobacteria or certain fungi/parasites. This may cause type IV hypersensitity (delayed-type) but has low toxicity. This is a granulomatous inflammation
  • Prolonged exposure to exogenous or endogenous (potentially toxic) agents
  • Autoimmunity where auto-antigens evoke a self-perpetuating immune reaction which results in chronic inflammation

The histological features of chronic inflammation:

  • Tissue section infiltrated with mononuclear cells (macrophages, lymphocytes, plasma cells)
  • There is tissue destruction which has been mainly induced by inflammatory cells
  • There are attempts at repair of this tissue, characterised by; connective tissue replacing the damaged tissue, proliferation of small blood vessels (angiogenesis – formation of new blood vessels) and fibrosis
Advertisements