Ringworm also known as Tinea or Dermatophytosis is actually a fungal infection of the skin. So why is it called ringworm, I hear you ask? The Ancient Greeks called it Herpes (which means circular or ring form) and the Romans associated the disease with the larval stage of Tinea, which is the genus for clothes moth. The two names were eventually combined to form the word “ringworm” before the actual cause of ringworm was known in the early 1800s.
Ringworm is given a specific name is depending on which area of the body is affected. The list below lists the various areas of the body that can be affected with ringworm (tinea) and the name given. In this article Tinea Capitis will be covered in the most detail.
Areas of the body where Ringworm can be found.
Beard -Tinea Barbae
Body- Tinea Corporis
Face- Tinea Faciei
Foot-Tinea Pedis (“athlete’s foot”)
Nail-Tinea Unguium (Onychomycosis)
The fungi involved in Tinea Capitis are saprophytic T tonsurans fungi. These fungi are able to invade and break down the keratinized tissues of the skin, hair and nails. Their keratinophilia (keratin loving) behaviour allows them to use keratin as a growth substrate (food). Tinea Capitis can be a highly contagious infection. Whether or not a person becomes infected depends on the individual’s age and the strength of their immune system. For example a young child may easily contract scalp ringworm and spread it to other children
Clinical features of Tinea Capitis
As mentioned above the fungus that is the current predominant cause of tinea capitis is T. tonsurans. Scalp infections caused by this fungus are hard to diagnosis because of the wide and varying clinical presentations. However there are six main features to look out for:
•Grey Type-Grey circular patches of alopecia with scaling scalp.
•Black dots- This is where the hair has broken off at the scalp, leaving small lengths of hair shaft above the surface of the hair. The broken hair shafts appear as small dots on the surface of the scalp within angular patches of alopecia.
•Kerion- This results from a marked inflammatory response to the fungi. The scalp is usually boggy and swollen. Patients with kerion often have associated enlarged lymph nodes in the neck (cervical lymphadenopathy) or face.
•Diffuse pustular pattern-Pustules are seen scattered across the scalp. Painful lymphadenopathy may also be present.
•Moth Eaten- This appears as patchy hair loss with scaly scalp.
•Diffuse scale-This clinical feature can resemble dandruff. The scalp has widespread scale.
Treatment for Tinea Capitis requires systemic antifungal drugs. The use of antifungal creams is unable to penetrate the hair shaft, and hence is not used to treat this infection.
If you suspect Tinea Capitis please visit your GP.
Chemical Procedures and Hair Breakage
Chemical procedures such as hair permanent hair dyes, bleaching, relaxers and perms can cause hair breakage. Below briefly describes common chemical procedures and how they could potentially cause hair breakage.
1.Permanent Hair dyes
Permanent colour contains an oxidising (hydrogen peroxide) agent, an alkalizing agent (ammonium hydroxide) and a pigment. The ammonium hydroxide opens up the cuticle by raising the pH to 8-9.5 allowing the pigment molecules to enter into the hair shaft. Ammonia also decomposes hydrogen peroxide into oxygen. The oxygen released from the hydrogen peroxide breaks down the melanin in the hair producing oxy-melanin, which is colourless. Large pigment molecules are produced when the pigment comes into contact with the oxygen released from the hydrogen peroxide. These large molecules of pigment are unable to leave the hair shaft and this results in permanent hair colour within the hair shaft.
A) Melanin+ Nascent Oxygen (released from hydrogen peroxide) =Oxy-Melanin (colourless)
B) Oxy-Melanin + Pigments (from hair dye) =Permanent hair colour.
The potential hair damage from permanent hair colouring arises when it is done too often or done without subsequent conditioning afterwards or carried out on weak hair to start with. The hair can become dry and brittle which can result in hair breakage.
Hydrogen peroxide is used to de-colourise the natural pigments in the hair. Ammonium hydroxide is also used in the process to speed up the release of oxygen from the hydrogen peroxide and to swell and open up the cuticle to allow the hydrogen peroxide to enter the hair shaft.
The damage done to hair during bleaching is listed below:
• Permanent loss of disulphide Bonds
Oxidation of cystine to cysteic acid in the disulphide bonds results in reduced tensile strength of the hair, which makes it more susceptible to breakage.
• Cuticle damage
If overlapping occurs during retouching then cuticle damage can occur. The cuticle can become rough and break away resulting in weak porous hair.
• Breakage of Polypeptide chains
Over bleaching can break polypeptide bonds in the hair which will result in hair shaft breakage.
During the perming process, hair bonds are broken through a chemical reaction called reduction. The reducing agents used in perms are called thiol compounds, usually ammonium thioglycollate is used. Another chemical used in perming is ammonium hydroxide, this opens up the cuticle to allow the thioglycollate to penetrate the hair shaft.
Once thioglycollate is in the cortex of the hair, it breaks the disulphide bonds in the hair by adding hydrogen atoms. The broken bonds are then reformed around perm rods (rollers) by oxidation using hydrogen peroxide.
Hair breakage during and after perming can be a result of the following:
• Cuticle damage caused when the ammonium hydroxide is applied the hair.
• Loss of protein during over- oxidation of the hair and lack of subsequent conditioning.
• Too much tension applied to the hair as it is curled around the rollers.
• Over-processing (reduction) results in too many cystine bonds broken. These broken bonds weaken the hair and make it susceptible to breaking.
• Over-neutralising with hydrogen peroxide results in cystine changing to cysteic acid which does not form linkages.
There two types of relaxers available, one type contains sodium hydroxide also known as lye relaxers and the other ‘No lye’ relaxer is based on two ingredients; calcium hydroxide and guanidine carbonate. The two ingredients in ‘No Lye’ relaxers are added together to form the alkaline relaxer (see fig 2 below).
Calcium hydroxide + guanidine carbonate →guanidine hydroxide (alkaline relaxer) + calcium carbonate
Relaxers break the disulphide bonds by a process called hydrolysis. The hair is permanently straightened and left very alkaline. When the relaxing process is complete the relaxer must be rinsed off using an acid balanced shampoo to neutralise the hydroxide ions and lower the pH of the hair.
Relaxers are very harsh alkaline chemicals which can cause breakage of the hair because of the following reasons:
• Relaxed hair is torsionally stressed and can break easily.
• Incomplete rinsing of the hair could leave the hair alkaline and result in dry brittle hair that breaks easily.
• Incorrect relaxing solutions and timing mistakes could also cause hair breakage. If relaxers are too alkaline and left on the hair too long they could have a depilatory action.
• Lack of conditioning treatments following relaxing.
The chemcials used in these procedures can be seriously damage your hair. Please make sure if you have any of the above procedures that they are carried out by a fully qualified professional.
J Norris-property of Roots2Ends
Hair breakage is not an uncommon thing to see on a daily basis, but there are different types and causes. The common types and their causes are covered below:
1.Idiopathic Trichoclasia (Gk-Thrix-Hair, Klasia-Breakage)
As the name suggests this type of hair breakage arises spontaneously or from an obscure unknown cause (idiopathic).
This hair condition is not classified to any particular age or nationality.The cause is usually attributed to harsh brushing or scratching of scalp.
2.Monilethrix (Latin-Monile-Necklace, GK-Thrix-Hair).
This hair breakage condition is also known as “beaded hairs” hence the name Monilethrix, because the hair can resemble beads on a necklace.
The hair is characterised by beaded hair fragile hair. This can be a lifelong disease which can spontaneously improve after puberty or during pregnancy.
This hair condition is often seen in infancy. It is not more prevalent in any sex or nationality.
This condition is due to a mutation in human hair keratin gene.
• The hair is fragile with varying degrees of breaking and alopecia
• The hair breaks to 0.5-2.5 cm and appears to be burnt 1.
• Usually occurs on scalp hair but can occasionally be seen in hair on other parts of the body such as the eyelashes, eyebrows, auxiliary and limb hairs.
• Lanugo hair appears normal after birth but is replaced after a few months with moniliform hair which is fragile, dry and lustless
There is currently no treatment for this hair condition, although retinoids, acitretin and minoxidil have shown limited and variable success. To minimise hair breakage, individuals with this hair condition should avoid hair trauma and chemical processing of the hair.
This is a self induced hair condition, in which the individual breaks of his or her hair. This condition is usually seen in neurotic patients hence the ‘mania’ part of word.
This condition is commonly known as ‘split ends’ (splitting of the hair shaft).
Below list the common causes of Trichoptiliosis:
• Over use of chemical treatments (relaxers, perming lotions, hair dyes)
• Excessive styling products especially products with high levels of alcohol (alcohol has the tendency to dry the hair out making it more susceptible to splitting).
• Heat damage (hairdryers, tong, flat irons etc)
• Improper detangling tools
• Improper detangling techniques
• Over washing
Regular trims help to prevent split ends and subsequent breakage.
5. Trichorrhexis Nodosa (Gk-Orrhexis-rupture, breaking, Nodosa-Nodes)
the picture shows Trichorrhexis Nodosa-fraying is seen at the site of a nodule or node.
This hair condition is diagnosed when small white dots are seen along the hair shaft.The hair will break very easily at these nodes.
Trichorrhexis Nodosa can either be caused by trauma (such as excessive brushing, back combing, heat styling or chemical procedures) or it can be congenital.
Treatment is aimed around minimising trauma to the hair from both chemical and physical avenues.
Alopecia areata (AA) is the name given to small circular patches of hair loss that occur on the scalp. Sometimes Alopecia Areata progresses to Alopecia Totalis, which is complete hair loss of the scalp or even Alopecia Universalis, which is complete hair loss of hair on the entire body (i.e. eye brows, eyelashes and body hair). The exact cause of AA is unknown but it is believed to be an autoimmune initiated disease. However not all scientists support this theory.
If we stick with the most widely accepted belief that alopecia areata is an autoimmune disease then the question that now has to be asked is what triggers the onset?
Psychological long-term stress and extreme shock have been reported as triggers for AA. But then another question has to be asked, and that is, why doesn’t everyone who goes through stress and or extreme shock develop AA? The answer to this question may lie in the fact that some people have a genetic predisposition to alopecia areata. It is generally believed that susceptibility to develop alopecia areata is polygenic, i.e. there are a number of genes that if inherited, result in the individual more likely to develop the disease. These genes are not reported to be mutations or defective genes, but normal functioning genes, with some genes carrying more weight or importance in promoting the susceptibility. The more genes inherited the more extensive the hair loss and the more persistent the alopecia areata.
Physical trauma has also been linked with alopecia areata. Cells under physical stress can produce heat shock proteins (HSPs). These proteins have been implicated in the autoimmune diseases lupus, ankylosing spondylitis and rheumatoid arthritis.
Chemicals have also reported as a trigger of alopecia areata. Workers in a paper factory developed alopecia areata after long-term exposure to the chemical acrylamide. Isolated cases have also been reported between HIV drug Zidovudine and the anti-depressant drug Fluvoxamine.
The good and bad news is that Alopecia Areata can be treated but not cured (yet). There is currently no conclusive diagnostic test for alopecia areata. Typically, the initial alopecia areata lesions appear as a smooth bald patch sometimes appearing within 24 hours. Some people describe irritation, tenderness or paresthesia (burning, tingling, numbness) in the affected area or in an area preceding the development of a new patch. Also small broken off hairs called ‘Exclamation Mark Hairs’ can be seen circumscribing the patch.
Corticosteroids, 8-methoxypsoralen plus ultra violet A light (PUVA), immune cell distractors and minoxidil are some of the documented treatment options for alopecia areata.
Seek advice from a qualified TTS Trichologist for a consultation and treatment. Treatment should only be done by a qualified professional.
Traction alopecia was first recorded in 1907 in Greenland in woman and girls who styled their hair in tight pony tails.
In the 21st century traction alopecia is commonly seen in Sikh men who grow their hair and beard very long and tightly wrap them up. It’s also seen in women who continuously wear weaves, hair extensions and those who tightly braid their hair.
This hair loss condition is caused by sustained tension of the scalp hair. Hair loss is usually symmetrical along the frontotemperal hairline and vellus hair (fine baby type hair) is usually seen in the affected area.
Hair loss can be permanent if traction persists over a long period of time resulting in atrophy (dying) of the hair follicles.
Do you have Traction Alopecia or could you be causing it?
In order to answer the above question you have to ask yourself the following questions:
A-Do you continuously put strain on your hair by tightly braiding your hair or by wearing long weaves/extensions without a least a months break?
B-When you have your hair braided or hair extensions applied, does your scalp ache for days after even weeks afterwards, and do you have to pat your head to try and relieve the ache?
C-Have you recently removed braids, a weave or hair extensions after a long period of time and noticed hair loss, especially along the hair line or temples?
If you answered yes to question A or B then you could be putting too much strain on your hair which could result in traction alopecia and then permanent hair loss.
If you answered yes to questions C then it would be advisable to stop wearing any hair extensions and to see a Trichologist. Myipaddress ask the eight ball A Fully qualified Trichologist (The Society of Trichologists) will be able to examine your scalp microscopically to determine if your hair follicles have been permanently damaged or not.
If the follicles are not permanently damaged then there are methods to stimulate hair growth.
If they are damaged then there are hair replacement systems that can be worn that will not apply any further strain on the hair or the hair can be styled naturally.
J.Norris-article property of Roots2Ends
Some women may have noticed that during pregnancy they had thicker healthier looking hair, but then shortly (3-4 months) after pregnancy their hair started to shed more than normal.This type of hair loss is called Telogen Effluvium.
(The word Effluvium comes from the Latin effluere which means to flow out and the word Telogen is the word used to describe the stage in the hair growth cycle when hair is naturally shed).
So why does it happen?
During pregnancy the hormone Oestrogen increases in the body and this causes the majority of hair on your scalp to remain in the growing phase (anagen phase) for the whole of your pregnancy. This is why pregnant women appear to have thicker hair because more hair is in the growth phase than normal. After pregnancy the hormones begin to return to normal, and hair that should have been shed during pregnancy (hair that has grown beyond its normal growth span) then enters the telogen phase (sheding phase) and a few months later they are shed. If the mother is breast feeding then hair loss can be delayed because the hormone Prolactin (breasting-feeding hormone) can prolong the hairs in the anagen phase (growing phase) even longer.
The Good News
Hair shed after pregnancy will appear to be a lot but shedding will decrease over the subsequent months and hair growth will return to normal. It’s important to remember that after pregnancy Telogen Effluvium doesn’t decrease scalp hair numbers. As soon as telogen hair is lost it is replaced by anagen hair (growing hair).
If you’re worried and hair loss prolongs.
If hair loss is prolonged (longer than 6 months) blood tests such as a full blood count, thyroid and serum ferritin test can be advisable (contact your GP).
J.norris-Property of Roots2Ends.