Archive for December, 2009

Immunity To Parasites

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A parasite is an organism which lives on or in another organism called the host. The parasite needs the host to live, but the host gains no benefit from having the parasite. The 3 main classes of parasite are protozoa (unicellular organisms), worms, and arthropods (insects and arachnids).

In comparison to acute bacterial or viral infections, a parasitic infection lasts much longer due to their well-evolved and effective methods of avoiding the immune system, a parasite is successful if it can successfully avoid or subvert immune responses directed against it. Many parasites are able to survive years in a host causing little or minimal harm, however for some parasites it is beneficial to cause disease in the host.

Parasites can cause harm to the host by:

  • Competing for nutrients in the host
  • Disrupting host tissue
  • Destroying host cells
  • Mechanical blockage

Endoparasties – Live inside the host

Ectoparasites – Live outside of the host

Protozoan Parasite Immunity

Protozoa are defined as single celled, eukaryotic microorganisms that lack cell walls. Not all protozoa are parasitic however.

Innate Immunity against Protozoa

Similar mechanisms to the removal of bacteria and viruses are in place to remove protozoa threats; this includes the complement system, NK cells and phagocytosis. However, many protozoa are breed and species specific, different species can be more susceptible to different pathogens.

Acquired Immunity against Protozoa

The acquired immune response to protozoa includes both humoral (antibodies, Helper T-cells and B cells) and cell mediated responses (Cytotoxic T-cells, macrophages, NK cells and cytokines).

Antibodies specific to protozoa surface antigens are released to control parasite numbers in the blood and tissues; this is aided by TH2 (T-helper 2 cells).

The cellular mediated immunity targets the intracellular infections and is mainly TH1 (T-helper 1 cell) driven. For the effective removal of most protozoa, the combination of TH1 and TH2 aided responses are required to target the protozoa at different stages of their life cycle.

Protozoa Evasion of Immunity

The mechanisms that protozoa have evolved to avoid the immune system are:

  • The avoidance of attachment and phagocytosis
  • Immunosuppression of the host immune system (e.g. destruction of T cells)
  • The blockage of antigen presentation (Expression in association with MHC Class II)
  • Alter surface antigens (Antigenic variation)
  • Block surface antigen expression to avoid detection (Parasite coats itself with host proteins)

Vaccinations to prevent possible protozoa infections have provided limited success, frequent boosters are needed and the vaccine must contain a mix of species and strains of protozoa to maximise its success.


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Spermatogenesis is the biological process whereby spermatogonia (the germ cell) develop into spermatozoa (the mature sperm cells). This process takes place in the seminiferous tubules of the testes; this is the starting point for spermatogenesis. Stem cells adjacent to the inner tubule wall divide, beginning at the walls and proceeding into the innermost part, or lumen producing immature sperm. Maturation occurs in the epididymis where sperm develop a tail and become motile.

Anatomy of the Testes

Seminiferous tubules comprise the majority of the structure of the testes. The remaining spaces between the tubules are occupied by interstitial tissue.

Interstitial Tissue

The interstitial tissue comprises mainly of blood vessels, lymph gaps, connective tissue and Leydig cells (specialised cells found in interstitial tissue adjacent to seminiferous tubules). Mast cells and macrophages are also present in small numbers.

Leydig Cells – These cells have an abundance of smooth endoplasmic reticulum and no rough endoplasmic reticulum, along with large amounts of mitochondria, lipid droplets and centrioles. They also have a prominent Golgi complex. Another cell specific feature is the receptors they have on their cell membrane that are highly specific to luteinising hormone (LH) – This differentiates them from other testicular cells, as they are the only cells to have these receptors.

Follicle-stimulating hormone (FSH) increases the response of Leydig cells by increasing the number of LH receptors expressed on their surface. The LH receptors when stimulated secrete steroidal hormones such as testosterone. Testosterone has a key role in the development of spermatozoa (spermatogenesis).

Seminiferous Tubules

Typical seminiferous tubules include the Sertoli cells and germ cells. The epithelium of these tubules is known as the germinal epithelium. The seminiferous tubules have a fluid filled lumen; mature spermatids are released into this lumen as fully mature spermatozoa. Myoid cells surround the basement membrane of seminiferous tubules; they are contractile in nature and their contractions move sperm along the seminiferous tubules.

Sertoli Cells

Sertoli cells have a main function in the nurturing of spermatozoa through their early stages of development from germ cells right up to their mature spermatid form (before being released into the seminiferous tubules to become spermatozoa). Sertoli cells therefore have a prime role in the co-ordinating of spermatogenesis – without Sertoli cells, spermatogenesis cannot take place.

Near the base of the cells in their lateral walls, tight junctions join Sertoli cells to one another. The formation of tight junctions means that inter-cellular diffusion of material is prevented. The tight junctions form a complete barrier that divides the tubule into a basal compartment and an adluminal compartment. Different types of germ cells occupy the different compartments. This barrier forms a blood-testes barrier, which isolates spermatocytes from the rest of the body, allowing for the environmental conditions required for spermatogenesis.

An important feature of the blood-testes barrier is that it prevents immune cells from reaching the haploid cells produced during spermatogenesis. This is important because the haploid cells are not recognisable as ‘self’ cells, meaning if the immune cells could reach them, they would destroy them. If damage were to occur to the tight junctions forming the blood-testes barrier, immune cells would be able to come into contact with the germ cells triggering an immune response and the production of antibodies causing the sperm cells to become non-functional – resulting in infertility of the male. Sertoli cells are also unable to proliferate; the body is unable to replace any lost Sertoli cells.

Sertoli cells have cell-membrane receptors specific for FSH, which when stimulated increases production of cyclic AMP

They are also able to convert cholesterol to pregnenolone, which is then converted to testosterone. They also produce specific proteins such as androgen binding protein under the influence of FSH and testosterone.


Below is only the introduction to this article on cryptorchidism, if you are interested and this is what you were looking for, then head over to our website, where you can download this article and many more for free! If you don’t want to download them, then it is possible for you to view them online in your browser!

Also remember to check out the new questions being added all the time, you can see which articles have questions by searching the index, where you will see a link next to the article like this [Questions]


Cryptorchidism is a disorder where either one or both testes fail to descend and are therefore absent from the scrotum.  This usually occurs during foetal development when the testes begin their movement or descent from an abdominal position through the inguinal canal into the scrotum. Because the testes have failed to descend and therefore remain within the body, the temperature is too hot for sperm production to occur, rendering the male infertile.

There are however varying levels of cryptorchidism:

• Undescended testicles may later fully descend (usually within 1 year) leaving the male without fertility problems

• Testicles which have not fully descended but have partially reached the scrotum may be able to produce some sperm

• Only on testicle may not descend, but as the other will have fully descended the male will be fertile

• If both testicles fail to descend (bilaterally cryptorchid testes) then the male is infertile

Only sperm production is affected however (due to the high body temperature) which means that the natural hormone production of the testes are unaffected, the male will still behave normally therefore and express normal sexual behaviour.

The possible outcomes of testes failure to descend:

• Testis could be found anywhere along the “path of descent” from high in the posterior (retroperitoneal) abdomen, just below the kidney, to the inguinal ring

• Testis could be found in the inguinal canal

• Testis could be ectopic, that is, found to have “wandered” from that path, usually outside the inguinal canal and sometimes even under the skin of the thigh, the perineum, the opposite scrotum, and femoral canal

• Testis could be undeveloped (hypoplastic) or severely abnormal (dysgenetic);

• Testis could have vanished – May therefore be anorchid or monorchid (Not formed)

The Oestrous Cycle

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The oestrous cycle is the reproductive cycle found in most mammalian placental females whereby there are recurring periods when the female is fertile and sexually receptive (oestrus) interrupted by periods in which the female is not fertile and sexually receptive (anoestrus). Animals that have oestrous cycles reabsorb the endometrium (inner membrane of the mammalian uterus) if conception does not occur during that cycle. The oestrous cycle is contrasted with the menstrual cycle in which the endometrium is shed through menstruation when pregnancy does not occur and in which the female may be sexually receptive at any time during the cycle.

There are many variations among animals in terms of their oestrous cycles. Some may undergo oestrous only one time a year during a particular season (white-tailed deer, foxes), while others may undergo a succession of cycles during a certain time of the year if they do not become pregnant (horses, sheep), and others may undergo cycles throughout the whole year (mice, cows, pigs).

Below is an overview of the hormonal changes during the oestrous cycle: (Download article to see this)

More Questions

Even more questions uploaded onto you can check them out now. See the previous blog post for how to get the best from those questions using flash-card software (This isn’t necessary as you can always use excel to view them). Remember to right click the question link and then click ‘Save Target As…’ otherwise the questions will appear in your browser window (Not ideal for viewing/printing etc.)

Also, if you have any ideas or suggestions for future articles or questions, drop a message on the comments page (There is a link at the top of the main page)

Hope you all had a good christmas and get in touch to ensure the website moves in a direction which will benefit you!

Question Time! has been updated and now questions are starting to appear for you to download! These questions are short answer/MCQ style.

Navigate to the index page where you will find a list of all the currently published articles (which are free to view/download/print) and if the article has questions available there will be a link next to it saying this. You can either:

  1. Click the Link to view the questions in your browser (Not really recommended)
  2. Right click the link, then click – ‘Save Target as…’ to save the file to your hard drive as a .csv file which you can open in excel
  3. Or probably the best, if you have some form of flash-card software (e.g. mental case, cram, gFlash, etc.) you can download the file and import it directly into the software which makes the questions look a lot more appealing. Such software is also available for mobile devices – so you can download them and quiz yourself on the go!

At the time of writing, only one set of questions is currently available (The complement system questions) but many more will be coming in future updates so be sure to follow us on twitter so you know when more are added!

If you would like to ask a question about any of this, where to get such flash-card software, how to view etc. or if you would like to suggest a topic for future downloadable questions to be based on, then visit the comments section of and be sure to leave a comment there!

Immunity Against Viruses


Viruses are small particles which infect living cells; this makes them obligate intracellular parasites. They have no reproductive mechanisms of their own so instead must use host cells to replicate. There are two main threats for a virus; the host’s immunity and the death of the host. Both of which will typically prevent the virus from propagating.

Many viruses are able to survive within the host for a long time without causing disease to the primary host. However when this virus is transferred to a secondary host, it is possible for a lethal disease to arise as a result. (An example is the transmission of the rabies virus to man). Vaccinating against the harmful effects of a virus therefore works best in the secondary host where the virus is not well adapted.

Structure of a Virus

Particles of a virus are known as virions. Virions encapsulate the nucleic acid core, which is surrounded by a layer of lipoprotein (or protein); this is known as the capsid. The degree of complexity of a virus can differ greatly. Viruses can contain either RNA or DNA and they can be either single stranded or double stranded, any combination of these still allows the virus (once in the host cell) to replicate.

Viral Pathogenicity

The virion is able to bind to a wide range of molecules to mediate attachment and internalisation by a host cell (by endocytosis). Once inside the cell, the capsid of the virion breaks down releasing the viral nucleic acid into the cytoplasm of the host cell. Once inside the cytoplasm, the viral nucleic acid is able to replicate and at the same time, it is also able to inhibit the production of DNA/RNA (thus protein synthesis) of the host cell.

Possible outcomes for a cell infected by a virus:

Lytic Infection – Host cell is destroyed, this is caused by virulent viruses

Persistent Infection – Host cell is not lysed, but virions are released slowly, over a longer period

Latent Infection – Occurs when there is a delay between the infection by the virus and the onset of symptoms

Transformation – Some viruses are able to transform a normal cell into a tumour cell