Warung Bebas

Sunday, 5 June 2011



Mbah Dukun listen the music, oldies song, do you know Michael Jackson? King of Pop? Yeah he was famous singer, everybody know who he is. He was a Afro American, however his skin changes to be white? How could it be happened? The anwer is…..

Vitiligo is a non contagious acquired pigmentation disorder characterized by sharply-defined white or loss the pigment of patches  variable shape and dimensions, increasing in size and number with time.
The exact cause of vitiligo is not known. It is an autoimmune disease that is believed to be hereditary. The proposed theories are that stress, thyroid dysfunction, skin injury, severe sunburns, chemicals, and medicines combined with the genetic tendency towards vitiligo can all contribute to the condition. However, these are theories that have not yet been substantiated.

Differential diagnosis
Differential diagnosis is made versus:
1) piebaldism, which is a rare depigmentation disorder due to a mutation of c-kit protooncogene affecting the differentiation and migration of melanocytes. It is characterized by stable and circumscribed white patches (with absence of melanocytes) present at birth, affecting the face (especially the central area with localized poliosis), sternal and abdominal zones, knees and elbows;
2) achromic nevus, which is a well-limited depigmented area, stable and evident at birth, in which melanocytes are either normal or reduced;
3) post-inflammatory leukoderma (e.g., after psoriasis or syphilis) in which patients have a history of pre-existing dermatosis;
4) pytiriasis versicolor, where mycologic examination reveals hyphae and spores;
5) depigmented lesions in leprosy, which shows anesthetic disturbance of sensibility.

Clinical description
The clinical picture consists of one or more well-demarcated and white maculae, progressing in size and number. They are asymptomatic generally. The lesions usually appear on sun-exposed or constitutionally hyperpigmented areas or on sites of stretch and pressure (face, dorsum of hands and fingers, external genitalia, knees and elbows). The margins of the patches are often hyperpigmented; hypopigmented areas sometimes occur together with the depigmented lesions and the normally pigmented skin (trichrome vitiligo). Rarely an inflammatory border may be found around the vitiligo patch resulting in a raised and erythematous edge (inflammatory vitiligo). Poliosis circumscripta, as well as canities and premature graying, can be observed; mucosae are rarely involved.
A. Vitiligo classification by Nordlund
Nordlund established a clinical classification based on distribution and extension of lesions (3). Three types have been delineated: localized, generalized and universal vitiligo.
1. Localized vitiligo
Localized vitiligo is classified into focalis (one or more patches in one area but not in a segmental pattern) and segmental (one or more maculae in dermatomal distribution) forms.
2. Generalized vitiligo
Generalized vitiligo can be subdivided into acrofacial (affecting face and distal extremities), vulgaris (the most common variety, with a symmetrical distribution of lesions in typical zones) and mixed (segmental plus vulgaris or acrofacial) types.
3. Universal vitiligo
Universal vitiligo involves more than 80% of the body.
B.Vitiligo classification by Koga
This is a more recent classification subdividing vitiligo into two clinical types: vitiligo non segmentalis (type A) and vitiligo segmentalis (type B) and (4).
1.Type A
Type A is more common, has a potential lifelong evolution and is associated with Koebner phenomenon and frequently with autoimmune diseases, such as Sutton nevus, thyroid disorders, juvenile diabetes mellitus, pernicious anemia and Addison’s disease.
2. Type B
Type B is rarer and has a dermatomal distribution; after rapid onset and evolution it usually exhibits a stable course.
The natural course of the disease is generally unpredictable, but it is often progressive; some degree of spontaneous repigmentation occurs in 10-20% of patients, but it is rarely cosmetically acceptable (5), often occurring in a perifollicular pattern.

Vitiligo is a challenging disease to treat. Most of the available treatments are not 100% successful. General aspects of treatments that need to be addressed include psychological support, use of sunscreens and camouflage cosmetics. There are a range of treatment modalities for re-pigmentation, which is discussed below.
a. General aspects
Psychosocial support-vitiligo can have a devastating effect on sufferers, affecting self-esteem and consequently, the ability of individuals to form and maintain relationships. Thus, it is important that psychological help is sought and given to sufferers. There are various support groups worldwide and joining this may be of help. Please click on our educational link for details of vitiligo support groups. Camouflage cosmetics can help to disguise the pigmentary abnormalities, especially for localized patches on the face. It is important that the right shade is used and proper application techniques are taught. The use of high factor broad-spectrum sunscreens is advisable in vitiligo sufferers. Other camouflage techniques, which can be used for this disorder, include self-tanning preparations, topical dyes and tattooing. These techniques generally do not result in an ideal colour match.
b. Re-pigmentation Techniques
The choice of re-pigmentation techniques depends on the location and size of the white patches. Treatment options that are of use in current clinical practice are discussed below.
1. Corticosteroids
Corticosteroids can be applied to lesional skin as a cream. It is efficacious in the treatment of localized patches of vitiligo and works by modifying the immune cells in lesional skin. The correct strength must be used on the appropriate sites of the body for the right time. Hence, steroid creams must be used under medical supervision.
2. Topical Calcipotriene
These agents when used as monotherapy have minimal effect in inducing re-pigmentation of vitiliginous lesions. When combined with phototherapy (such as PUVA) or with topical steroids (compound creams are available), they can be useful in selected patients.
3. Ultraviolet radiation
Ultraviolet radiation can induce re-pigmentation of the skin in patients with vitiligo. The mode of action is via modulation of the immune system. Natural sunlight can be used, as well as UVA with a psoralen (PUVA) and UVB. PUVA and UVB are types of ultraviolet radiation, distinguished by their wavelength. With PUVA, a psoralen, which absorbs the UVA, is given as a tablet (oral PUVA) or applied topically to the skin. UVB, especially narrow-band UVB (NBUVB)
is more efficacious for treating widespread vitiligo. Furthermore, evidence to date, indicates that it is associated with fewer side effects compared to PUVA. For an in-depth discussion on the uses of PUVA and UVB, please read our upcoming article on ‘the uses of phototherapy in blacks’.
4. Excimer laser
This is a targeted laser, with a wavelength of 305nm, similar to the spectrum of UVB. Studies have shown that this laser promotes re-pigmentation in vitiligo when used as monotherapy or in combination with topical tacrolimus. It is an alternative therapy for treating localized patches of vitiligo in units where it is available. For an in-depth review of the excimer laser, please read the article ‘lasers and light therapy in blacks’.
5. Surgical techniques
There are various surgical techniques, which can be used for grafting normal skin onto affected sites of vitiligo. This allows melanocytes (pigment producing cells of the skin) to be transplanted onto lesional sites, thereby inducing re-pigmentation of the affected sites.
Practitioners performing these techniques must be well trained, as complications may arise. To have success with this technique, appropriate selection of patients is mandatory. In fact, a number of studies have shown that surgical treatments are satisfactory when they are implemented to patients with stable type vitiligo, which is unresponsive to conventional therapies. The surgical techniques available include suction blister grafting, split-thickness skin grafting, punch grafting, follicular grafting, injection of cultured melanocytes and non-cultured melanocytes transplantation. This will be discussed in-depth in an upcoming article on surgical procedures in dermatology.
c. De-pigmentation Therapy
Where a large proportion of the skin is affected by vitiligo, another mode of treatment is to de-pigment unaffected skin using potent agents (monobenzones). Once this is done, the skin will be more sensitive to light and for this reason, general sun protection advice should be given. This will include the use of a high factor broad-spectrum sunscreen.
d. Special Issue-Topical Calcineurin Inhibitors
The calcineurin inhibitors, Tacrolimus and Elidel (pimecrolimus), are approved for the treatment of atopic dermatitis. Their mechanism of action is via modulation of the immune system. Recently both have had a black box warning of cancer risk applied to them by the US Food and Drug Administration (FDA). Although there has been published data indicating both medications are successful in treating localized patches of vitiligo, the FDA has not approved the use of either medication for treating vitiligo. Accordingly, treating vitiligo with them is an off label use. We advice our readers to discuss with their skin care physicians about the risks and benefits of their use for vitiligo prior to use.

1. http://blackhealthmatters.org/Vitiligo.pdf
2. http://www.hcvadvocate.org/hepatitis/factsheets_pdf/Vitiligo_09.pdf
3. http://www.orpha.net/data/patho/GB/uk-vitiligo.pdf

Saturday, 4 June 2011

Hutchinson-Gilford Progeria syndrome

Mbah Dukun watched Bollywood movie, “PAA”. Story of Auro ( Amitabh Bachchan ), a 12 years old boy who because of genetic abnormalities called progeria have sightings like people aged 60 years. So what is Progeria?

Disease name and synonyms
• Progeria
• Hutchinson-Gilford progeria syndrome
Hutchinson-Gilford progeria syndrome is a rare genetic disorder characterized by many features reminiscent of marked premature ageing. The characteristic features include short stature, prominent eyes, micrognathia, craniofacial disproportion, loss of subcutaneous fat, alopecia, beaked nose, "plucked-bird" appearance, coax valga, pathologic bone fractures, atherosclerosis, and cardiovascular disorders. Other clinical features include abnormal and delayed dentition, thin and highpitched voice, pyriform thorax, and short dystrophic clavicles.
At birth, the appearance of patients with Hutchinson-Gilford progeria syndrome is generally normal, but by the first year of age patients show severe growth retardation, balding and sclerodermatous skin changes. Affected children are usually short and thin with an average height of 100 cm or so and average weight of 12-15 kg or even less. Death usually occurs from 7 to 28 years, with a median age of 13.4 years. Over 80% of deaths are due to heart attacks or congestive heart failure.
Molecular Genetics
Hutchinson-Gilford progeria syndrome is caused by mutation in the lamin A (LMNA) gene. Lamins are type V intermediate filament proteins and have a short N-terminal "head" domain, an alpha-helical "central rod" domain, and a globular tail domain. Lamins are classified as either A or B type according to their primary sequence, expression pattern, and biochemical properties. B-type lamins are expressed in all cells during development and in adult animals, whereas A-type lamins are expressed in differentiated cells. The LMNA gene encodes three A-type lamins: lamin A (LA), lamin C, and lamin A delta-10. Lamin A contains a C-terminal CAAX box, which undergoes methyl esterification and farnesylation. In the process of LA maturation, the C-terminal 18 residues, which include the modified C-terminal cysteine, are removed in two specific cleavage steps.
The most frequent LMNA mutation in Hutchinson-Gilford progeria syndrome is a nucleotide substitution at position 1824, C-to-T, resulting in a silent gly-to-gly mutation at codon 608 (G608G) within exon 11 of the LMNA gene. This predicts a deletion of 50 basepairs of prelamin A near the C terminus. Low levels of both the mutant mRNA and the mutant protein, LA delta-50, are expressed in fibroblasts derived from Hutchinson-Gilford progeria syndrome patients. In addition, Hutchinson- Gilford progeria syndrome cell nuclei frequently display irregular shapes.

Hutchinson-Gilford Progeria Syndrome (HGPS) is a childhood disorder caused by a point mutation in position 1824 of the LMNA gene, replacing cytosine with thymine, creating a form of the Lamin A protein which can not be processed properly and accumulates in the cell nucleus. Lamin A is a major structural protein of the human cell nucleus. Before the late 20th century, research on progeria yielded very little information about the syndrome. In 2003, the cause of progeria was discovered. The LMNA gene is responsible for producing lamin proteins, which provide strength and stability in cells. Lamin A and Lamin C support the nuclear envelope. When Lamin A is altered, it affects the shape and the function of the nuclear envelope. These changes cause other cells to die prematurely.
Unlike "accelerated aging diseases" (such as Werner's syndrome, Cockayne's syndrome, or xeroderma pigmentosum), progeria is not caused by defective DNA repair. Because these diseases display what are considered different aspects of aging but never every aspect, they are often called "segmental progerias".

Signs and symptoms
Diagnosis is suspected according to signs and symptoms, such as skin changes, abnormal growth, and loss of hair. It can be confirmed through a genetic test.

Clinical Diagnosis
The diagnosis of classic Hutchinson-Gilford progeria syndrome (HGPS, progeria) is based on recognition of common clinical features and detection of the classic c.1824C>T (p.Gly608Gly) heterozygous LMNA mutation; the diagnosis of atypical HGPS is made in individuals with more or less severe features or the non-classic LMNA mutations, for example, c.1822 G>A (p.Gly608Ser), c.1821G>A (p.Val607Val), or c.1968+1G>A.
Individuals having the p.Gly608Gly LMNA silent mutation and most of the following features after age three years are considered to have the classic Hutchinson-Gilford progeria syndrome:
•    Growth
o    Short stature (<3rd percentile), lifelong
o    Weight (<3rd percentile), lifelong
o    Weight distinctly low for height
o    Head disproportionately large for face
o    Thin, high-pitched voice
•    Body fat. .Diminished subcutaneous fat globally, with the following sequellae:
o    Prominent scalp veins
o    Prominent veins over most of body
o    Irregular small outpouchings of skin over lower abdomen and/or proximal thighs
o    Circumoral cyanosis
o    Prominent eyes
o    Lack of ear lobes, in some but not all cases
•    Skin/hair/nails
o    Taut, dry skin that is variably pigmented (spotty)
o    "Sclerodermatous" skin over lower abdomen and proximal thighs
o    Generalized alopecia with sparse downy hairs on the occiput
o    Loss of eyebrows and sometimes eyelashes
o    Dystrophic fingernails and toenails
o    Lagophthalmos (the inability to fully close the eye) and, in a minority of cases, corneal ulceration
o    Thin lips
•    Teeth
o    Delayed eruption of primary teeth
o    Delayed loss of erupted primary teeth
o    Partial secondary tooth eruption
o    Dental crowding as a result of small mouth, lack of primary tooth loss, and secondary tooth eruption behind primary teeth
•    Skeletal system/joints
o    Narrow nasal bridge, pointed nasal tip
o    Osteolysis of the distal phalanges
o    Delayed closure of the anterior fontanelle
o    Pear-shaped thorax
o    Retrognathia and micrognathia
o    Short, dystrophic clavicles
o    Osteoarthritis
o    "Horse-riding" stance and wide-based, shuffling gait
o    Coxa valga
o    Low bone density
o    Thin limbs
o    Tightened joint ligaments globally but variable in severity
•    Cardiovascular/neurovascular
o    Severe progressive atherosclerosis with variable age of clinical manifestation resulting in:
    Cardiac manifestations: angina, congestive heart failure, myocardial infarction
   Stroke, including transient ischemic attacks and silent strokes that are seen on MRI or CT of the head but do not manifest as clinical deficits
o    Raynaud phenomenon in fingers of some but not all individuals
•    Audiologic. Low-frequency conductive hearing loss
•    Endocrine
o    Failure to complete secondary sexual development
o    Low serum leptin concentration
o    Insulin resistance in up to 50% of individuals. Note that frank diabetes mellitus is unusual.


There's no cure for progeria. Regular monitoring for cardiovascular disease may help with  managing your child's condition. Some children undergo coronary artery bypass surgery or dilation of cardiac arteries (angioplasty) to slow the progression of cardiovascular disease.
Certain therapies may ease or delay some of the signs and symptoms. They include:
•    Low-dose aspirin. A daily dose may help prevent heart attacks and stroke.
•    Other medications. Depending on your child's condition, your doctor may prescribe other medications, such as statins to lower cholesterol or anticoagulants to help prevent blood clots. The use of growth hormone may help increase height and weight.
•    Physical and occupational therapy. These may help with joint stiffness and hip problems and may allow your child to remain active.
•    Extraction of primary teeth. Your child's permanent teeth may start coming in before his or her baby teeth fall out. Extraction may help prevent problems associated with the delayed loss of baby teeth, including overcrowding and developing a second row of teeth when permanent teeth come in.

There is no known cure. Few people with progeria exceed 13 years of age. At least 90% of patients die from complications of atherosclerosis, such as heart attack or stroke.
Mental development is not affected. With respect to the features of aging that progeria appears to manifest, the development of symptoms is comparable to aging at a rate eight to ten times faster than normal. With respect to features of aging that progeria does not exhibit, patients show no neurodegeneration or cancer predisposition. They also do not develop the so-called "wear and tear" conditions commonly associated with aging, such as cataracts (caused by UV exposure) and osteoarthritis (caused by mechanical wear).[
Although there may not be any successful treatments for progeria itself, there are treatments for the problems it causes, such as arthritic, respiratory, and cardiovascular problems.

1.    http://www.ncbi.nlm.nih.gov/books/NBK1121
2.    http://www.answers.com/topic/progeria
3.    http://www.cags.org.ae/pdf/176670.pdf

Friday, 3 June 2011

Serology Diagnostic for Syphilis

Diagnosis of Syphilis
Diagnosis of syphilis is based on history, physical examination, and laboratory investigation. It is essential that the stage of syphilis be accurately assessed and documented in order to ensure appropriate management of cases and contacts.

Darkfield Microscopy & Direct or Indirect

1. Fluorescent Antibody Test (DFA/IFA):
Darkfield microscopy and DFA/IFA testing of lesion exudates or tissues are the definitive methods for diagnosing early syphilis when an active chancre, mucous patch, or condyloma latum is present. It is also useful for testing nasal discharge in a neonate with snuffles.
Darkfield microscopy is often not practical (it is not available in most labs including CPL) as it requires a skilled technician on-site. In addition, specimens must be appropriately collected and quickly examined within 5-20 minutes of collection. Positive tests on these materials for immunofluorescent (DFA) testing are diagnostic.
Samples collected from serous exudates from a chancre or secondary skin or mucous membrane lesions for DFA testing should be submitted on a slide and sent to CPL. CPL requests an additional dry Dacron swab be collected for nucleic acid amplification testing (NAAT), and transported in a dry sterile urine container. NAAT is used for syphilis subtyping and not for diagnosis. Prior arrangements are generally not required.
Serologic tests for syphilis are essential for diagnosis of individuals, for following the efficacy of therapy, and for screening purposes. They detect antibodies formed during the course of syphilitic infection. A presumptive diagnosis is possible with the use of two types of serologic tests for syphilis; nonspecific nontreponemal antibody tests (VDRL and RPR) and specific treponemal antibody tests (FTA-ABS and TP-PA). To establish a diagnosis of syphilis, both types of serologic tests are usually necessary. It should be emphasized that serologic test results for syphilis on rare occasions may be negative in active cases, especially in older patients, or very early in primary infections. After hours testing is conducted for transplant and other emergent purposes. An appropriate sample is 5-10 ml of
blood collected in a red-stoppered tube which should be sent to CPL with a request for “serum for VDRL”. The CPL lab requisition should also provide information on the reason for testing (sexual contact to case, genital ulcer, clinical findings, etc). It is extremely important to include the relevant history on the lab requisition.
Routine screening of umbilical cord blood is NOT recommended for serological testing where a diagnosis of congenital syphilis is considered.
Testing of maternal serum is preferred to testing infant serum because infant serum can be
nonreactive if maternal serology is low titre or if the infection was late in pregnancy. Cord blood that is contaminated with maternal blood may lead to a
false positive test result.

2. Nontreponemal Tests (VDRL and RPR):
Syphilitic infection leads to the production of nonspecific antibodies (IgM and IgG) directed against a lipoidal antigen resulting from the interaction of host tissues with T. pallidum or from T. pallidum itself. This antibody-antigen reaction is the basis of nontreponemal tests such as the Venereal Disease Research Laboratory slide test (VDRL) and the rapid plasma reagin test (RPR).
The RPR test is more sensitive than the VDRL. CPL uses the rapid plasma reagin card test (RPR). After adequate treatment of syphilis, nontreponemal tests (NTT) eventually become nonreactive. However, even with sufficient treatment, patients sometimes have a persistent low-level positive nontreponemal test referred to as a serofast conversion. Nontreponemal test titres of persons who have been treated for latent or late stages of syphilis or who have become reinfected do not decrease as rapidly as do those of persons in the early stages of their first infection. In fact these persons may remain serofast for life.
VDRL and RPR become positive one to four weeks after the appearance of the primary chancre or six weeks after exposure. Biologic false positive reactions occur at a rate of 1-2% in the general population. Acute false positive tests lasting less than six months can occur following a febrile illness or immunization. As a rule, 90% of false positive titres are less than 1:8, but low titres are also seen in latent infection. False positive rates in pregnancy are similar to the general population. More than 10% of IDU may have false positive results (18). HIV infection has not been associated with increased false positive NTT in individuals at low risk of IDU.
Serial nontreponemal tests are useful to determine the stage of the disease; a four-fold rise in titre may indicate recent infection, reinfection in an adequately treated person, or relapse in an inadequately treated person. Adequate treatment of infectious syphilis is indicated by a four-fold or greater decline in titre within one year. Titres should generally become non-reactive or weakly reactive within one year following treatment of primary syphilis and within two years after treatment for secondary syphilis. Treatment of late latent or late syphilis usually has little or no effect on the titre and should not be used to gauge the adequacy of the treatment. Titres tend to become lower with time, but serum frequently remains reactive, usually in low titre. As with all quantitative serologic tests, only a four-fold or greater change in titre is meaningful.

3. Specific Treponemal Tests:
These tests measure antibodies against specific T. pallidum antigens and are used primarily to confirm the diagnosis of syphilis in patients with a reactive nontreponemal test. The principal specific treponemal antibody tests performed in most laboratories are the T. pallidum particle agglutination tests (TP-PA) and fluorescent treponemal antibody-absorption test (FTA-ABS).
Most patients who have reactive treponemal tests will have reactive tests for the remainder of their lives, regardless of treatment or disease activity. However, reversion to a nonreactive status may occur in up to 10% of patients, especially in those who are treated early (3). Treponemal test antibody titres correlate poorly with disease activity and should not be used to assess treatment response.
False positive results can occur especially when the FTA-ABS test is used in patients with Lyme disease, HIV, pregnancy, drug addiction, toxoplasmosis, H. pylori, autoimmune disorders like lupus and rheumatoid arthritis, and in persons with other treponemal diseases such as yaws, pinta or bejel.
Confirmatory Test:
The TP-PA test is a specific treponemal test for the serologic detection of antibodies to various species and subspecies of treponemes. Reports from CPL refer to the TP-PA as a confirmatory test result.
Reference Test:
The FTA-ABS test is an indirect immunofluorescent antibody test using T. pallidum from rabbit testis as the antigen. Its interpretation is subjective and requires great attention to detail. Its principal use is to verify the diagnosis of syphilis. Reports from CPL refer to this as the reference test.

4. Tests for Neurosyphilis:
No single test is diagnostic for neurosyphilis; the CSF-VDRL is highly specific but it is insensitive; as low as 30%. Most other tests are both insensitive and nonspecific and must be interpreted in relation to other test results and the clinical assessment.
Diagnosis of neurosyphilis usually depends on the combination of patient history, physical examination, reactive serologic test results, and abnormalities of CSF (cell count, protein, or a reactive CSF-VDRL). The CSF leukocyte count is usually elevated (>5 WBC/mm3) in patients with neurosyphilis. The CSF leukocyte count can also be used as a sensitive measure of the effectiveness of therapy. A positive CSF-VDRL result in the appropriate clinical setting establishes the diagnosis of neurosyphilis although serum antibody contamination is possible. A negative CSF-VDRL does not rule out the possibility of neurosyphilis. Normalization of CSF markers is affected by the stage of syphilis at which treatment is initiated and pretreatment levels of particular CSF markers. In patients without HIV infection treated with penicillin regimens, the CSF pleocytosis and VDRL titre normalize within one year. Reversion of pleocytosis is more likely when pretreatment CSF WBC counts are high. CSF-VDRL normalization
is less likely when pretreatment CSF-VDRL titres are high. In HIV-infected patients, CSF WBC count, protein, and VDRL may be slow to normalize. CSF-VDRL titres are less likely to normalize after treatment when CD4+ counts are <200 cells/μL compared to CD4+ counts >200 cells/μL. Therefore in HIV-infected patients, it is not possible to exclude treatment failure and more intensive regimens may be required.
Examination of CSF should be considered in the following circumstances:
1. Congenital syphilis;
2. Neurologic, ophthalmic, or otologic signs and symptoms;
3. Tertiary syphilis;
4. Previously treated patients who fail to achieve an adequate serologic response;
5. HIV coinfection with late latent or syphilis of unknown duration;
6. Where HIV coinfection exists, a lumbar puncture
(LP) is strongly recommended when neurological signs or symptoms are present, VDRL/RPR ≥1:32 dilutions, CD4+ counts <350 cells/μL or treated syphilis with suboptimal decline in VDRL/RPR titre. Some experts recommend a LP for all syphilis cases with HIV coinfection. A LP may be considered in other patients on a case by case basis.

5. Tests for congenital syphilis:
Venous samples should be obtained from both mother and baby for serology (treponemal and nontreponemal tests). Cord blood is not suitable for testing. The interpretation of reactive antibodies in the neonate must take into consideration the maternal history, including stage of syphilis, history of treatment, and syphilis serology results.
Placenta, neonatal nasal discharge, or skin lesions may be examined by darkfield microscopy or DFA/IFA for T. pallidum. CSF examination should be performed on all infants with suspected congenital syphilis. Long bone x-rays should also be performed.


oh my God, whats a matter with this picture? there is something on gland? yes that is wound, like ulcus. Mbah Dukun will explain what that is. it's called syphillis
 1. Definition
2. Etiology
3. Symptoms
4. Therapy and Treatment
5. Mbah dukun's advices 

Syphilis is a chronic infectious disease caused by the spirochaete Treponema pallidum. It progresses in stages. Syphilis is easy to cure in its early stages. But without treatment, it can hurt your body’s organs, leading to severe illness and even death.

Syphilis caused by Treponema pallidum.  Treponema pallidum including Spirochaeta group which is shaped like a spiral with a length between 50-20 microns wide and 0.1 to 0.2 microns, easily visible with dark field microscope looks like a spiral that can perform movements such as rotation.  These organisms are easily killed by soap anaerobic, oxygen, sapranin, even by aquades.  In donor blood stored in the refrigerator Treponema pallidum will die within three days but can be transmitted through transfusion using fresh blood.

How is syphilis spread?
Syphilis is usually transmitted by sexual contact or from mother to infant, although endemic syphilis is transmitted by non-sexual contact in communities living under poor hygiene conditions. T. pallidum can also be transmitted by blood transfusion. In spite of provoking a strong humoral and cell-mediated immune response, T. pallidum is able to survive in the human host for several decades.After an incubation period of about 21 days, an ulcer (the primary chancre) appears at the site of inoculation. This resolves spontaneously and 6–8 weeks later is followed by the secondary stage, at which time the organism has disseminated via the blood stream and any organ can be affected.
Tertiary syphilis, which can affect the skin, bones or central nervous and cardiovascular systems, can occur many years later1. In pregnant women, syphilis can lead to stillbirth or congenital infection of the neonate, resulting in neonatal death or late sequelae.Parenteral penicillin remains the treatment of choice, and resistance to it has not been described.As T. pallidum divides slowly, a long-acting preparation is recommended.

Symptoms and signs
A. Primary syphilis
In the early stages of syphilis a sore can appear on the penis or in the rectum or, in women, on the cervix. In people co-infected with HIV, multiple sores can appear. Because the sores appear in hidden locations, early-stage syphilis might go unnoticed in both men and women. Lymph nodes in the groin may become swollen, usually within a week of the appearance of the syphilitic sore. Although the sore, sometimes called a chancre, can heal within four to six weeks, lymph nodes may remain swollen for several months.
Still, early-stage syphilis can have minimal symptoms and may go unnoticed by affected people. Troublingly, treponemes have been found in the spinal fluid of people with primary syphilis, regardless of HIV infection.



B. Secondary syphilis
In this stage, generally two to 12 weeks after the appearance of the chancre, symptoms of a widespread T. pallidum infection occur. Symptoms can vary considerably but the following can be common:
• skin rash;
• low-grade fever;
• lack of energy;
• sore throat;
• lack of appetite.
The skin rash can begin on the trunk but may also appear anywhere else, including on the palms of the hands and soles of the feet. If the rash affects a hairy area, temporary patchy hair loss can occur. For instance, thinning of the eyebrows, beard or parts of the head can be a feature of syphilitic rash. Painless lesions called mucous patches can appear on the wet tissues of the genitals, mouth, throat and tonsils. These lesions are teeming with treponemes and are highly infectious.
In up to 40% of people with secondary syphilis, the brain and spinal cord (CNS—central nervous system) can become infected, with or without symptoms. In some cases, symptoms such as the following may appear:
• ringing in the ears;
• decrease in the ability to hear clearly;
• difficulty seeing clearly;
• headache.
If left untreated, neurosyphilis can develop, leading to severe complications. The germs that cause syphilis can also infect the liver, causing liver damage or hepatitis, which can be detected by increased levels of liver enzymes in the blood.
Secondary syphilis can also turn into latent syphilis. At this stage, no symptoms are present and the infection is only detectable with blood tests. However, despite the lack of symptoms, the disease is still eating away at the body.

C. Late syphilis (tertiary syphilis)
In this stage of illness, any organ of the body may become slowly inflamed and affected by T. pallidum. Generally, late syphilis can affect the nervous system (neurosyphilis), the heart and blood vessels (cardiovascular syphilis) and just
about any organ/system where a syphilitic lesion can appear. These lesions, which are usually solitary, are called gummas.
If left untreated, late-stage syphilis can eventually lead to unpleasant and dreadful complications, including the following:
• difficulty falling asleep;
• peripheral neuropathy;
• problems getting and maintaining an erection;
• changes in personality;
• poor memory;
• decreased capacity for insight and good
• meningitis;
• poor control of muscles;
• damaged joints;
• seizures;
• stroke.
Given all of these, regular blood tests for syphilis (and other STIs) are important for sexually active people who wish to remain healthy.

Treatment and Teraphy
Unlike the case with many other diseases, one syphilis expert, writing in an infectious disease textbook, noted that “there have not been many well-controlled, carefully planned, prospective studies to determine [the best dose or length] of therapy.” Current recommendations for treatment of syphilis are based on extrapolations of older data. Despite these drawbacks, an antibiotic called benzathine penicillin G is considered the gold standard of anti-syphilis therapy.

Drug levels
Ideally, maintaining high levels of penicillin in the blood should keep T. pallidum from reproducing and still higher levels can help kill these germs. So, for treating early syphilis, high levels of penicillin G are needed for at least seven days. The most convenient way to achieve this while avoiding the issue of patient adherence is an injection of benzathine G penicillin into muscle. However, it is important to note that this dose is inadequate for neurosyphilis; indeed, levels of penicillin that can kill treponemes in the CNS are not reliably achieved with a single injection of benzathine penicillin G 2.4 million units. Yet, in cases of early diagnosis, where, in theory, there are fewer treponemes, the evidence shows that treatment with a single injection of penicillin is sufficient therapy for the average person with primary syphilis.
Other antibiotics
Antibiotics such as doxycycline impair the growth of treponemes and are sometimes used in patients who are allergic to penicillin. Bear in mind that unlike penicillin, doxycycline does not kill treponemes and may be less effective in people with severely weakened immune systems.
In cases of penicillin allergy, some experts prefer to desensitize their patients to penicillin—a course of action suggested by PHAC (Public Health Agency of Canada). Penicillin desensitization is also recommended for cases of syphilis in pregnant women.
Another potential treatment is the antibiotic azithromycin (Zithromax). However, reports have emerged of cases of syphilis resistant to azithromycin in the United States, Ireland and, recently, in the province of British Columbia. All of the BC cases of azithromycin-resistant syphilis were in MSM. PHAC does not  recommend the use of this antibiotic for the routine treatment of syphilis.

Mbah Dukun's Advice For You

There are steps you can take to lower your risk of getting syphilis:
• Don’t have sex. The surest way to keep from getting syphilis is to prac¬tice abstinence. This means not hav¬ing vaginal, oral, or anal sex.
• Be faithful. Having a sexual rela¬tionship with one partner who has been tested for syphilis and is not infected is another way to lower your risk of getting infected. Be faithful to each other. This means you only have sex with each other and no one else.
• Use condoms. Syphilis sores can occur in places that are covered by a condom, as well as areas that are not covered. So, using a condom the right way and every time you have vaginal, anal, or oral sex might lower your risk. For vaginal sex, use a latex male condom or a female polyure¬thane condom. For anal sex, use a latex male condom. For oral sex use a male latex condom. A dental dam might offer some protection during oral sex (mouth to vagina/anus).
• Know that some methods of birth control, like birth control pills, shots, implants, or dia¬phragms, will not protect you from STIs, including syphilis. If you use one of these methods, be sure to also use a latex condom every time you have sex.
• Talk with your sex partner(s) about STIs and using condoms. It’s up to you to make sure you are protected. Remember, it’s your body! For more information, call the Centers for Disease Control and Prevention at (800) 232-4636.
• Talk frankly with your doctor and your sex partner(s) about any STIs you or your partner has or has had. Talk about symptoms, such as sores or discharge. Try not to be embarrassed. Your doctor is there to help you with any and all health problems. Also, being open with your partners can help you protect your health and the health of others.
• Have a yearly pelvic exam. Ask your doctor if you should be tested for syphilis or other STIs, and how often you should be retested. Testing for many STIs is simple and often can be done during your checkup. The soon¬er syphilis is found, the more likely it can be cured quickly and easily.
• Avoid using drugs or drinking too much alcohol. These activi¬ties may lead to risky sexual behavior such as not wearing a condom.

1. http://www.womenshealth.gov/faq/syphilis.pdf
2. http://www.catie.ca/pdf/facts/syphilis.pdf
3. http://www.gov.mb.ca/health/publichealth/cdc/protocol/syphilis.pdf
4. http://www.hpa.org.uk/cdph/issues/CDPHvol3/No3/guidelines.pdf
5. http://www2a.cdc.gov


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