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).

Advertisements

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

Types of Inflammation

An extensive list of the types of inflammation you may encounter and the part of the body which they affect. If you have any additions or notice any which are incorrect then please comment at the end of this post!

This was brought to you by www.jameswatts.co.uk

Types of Inflammation

  • Adenitis – Inflammation of the adenoids
  • Adnexitis – Inflammation of the adnexa uteri
  • Alveolitis – Inflammation of the alveoli
  • Angiitis – Inflammation of  blood or lymph vessels
  • Appendicitis – Inflammation of the appendix
  • Arthritis – Inflammation of the joints
  • Balanitis –  Inflammation of the glans penis
  • Blepharitis – Inflammation of the eye
  • Bronchiolitis –  Inflammation of the bronchioles
  • Bronchitis – Inflammation of the bronchi of the lungs
  • Bronchoalveolitis – Inflammation of the bronchioles of the lungs
  • Bursitis – Inflammation of a bursa
  • Cellulitis – Inflammation of subcutaneous or connective tissue
  • Cholangitis –  An inflammation of the bile duct
  • Cholecystitis –  An inflammation of the gallbladder
  • Colitis – Inflammation of the colon
  • Conjunctivitis – Inflammation of the conjunctiva
  • Cystitis –  Inflammation of the urinary bladder
  • Dermatitis – Inflammation of the skin
  • Diverticulitis – Inflammation of the diverticulum
  • Encephalitis – Inflammation of the brain
  • Endocarditis – Inflammation of the endocardium and possibly the heart valves
  • Endocervicitis – Inflammation of the mucous membrane of the uterine cervix
  • Enteritis – Inflammation of the intestines, generally the small intestine
  • Enterocolitis – Inflammation of the mucous membranes of the small intestine and of the colon
  • Epicondylitis – Inflammation of the elbow or knee
  • Gastritis –  Inflammation of the lining of the stomach
  • Gastroenteritis – Inflammation of the mucous membranes of the stomach and intestine
  • Gingivitis – Inflammation of the gums or gingivae
  • Glomerulonephritis – Inflammation of the glomeruli
  • Glossitis – Inflammation of the tongue
  • Hepatitis – Inflammation of the liver
  • Ileitis – Inflammation of the ileum
  • Iritis – Inflammation of the iris
  • Keratitis – Inflammation of the cornea
  • Keratoconjunctivitis – Inflammation of the cornea and the conjunctiva
  • Laryngitis – Inflammation of the larynx
  • Lymphangitis – Inflammation of the lymph glands
  • Mastitis – Inflammation of a breast or udder
  • Mastoiditis – Inflammation of the ear
  • Meningitis – Inflammation of the meninges
  • Myocarditis – Inflammation of the myocardium
  • Myositis – Inflammation of the muscles
  • Nephritis – Inflammation of the kidney
  • Neuritis – Inflammation of one or more nerves
  • Oesophagitis – Inflammation of the oesophagus
  • Oophoritis – Inflammation of the ovaries
  • Osteomyelitis – Inflammation of the bone
  • Otitis – Inflammation of the ear
  • Pancreatitis – Inflammation of the pancreas
  • Parotitis – Inflammation of one or both parotid glands
  • Pericarditis – Inflammation of the pericardium, the membrane that surrounds the heart
  • Peritonitis – Inflammation of the peritoneum
  • Pharyngitis – Inflammation of the pharynx
  • Phlebitis – Inflammation of a vein
  • Polyneuritis – Inflammation of multiple nerves
  • Proctitis – Inflammation of the anus and the lining of the rectum
  • Prostatitis – Inflammation of the prostrate
  • Pyelonephritis – Inflammation of the urinary tract which has reached the kidney
  • Retinitis – Inflammation of the retina
  • Rhinitis – Inflammation of the mucous membranes of the nose.
  • Salpingitis – Inflammation of the fallopian tube
  • Sinusitis – Inflammation of the paranasal sinuses
  • Spondylitis – Inflammation of the spine
  • Stomatitis – Inflammation of the mucous membrane lining of the mouth
  • Synovitis – Inflammation of the synovium
  • Tendinitis – Inflammation of a tendon
  • Tenosynovitis – Inflammation of the fluid-filled sheath (the synovium) that surrounds a tendon
  • Thyroiditis – Inflammation of the thyroid gland
  • Tonsillitis – Inflammation of the tonsils
  • Tracheitis – Inflammation of the trachea
  • Urethritis – Inflammation of the urethra
  • Uveitis – Inflammation of the middle layer of the eye – the uvea
  • Vaginitis – Inflammation of the vagina
  • Vasculitis – Inflammation of the wall of blood vessels
  • Vulvovaginitis – Inflammation of the vulva and vagina

Acute Inflammation

From now on I intend to only include the introduction of learning articles, that way you dont have to scroll for ages to get the information you need. To view and download this 9 page article on acute inflammation, visit http://www.jameswatts.co.uk/VetSci/Learn/Learn.html

Introduction

Acute inflammation is the immediate response to an inflammatory agent (such as a pathogen or foreign material) or necrotic cells/tissue caused by cell injury and death. It undergoes many vascular changes in order to increase the amount of antibodies and leukocytes at the site of inflammation. The major contributing factors are:

  1. Alterations in the vascular flow and calibre – increasing blood flow
  2. Structural changes of the microvasculature (capillaries, arterioles and venules) – Resulting in the leakage of plasma proteins (e.g. fibrin) and the evasion of leukocytes
  3. Emigration of leukocytes from the microcirculation – Resulting in the accumulation of leukocytes in the area of injury

An Introduction to Inflammation

Introduction

Inflammation can be characterised by 5 main features (names in brackets are the Latin), these are:

  • Swelling (tumour)
  • Heat (calor)
  • Redness (rubor)
  • Pain (dolor)
  • Loss of function (functio laesa)

Inflammation is a protective response by the body towards cell injury. Cell injury may be due to; necrotic cells or tissue, the introduction of microbes (such as viruses or bacteria), toxins, hypoxia, etc. Inflammation is therefore the body’s way of attempting to remove the primary cause of inflammation and any damage that may have occurred as a result (Healing and repair). However if inflammation did not occur, then the body would be unable to deal with wounds and infections letting them go unchecked and progressively destroy the tissue. All injured organs would therefore be unable to regain function, eventually leading to mortality.

Inflammation is a complicated series of biological reactions, only taking place in vascularised tissue, simply however it works by attempting to remove, dilute or barricade the injurious/pathogenic agent or tissue. Its secondary role is to induce the healing and the repair of the damaged tissue. The result of this is an accumulation of leukocytes and fluid in the vascularised tissue.

It is also important to remember that chronic inflammation may pose problems to the body; these may be hypersensitivity reactions, autoimmune reactions or organ dysfunction due to the formation of scars/obstructions caused by fibrosis e.g. hay fever (hypersensitivity) or arthritis (autoimmune response).

The Inflammatory Response

As said before, an inflammatory response will only occur in vascularised connective tissue. A typical inflammatory response will involve the utilisation of plasma, circulating cells (leukocytes), blood vessels (endothelial cells) and other cells/extracellular matrix in the connective tissue.

The inflammatory response is mediated by chemical factors which are derived from the plasma or from the cells. The chemical mediators are triggered by an inflammatory stimulus which could include anything from a splinter (foreign material) to necrotic cells. Necrotic tissue/cells are able to contribute to inflammation (as opposed to triggering the inflammatory system) by producing their own inflammatory mediators. The chemical factors involved in the whole process both amplify the inflammatory response and impact on its progression.

The inflammatory response will only stop when the initial stimulus is removed and all the chemical mediators which arose as a result are inhibited (or dissipated).

Components of Inflammation

Some of the main components of inflammation include:

Connective tissue layer:

  • Mast cells – Resident cells of tissues which contain many granules rich in histamine and heparin. They play an important protective role as well, being intimately involved in wound healing and defence against pathogens.
  • Fibroblasts – A type of cell which synthesizes the extracellular matrix and collagen and also plays a critical role in wound healing.
  • Macrophages – Resident large phagocytes (Some also circulate in the blood stream)

The Circulating Cells:

  • Polymorphonuclear Leukocytes (Neutrophils)
  • Lymphocytes
  • Monocytes
  • Eosinophils
  • Basophils
  • Platelets

The Extracellular Matrix:

  • Collagen and Elastin fibres – These are structural fibrous proteins
  • Proteoglycans
  • Adhesive glycoproteins (Fibronectin, laminin, non-fibrillar collagen, tenascin and others)

The Extracellular Matrix (ECM)

The ECM is a network of locally secreted and assembled proteins, such as collagen and elastin. It forms in the spaces surrounding cells and linkage occurs between cells and the ECM by adhesive glycoproteins (such as Fibronectin, laminin, non-fibrillar collagen, tenascin and others). It also consists of proteoglycans which are usually attached to the proteins. They have a net negative charge that attracts water molecules, keeping the ECM and resident cells hydrated. Proteoglycans may also help to trap and store growth factors within the ECM.

The function of the ECM is to sequester molecules such as water (using the mechanism described above), it also acts as a reservoir for growth factors and a substratum for cells to adhere, migrate and proliferate.

Terms Associated With Inflammation

The inflammatory response can be classified as either:

  • Acute inflammation – Typically these are of relatively short duration, from a few minutes to a few days. The main characteristics of acute inflammation are; exudation (see below) of fluid and plasma proteins (oedema) and the emigration of leukocytes (predominantly neutrophils)
  • Chronic inflammation – Chronic inflammation is of longer duration and is associated with:
    • The presence of lymphocytes and macrophages
    • Proliferation of blood vessels
    • Fibrosis
    • Tissue necrosis

Definitions:

  • Exudation – The escape of fluid, proteins and blood cells from the vascular system into the interstitial tissue or body cavities
  • Exudate – Inflammatory extravascular fluid which contains; a high protein concentration, much cellular debris and a specific gravity (density in relation to water) of >1.012. The specific gravity of >1.012 is due to the increased permeability of small blood vessels in the area of injury.
  • Transudate – This is fluid with a low protein content (of which the main constituent is albumin) and it has a specific gravity of <1.012 due to the ultrafiltrate of blood plasma which results in a hydrostatic imbalance across the vascular endothelium. Permeability of the endothelium is not altered.
  • Oedema – Excess fluid in the interstitial or serous cavities (The fluid can be either transudate or exudate)
  • Pus – Inflammatory exudate rich in leukocytes (predominantly neutrophils) and cell debris.
Advertisements