TONSILITIS

Today, Mbah Dukun Bagong Lee, the shaman medical, visit his blog. He reads comment from visitor. Please post about tonsillitis!!! Before mbah dukun explains about tonsillitis, we must know what tonsil is.

Definition
The palatine tonsil represents the largest accumulation of lymphoid tissue in the head and neck region. Each tonsil has a compact body with a definite thin capsule on its deep surface. A stratified squamous epithelium lines the outer surface of the tonsil and invaginates deeply into the lymphoid tissue to form multiple crypts.

Anatomy of the tonsils
The tonsillar fossa is composed of three muscles: the palatoglossus muscle, the palatopharyngeal muscle, and the superior constrictor muscle. The palatoglossus muscle forms the anterior pillar and the palatopharyngeal muscle forms the posterior pillar. The tonsillar bed is formed by the superior constrictor muscle of the pharynx. The arterial blood supply of the tonsil enters primarily at the lower pole and is derived from the tonsillar branch of the dorsal lingual artery, the scending palatine artery and the tonsillar branch of the facial artery. The ascending pharyngeal artery and the lesser palatine artery also contribute to the vascular supply at the upper pole. Venous blood drains through the peritonsillar plexus around the capsule. The plexus then drains into the lingual and pharyngeal veins, which in turn drain into the internal jugular vein.
The nerve supply of the tonsillar region is through the tonsillar branches of the glossopharyngeal nerve and the descending branches of the lesser palatine nerves. The cause of referred otalgia with tonsillitis is through the tympanic branch of the glossopharyngeal nerve. The lymphatic drainage courses through the upper deep cervical lymph nodes.

What function do tonsils serve?
The tonsils are predominantly ß-cell organs with ßlymphocytes comprising 50% to 65% of all tonsillar lymphocytes. T-cell lymphocytes comprise approximately 40% of tonsillar lymphocytes and 3% are mature plasma cells. Tonsils are involved in inducing secretory immunity and regulating immunoglobulin production. The tonsils are favourably located to mediate immunologic protection of the upper aerodigestive tract as they are exposed to airborne antigens. Moreover, there are 10 to 30 crypts in each tonsil that are ideally suited to trapping foreign material and transporting it to the lymphoid follicles. The proliferation of ß cells in the germinal centres of the tonsils in response to antigenic signals is one of the most important tonsillar functions.
The human tonsils are immunologically most active between the ages of four and 10. Involution of the tonsils begins after puberty, resulting in a decrease in the ß-cell population and a relative increase in the ratio of T- to ß-cells.
Although the overall immunoglobulin production is reduced, there is still considerable ß-cell activity if seen in clinically healthy tonsils. The immunologic consequences of tonsillectomy are unclear. It is evident, however, that tonsillectomy does not result in a major immunologic deficiency.

What are tonsils and what is tonsillitis?
Tonsils are made of soft glandular tissue and are part of the immune system. You have two tonsils, one on either side at the back of the mouth. The picture shows normal non-infected tonsils.
Tonsillitis is an infection of the tonsils. A sore throat is the common symptom. In addition, you may also have a cough, fever, headache, feel sick, feel tired, find swallowing painful, and have swollen neck glands. The tonsils may swell and become red. Pus may appear as white spots on the tonsils.

What are the types of tonsillitis?
o Acute Tonsillitis – those affected usually have fever, sore throat, foul breath, difficulty or painful swallowing, and tender, enlarged lymph nodes. These symptoms usually resolve in 5 – 7 days, but may persist up to two weeks despite therapy
o Recurrent Tonsillitis – same symptoms, with multiple episodes over time
o Chronic Tonsillitis – chronic sore throat, bad breath, soreness with swallowing, perhaps, enlarged and tender neck lymph nodes
o Peritonsillar Abscess – severe sore throat, fever, bad breath, difficulty opening the mouth, usually with a muffled (hot potato) voice. This is due to infection around the tonsil, and typically occurs seven to ten days after the onset of symptoms

Etiology
Many viruses and many bacteria can cause tonsillitis. The most common include:
o Herpes simplex virus
o Streptococcus pyogenes – “strep throat”
o Epstein-Barr virus – the cause of infectious mononucleosis (mono)
o Adenovirus
o Cytomegalovirus
Bacteria cause between 15 and 30 percent of cases of acute tonsillitis. To determine the cause, many tests are commonly performed. While most episodes are viral in origin, only a throat culture helps determine whether the infection is viral or bacterial in origin. The symptoms and signs of viral versus bacterial tonsillitis are very similar. To the observer, the condition looks the same in most individuals.

Symptoms
The Following are the most common symptoms dor tonsillitis include  the following however, individuals may experience symptoms differently:
a.    Swollen, red tonsils (often coated with a yellow, gray, or white membrane)
b.    Blisters or painful ulcerated areas on the throat
c.    Sudden onset of sore throat
d.    Pain while swallowing
e.    Headache
f.    Malaise
g.    Chills
h.    Fever
i.    Swollen and tender lymph nodes in the neck or jaw area
 Also you will find these symptoms when repeated infections or irritation causes enlargement, You may notice:
a.    Difficulty breathing through the nose
b.    Mouth breathing
c.    A muffled sound to the voice (hot potato voice)
d.    Noisy breathing
e.    Snoring while sleeping
f.    A chronic sensation of drainage in the back of the nose and upper throat

What are the complications of tonsillitis?
The complications of tonsillitis may be classified into suppurative and nonsuppurative complications. The nonsuppurative complications include scarlet fever, acute rheumatic fever, and post-streptococcal glomerulonephritis. Suppurative complications include peritonsillar, parapharyngeal and retropharyngeal abscess formation.
Scarlet fever is secondary to acute streptococcal tonsillitis or pharyngitis with production of endotoxins by the bacteria. Clinical signs include an erythematous rash, severe lymphadenopathy, fever, tachycardia, and a yellow exudate overlying erythematous tonsils. Acute rheumatic fever is a syndrome that follows Group A Streptococcal Pharyngitis for one to four weeks. Certain proteins found in heart muscle appear to be antigenetically similar to protein found on the streptococcus.
This is believed to be the method of infection of cardiac tissue. Post-streptococcal glomerulonephritis may be seen after both pharyngeal and skin infections. The typical patient develops an acute nephritic syndrome one to two weeks after a streptococcal infection. The infection is secondary to the presence of a common antigen in the glomerulus and in the streptococcus. Antibiotic therapy may not necessarily alter the natural history of glomerulonephritis. A tonsillectomy may be necessary to eliminate the source of infection.
Peritonsillar abscess most commonly occurs in patients with recurrent tonsillitis or in those with chronic tonsillitis who have been inadequately treated. The spread of infection is from the superior pole of the tonsil with pus formation between the tonsil bed and the tonsillar capsule. peritonsillar cellulitis and abscess respectively. This infection usually occurs unilaterally and the pain is quite severe.
Drooling is caused by odynophagia and dysphagia. Trismus is frequently present as a result of irritation of the pterygoid musculature by the pus and inflamma on. There is gross unilateral swelling of the palate and anterior pillar with displacement of the tonsil downward and medially with deviation of the uvula toward the opposite side. Cultures of peritonsillar abscess usually show a polymicrobial infection, both aerobic and anaerobic.
An abscess in the parapharyngeal space can develop if infection or pus drains from either the tonsils or from a peritonsillar abscess through the superior constrictor muscle. The abscess is located between the superior constrictor muscle and the deep cervical fascia and causes displacement of the tonsil on the lateral pharyngeal wall toward the midline.
Involvement of the adjacent pterygoid and paraspinal muscles with the inflammatory process results in trismus and a stiff neck. Progression of the infection of the abscess may spread down the carotid sheath into the mediastinum. As with most softtissue infections of the neck, lateral pharyngeal space infections are polymicrobial and reflect the oropharyngeal flora.
A retropharyngeal abscess may also result from a peritonsillar abscess. The source of the abscess is a chain of lymph nodes on either side of the midline in the retropharyngeal space. These lymph nodes receive drainage from the nose, paranasal sinuses, pharynx and Eustachian tube. Children usually present with irritability, fever, dysphagia, muffled speech, noisy breathing, stiff neck, and cervical lymphadenopathy.


What is the treatment for tonsillitis?
•    Not treating is an option as many tonsil infections are mild and soon get better.
•    Have plenty to drink. It is tempting not to drink very much if it is painful to swallow.
•    You may become mildly dehydrated if you don't drink much, particularly if you also have a fever. Mild dehydration can make headaches and tiredness much worse.
•    ANALGESIC include Paracetamol or ibuprofen to remove pain, headache, and fever. To keep symptoms to a minimum it is best to take a dose at regular intervals as recommended on the packet of medication rather than 'now and then'. For example, take paracetamol four times a day until symptoms ease.
•    Aspirin gargles may ease the soreness. (There is little research evidence that confirms this. However, it is a popular treatment and may be worth a try.) Dissolve some soluble aspirin in water and gargle for 3-4 minutes. You can do this 3-4 times a day. Spit out the aspirin after gargling. (You should not give aspirin to children under 16.)
•    Other gargles, lozenges, and sprays that you can buy at pharmacies may help to soothe a sore throat. However, they do not shorten the illness.

What are indications for tonsil removed or tonsillectomy
Tonsillectomy is still commonly performed in children, occasionally in adults. The actual
procedure performed does not vary with the age of the patient.
Reasons tonsils are removed – tonsillectomy -- include:
A. Infection
1. Recurrent tonsillitis (more than seven per year or five per year for two years or three per year for three years).
2. Persistent, chronic tonsillitis.
3. Recurrent otitis media unresponsive to medical or previous placement of PETubes.
4. Chronic/recurrent nasopharyngitis.
5. Chronic/recurrent sinusitis.

B. Obstruction
1. Hypertrophy with obstruction unresponsive to antibiotics with or without obstructive apnea, severe
dysphagia, and failure to thrive.
-If adenoids enlarged only.
-If tonsils enlarged only.
-If tonsils and adenoides are enlarged.
2. Nasal obstruction with speech abnormalities, orodental abnormalities.

C. Miscellaneous
1. Recurrent peritonsillar abscess or peritonsillar abscess with previous history of recurrent or persistent
tonsillitis.
2. Unilateral tonsillar hypertrophy.
3. Hemorrhagic tonsillitis.
4. Chronic tonsillolithiasis.


Why are adenoids removed – adenoidectomy?
Reasons adenoids are removed – adenoidectomy -- include:
1.    Often removed at the same setting as tonsils in children with chronic upper airway obstruction;
2.    Chronic mouth breathing;
3.    Chronic, recurrent sinus infections in children, under age 10;
4.    Abnormalities in dental growth – high arched palate;
5.    Need for more than one set of eardrum tubes for recurrent ear infections

About tonsillectomy & adenoidectomy
1.    The surgery is performed under general anesthesia, that is, the patient is put to sleep for  short time
2.    The duration of surgery is generally 20 – 30 minutes, and is performed in an outpatient surgical facility or hospital operating room
3.    The adenoids are removed through the back of the throat, with the surgeon seated at the patient’s head. No external skin incisions are made.
Ue a technique called Coblation® Tonsillectomy. I feel this technique results in less discomfort after surgery. Most patients resume a normal diet in 3 – 5 days after surgery, compared to 7 – 10 days using the outdated electrocautery technique.


refferences
1. http://www.homoeopathyclinic.com/articles/diseases/Tonsillitis.pdf
2. ttp://www.woodlandsmedicalcentre.com/Portals/0/Tonsilitis.pdf

3. http://farm3.static.flickr.com
4. http://www.stacommunications.com/journals/diagnosis/2003/02_February/tonsilitis.pdf

TYPHOID FEVER

DEFINITIONS
Typhoid fever is an acute infectious disease caused by gram-negative bacteria Salmonella typhi. During an infection, the germs multiply in phagocytic cells mononuclear and continuously released into the bloodstream.

Etiology
The cause of typhoid fever is S. typhi, the gram-negative bacteria that don’t have capsule, have flagella that it's almost always on the move by using flagella peritrichous. There are several other species paratyphi A, B, and C which is the cause of paratyphoid fever. Having a somatic antigen (O) of the oligosaccharide, flagellar antigen (H) consisting of protein and envelope antigen (K) consisting of polysaccharides.

Pathogenesis
1. S. typhi: transmission occurs via oral (food or water contaminated with S. typhi)
a. Passing through the "barrier" of gastric acid resulting in the decrease of acidity of gastric acid-alkaline food.
b. Passing through the "barrier" small intestine, (decrease in intestinal peristalsis) and disruption of production or function of intestinal mucosal IgA
c. Stick and into the small intestine epithelial cells, basolateral move in the direction, out of the small intestine epithelial cells, into the lamina propria.
d. Phagocyted by macrophage cells, but was able to continue to live in it, carried on in mesenteric lymph nodes, and then through the ductus thoracicus into the general blood circulation / circulation, resulting bacteremia I which showed no clinical symptoms (asymptomatic)
2. In addition to the epithelial cells lining the small intestine, S. typhi can enter through the cell-M which is above the "Plaque de Peyer" small intestine, phagocyted by macrophage cells, carried to the mesenteric lymph nodes, and then go into the general blood circulation.
3. Bacteremia occurs 24-72 hours after infection.
4. Most S. typhi in macrophages out of circulation into the tissues and organs nonlimfoid breed therein.
5. S. typhi that is in the macrophages can survive and multiply inside macrophages fagosom. Tues finally experienced lysis, S. typhi out into the general blood circulation, occurs bacteremia II is accompanied by clinical symptoms (symptomatic) fever, headache, muscle joints etc.. Clinical symptoms are caused by the influence of endotoxin on the hypothalamus, as well as the influence of proinflammatory cytokines produced by macrophages infected with S. typhi.

CLINICAL SYMPTOMS
The period of typhoid fever shoots last between 10-14 days. Clinical symptoms that arise are very varied from mild to severe, from asymptomatic until the disease is typically accompanied by a picture of complications up to death.
1. In the first week of clinical symptoms of the disease is found in the complaints and symptoms similar to acute infectious diseases in general are fever, headache, dizziness, muscle pain, anorexia, nausea, vomiting, or diarrhea obstipation, bad feeling in lower stomach, cough and epistaxis.
2. On physical examination found only body temperature to rise. The nature of the fever is rising slowly, especially in the afternoon until the evening. In the second week of the symptoms become more obvious in the form of fever, relative bradycardia (increase in body temperature is not followed by increase in pulse rate 8 times per minute), a webbed tongue (gross in the middle, edge and red tip and tremor), hepatomegaly, splenomegaly, and meteorismus
 .3. Somnolen of central nervous disorders, stupor, delirium or psychosis and even coma. Roseolae rarely found in people in Indonesia.


DIAGNOSTIC STEPS
1. Anamnesis
2. Clinical Alerts
3. Laboratory
a. Leukopenia, anesonofilia
b. Bile culture (): blood at week I (in the second week may be negative); feces week II week III urine.
c. Widal reaction (): titer> 1 / 200. Usually positive for the week II
d. Identification of Antigen: Elisa, PCR, IgM S. Typhi


LABORATORY EXAMINATION
a. Blood
It often happens leukopenia, leukocytes can also be normal or leukocytosis. AST / ALT levels are often elevated but will return after recovery. Germs cultured highest at I-week illness, a definitive diagnosis of typhoid fever. Week I: 80-90%, week II: 20-25%, week III: 10-15%.
b. Urine
Urine culture was highest at week II / II, a definitive diagnosis or illness (carrier).
c. Feces
Found a lot of erythrocytes in the stool. Germs cultured in the week II / II, a definitive diagnosis or carrier post typhi.
d. Serology
Is often done Widal test. Widal test done to detect antibodies to the germ S. Typhi with an antibody called aglutinin. Used as aglutinin is aglutinin O and H. The higher the titer the more likely it is infected. Currently there is no common opinion on a significant aglutinin diagnostic titer for typhoid fever.
e. Bone Marrow
Creating a culture of bone marrow. Highly sensitive (95%), not affected by administration of antibiotics and disease phase.


DIFFERENTIAL DIAGNOSIS
1. Viral hepatitis
2. Malaria
3. Cytomegalovirus
4. Leptospirosis
5. Influenza
6. Bronchitis
7. Bronchopneumonia
8. Gastroenteritis
9. TBC
10. UTI



MANAGEMENT
a. Bed rest
b. Diets low in fiber, high calorie and protein
c. Antimicrobial, which is often used is as follows:
1.    Chloramphenicol, a dose of 4 x 500 mg per day given up to 7 days free of heat.
2.    Tiamfenikol, the same dose of chloramphenicol
3.    Cotrimoxazole, 2 x 2 tablet (1 tablet contains 400 mg sulfamethoxazole and trimethoprim 80 mg) was given for 2 weeks.
4.    Ampicillin or amoxicillin, the dose of 50-150 mg / KgBW for 2 weeks
5.    Third-generation cephalosporin, for example ceftriaxonewith 3-4 grams daily dose for 3-5 days
6.    Fluoroquinolone class:
-    Norfloxacin dose of 2 x 400 mg / day for 14 days
-    Ciprofloxacin dose of 2 x 500 mg / day for 6 days
-    Ofloxacin dose of 2 x 400 mg / day for 7 days
-    Pefloxacin dose of 400 mg / day for 7 days
-    Fleroxacindose of 400 mg / day for 7 days
-    In pregnant women that can be used are ampicillin, amoxicillin and ceftriaxone

PREVENTION
Cleanliness
-    • Personal: with hand washing.
-    • The disposal of feces and urine.
-    • Provision of clean water.
-    Immunization
• Children over 2 years.
-    • Contact with patients.
-    • Events outside the Ordinary.
-    • Travelling to endemic areas.
-    • Tyvium - Typherix ® i.m ® 3 years.
-    • Vivotif ® Oral.


COMPLICATIONS
a. Intestinal
1. Intestinal bleeding
In the intestine of infected Peyeri plaque (particularly the terminal ileum) can form ulcers / wound oval-shaped and extends to the axis of the intestine. If the wound penetrates the gut lumen and the blood vessels so there is bleeding.
2. Intestinal Perforation
Occurs in approximately 3% of patients treated. Usually arise in the third week but can also occur in the first week. In addition to common symptoms of typhoid is common, the patient complained of typhoid fever with perforation of severe abdominal pain especially in the lower right quadrant which then spread throughout the abdomen and is accompanied by signs of ileus. Weaken bowel sounds in 50% of deaf patients and sometimes the liver is not found because of abdominal free air. Other signs of perforation are rapid pulse, blood pressure down and may even shock. Leukocytosis with a shift to the left to bolster the perforation

b. EXTRA intestinal Complications Hematological
Complications hematological form of thrombocytopenia, hipofibrino-genemia, increased prothrombin time, increased partial thromboplastin time, increased fibrin degration product until disseminate intravascular coagulation (KID) can be found in most patients with typhoid fever. Trombositoponia have often found, this may occur because of decreased production of platelets in bone marrow during the process of infection or increased destruction of platelets in the reticuloendothelial system. Drugs also play a role.

1. Typhoid hepatitis
Mild to moderate swelling of the liver are found in 50% of cases with typhoid fever and more prevalent due to S typhi than S. Paratyphi. To distinguish whether hepatitis due to typhoid, viral, malaria or Amoeba then need to be considered physical, laboratory parameters, and if necessary histopathological liver. In typhoid fever increased transaminase enzymes are not relevant to the increase in serum bilirubin (to differentiate it by because of viral hepatitis.) Typhoid hepatitis can occur in patients with malnutrition and poor immune system. Although very rare, complications can occur hepatoencephalopathy
2. Myocarditis
Myocarditis occurs in 1-5% patients with typhoid fever while electrocardiographic abnormalities may occur in 10-15% sufferer. Patients with myocarditis are usually without symptoms of cardiovascular or chest pains, arrhythmia and congestive heart failure, or cardiogenic shock. While pericarditis is very rare. Persistent electrocardiographic changes accompanied by arrhythmias have a poor prognosis. The disorder is caused by damage of myocard by the germ S. tyhphi and myocarditis frequently as a cause of death. Usually seen in severely ill patients, a state of acute and fulminant.
3. Neuropsychiatric / Typhoid Toxic
Delerium neuropsychiatric manifestations can be either with or without seizures, a semi-coma, Parkinsonism Parkinson rigidytyltransient acute brain syndrome, generalized mioclonus, meningismus, cyitotoxic schizophrenia, acute mania, hipomania, encephalomyelitis, meningitis, peripheral polineuritis, Guillain-Barre syndrome and psychosis.