Chronic Supurative Otitis Media (CSOM)

3 days ago Mbah Dukun posted about Ear disease, Acute Otitis Media. Today, Mbah Dukun posts about complication of Acute Otitis Media. Yes from the title all of you know what Mbah Dukun means, Chronic Supurative Otitis Media. Is it dangerous? find the answer below.

1. Definition

2. Classification

3. Etiology

4. Pathology

5. Clinical manifestations

6. Management (treatment and therapy)

7. Complications

DEFINITION

CSOM is chronic inflammation of the middle ear cavum, mastoid and tympanic membrane is intact (perforated) also found an intermittent purulent secretions (othorea).  Secretions may be watery or thick, clear or in the form of pus and lasted more than 2 months. 

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CLASSIFICATION

CSOM can be divided into two types :

1.  Tubotympany = benign type = rhinogen safe.

Tubotympany characterized by the presence of a central perforation or pars Tens and clinical symptoms that vary depends on wide and severity of disease.  Clinically divided into:

a.  active

In this type, there are secretions of the ear and deafness.  Usually preceded by the expansion of the upper respiratory tract infections through the eustachius tube or after swimming where germs enter through the outer ear canal.  Secretions varied from mucoid to mucopurulent.

b.  not active

From examination the ear found total dry perforation with middle ear mucosa is pale.  Symptoms encountered a mild conductive deafness.  Other symptoms are encountered, such as vertigo, tinnitus, or a feeling of fullness in the ear.

2.  Type aticoantral = wild type = danger =  bone type

In this type were found Cholesteatoma and dangerous.  Aticoantral type is more often about flaccida pars and the trademark is the formation of retraction pockets, which is where the accumulation of keratin to produce Cholesteatoma.

Cholesteatoma can be divided

above two types, namely:

a.  Congenital

b.  Obtained.

In general, there Cholesteatoma in chronic otitis media with perforation marginal, but some are located in the pars flaccida (Attic retraction cholesteatom).

ETIOLOGY

CSOM occurs almost always starts with recurrent otitis media in children, rarely in the adult.  Infection factor usually comes from the nasopharynx (adenoiditis, tonsillitis, rhinitis, sinusitis), reaching the middle ear through the tube of Eustachius.  Eustachius tube abnormal function are predisposing factors which found in children with cleft palate and Down's syndrome.  Presence of tubal pathology, causing reflux of contents nasopharynx which is a factor of the high incidence of CSOM in the United States.  Humoral abnormalities (such as hipogammaglobulinemia) and cell-mediated (such as HIV infection) can manifest as chronic ear secretion.

Causes of CSOM among others:

1.  Environment

2.  Genetic

3.  history of otitis media.

4.  Infection

5.  Upper respiratory tract infection

6.  Autoimmune

7.  Allergy

8.  Eustachius tube disfunction.

Some of the factors that cause persistent tympanic membrane perforation in CSOM:

• Infections that persist in the middle ear mastoid resulting in the production of purulent ear discharge persists.

• The continued obstruction Eustachius tube which reduces the spontaneous closure of the perforation.

• Several large perforations suffered through the mechanism of spontaneous closure of epithelial migration.

• At the edge of the perforation of squamous epithelium can experience rapid growth over the medial side of the tympanic membrane.  This process also prevents the spontaneous closure of the perforation.

Factors that cause middle ear infections become chronic suppurative compound, among others:

1.  Eustachius tube dysfunctions chronic or recurrent.

a.  Nose and throat infections are chronic or recurrent.

b.  Partial or total anatomic obstruction tube Eustachius

2.  Persistent tympanic membrane perforation.

3.  The occurrence of squamous metaplasia or other permanent pathological changes in the middle ear.

4.  Persistent obstruction of the aeration of the ear or mastoid cavity.

5.  There are areas with sekuester or persistent osteomyelitis in the mastoid.

6.  Basic constitutional factors such as allergies, general weakness or changes in the body's defense mechanisms.

Pathogenesis

CSOM Patogensis not yet fully known, but in this case is the chronic stage of acute otitis media (OMA) with a perforation that has been formed, followed by the release of secretions that keep menerus1.  OMA perforation can occur secondary to chronic uneventful middle ear infection in eg dry perforations.  Some authors claim this as an inactive state of chronic otitis media.

PATHOLOGY

CSOM is more often a recurrent disease.  This chronic condition is more time-based rather than pathology, and staging.  In general, the picture found is:

1.  There is a perforated tympanic membrane in the central part.

2.  Mucosa varies according to disease stage

3.  The bones of hearing can be damaged or not, depending on the severity of infection

previously.

4.  Mastoid pneumatization

CSOM most often in childhood.  Most recent mastoid pneumatization occurs between 5-10 years.  When chronic infection persists, the mastoid had sclerotic process, thereby shrinking the size of the mastoid processes.

CLINICAL MANIFESTASIONS

1.  Discharge Ear (Otorrhoe)

Purulent or mucoid secretions is dependent stage of inflammation.  In CSOM benign type, the liquid that comes out muco pus that do not stink, often as a reaction to irritation of the mucosa of the middle ear by the tympanic membrane perforation and infection.

The exit discharge is usually intermittent.  In the inactive stage CSOM not found adannya ear secretions.  In CSOM wild type, element and mucoid middle ear secretions reduced or lost due to widespread destruction of the mucosal lining.  Secretions are mixed with blood-related presence of granulation tissue and ear polyps and a sign of Cholesteatoma.  If secretions are watery watery without the possibility of tuberculosis leads to pain.

2.  Hearing Loss

Conductive deafness is usually encountered but can also be mixed.  Severity of deafness depends on the magnitude and location of tympanic membrane perforation and mobility sound delivery system into the middle ear.  In CSOM malignant type, usually obtained severe conductive deafness.

3.  Otalgia (Ear Pain)

In CSOM, complaints of pain caused dammed pus drainage.  Pain may mean the threat of complications due to drainage constraints secretions, exposure durameter or lateral sinus wall, or the threat of brain abscess formation.  Pain is a sign of developing complications such as Petrositis CSOM, subperiosteal abscess or lateral sinus thrombosis.

4.  Vertigo

vertigo often appears, is a sign of labyrinthine fistula caused by the occurrence of erosion of the walls of the maze by Cholesteatoma.  Vertigo that arises usually due to a sudden change in air pressure or the sensitive patient.  vertigo can occur simply because a large perforation of tympanic membrane, causing a maze more easily aroused by the temperature difference.  The spread of infection into the labyrinth will also be led to complaints of vertigo.  Vertigo can also occur from complications of the cerebellum.

CLINICAL SIGNS

Clinical signs of malignant type CSOM

1.  Presence of abscess or fistula retroauricular

2.  Granulation tissue or polyps in the ear canal from the tympanic cavity.

3.  Pus is always active or foul smelling (smell Cholesteatoma)

4.  X-ray mastoid Cholesteatoma the picture.

CLINICAL EXAMINATION

To complete the examination, clinical examination can be performed as

follows:

Audiometric examination

In patients with CSOM audiometric examination is usually found to conductive deafness.  But it can also be found there sensorineural deaf, deafness severity depending on the size and location of the tympanic membrane perforation as well as the integrity and mobility

The degree of hearing loss threshold of hearing

Normal: -10 dB to 26 dB

Mild : 27 dB to 40 dB

Moderate: 41 dB to 55 dB

Moderat to Severe: 56 dB to 70 dB

Severe: 71 dB to 90 dB

Total deafness: more than 90 dB.

To evaluate, the following observations :

1.  Perforation usually cause deafness conductive generally no more than 15-20 dB

2.  Damage to the bones of the circuit causing deafness conductive hearing loss 30-50 dB when accompanied by perforation.

3.  Discontinuity of bone behind of intact tympanic membrane causing conductive deafness 55-65 dB.

4.  Weaknesses and low discrimination speech, no matter what the conductive of bone, showed severe damage cochlea.

Radiological examination.

1.  Projection Schuller

Shows the extent of mastoid pneumatization of the lateral direction and over.  This photo is useful for surgery because it shows the position of the lateral sinus and the tegmen.

2.  Projection Mayer or Owen,

Taken from the middle ear and anterior direction.  Will look picture the bones of hearing and tweaking so it can be known whether the bone damage has on structures.

3.  Projection Stenver

Shows a picture along the petrosal pyramid and more clearly shows the internal auditory canal, vestibule and semicircular canals.  These projections put the antrum in cross section so as to show the existence of enlargement.

4.  Projection Chause III

Give an especial longitudinally so that it can show early damage to the lateral wall of tweaking.  Politomografi and or CT scans can depict bone damage because Cholesteatoma.

Bacteriology

Bacteria are often found in CSOM are Pseudomonas aeruginosa, Staphylococcal aureus and Proteus.  While the OMSA streptococcus bacteria pneumonie, H.  influenza, and Morexella kataralis.  Other bacteria found in CSOM E.  Coli, Difteroid, Klebsiella, and anaerobes are Bacteriodes sp.

1.  Specific bacteria

Eg Tuberculosis.  Otitis tuberculosis is very rare (less than 1%).  In adults is usually caused by advanced lung infection.  These infections enter the middle ear through the tube.  Tuberculous otitis media can occur in children who are relatively healthy as a result of drinking milk that is not pasteurized

2.  Non-specific bacteria both aerobic and anaerobic.

Aerobic bacteria are often met by Pseudomonas aeruginosa, Staphylococcus aureus and Proteus sp.  Antibiotics are sensitive to ceftazidime and Pseudomonas aeruginosa is ciproflokxacin, and is resistant to penicillins, cephalosporins and macrolides.  While Proteus mirabilis sensitive to antibiotics except for macrolides.  Staphylococcus aureus resistant to sulphonamides and trimethoprim and sensitive to cephalosporin generations I and gentamicin

MANAGEMENT

The principle of treatment depends on the type and extent of infectious diseases, where treatment can be divided into:

1.  Conservative

2.  Surgery

CSOM benign INACTIVE

This situation does not require treatment, and advised not to scrape the ears, the water should not enter the ear during bathing, swimming is prohibited and immediately seek treatment when suffering from upper respiratory tract infection.  If the facility allows reconstruction surgery should be performed (miringoplasty, tympanoplasty) to prevent recurrent infections and hearing loss.

CSOM benign ACTIVE

The principle of treatment of CSOM is:

1. Clean ear canal and tympanic cavity.

2. antibiotics:

- Topical antibiotics (antimicrobial)

- Systemic.

Topical antibiotics

Antibiotics topically in the ear and a lot of secretions without cleaning first, is not effective.  If the discharge is reduced / no longer progressive but given

drops containing antibiotics and topical drug delivery kortikosteroid.4 Given meant to go to the middle ear, it is not recommended that antibiotics such as neomycin and duration ototoxic not more than 1 week.  How to best selection of antibiotics based on culture, and resistency test.

Ear powder used as:

a.  Acidum boricum with or without iodine

b.  Terramycin.

c.  Asidum borikum chloromicetin 2.5 grams mixed with 250 mg

Topical antibiotic treatment can be widely used for active CSOM combined with ear cleaning.  Topical antibiotics that can be used in chronic otitis media is:

1.  Polymyxin B or polymyxin E

These drugs are bacterisid against gram-negative bacteria, Pseudomonas, E.

Koli Klebeilla, Enterobakter, but the resistant gram-positive, Proteus, B.  fragilis Toxic to kidneys and nervous system.

2.  Neomycin

bactericid drugs on gram-positive and negative, for example: Staphylococcal aureus, Proteus sp.  Resistant to all anaerobes and Pseudomonas.  Toxic to the kidneys and ears.

3.  Chloramphenicol

These drugs are bactericid

Systemic antibiotics

Antibiotics are not more than 1 week and must be accompanied cleaning profus secretions.  In the event of treatment failure, keep in mind that there are reasons of failure in these patients.  Antimicrobials can be divided into 2 groups.  The first class of power killed him dependent measure.  The higher levels of the drug, the more germs were killed, for example with the quinolone class of aminoglycosides.

The second category is a particular concentration of antimicrobial that killed her best resources.  Elevation does not increase the dose of killing power of this class of antimicrobials, such as beta-lactam class.

Systemic antibiotic therapy is recommended in chronic otitis media is.

Pseudomonas: Aminoglycosides ± carbenicillin

P.  mirabilis: Ampicillin or cephalosporin

P.  morganii, P.  vulgaris: Aminoglycosides ± carbenicillin

Klebsiella: Cephalosporin or aminoglycosides

E.  coli: Ampicillin or cephalosporin

S.  Anti-stafilikokus aureus: penicillin, cephalosporin, erythromycin, aminoglycosides

Streptococci: Penicillin, cephalosporin, erythromycin, aminoglycosides

B.  fragilis: clindamycin

Class of quinolone antibiotics (ciprofloxacin and ofloxacin) are able to nalidixic acid derivate that has anti-pseudomonal activity and can be administered orally.  But it is not recommended for children under the age of 16 years.  Cephalosporin Group III generation (cefotaxime, and ceftriaxone seftazidinm) are also active against Pseudomonas, but must be administered parenterally.  This therapy is very good for the OMA, while for CSOM is uncertain enough, although it can cope with CSOM.  Have the effect of metronidazole for anaerobic bactericid.  According to Browsing et al metronidazole can be given with and without antibiotics (cephalexin and cotrimoxazol) on active CSOM, a dose of 400 mg per 8 hours for 2 weeks or 200 mg per 8 hours for 2-4 weeks.

Malignant CSOM

Treatment for Malignant CSOM is surgery.  Conservative medical treatment is only a temporary treatment before surgery.  If there is a subperiosteal abscess, the abscess incision should be done separately before then performed mastoidektomy.

There are several types of surgery or surgery techniques that can be done in CSOM with chronic mastoiditis, either benign or malignant type, among others:

1.Mastoidektomy simple (simple mastoidectomy)

2. radical Matoidectomy

3.radical with modifications mastoidectomy

4.Miringoplasty

5.Timpanoplasty

6. Combined approach tympanoplasty)

The goal is to stop operating permanently infection, tympanic membrane perforation repair, prevent complications or more severe hearing damage, and improve hearing.

COMPLICATIONS

Tendency of complications of otitis media gets depends on the pathological abnormalities that cause otorrhoea.  Nevertheless resistant organisms and lack of effective treatment, would lead to complications.  usually obtained in patients with CSOM complications malignant type, but an acute otitis media or an acute exacerbation by a virulent bacteria in CSOM benign type can cause complications.

Serious intra-cranial complications more often seen in acute exacerbation of CSOM associated with Cholesteatoma.

A.  Complications of middle ear:

1.  Persistent tympanic membrane perforation

2.  Erosion of bone loss

3.  Facial nerve paralysis

B.  Ear complications in

1.  Labyrinth fistula

2.  Labyrinitis suppurative

3.  Nerve deafness (sensorineural)

C.  Complications of Extradural

1.  Extradural abscess

2.  Lateral sinus thrombosis

3.  Petrositis

D.  Complications to the central nervous system

1.  Meningitis

2.  Brain abscess

3.  Hindrocephalus otitis

Complication of middle ear infections trip to the intra-cranial must pass through three kinds of trajectories:

1.  From the middle ear cavity to the brain membrane

2.  Penetrate the lining of the brain.

3.  brain expansion.

ACUTE OTITIS MEDIA

Today Mbah Dukun share information about kind of ear disease. what is that, mbah? it's called ACUTE OTITIS MEDIA. maybe you've never heard about this disease, but you might have it before. Okey mbah dukun start to explain. Just click options below

 1. DEFINITION

2. ETIOLOGY 

3. PATHOGENESIS

4. DIAGNOSIS

5. TREATMENT AND THERAPY

6. COMPLICATIONS

DEFINITION
 Acute otitis media is an inflammation of the mucosa of the middle ear cavity, eustachius tube, and aditus ad antrum caused by bacterial or viral infection with clinical symptoms of ear pain, fever, and even hearing loss, tinnitus and vertigo.  generally takes place within 3-6 weeks.


Etiology
The main cause of acute otitis media (AOM) is the invasion of pyogenic bacteria into the middle ear in a state that is normally sterile.  Common bacterial causes of AOM include hemolytic streptococcus, Staphylococcal aureus, Pnemococcus.  In addition, occasionally found also Haemofilus influenza, Escherichia coli, Streptococcus anhemolitikus, Proteus vulgaris and Pseudomonas aurogenosa.  Haemofilus influenza is often found in children aged under 5 years old.  Upper respiratory tract infections are recurrent and tubal dysfunction eustachii also be the cause of the AOM in children and adults.

Incidence
Acute otitis media most commonly suffered by children ages 3 months-3 years.  But not infrequently also the adults.  Children are more often exposed to AOM due to several things, including:
1.  Child's immune system is not perfect
2.  Tuba eusthacius children are shorter, wider and lies horizontally
3.  Adenoid children relatively larger and situated adjacent to the mouth of the fallopian tubes so that disrupt the opening of the eustachii tube eusthachii.  Adenoids are easy to track the spread of infected bacteria and viruses into the middle ear.

Pathogenesis
AOM trigger factors can be initiated by the occurrence of upper respiratory tract infection accompanied by the repeated disruption of the body by the cilia of the tubal mucosa eusthachii, enzymes and antibodies that cause negative pressure resulting in bacterial invasion of the mucosa of the nasopharynx into the middle ear through the eustachii tube and settled in  in the middle ear becomes acute otitis media.

There are 5 stages of acute otitis media (AOM) based on changes in middle ear mucosa, namely:
1.  tubal occlusion Stadium
Marked with a picture of the tympanic membrane retraction due to negative middle ear pressure.  Sometimes the tympanic membrane appears normal or pale cloudy color.  Effusions may have occurred but difficult to detect.

2.  Hiperemia Stadium

 


Dilated blood vessels that appear in some or all of the tympanic membrane accompanied by edema.  Secretions are beginning to form serous exudate is still so difficult to assess.




3.  Suppuration Stadium

 
Severe edema of the mucosa of the middle ear accompanied by the destruction of superficial epithelial cells and the formation of purulent exudate in the tympanic cavity causing the tympanic membrane protruding toward the outer ear canal (bulging).  Clinical symptoms, the patient seems to ache, pulse, fever, and pain in the ear intensified.  In the circumstances further, ischemia can occur due to the pressure of growing purulent exudate, thrombophlebitis in the veins of small even to necrosis of the mucosa and submucosa.


4.  Perforation Stadium
Rupture of the tympanic membrane so that the pus out of the middle ear into the outer ear canal.  Sometimes the secret expenditures are pulsation.  This stage is often caused by late delivery of antibiotics and the high virulence of germs.







5.  Resolution Stadium
Characterized by a gradual normal tympanic membrane perforation of the tympanic membrane to close the back and no purulent secretions.  This occurs if the tympanic membrane was intact, good endurance and low-virulence bacteria.

DIAGNOSIS
Diagnosis AOM should meet the following 3 things:
1.  sudden onset (acute)
2.  The discovery of signs of effusion (effusion: fluid collection in a body cavity) in the middle ear.  Effusions evidenced by observing the following signs:
a.  Deployment tympanic membrane
b.  Limited / lack of movement of the tympanic membrane
c.  The existence of the shadow of fluid behind the tympanic membrane
d.  Discharge from the ear
3.  Signs / symptoms of inflammation of the middle ear as evidenced by the presence of either one of the following signs:
a.  Redness of the tympanic membrane
b.  Ear pain that interferes with sleep and normal activity
Children with AOM may experience ear pain, discharge from the ear, decreased hearing, fever, difficulty eating, nausea and vomiting and cranky.  However these symptoms are not specific to that diagnosis AOM AOM can not be based on history alone.  Middle ear effusions examined with otoscope to see clearly the situation in the tympanic membrane / tympanic membrane is bulging, erythema and even yellow and dingy and the presence of yellowish fluid in the ear canal.  If confirmation is required, generally performed with a pneumatic otoscope (an instrument used to see the tympanic membrane which is equipped with a small air pump to assess tympanic membrane response to changes in air pressure).  Movement of the tympanic membrane is less visible with this examination.  This examination can be used as additional tests to confirm the diagnosis of AOM.  But generally AOM can already be enforced by ordinary otoscope examination.  Middle ear effusions can also be proved by tympanosyntesis (stabbing of the tympanic membrane).  But this examination is not performed on any child.  Among other indications of the need tympanosyntesis AOM in infants younger than 6 weeks with a history of intensive care in hospital, children with immune disorders, children who are not members of the response to some antibiotics or with very severe symptoms and complications.

TREATMENT of  ACUTE OTITIS MEDIA
1.  Antibiotics
AOM is generally a disease that will heal by itself. About 80% of AOM cured in 3 days without antibiotics.  Use of antibiotics does not reduce complications, including decreased hearing.
If symptoms do not improve within 48-72 hours or there is worsening of symptoms, antibiotic given.  American Academy of Pediatrics (APP) which categorize AOM observable and should be treated with antibiotics as following;
a. <6 months of Antibiotics
b. 6 months - 2 years of Antibiotics
c. > 2 years of antibiotics if symptoms are severe. if symptoms are mild, do observations

Mild Symptoms if mild ear pain and fever <39 C in 24 last hour.  While the severe symptoms are moderate to severe ear pain or fever 39 C.
Options observation for 48-72 hours can only be performed on children age 6 months-2 years with mild symptoms during the examination or diagnosis of doubtful in children over 2 years.  Analgesia should still be given during the observation.
The first choice of antibiotics in AOM is amoxycilin. American Academy of Family Physicians (AAFP) recommends dosing 40mg/kgweight/daystandards in children with low risk (age> 2tahun, not in intensive care, had not received antibiotic treatment within 3 last month).  While high doses administered 80mg/kgweight/day in children with high risk (age <2 years, in treatment, there is a history antibiotics in the last 3 months and are resistant to giving amoxycilin low dose).  Meanwhile, The Centre for Disease Control and Prevention (CDC) recommends antibiotic therapy on the AOM as follows:

CONDITIONS OF TREATMENT
Otitis media with bulging tympanic membrane  High-dose amoxycilin (80 - 100mg/kgweight/day per oral) for 7 days
Otitis media without bulging tympanic membrane  Delays antibiotics, (Spontaneously cured)
recurrent otitis media  delays antibiotics, used influenza vaccine
Otitis media bacterial resistance e.c against high-dose amoxycilin  High-dose clavulanate amoxycilin (80-90 mg / kg / day orally for 7 days), cefuroxime axetil (30 mg / kg 2 times / day orally); ceftriaxone (IM 50mg/kgweight/day during 3 days)

Delays antibiotics and antibiotic treatment settings performed to otitis media without bulging because, generally, it recover spontaneously without antibiotic treatment. Setting prescribing can be done by administering acetaminophen in case of otalgia and fever, and if after giving it, a fever still on going and no improvement of clinical symptoms for 3 days, so amoxycilin just given in high doses.  Antibiotics in the AOM will produce symptAOMtic improvement in 48-72 hours.  In the first 24 hours occurred stabilization, while the 24 second hours began repairs.  If the patient does not improve in 3 days or re-emerged in 14 days there may be other diseases or treatment provided is not adequate / inadequate or has even happened bacterial resistance to antibiotics. If the patient is allergic to alternative antibiotics Penicilin class used were cefuroxime axetil, ceftriaxone injection (2-3x50mg/kgweight/day) or second-generation cephalosporins such as cefdinir, cefpodoxime or cefuroxime. Another option is a class of macrolides such as azithromycin and clarithromicyn.
2.  Analgesia / pain relief
Besides antibiotics, treatment should be accompanied AOM pain relievers. Analgesia is commonly used is simple analgesia such as paracetamol or ibuprofen.  However, it should be noted that the use of ibuprofen should be ensured that the children do not have indigestion Since the granting of ibuprofen can aggravate the situation.

COMPLICATIONS
Acute otitis media is not treated promptly with antibiotics can be continued become chronic otitis media (COM) and mastoiditis.  Another complication that can periosteal abscess occurs as up to meningitis and brain abscess even can also result in permanent hearing loss due to rupture tympanic membrane and if it has to disrupt auditory function will also cause problems in speech and language in children.

Laryngeal Papilloma

Inul Daratista, dangdut singer, came to Mbah Dukun,s house. She complained to mbah dukun about her voice. use laryngoscope direct methode, mbah dukun found something in Inul's laryng. what is that? it called Laryngeal Papilloma. Do you wanna know about Laryngeal Papilloma? just click options below.

1. Definition
2. Etiology
3. Histopatology
4. Clinical manifestations
5. Diagnose
6. Therapy and treatment (management)
7. Complications
 





definition
Laryngeal papilloma is a benign proliferative squamous epithelial cell larynx which most often found. Papillomavirus is the type of tumor that develops rapidly, although not malignant. These tumors can migrate to the oral cavity, nose, trachea and lungs, but the most common location is larynx.



There are two types of laryngeal papillomas: one is the laryngeal papilloma juvenilis usually multiple and tend to be aggressive. The other is a solitary senile larynx papilloma and less aggressive but can develop into malignant.

etiology
The cause of laryngeal papilloma is a " human papilloma virus ' ( HPV ) types 6.11 which infect epithelial cells. It is estimated that the spread of the disease is present at birth from mothers exposed by " genital warts ".
In the normal mucosa cells adjacent to the papilloma, also contain viral DNA that can be activated recurrent lesions. Papilloma in children is more often multiple and recur than adults. While the papilloma in adults is usually single but it tends to become malignant with a specific subtype found that HPV 16.

histopathology
Macroscopic : eksofitik lesions, such as cauliflower, gray or red and bleed easily. This type of lesion is aggressive and easily relapse, but may disappear  spontaneously.
Microscopic: showing a group of connective tissue stroma and blood vessels such as the fingers are coated with a layer of squamous epithelial cells or parakeratotik keratotic surface. Sometimes a picture appeared that bermitosis cells.

clinical manifestations
Initial symptoms are the form of hoarse voice phonation disorders, disfoni even afoni. If the papilloma is large enough can cause respiratory problems such as cough, shortness, and stridor inspiration. In children, the bias occurs misdiagnosis, because often show symptoms of hoarseness, stridor, and respiratory distress after failed treatment of severe asthma or bronchitis.

diagnosis
anamnesis:
Found symptoms of hoarseness until afoni arise even respiratory distress. At the sound of crying children can appear abnormal. Found also a history of progressive hoarseness changes slowly, especially in patients who have a history of the parents had suffered Condyloma akuminata.
physical examination
Usually there is stridor on inspiration and direct laryngoscopy examination of the tumor that resembles the picture looks cauliflower, red, brittle, and bleed easily

Differential Diagnoses
1. Vocal cord polyp.
2. Vocal cord cyst.
3. Vocal cord nodules
4. bronchial asthma
5. bronchitis
6. laryngomalaise

Management
Laryngeal papilloma therapeutic goal is to maintain the airway, maintaining voice quality and eliminates the mass of papilloma and prevent recurrence.
a. Surgery
Some techniques used include: tracheostomy, laryngofissure, microlaryngoscope and extirpation by forceps, microcauter, microlaryngoscope with diathermy or ultrasound, cryosurgery, CO2 surgical laser.
b. medical
Drugs used: antivirus, hormone ( diethylstilbestrol ), steroids, and topical podophyllin
c. immunologically
using interferon
d. photodynamic therapy
This therapy uses dihematoporfirin ether which are activated with the appropriate wavelength (630 nm ).

Post-operative care including total voice rest during the first week, spoke softly during the second week, and gradually to normal in the third week. To speed healing and prevent mucosal dryness is important given the cold mist inhalation (cool mist ) during the first week.

complication
In general, laryngeal papillomas in children may heal spontaneously when puberty, but can be extended to the trachea, bronchus, and lung, believed to tracheostomy or extirpation due to action is not perfect.

prognosis
Prognosis is generally good, early diagnosis and appropriate treatment is a factor thought to affect recurrence. The cause of death is usually due to spread to the lungs.

Vitiligo

 

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.

Etiology

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.

Treatment

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.


refferences
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

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

(HGPS)

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.

Etiology

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
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.


Treatment
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.

Prognosis
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.

Refferences
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

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.
Serology:
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.

Syphilis

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 






 
Definition
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.

Etiology

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
judgment;
• 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.

refferences
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