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Wednesday, October 31, 2007

Vitamin D has no effect on Overall Cancer Death Risk

A new US study has concluded that Vitamin D has no effect on the overall risk of dying from cancer although higher levels of the vitamin may be linked with a decreased risk of dying from colorectal cancer. This finding contradicts the findings of some other studies.

The study is published in the early online issue of the Journal of the National Cancer Institute and is the work of Dr. D. Michal Freedman, of the National Cancer Institute in Bethesda, Maryland, and colleagues.

The researchers wrote that:

"To our knowledge, this study is the first to examine the relationship between measured serum vitamin D levels and cancer mortality for selected site and for all sites combined."

Diet and exposure to sunlight are the main source of vitamin D in the body. Some epidemiological studies have suggested there is a link between higher levels of vitamin D and increased survival or reduced risk of dying from cancer. Also studies on animal and human cells have suggested the vitamin shrinks tumors and triggers the death of cancer cells.

Freedman and colleagues analyzed data on 16,818 people who took part in the third national Health and Nutrition Examination Survey. The participants were aged 17 or older and were followed from between 1988 and 1994 up to 2000. Levels of Vitamin D, or more specifically serum 25(OH)D, circulating in the blood at time of enrollment (baseline) were measured using a process known as radioimmunoassay. Levels of vitamin A were also measured for comparison.

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Pap Smear Video

Researched and Presented by Anthony
Description: Obtaining a pap smear from the cervix and cervical canal.
Note: You need the latest Flash Player in order to view the video. Download it here.

This is how a pap smear is done, however, for a complete summary of information, here are the things you need to know about the procedure.

What is a Pap Smear?

A Pap smear (also known as the Pap test) is a medical procedure in which a sample of cells from a woman's cervix (the end of the uterus that extends into the vagina) is collected and spread (smeared) on a microscope slide. The cells are examined under a microscope in order to look for pre-malignant (before-cancer) or malignant (cancer) changes.

A Pap smear is a simple, quick, and relatively painless screening test. Its specificity - which means its ability to avoid classifying a normal smear as abnormal -- while very good, is not perfect. The sensitivity of a Pap smear - which means its ability to detect every single abnormality -- while extremely good, is also not perfect. Thus, a few women develop cervical cancer despite having regular Pap screening.

In the vast majority of cases, a Pap test does identify minor cellular abnormalities before they have had a chance to become malignant and at a point when the condition is most easily treatable. The Pap smear is not intended to detect other forms of cancer such as those of the ovary, vagina, or uterus. Cancer of these organs may be discovered during the course of the gynecologic (pelvic) exam, which usually is done at the same time as the Pap smear.

How is a Pap smear done?

A woman should have a Pap smear when she is not menstruating. The best time for screening is between 10 and 20 days after the first day of her menstrual period. For about 2 days before testing, a woman should avoid douching or using spermicidal foams, creams, or jellies or vaginal medicines (except as directed by a physician). These agents may wash away or hide any abnormal cervical cells.

A Pap smear can be done in a doctor's office, a clinic, or a hospital by either a physician or other specially trained health care professional, such as a physician assistant, a nurse practitioner, or a nurse midwife. With the woman positioned on her back, the clinician will often first examine the outside of the patient's genital and rectal areas, including the urethra (the opening where urine leaves the body), to assure that they look normal. A speculum is then inserted into the vaginal area (the birth canal). The speculum is an instrument that allows the vagina and the cervix to be viewed and examined. A cotton swab is sometimes used to clear away mucus that might interfere with an optimal sample.

A small brush called a cervical brush is then inserted into the opening of the cervix (the cervical os) and twirled around to collect a sample of cells. This sample, because it comes from inside the cervix, is called the endocervical sample ("endo" meaning inside). A second sample is also collected as part of the Pap smear and is called the ectocervical sample ("ecto" meaning outside). These cells are collected from a scraping of the area surrounding, but not entering, the cervical os. Both the endocervical and the ectocervical samples are gently smeared on a glass slide and a fixative (a preservative) is used to prepare the cells on the slide for laboratory evaluation.

A bimanual (both hands) exam usually follows the collection of the two samples for the Pap smear. The bimanual examination involves the examiner inserting two fingers of one hand inside the vaginal canal while feeling the ovaries and uterus with the other hand on top of the abdomen (belly).

The results of the Pap smear are usually available in 2 to 3 weeks. At the end of Pap smear testing, each woman should ask how she should expect to be informed about the results of her Pap smear. If a woman has not learned of her results after a month, she should contact her clinician's office.

What are the possible recommendations for follow-up after a Pap smear?

Once the final diagnosis has been made, the follow-up recommends what the appropriate next step(s) might be. For example, if the final diagnosis states that the smear was "within normal limits," the appropriate follow-up might be "recommend routine follow-up."

An abnormal Pap smear is one in which the laboratory interprets the cellular changes to be different from those normally seen on a healthy cervix. There are a number of possible follow-up scenarios for an abnormal Pap smear.

Metzenbaum Scissors

Researched by Anthony

Metzenbaum scissors are surgical scissors designed for cutting delicate tissue. The scissors come in variable lengths and have a relatively long handle-to-blade ratio. They are constructed of tungsten carbide and its blades can be curved or straight. Also, the blade tips can be either sharp or blunt.

Source: Wikipedia - the Free Encyclopedia

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Painless Penile Lesion in a 52-Year-Old Man

By Anthony
This is another one of those interesting Guess my diagnosis game. If you're up to it, check this out...


A 52-year-old man with no clinically significant medical history presents to the emergency department (ED) with a chief complaint of a “rash” on his penis. The patient states that the rash first appeared 1 week before presentation. He denies any dysuria, urethral discharge, pruritus or pain in the area of the lesion. This is the first time he has had such a rash. He admits to having had several recent sexual partners.

On physical examination, his vital signs are normal. The patient has a well-demarcated, ulcerated lesion on the ventral aspect of his penis (see Image). The lesion is not tender to palpation. No other lesions are noted, and no discharge is observed from the urethra. The findings of his testicular examination are unremarkable, with the exception of bilateral prominent inguinal lymphadenopathy. The remaining physical findings, including the cardiac and abdominal findings, are unremarkable.

What do you think is the diagnosis, and what empiric treatment is necessary?


The lesion is characteristically painless.


See Answer


Researched by Anthony
Thoracentesis (also known as thoracocentesis or pleural tap) is an invasive procedure to remove fluid or air from the pleural space for diagnostic or therapeutic purposes. A cannula, or hollow needle, is carefully introduced into the thorax, generally after administration of local anesthesia. The procedure was first described in 1852.

The recommended location varies depending upon the source. Some sources recommend the midaxillary line, in the sixth, seventh, or eighth intercostal space.

See Actual Video


This procedure is indicated when unexplained fluid accumulates in the chest cavity outside the lung. In more than 90% of cases analysis of pleural fluid yields clinically useful information. If a large amount of fluid is present, then this procedure can also be used therapeutically to remove that fluid and improve patient comfort and lung function.

The most common causes of pleural effusions are cancer, congestive heart failure, pneumonia, and recent surgery. In countries where tuberculosis is common, this is also a common cause of pleural effusions.

When cardiopulmonary status is compromised (i.e. when the fluid or air has its repercussions on the function of heart and lungs), due to air (significant pneumothorax), fluid (pleural fluid) or blood (hemothorax) outside the lung, then this procedure is usually replaced with tube thoracostomy, the placement of a large tube in the pleural space.


An uncooperative patient or a coagulation disorder that can not be corrected are absolute contraindications.

Relative contraindications are site of insertion has known bullous disease (e.g. emphysema), use of positive end-expiratory pressure (PEEP) and only one functioning lung (due to diminished reserve).


Major complications are pneumothorax (3-30%), hemopneumothorax, hemorrhage, hypotension (low blood pressure due to a vasovagal response) and re-expansion pulmonary edema.

Minor complications include a dry tap (no fluid return), subcutaneous hematoma or seroma, anxiety, dyspnea and cough (after removing large volume of fluid).

Interpretation of pleural fluid analysis

Several diagnostic tools are available to determine the etiology of pleural fluid.

Transudate versus exudate

First the fluid is either transudate or exudate.

A transudate is defined as pleural fluid to serum total protein ratio of less than 0.5, pleural fluid to serum LDH ratio < style="font-style: italic;">Amylase

A high amylase level (twice the serum level or the absolute value is greater than 160 Somogy units) in the pleural fluid is indicative of either acute or chronic pancreatitis, pancreatic pseudocyst that has dissected or ruptured into the pleural space, cancer or esophageal rupture.


This is considered low if pleural fluid value is less than 50% of normal serum value. The differential diagnosis for this is:

* rheumatoid effusion
* lupus effusion
* bacterial empyema
* malignancy
* tuberculosis
* esophageal rupture (Boerhaave syndrome)


Normal pleural fluid pH is approximately 7.60. A pleural fluid pH below 7.30 with normal arterial blood pH has the same differential diagnosis as low pleural fluid glucose.

Triglyceride and cholesterol

Chylothorax (fluid from lymph vessels leaking into the pleural cavity) may be identified by determining triglyceride and cholesterol levels, which are relatively high in lymph. A triglyceride level over 110 mg/dl and the presence of chylomicrons indicate a chylous effusion. The appearance is generally milky but can be serous.

The main cause for chylothorax is rupture of the thoracic duct, most frequently as a result of trauma or malignancy (such as lymphoma).

Cell count and differential

The number of white blood cells can give an indication of infection. The specific subtypes can also give clues as to the type on infection. The amount of red blood cells are an obvious sign of bleeding.

Cultures and stains

If the effusion is caused by infection, microbiological culture may yield the infectious organism responsible for the infection, sometimes before other cultures (e.g. blood cultures and sputum cultures) become positive. A Gram stain may give a rough indication of the causative organism. A Ziehl-Neelsen stain may identify tuberculosis or other mycobacterial diseases.


Cytology is an important tool in identifying effusions due to malignancy. The most common causes for pleural fluid are lung cancer, metastasis from elsewhere and mesothelioma. The latter often presents with an effusion. Normal cytology results do not reliably rule out malignancy, but make the diagnosis more unlikely.

Source: Wikipedia - the Free Encyclopedia

If you find an error, please let us know.


Compiled and Summarized by Anthony
Chickenpox is the common name for Varicella zoster, classically one of the childhood infectious diseases caught by and survived by almost every child.

Chickenpox is caused by the varicella-zoster virus (VZV), also known as human herpes virus 3 (HHV-3), one of the eight herpes viruses known to affect humans. It starts with conjunctival and catarrhal symptoms and then characteristic spots appearing in two or three waves, mainly on the body and head rather than the hands and becoming itchy raw pox (pocks), small open sores which heal mostly without scarring.

Chickenpox has a 14-16 day incubation period and is highly contagious through physical contact two days before symptoms appear. Following primary infection, there is usually lifelong protective immunity from further episodes of chickenpox. Recurrent chickenpox, commonly known as shingles, is fairly rare but more likely in people with compromised immune systems.

Chickenpox is rarely fatal (usually from varicella pneumonia), with pregnant women and those with a suppressed immune system being more at risk. Pregnant women not known to be immune and who come into contact with chickenpox may need urgent treatment as the virus can cause serious problems for the baby. This is less of an issue after 20 weeks.

Later in life, viruses remaining dormant in the nerves can reactivate causing localized eruptions of shingles. This occurs particularly in people with compromised immune systems, such as the elderly, and perhaps even those suffering sunburn. Unlike chickenpox which normally fully settles, shingles may result in persisting post-herpetic neuralgia pain.

Signs and Symptoms

Chickenpox is a highly contagious disease that spreads from person to person by direct contact or through the air from an infected person's coughing or sneezing. Touching the fluid from a chickenpox blister can also spread the disease. A person with chickenpox is contagious from one to two days before the rash appears until all blisters have formed scabs. This may take five to 10 days. It takes from 10-21 days after contact with an infected person for someone to develop chickenpox.

The chickenpox lesions (blisters) start as a two to four millimeter red papule which develops an irregular outline (a rose petal). A thin-walled, clear vesicle (dew drop) develops on top of the area of redness. This "dew drop on a rose petal" lesion is very characteristic for chickenpox. After about eight to 12 hours the fluid in the vesicle gets cloudy and the vesicle breaks leaving a crust. The fluid is highly contagious, but once the lesion crusts over, it is not considered contagious. The crust usually falls off after seven days sometimes leaving a crater-like scar. Although one lesion goes through this complete cycle in about seven days, another hallmark of chickenpox is the fact that new lesions crop up every day for several days. Therefore, it may take about a week until new lesions stop appearing and existing lesions crust over. Children are not to be sent back to school until all lesions have crusted over.

Secondary infections, such as inflammation of the brain, can occur in immunocompromised individuals. This is more dangerous with shingles.

Chickenpox is highly contagious and is spread through the air when infected people cough or sneeze, or through physical contact with fluid from lesions on the skin. Zoster, also known as shingles, is a reactivation of chickenpox and may also be a source of the virus for susceptible children and adults. It is not necessary to have physical contact with the infected person for the disease to spread. Those infected can spread chickenpox before they know they have the disease - even before any rash develops. In fact, people with chickenpox can infect others from about two days before the rash develops until all the sores have crusted over, usually four to five days after the rash starts.

Congenital defects in babies

These may occur if the child's mother was exposed to the zoster virus during pregnancy. Effects on the fetus may be minimal in nature but physical deformities range in severity from under developed toes and fingers, to severe anal and bladder malformation. Possible problems include:

· Damage to brain: encephalitis, microcephaly, hydrocephaly, aplasia of brain
· Damage to the eye (optic stalk, optic cap, and lens vesicles), microphthalmia, cataracts, chorioretinitis, optic atrophy
· Other neurological disorder: damage to cervical and lumbosacral spinal cord, motor/sensory deficits, absent deep tendon reflexes, anisocoria/Horner's syndrome
· Damage to body: hypoplasia of upper/lower extremities, anal and bladder sphincter dysfunction
· Skin disorders: (cicatricial) skin lesions, hypopigmentation

Causative Agent

Human herpesvirus 3 (alpha) or varicella zoster virus (VZV) is the causative agent.

Mode of Transmission

Chickenpox transmission is mainly person to person by airborne respiratory droplets but also by direct contact with vesicle fluid of chickenpox cases, or contact with the vesicle fluid of patients with herpes zoster. Indirect contact occurs through articles freshly soiled by discharges from vesicles of infected persons. Scabs are not infective.


Confirmation of the diagnosis is generally only required when the clinical picture is atypical. It is made by:

· isolation of the virus in cell cultures
· visualisation by electron microscopy
· serological tests for antibodies
· immunofluorescence on lesion swab or fluid
· nucleic acid testing or PCR.

Incubation Period

14-16 days (13-17 days in some books)


Little is known about the route and the source of transmission of the virus. VZV is certainly transmissible through the airborne route and does not require close personal contact. The skin lesions are certainly full of infectious virus particles whilst in contrast, it is almost impossible to isolate virus from the upper respiratory tract. It is possible that aerial transmission originates from symptomless oral lesions. The virus is thought to gain entry via the respiratory tract and spreads shortly after to the lymphoid system. After an incubation period of 14 days, the virus arrives at its main target organ, the skin. The virus probably spreads to other organ systems in the body without any ill effect. However, in immunocompromised individuals and neonates, dissemination can cause serious infection of the lungs and brain. Recovery from infection is thought to result in lifelong immunity.

Following the primary infection, the virus remains latent in the cerebral or posterior root ganglia. In 10 - 20% of individuals, a single recurrent infection occurs after several decades. The virus reactivates in the ganglion and tracks down the sensory nerve to the area of the skin innervated by the nerve, producing a varicellaform rash in the distribution of a dermatome. The failure of the host defense mechanisms to contain the virus in the ganglia after such prolonged periods of time is not understood. In immunocompetent individuals, it is probably due to the decline effectiveness of previously acquired immunity with advancing age. Herpes zoster also appears in increasing frequency in immunocompromised individuals such as those with Hodgkin's disease and AIDS, who have defective CMI. Also disseminated herpes zoster is more likely to occur in such people.


Chickenpox is usually acquired by the inhalation of airborne respiratory droplets from an infected host. The highly contagious nature of VZV explains the epidemics of chickenpox that spread through schools as one child who is infected quickly spreads the virus to many classmates. High viral titers are found in the characteristic vesicles of chickenpox; thus, viral transmission may also occur through direct contact with these vesicles, although the risk is lower.

After initial inhalation of contaminated respiratory droplets, the virus infects the conjunctivae or the mucosae of the upper respiratory tract. Viral proliferation occurs in regional lymph nodes of the upper respiratory tract 2-4 days after initial infection and is followed by primary viremia on postinfection days 4-6. A second round of viral replication occurs in the body's internal organs, most notably the liver and the spleen, followed by a secondary viremia 14-16 days postinfection. This secondary viremia is characterized by diffuse viral invasion of capillary endothelial cells and the epidermis. VZV infection of cells of the malpighian layer produces both intercellular edema and intracellular edema, resulting in the characteristic vesicle.

Exposure to VZV in a healthy child initiates the production of host immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) antibodies; IgG antibodies persist for life and confer immunity. Cell-mediated immune responses are also important in limiting the scope and the duration of primary varicella infection. After primary infection, VZV is hypothesized to spread from mucosal and epidermal lesions to local sensory nerves. VZV then remains latent in the dorsal ganglion cells of the sensory nerves. Reactivation of VZV results in the clinically distinct syndrome of herpes zoster (shingles).


The varicella-zoster virus is spread through direct contact with a person that is infected and through the air with fluid from the rash or respiratory secretions. An infected person can spread the virus from 5 days before the rash develops until all lesions have crusted.

Currently, the best way to prevent illness is by vaccine, which is 85% effective.

People with chickenpox should remain at home until no new lesions are forming and all present lesions have crusted. This is generally a period of four to five days for persons with a healthy immune system.

Infected persons with compromised immune systems may continue to form new lesions and remain infectious for a longer period of time.

People with shingles should cover their rash before leaving the house. Care should be taken to wash hands after touching chickenpox or shingles rashes.


For most health children, chickenpox symptoms can be controlled with soothing baths or antihistamines to decrease itching. Acetaminophen may help control fever, headache, or muscle pain. Do not give aspirin to children with chickenpox, because this can increase the child's risk of Reye syndrome.

A prescription drug called acyclovir is FDA approved to treat the symptoms of chickenpox in persons older than age 2. The drug should help reduce the severity of chickenpox symptoms, especially in older children and teenagers, if taken within 24 hours of the rash's first appearance. However, this drug is generally only used in severe cases of chickenpox and in patients who have weakened immune systems, such as persons with cancer and who have had an organ transplant.

A vaccine to prevent chickenpox is available for children over age 1.

Drug-related information can be found here.


Secondary bacterial infection of skin lesions, manifesting as impetigo, cellulitis, and erysipelas, is the most common complication in healthy children.

o Staphylococci and streptococci are the most commonly implicated bacterial pathogens.
o Bacterial superinfection may predispose to scarring. Localized bacterial superinfection rarely may manifest in septicemia, culminating in secondary bacterial pneumonia, otitis media, or necrotizing fasciitis.

Disseminated primary varicella infection, usually seen in the immunocompromised or adult populations, may have high morbidity. Ninety percent of cases of varicella pneumonia occur in the adult population. Rarer complications of disseminated chickenpox also include myocarditis, hepatitis, and glomerulonephritis.

Central nervous system complications of primary VZV infection may occur, albeit very rarely. Reye syndrome, Guillain-Barré syndrome, acute cerebellar ataxia, and encephalitis have all been documented to occur after VZV infection.

Thrombocytopenia and purpura secondary to VZV infection have been described in more than 100 patients.

o Hemorrhagic complications are more common in the immunocompromised or immunosuppressed populations, although healthy children and adults have been affected. Five major clinical syndromes have been described: febrile purpura, malignant chickenpox with purpura, postinfectious purpura, purpura fulminans, and anaphylactoid purpura.

o These syndromes have variable courses, with febrile purpura being the most benign of the syndromes and having an uncomplicated outcome. In contrast, malignant chickenpox with purpura is a grave clinical condition that has a mortality rate of greater than 70%. The etiology of these hemorrhagic chickenpox syndromes is not known, although an autoimmune pathophysiologic mechanism has been implicated.


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Tuesday, October 30, 2007

HIV arrived in US from Haiti, New Study

HIV, the virus that causes AIDS, probably came into the US from Haiti around the year 1969, a decade earlier than most scientists believed, says new research from the US.

The study is due to be published this week in the Early Online issue of the Proceedings of the National Academy of Sciences and is the work of Michael Worobey, an assistant professor of ecology and evolutionary biology at The University of Arizona in Tucson, and colleagues. The title of the study is "The emergence of HIV/AIDS in the Americas and beyond".

"Our results show that the strain of virus that spawned the US AIDS epidemic probably arrived in or around 1969. That is earlier than a lot of people had imagined," said Worobey in a prepared statement.

"Haiti was the stepping stone the virus took when it left central Africa and started its sweep around the world. Once the virus got to the US, then it just moved explosively around the world," added Worobey.

The researchers found that most HIV/AIDS strains in the US came from a single common ancestor that predates the well storied "Patient Zero" theory. The Patient Zero theory came from a misrepresentation for Patient O (Oh), for "Out of California", where early research on AIDS by the US Centers for Disease Control and Prevention (CDC) suggested HIV in the US spread in the late 1970s, early 1980s from one man in California.

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Monday, October 29, 2007

Thoracentesis Video

Researched and Presented by Anthony
Description: A full Detailed video on Thoracentesis.
Note: You need the latest Flash Player in order to view the video. Download it here.

The video will explain everything you need to know about Thoracentesis, however, here are a few things you need to take note.


Thoracentesis is a procedure to remove fluid from the space between the lining of the outside of the lungs (pleura) and the wall of the chest. Normally, very little fluid is present in this space. An accumulation of excess fluid between the layers of the pleura is called a pleural effusion.

How the Test is Performed

A small area of skin on your chest or back is washed with a sterilizing solution. Some numbing medicine (local anesthetic) is injected in this area. A needle is then placed through the skin of the chest wall into the space around the lungs called the pleural space. Fluid is withdrawn and collected and may be sent to a laboratory for analysis (pleural fluid analysis).

How to Prepare for the Test

A consent is necessary. Failure to do so will really put the blame on you.

A chest x-ray may be performed before and after the test.

Tell the patient/client not to cough, and tell the client not to breathe deeply, or move during the test to avoid injury to the lung.

How the Test Will Feel

The client will be on a bed or may sit on the edge of a chair or bed with his/her head and arms resting on a table. The skin around the procedure site is disinfected and the area is draped. A local anesthetic is injected into the skin. The thoracentesis needle is inserted above the rib into the pleural space.

There will be a stinging sensation when the local anesthetic is injected, and the client may feel a sensation of pressure when the needle is inserted into the pleural space.

Tell the client to inform the health care provider if he/she develops shortness of breath or chest pain.

Why the Test is Performed

The test is performed to determine the cause of the fluid accumulation or to relieve the symptoms associated with the fluid accumulation.

Normal Results

Normally the pleural cavity contains only a very small amount of fluid.

What Abnormal Results Mean

The analysis of the fluid will indicate possible causes of pleural effusion such as infection, cancer, heart failure, cirrhosis, and kidney disease. If infection is suspected, a culture of the fluid is often done to determine whether microorganisms are present and if so, to identify them.

Additional conditions under which the test may be performed include the following:

* Pneumonia
* Hemothorax
* Pulmonary veno-occlusive disease
* Pancreatitis
* Pulmonary embolism
* Thyroid disease
* Collagen vascular disease
* Asbestos-related pleural effusion
* Drug reactions


* Pneumothorax (collapse of the lung)
* Fluid re-accumulation
* Pulmonary edema
* Bleeding
* Infection
* Respiratory distress


A chest x-ray is often done after the procedure to detect possible complications.


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Compiled and Summarized by Anthony
Leprosy, or Hansen's disease, is a chronic infectious disease caused by the bacterium Mycobacterium leprae. Leprosy is primarily a granulomatous disease of the peripheral nerves and mucosa of the upper respiratory tract; skin lesions are the primary external symptom. Left untreated, leprosy can be progressive, causing permanent damage to the skin, nerves, limbs, and eyes. Contrary to popular conception, leprosy does not cause body parts to simply fall off, and it differs from tzaraath, the malady described in the Hebrew scriptures and previously translated into English as leprosy.

Historically, leprosy has affected humanity since at least 300 BC, and was well-recognized in the civilizations of ancient China, Egypt and India. In 1995, the World Health Organization (WHO) estimated that between two and three million individuals were permanently disabled because of leprosy. Although the forced quarantine or segregation of patients is unnecessary—and can be considered unethical—a few leper colonies still remain around the world, in countries such as India, and Vietnam.

The age-old social stigma associated with the advanced form of leprosy lingers in many areas, and remains a major obstacle to self-reporting and early treatment. Effective treatment for leprosy appeared in the late 1940s with the introduction of dapsone and its derivatives. However, leprosy bacilli resistant to dapsone gradually evolved and became widespread, and it was not until the introduction of multidrug therapy (MDT) in the early 1980s that the disease could be diagnosed and treated successfully within the community.

Mycobacterium leprae, the causative agent of leprosy, was discovered by G. H. Armauer Hansen in Norway in 1873, making it the first bacterium to be identified as causing disease in man. Historically, individuals with Hansen's disease have been known as lepers, however, this term is falling into disuse as a result of the diminishing number of leprosy patients and the pejorative connotations of the term. The term most widely accepted among people and agencies working in the field of Hansen's disease is "people affected by Hansen's disease."

In particular tinea capitis (fungal scalp infection) and related infections on other body parts caused by the dermatophyte fungus Trichophyton violaceum are abundant throughout the Middle East and North Africa today and might also have been common in biblical times. Similarly, the related agent of the disfiguring skin disease favus, Trichophyton schoenleinii, appears to have been common throughout Eurasia and Africa before the advent of modern medicine. Persons with severe favus and similar fungal diseases (and potentially also with severe psoriasis and other diseases not caused by microorganisms) tended to be classed as having leprosy as late as the 17th century in Europe. This is clearly shown in the painting Governors of the Home for Lepers at Haarlem 1667 by Jan de Bray (Frans Hals Museum, Haarlem, the Netherlands), where a young Dutch man with a vivid scalp infection, almost certainly caused by a fungus, is shown being cared for by three officials of a charitable home intended for leprosy sufferers. The use of the word "leprosy" before the mid-19th century, when microscopic examination of skin for medical diagnosis was first developed, can seldom be correlated reliably with Hansen's disease as we understand it today.

The word "leprosy" derives from the ancient Greek words lepros, a scale, and lepein, to peel. The word came into the English language via Latin and Old French.

Signs and Symptoms

The clinical manifestations of leprosy vary but primarily affect the skin, nerves, and mucous membranes. Patients with this chronic infectious disease are classified as having paucibacillary (tuberculoid leprosy), multibacillary Hansen's disease (lepromatous leprosy), or borderline leprosy.

Borderline leprosy (also termed multibacillary), of intermediate severity, is the most common form. Skin lesions resemble tuberculoid leprosy but are more numerous and irregular; large patches may affect a whole limb, and peripheral nerve involvement with weakness and loss of sensation is common. This type is unstable and may become more like lepromatous leprosy or may undergo a reversal reaction, becoming more like the tuberculoid form.

Paucibacillary Hansen's disease is characterized by one or more hypopigmented skin macules and anesthetic patches, i.e., damaged peripheral nerves that have been attacked by the human host's immune cells.

Multibacillary Hansen's disease is associated with symmetric skin lesions, nodules, plaques, thickened dermis, and frequent involvement of the nasal mucosa resulting in nasal congestion and epistaxis (nose bleeds) but typically detectable nerve damage is late.

Contrary to popular belief, Hansen's bacillus does not cause rotting of the flesh; rather, a long investigation by Paul Brand yielded that insensitivity in the limbs extremities was the reason why unfelt wounds or lesions, however minute, lead to undetected deterioration of the tissues, the lack of pain not triggering an immediate response as in a fully functioning body. Recently, leprosy has also emerged as a problem in HIV patients on antiretroviral drugs.

Causative Agent

Mycobacterium leprae is the causative agent of leprosy. An intracellular, acid-fast bacterium, M. leprae is aerobic, gram-positive, and rod-shaped, and is surrounded by the waxy cell membrane coating characteristic of Mycobacterium species.

Due to extensive loss of genes necessary for independent growth, M. leprae is unculturable in the laboratory, a factor which leads to difficulty in definitively identifying the organism under a strict interpretation of Koch's postulates.[9] The use of non-culture-based techniques such as molecular genetics has allowed for alternative establishment of causation

Mode of Transmission

The mode of transmission is not clearly established. The disease is probably transmitted from person to person by aerosol with a high subclinical rate of infection. Household and prolonged close contact seem important. There is anecdotal evidence that rarely it may be transmitted by inoculation, such as by contaminated tattoo needles.


Clinical suspicion is the crucial factor in making an early diagnosis of leprosy in non-endemic areas. Leprosy should always be considered in any undiagnosed patient with chronic skin lesions or a peripheral neuropathy. This is particularly important if they have spent more than brief periods in areas where the disease is endemic, or they have been a contact of a patient known to have leprosy.

Confirmation of diagnosis depends on the form:

· lepromatous disease requires demonstration of plentiful acid-fast bacilli in skin or nasal smears. Skin smears are made by scraping a small amount of tissue fluid from a superficial scalpel cut over a lesion and smearing it on a glass slide.

· tuberculoid disease requires demonstration of typical granulomata with sparse acid-fast bacilli, in biopsies of either skin or nerve lesions.

Incubation Period

In leprosy, the incubation period and the times of infection and onset of disease are difficult to define; the former because of the lack of adequate immunological tools and the latter because of the disease's slow onset. Even so, several investigators have attempted to measure the incubation period for leprosy. The minimum incubation period reported is as short as a few weeks and this is based on the very occasional occurrence of leprosy among young infants. The maximum incubation period reported is as long as 30 years or more, or over, as observed among war veterans known to have been exposed for short periods in endemic areas but otherwise living in non-endemic areas. It is generally agreed that the average incubation period is between 3 to 5 years.


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Leprosy is not a highly infectious disease. The principal means of transmission is by aerosol spread from infected nasal secretions to exposed nasal and oral mucosa. Leprosy is not generally spread by means of direct contact through intact skin, though close contacts are most vulnerable. The incubation period is 6 months to 40 years or longer. The mean incubation period is 4 years for tuberculoid leprosy (TT) and 10 years for lepromatous leprosy (LL).

The areas most commonly affected are the superficial peripheral nerves, skin, mucous membranes of the upper respiratory tract, anterior chamber of the eyes, and testes. These areas tend to be cool parts of the body. Tissue damage depends on the degree to which cell-mediated immunity is expressed, the type and extent of bacillary spread and multiplication, the appearance of tissue-damaging immunologic complications (ie, lepra reactions), and the development of nerve damage and its sequelae.

M. leprae is an obligate intracellular acid-fast gram-positive bacillus with an affinity for macrophages and Schwann cells. For Schwann cells in particular, the mycobacterium binds to the G domain of the alpha-chain of laminin 2 (found only in peripheral nerves) in the basal lamina. Its slow replication within the Schwann cell will eventually stimulate a cell-mediated immune response, which creates a chronic inflammatory reaction. As a result, swelling occurs in the perineurium, leading to ischemia, fibrosis, and axonal death.

The genomic sequence of M. leprae was only recently completed. One important discovery is that though it depends on its host for metabolism, the microorganism retains genes for the formation of a mycobacterial cell wall. Components of the cell wall stimulate a host immunoglobulin M (IgM) antibody and cell-mediated immune response, while also moderating the bactericidal abilities of macrophages.

The strength of the host's immune system influences the clinical form of the disease. A strong cell-mediated immunity and a weak humoral response results in mild forms of disease, with a few well-defined nerves involved and lower bacterial loads. A strong humoral response but relatively absent cell-mediated immunity results in LL, with widespread lesions, extensive skin and nerve involvement, and high bacterial loads. Therefore, a spectrum of disease exists such that cell-mediated immunity dominates in mild forms of leprosy and decreases with increasing clinical severity. Meanwhile, humoral immunity is relatively absent in mild disease and increases with the severity of disease.

Toll-like receptors (TLRs) may also play a role in the pathogenesis of leprosy. M. leprae activate TLR2 and TLR1, which are found on the surface of Schwann cells, especially with TT. Although this cell-mediated immune defense is most active in mild forms of the disease, it is also likely responsible for the activation of apoptosis genes and consequently the hastened onset of nerve damage found in mild disease. Alpha-2 laminin receptors found in the basal lamina of Schwann cells are also a target of entry for M. leprae into these cells, while activation of ErbB2 receptor tyrosine kinase signaling pathway has been identified as a mediator of demyelination in leprosy.

The activation of macrophages and dendritic cells, both antigen-presenting cells, is involved in the host immune response to M. leprae. Interleukin-1 beta produced by antigen-presenting cells infected by mycobacteria has been shown to impair the maturation and function of dendritic cells. Because bacilli have been found in the endothelium of skin, nervous tissue, and nasal mucosa, endothelial cells are also thought to contribute to the pathogenesis of leprosy.

A sudden increase in T-cell immunity is responsible for type I reversal reactions. Type II reactions result from activation of tumor necrosis factor-alpha (TNF-alpha) and deposition of immune complexes in tissues with neutrophilic infiltration and from complement activation in organs. One study found that cyclooxygenase 2 was expressed in microvessels, nerve bundles, and isolated nerve fibers in the dermis and subcutis during reversal reactions.


Household contacts of patients with lepromatous disease should be monitored annually for 5 years after diagnosis.

· Children especially should be observed for the development of disease.

· In endemic countries, chemoprophylaxis may be useful in controlling the disease.

· In the United Kingdom, close contacts of LL patients younger than 12 years are given rifampin 15 mg/kg once a month for 6 months as prophylaxis.

Attempts have been made to develop a vaccine against leprosy. Although not widely used, antileprosy vaccination can be immunoprophylactic and therapeutic. Current vaccines with various degrees of use are the bacille Calmette-Guérin (BCG) vaccine; the Mycobacterium w vaccine; the Mycobacterium avium-intracellulare complex (Mycobacterium ICRC) vaccine; the BCG plus heat-killed M. leprae, Mycobacterium tufu, and Mycobacterium habana vaccine.

· The BCG vaccine has variable results in protecting certain populations; therefore, it is not widely prescribed. However, repeat immunization with BCG may result in further protection. In the United Kingdom, the BCG vaccine is given to household contacts younger than 12 years.

· In India, the Mycobacterium w and Mycobacterium ICRC vaccines are given. Mycobacterium w has a synergistic effect with chemotherapy, with accelerated clearing of the infection and shortening of treatment.


Until the development of dapsone, rifampin, and clofazimine in the 1940s, there was no effective cure for leprosy. However, dapsone is only weakly bactericidal against M. leprae and it was considered necessary for patients to take the drug indefinitely. Moreover, when dapsone was used alone, the M. leprae population quickly evolved antibiotic resistance; by the 1960s, the world's only known anti-leprosy drug became virtually useless.

The search for more effective anti-leprosy drugs to dapsone led to the use of clofazimine and rifampicin in the 1960s and 1970s. Later, Shantaram Yawalkar and colleagues formulated a combined therapy using rifampicin and dapsone, intended to mitigate bacterial resistance. Multidrug therapy (MDT) and combining all three drugs was first recommended by a WHO Expert Committee in 1981. These three anti-leprosy drugs are still used in the standard MDT regimens. None of them are used alone because of the risk of developing resistance.

Because this treatment is quite expensive, it was not quickly adopted in most endemic countries. In 1985 leprosy was still considered a public health problem in 122 countries. The 44th World Health Assembly (WHA), held in Geneva in 1991 passed a resolution to eliminate leprosy as a public health problem by the year 2000 — defined as reducing the global prevalence of the disease to less than 1 case per 100,000. At the Assembly, the World Health Organization (WHO) was given the mandate to develop an elimination strategy by its member states, based on increasing the geographical coverage of MDT and patients’ accessibility to the treatment.

The WHO Study Group's report on the Chemotherapy of Leprosy in 1993 recommended two types of standard MDT regimen be adapted. The first was a 24-month treatment for multibacillary (MB or lepromatous) cases using rifampicin, clofazimine, and dapsone. The second was a six-month treatment for paucibacillary (PB or tuberculoid) cases, using rifampicin and dapsone. At the First International Conference on the Elimination of Leprosy as a Public Health Problem, held in Hanoi the next year, the global strategy was endorsed and funds provided to WHO for the procurement and supply of MDT to all endemic countries.

Since 1995, WHO has supplied all endemic countries with free MDT in blister packs, supplied through Ministries of Health. This free provision was extended in 2000, and again in 2005, and will run until at least the end of 2010. At the national level, non-government organizations (NGOs) affiliated to the national program will continue to be provided with an appropriate free supply of this MDT by the government.

MDT remains highly effective and patients are no longer infectious after the first monthly dose. It is safe and easy to use under field conditions due to its presentation in calendar blister packs. Relapse rates remain low, and there is no known resistance to the combined drugs. The Seventh WHO Expert Committee on Leprosy, reporting in 1997, concluded that the MB duration of treatment—then standing at 24 months—could safely be shortened to 12 months "without significantly compromising its efficacy."

Persistent obstacles to the elimination of the disease include improving detection, educating patients and the population about its cause, and fighting social taboos about a disease for which patients have historically been considered "unclean" or "cursed by God" as outcasts. Where taboos are strong, patients may be forced to hide their condition (and avoid seeking treatment) to avoid discrimination. The lack of awareness about Hansen's disease can lead people to falsely believe that the disease is highly contagious and incurable.

See List of Medications and their dosage here.


Reactional states occur in about one third of patients and are acute inflammations of the disease. A leprous reaction should be considered a medical emergency requiring immediate care. These states can result in permanent neurologic sequelae, resulting in disability and deformity. Patients at the highest risk are those with multibacillary leprosy and/or preexisting nerve impairment.

o Lepra type I (reversal) reactions usually affect patients with borderline disease. Reversal reactions are a shift toward the tuberculoid pole after the start of therapy, and they are type IV cell-mediated allergic hypersensitivities. Puberty, pregnancy, and childbirth can also precipitate type I reactions. These reactions usually result in skin erythema, with edema and tenderness of peripheral nerves. The peak time for type I reactions is during the first 2 months of therapy and for up to 12 months. Corticosteroid treatment is aimed at controlling acute inflammation, relieving pain, and reversing nerve and eye damage. With treatment, approximately 60-70% of the patient's nerve function is recovered. If neuritis is absent, nonsteroidal anti-inflammatory drugs (NSAIDs) may be helpful.

o Lepra type II reactions, or ENL, occur in about 10% of patients with BL and in 20% of patients with LL. These reactions are type III humoral hypersensitivities, with a systemic inflammatory response to immune complex deposition. The most common presenting symptoms are crops of painful erythematous nodules of the skin and subcutaneous tissue. Bullae, ulcers, and necrosis may also occur. The reaction usually manifests after a few years of therapy, and, although a single acute episode is possible, relapses occur intermittently over several years. Associated fever, malaise, arthralgias, neuralgia, iridocyclitis, dactylitis, orchitis, and proteinuria may be present.

· · The use of clofazimine in MDT substantially reduces the incidence of ENL to 5%. Clofazimine has also been used to treat ENL.

· · Thalidomide is effective except in the case of neuritis or iritis, in which case, corticosteroids should be used.

· · Other treatment therapies reported to be effective include colchicine, pentoxifylline, cyclosporine A, intravenous immunoglobulin (IVIG), and infliximab.

· · Lowering the dose of dapsone may decrease the severity of bullae and ulcers.

o Lucio phenomenon is an unusual type II reaction that is sometimes designated a type II reaction. It is common in Mexico and Central America and is characterized by cutaneous hemorrhagic infarcts in patients with diffuse LL. Thalidomide is ineffective in treating this type of reaction. Azathioprine or cyclophosphamide with corticosteroids with or without plasmapheresis has been used.

The real challenge in managing leprosy is the treatment of reactional states.

o If the course of MDT is not complete, continue taking those medications as directed.

o Systemic steroids are effective in reducing inflammation and edema in reversal reactions; therefore, they are the most helpful medications in preventing nerve damage.

o Prednisone 40-80 mg/d should be given for 5-7 days then tapered slowly over 3-6 months. This long course is necessary to decrease the severity of disabilities and deformities. One study recommended a low-dose (30 mg/d) regimen for 20 weeks for controlling type I reactions.

o Clofazimine can also be used as a steroid-sparing agent for reversal reactions, alone or with corticosteroids.

o Although the WHO does not support its use for ENL, thalidomide is highly effective with ENL. It is ineffective for the treatment of reversal reactions.

Neuropathy induced by leprosy can result in trauma, pressure necrosis, or secondary infection that goes unnoticed, leading to amputation of digits or limbs. Wrist and foot drop are also common. Silent neuropathy can occur in the absence of overt signs of nerve or skin inflammation. Even with corticosteroid treatment, only about 60% of nerve function is recovered. Cyclosporine A may be useful in controlling nerve impairment and pain.

Injuries can result in ulcerations, cellulitis, scarring, and bony destruction. Foot ulcers caught early should be treated with rest because they heal if they are not subject to weightbearing.

Osteoporosis and fractures can result from bony changes due to leprosy. Risedronate and other bisphosphates may help improve lumbar bone mineral density.

Contractures can develop and result in fixation. Common sequelae include clawing of hands and feet.

Eye damage can result in loss of the corneal reflex, lagophthalmos, ectropion, entropion, and blindness. One study found the risk of ocular complications in patients with multibacillary disease, after completion of MDT, to be 5.6% with eye-threatening complications to be 3.9%.

Skin drying and fissures can be caused by autonomic disruption.


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Saturday, October 27, 2007

Romantic Novels commonly include Passionate Romance in Emergency Medicine Settings

Emergency medicine departments are popular venues for passionate romance in numerous romantic novels, according to a Correspondence in The Lancet, this week's issue.

According to Dr. Brendan Kelly, University College Dublin and Mater Misericordiae University Hospital, Dublin, Ireland "Romantic fiction generates US$1.2 billion in sales annually and accounts for 39.3% of all fiction sold in the USA. In recent decades, medical romance has emerged as a substantial subgenre within romance fiction, and, to explore this area further, I studied 20 randomly selected medical romance novels."

Dr. Kelly explains that he found that the majority of plots took place in emergency and primary care settings, including emergency departments and airborne medical teams. The most popular pair that writers seem to go for are a male doctor with a female doctor, the second most popular being a male doctor with a female nurse.

"There was a marked preponderance of brilliant, tall, muscular male doctors with chiseled features, working in emergency medicine; they were commonly of Mediterranean origin and had personal tragedies in their pasts. Female doctors and nurses ended to be skilled, beautiful, and determined, but still compassionate; many had overcome substantial personal and profession obstacles in their lives. Protagonists of both sexes had frequently neglected their personal lives to care better for their patients, many of whom had life-threatening illnesses from which they nonetheless managed to recover," Kelly writes.

"These novels draw attention to the romantic possibilities of primary care settings and the apparent inevitability of uncontrolled passions in the context of emergency medicine, especially as practiced on airplanes. These novels suggest that there is an urgent need to include instruction in the arts of romance in training programs for doctors and nurses who intend working in these settings," Kelly concludes.

See Full Article

Friday, October 26, 2007

ANF Seeks Fair Treatment for Victorian Nurses

The ANF (Federal Office) urged Premier Brumby to begin negotiating in good faith with the Victorian Branch of the ANF to end the current nursing dispute.

ANF Assistant Federal Secretary Ged Kearney said the ANF is "appalled" by the Victorian Labor Government's use of the harsh WorkChoices legislation to punish nurses.

The ANF says Mr. Brumby is aware that nurse patient ratios are the most important issue at stake in the dispute and he also knows that the AIRC cannot rule on this issue.

"This is a blatant attempt to get rid of ratios," Ms. Kearney said. "It is ratios in Victoria that have attracted so many nurses back into the public system and allowed nurses to provide a high quality of patient care. If ratios are cut, nurses will leave the profession, and the level of patient care will deteriorate. Surely the Brumby Government understands this."

Research by the University of Sydney completed earlier this month, confirms that two thirds of nurses would consider cutting their working hours or leaving the public health system or nursing altogether if nurse patient ratios were scrapped.

"The research by the Workplace Research Center at the University of Sydney revealed 73% of nurses' workload had increased every year for the past three years, compared to the 56% who were surveyed in 2003," Ms. Kearney said. "Nurse patient ratios mean that nurses can, to an extent, manage to provide safe quality care in a high pressured environment."

This dispute shows that WorkChoices is not about resolving disputes.

"The Federal ALP is campaigning against WorkChoices in this election so it must be very disappointing to see the legislation being used against nurses in Victoria," Ms. Kearney said.

The ANF, representing 150,000 members, is the professional and industrial voice for nurses and midwives in Australia.

Source: http://www.medicalnewstoday.com

h.s. (on prescription)

h.s. or HS stands for hora somni, which means before sleep or at bedtime.

Tachycardia (pedia)

In pediatrics, the normal heart rates are:

Infant: 100-160 bpm
Toddler: 90-150 bpm
Preschooler: 80-140 bpm
School-age: 70-120 bpm

If the heart rate goes above the normal range, this is already called Tachycardia.

Source: http://www.health.state.ny.us

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Bradycardia (pedia)

In pediatrics, the normal heart rates are:

Infant: 100-160 bpm
Toddler: 90-150 bpm
Preschooler: 80-140 bpm
School-age: 70-120 bpm

If the heart rate goes below the normal range, this is already called Bradycardia.

Note that a drop in heart rate may still be considered normal if the heart rate returns to normal within five to 10 seconds without any aid.

Source: http://www.health.state.ny.us

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Thursday, October 25, 2007

Operating Scissors

Researched by Anthony
Operating scissors are general medical scissors that are available with a variety of blade styles, in various sizes and designs. An essential component of any first-aid kit, operating scissors are floor grade which means they are for regular use and they are also autoclavable, which means that they can be used for any surgical procedure. Operating scissors are very sharp blunt tip scissors. They have a screw lock. They are used in general surgery for cutting sutures, gauze and other such material. They need to be sharpened regularly.


These scissors are made of high-quality stainless steel. They are also made of other metals like chrome, aluminum etc. However, stainless steel operating scissors with sand finish are very popular.

Types of operating scissors

* Operating scissors, straight
* Operating scissors, curved
* Mayo operating scissors, straight
* Mayo operating scissors, curved

Types of blades in operating scissors

* Sharp/blunt
* Blunt/blunt
* Sharp/sharp
* Blunt/sharp

Source: http://www.surgicalsindia.com

Tachycardia (adult)

Researched by Anthony
A normal adult heart beats between 60 and 100 times a minute. A heart rate over 100 beats a minute is called tachycardia. Some tachycardias are relatively harmless and need no treatment, but others can be life-threatening. Treatment for recurrent tachycardia can range from daily medication to open-heart surgery. A specific diagnosis is necessary before finding the right treatment for the tachycardia.

Signs and symptoms

When the heart rate is too rapid, it may not effectively pump blood to the rest of the body, depriving organs and tissues of oxygen. This can cause these signs and symptoms:

· Dizziness
· Shortness of breath
· Lightheadedness
· Rapid heartbeat
· Heart palpitations — a racing, uncomfortable or irregular heartbeat or a sensation of "flopping" in the chest
· Chest pain
· Blackouts
· Visual problems
· Fainting (syncope)

Some people with tachycardia have no symptoms and don't realize they have this condition until a doctor discovers it during a physical examination.


The heart is a muscular pump that circulates blood all around the body. There are four hollow chambers in the heart — the two upper chambers are the atria, and the lower, more muscular chambers are the ventricles. Each heartbeat begins in the right atrium. There, the heart's natural pacemaker, called the sinus node, sends an electrical signal that causes the atria to contract, filling the ventricles with blood. A split second later, the electrical impulse travels across the atrioventricular (AV) node into the ventricles. This makes the ventricles contract, sending blood throughout the body. In people with tachycardias, this normal rhythm is disrupted somewhere along the electrical path, causing the heart to beat too quickly.

Types of Tachycardias

Tachycardias are classified according to where they originate — in the atria or in the ventricles.

Tachycardias originating in the upper heart chambers

Atrial fibrillation. In this most common arrhythmia in the U.S., electrical impulses make the atria beat extremely quickly — up to 400 beats a minute. Only some of these electrical impulses travel across the AV node and reach the ventricles, causing a rapid and irregular heartbeat. This tachycardia is most common in people over 60 years of age.

Atrial flutter. Atrial flutter is similar to atrial fibrillation, except the extremely fast beating is more controlled and rhythmic. The most common symptom of atrial flutter is chest pain.

Supraventricular tachycardia (SVT). SVT is a broad term that includes many forms of arrhythmia originating above the ventricles (supraventricular). SVTs usually cause a burst of rapid heartbeats that begin and end suddenly and can last from seconds to hours. These often start when the electrical impulse from a premature heartbeat begins to circle repeatedly through an extra pathway. SVT may cause the heart to beat 160 to 200 times a minute. Although generally not life-threatening in an otherwise normal heart, symptoms from the racing heart may feel quite uncomfortable. These arrhythmias are common in young people.

Tachycardias originating in the ventricles

Because the ventricles supply blood to the entire body, a tachycardia that starts in the ventricles can be a medical emergency. Types include:

Ventricular tachycardia. This is a rapid, rhythmic heartbeat that most often affects people with structural heart disease with damage to the heart muscle (myocardium), such as occurs with a heart attack. Ventricular tachycardia can be life-threatening by itself, and without treatment it can rapidly turn into fatal ventricular fibrillation.

Ventricular fibrillation. During ventricular fibrillation, rapid, chaotic electrical impulses cause the ventricles to quiver uselessly instead of pumping necessary blood to the body. This serious malfunction results in death if the heart isn't restored to a normal rhythm within minutes.

Tachycardia Triggers

In some people, external substances can affect the heart's electrical system and cause a tachycardia to develop. People with sensitivities to the substances can develop tachycardias after moderate exposure, but abuse of these substances can also cause the arrhythmia directly.

Substances include:

* Caffeine
* Alcohol
* Tobacco
* Dietary supplements and over-the-counter medications
* Illicit drugs
* Prescription drugs
* Environmental pollutants, such as automobile emissions and paint thinner

Risk factors

Certain factors can increase the risk of developing tachycardias. They include:

Coronary artery disease. Hardening or narrowing of the heart's arteries, a previous heart attack or heart damage puts one at higher risk of developing an arrhythmia.

Damaged heart muscle (cardiomyopathy). When cardiomyopathy damages the heart muscle, the electrical pathways can be affected.

Damaged heart valves. The heart valves can become damaged due to cardiovascular disease, increasing the tachycardia risk.

Older age. Aging-related wear on the heart makes one more susceptible to developing an arrhythmia.

Genetics. If a person have a family history of arrhythmia disorders or heart disease, that person is at higher risk.

Overactive thyroid (hyperthyroidism). An overactive thyroid gland releases excess hormones, causing metabolism to speed up. This can lead to fast or irregular heartbeats.

Sleep apnea. When this sleep disorder causes one to stop breathing repeatedly during sleep, the lack of oxygen can lead to bursts of atrial fibrillation.

Electrolyte imbalance. An imbalance of minerals in the blood, such as potassium, sodium, calcium and magnesium can affect the heart's electrical system, leading to irregular heartbeats.

High blood pressure (hypertension). High blood pressure, especially if poorly controlled, puts a strain on the heart and can result in enlargement of the heart chambers or weakness of the heart muscle with an increased risk of tachycardia or both.

Screening and Diagnosis

To diagnose and treat an arrhythmia, the doctor needs to document the type of abnormal rhythm. This can be done by monitoring the heart of the patient in the doctor's office or hospital or as he/she go about his/her daily activities, or by actively triggering tachycardia while being closely watched by a doctor.

Tests that monitors heart rate

Electrocardiogram (ECG). Sensor pads with wires attached, called electrodes, are placed on the chest and sometimes, the limbs to measure the heart's electrical impulses.

Holter monitor. This small, portable ECG device is worn for 24 hours of continuous monitoring of the heart's electrical signals.

Event monitor. An event monitor can help doctors evaluate more sporadic tachycardias. A patient wears this portable ECG device at home and activate it when he's/she's experiencing symptoms. The doctor can then evaluate the ECG strip to determine if there's an association between the symptoms and the heart's rhythm.

Tests that trigger the arrhythmia include

Stress test. Some tachycardias are triggered or made worse with exercise. During a stress test, a patient is made to walk or run on a treadmill, or ride a stationary bike, while his/her heart's rhythm is monitored with an electrocardiogram. Stress tests also try to determine if there is coronary artery disease.

Electrophysiological mapping and testing. While a patient is under light sedation, a specialist in heart rhythm disorders (electrophysiologist) threads thin, flexible tubes (catheters) tipped with electrodes through the patient's blood vessels to various places inside the heart. From there, the electrodes precisely map the heart's electrical impulses. During testing, the electrodes stimulate the heart to trigger or halt the tachycardia, revealing its type and location.

Tilt table test. This test may be used if a patient have recurrent fainting spells. A patient is made to lie flat on a special table, and then the table is tilted as if he/she is standing up. The doctor observes how the heart and nervous system respond to these changes in position.

Tests that check the structure and function of the heart

Echocardiogram. This test uses soundwaves to produce detailed images of the heart's structure, size and motion, which can give the doctor valuable information about arrhythmia.

Coronary angiogram. During coronary angiography, a type of dye that's visible by X-ray machine is injected into the blood vessels of the heart. The X-ray machine rapidly takes a series of images (angiograms), offering a detailed look at the inside of blood vessels to see if coronary artery disease is causing a tachycardia.


In a heart arrhythmia, heartbeat irregularities may put one at higher risk of developing blood clots in the heart, which can dislodge and lead to a heart attack or stroke. Some people with known arrhythmias take blood-thinning medications called anticoagulants to prevent blood clots from forming.

Tachycardias can be mild and cause no symptoms. They can also happen suddenly with potentially serious and even fatal results. Even a relatively harmless tachycardia can quickly turn into something deadly, or at least predict that one would have a more significant arrhythmia in the future. Proper diagnosis and treatment are key in preventing these complications.


Treatment of a tachycardia depends on the symptoms, how often a person have episodes of tachycardia and whether they have any underlying heart conditions. The doctor may prescribe medications to control the heart rate, use minimally invasive procedures to destroy tachycardia trigger spots, or suggest the placement of a heart device that monitors and resets the heart rhythm as needed.


Doctors often use medications in tachycardia emergencies, and they also prescribe them for long-term control of the arrhythmia. Medications may be used alone or in combination with other treatments.

Anti-arrhythmic medications. These medications work to slow the conduction of electrical signals or prolong the time it takes the heart muscle to recharge after a beat. In some people with tachycardia, however, these medications can make arrhythmias worse.

Calcium channel blockers, potassium channel blockers and beta blockers. These medications work in various ways to slow nerve impulses in the heart muscle or reduce the workload on the heart. These medications are also used to treat high blood pressure, coronary artery disease and chest pain.

Blood thinners. Also called anticoagulants, these medications are not used to treat the abnormal heart rhythm, but rather to reduce the risk that the abnormal rhythm will trigger a blood clot that may lead to a stroke or heart attack. Anticoagulants make it more difficult for blood to clot.

Nonsurgical Procedures

Nonsurgical techniques may be used if medications don't work. Some examples include:

Cardioversion. Most effective for atrial tachycardias, this technique uses either drugs or an electrical shock to restore a normal rhythm. In electric cardioversion, the doctor shocks the heart to stop its beat for a split second to "reset" it. Cardioversion drugs may be given through an intravenous (IV) line to reset the heart.

Radiofrequency catheter ablation. In this procedure done under mild sedation, several electrode-tipped tubes (catheters) are threaded through the blood vessels to specific electrical pathways in the heart. Then radiofrequency energy is used to destroy the area of heart tissue responsible for the arrhythmia.

Implantable cardioverter-defibrillator

If the underlying heart condition puts one at high risk of having a life-threatening tachycardia, the doctor may recommend an implantable cardioverter-defibrillator (ICD).

An implantable cardioverter-defibrillator — a pager-sized device implanted in the chest like a pacemaker — detects and stops dangerous arrhythmias. The ICD continuously monitors the heartbeat and delivers precisely calibrated electrical shocks to restore a normal heart rhythm.

Surgical treatments

If a patient does not respond to other treatments or needs a treatment for an underlying heart condition, surgery may be an option.

Maze procedure. The maze procedure is often done during an open-heart surgery. Using a scalpel, doctors create several precise incisions in the atria to create a pattern or maze of scar tissue. Because scar tissue doesn't carry electricity, it interferes with stray electrical impulses that cause atrial fibrillation. Radiofrequency or cryotherapy also can be used, and there are several variations of the surgical maze technique. The procedure has a high success rate, but because it usually requires open-heart surgery, it's generally reserved for people who don't respond to other treatments or when it can be done during other necessary heart surgery, such as coronary artery bypass surgery or heart valve repair. Some people require a pacemaker after the procedure.


The most effective way to prevent tachycardias is to reduce the risk of developing heart disease. If one already have heart disease, he/she needs to monitor it and follow his/her treatment plan to lower his/her tachycardia risk.

Prevent heart disease

Treat or eliminate risk factors that may lead to heart disease. The following steps may be taken:

Exercising and eating a healthy diet. Living a heart-healthy lifestyle by exercising regularly and eating a healthy, low-fat diet that's rich in fruits, vegetables, whole grains and antioxidants.

Maintaining a healthy weight. Obesity puts one at higher risk of developing heart disease and tachycardias.

Keeping blood pressure and cholesterol under control. Making lifestyle changes or taking medications to correct high blood pressure (hypertension) or high cholesterol.

Cessation of smoking. Tobacco use increases the risk of cardiovascular disease and heart arrhythmias.

Stress Control. Avoiding unnecessary stress, and learning coping techniques to handle normal stress in a healthy way.

Constant Checkups. Having regular physical exams and reporting any signs or symptoms to a doctor.

Monitor and treat existing heart disease

If a person already have heart disease, there are steps he/she can take to lower his/her risk of developing a tachycardia or other arrhythmia:

Following the plan. Understanding the treatment plan, and taking all medications as prescribed.

Getting electrical system checked. One should talk to a doctor about whether a heart attack or another cause has compromised the heart's electrical system and put him/her at risk of sudden cardiac death.

Reporting changes immediately. If symptoms change, get worse or develop new symptoms, one should tell his/her doctor immediately.

Coping skills

If a person have tachycardia, he/she may feel like his/her heart could spin out of control any second. This uncertainty may leave him/her feeling anxious and stressed. The best thing he/she can do is to follow his/her treatment plan and talk with his/her doctor about any concerns he/she may have. It may also help to meet with a psychologist, a genetics counselor or a cardiologist.

Source: http://www.mayoclinic.com

If you find an error, please let us know.

Bradycardia (adult)

Researched by Anthony
Bradycardia, as applied to adult medicine, is defined as a resting heart rate of under 60 beats per minute, though it is seldom symptomatic until the rate drops below 50 beat/min. Trained athletes tend to have slow resting heart rates, and resting bradycardia in athletes should not be considered abnormal if the individual has no symptoms associated with it.

The term relative bradycardia is used to explain a heart rate that, while not technically below 60 beats per minute, is considered too slow for the individual's current medical condition.

This cardiac arrhythmia can be underlain by several causes, which are best divided into cardiac and non-cardiac causes. Non-cardiac causes are usually secondary, and can involve drug use or abuse; metabolic or endocrine issues, especially in the thyroid; an electrolyte imbalance; neurologic factors; autonomic reflexes; situational factors such as prolonged bed rest; and autoimmunity. Cardiac causes include acute or chronic ischemic heart disease, vascular heart disease, valvular heart disease, or degenerative primary electrical disease. Ultimately, the causes act by three mechanisms: depressed automaticity of the heart, conduction block, or escape pacemakers and rhythms.


There are generally two types of problems that result in bradycardias: disorders of the sinus node, and disorders of the atrioventricular node (AV node).

With sinus node dysfunction (sometimes called sick sinus syndrome), there may be disordered automaticity or impaired conduction of the impulse from the sinus node into the surrounding atrial tissue (an "exit block"). It is difficult and sometimes impossible to assign a mechanism to any particular bradycardia, but the underlying mechanism is not clinically relevant to treatment, which is the same in both cases of sick sinus syndrome: a permanent pacemaker.

Atrioventricular conduction disturbances (aka: AV block; 1° AV block, 2° type I AV block, 2° type II AV block, 3° AV block) may result from impaired conduction in the AV node, or anywhere below it, such as in the bundle of HIS.

Patients with bradycardia have likely acquired it, as opposed to having it congenitally. Bradycardia is more common in older patients.


There are two main reasons for treating any cardiac arrhythmias. With bradycardia, the first is to address the associated symptoms, such as fatigue, limitations on how much an individual can physically exert, fainting (syncope), dizziness or lightheadedness, or other vague and non-specific symptoms. The other reason to treat bradycardia is if the person's ultimate outcome (prognosis) will be changed or impacted by the bradycardia. Treatment in this vein depends on whether any symptoms are present, and what the underlying cause is. Primary or idiopathic bradycardia is treated symptomatically if it is significant, and the underlying cause is treated if the bradycardia is secondary.


Drug treatment for bradycardia is typically not indicated for patients who are asymptomatic. In symptomatic patients, underlying electrolyte or acid-base disorders or hypoxia should be corrected first. IV atropine may provide temporary improvement in symptomatic patients, although its use should be balanced by an appreciation of the increase in myocardial oxygen demand this agent causes.

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Typhoid Fever

Compiled and Summarized by Anthony
Typhoid fever, also known as enteric fever, is an illness caused by the bacterium Salmonella enterica serovar typhi. It is commonly transmitted through the fecal-oral route — the ingestion of food or water contaminated with feces or urine from an infected person. The bacteria then multiplies in the blood stream of the infected person and are absorbed into the digestive tract and eliminated with the waste.

Signs and Symptoms

Typhoid fever is characterized by a sustained fever as high as 40°C (104°F), profuse sweating, gastroenteritis, and diarrhea. Less commonly a rash of flat, rose-colored spots may appear.

Classically, the course of untreated typhoid fever is divided into four individual stages, each lasting approximately one week. In the first week, there is a slowly rising temperature with relative bradycardia, malaise, headache and cough. Epistaxis is seen in a quarter of cases and abdominal pain is also possible. There is leukopenia with eosinopenia and relative lymphocytosis, a positive diazo reaction and blood cultures are positive for Salmonella typhi or paratyphi. The classic Widal test is negative in the first week.

In the second week of the infection, the patient lies prostrated with high fever in plateau around 40°C and bradycardia (Sphygmo-thermic dissociation), classically with a dicrotic pulse wave. Delirium is frequent, frequently calm, but sometimes agitated. This delirium gives to typhoid the nickname of "nervous fever". Rose spots appear on the lower chest and abdomen in around 1/3 patients. There are rhonchi in lung bases. The abdomen is distended and painful in the right lower quadrant where borborygmi can be heard. Diarrhea can occur in this stage: six to eight stools in a day, green with a characteristic smell, comparable to pea-soup. However, constipation is also frequent. The spleen and liver are enlarged (hepatosplenomegaly) and tender and there is elevation of liver transaminases. The Widal reaction is strongly positive with antiO and antiH antibodies. Blood cultures are sometimes still positive at this stage.

In the third week of typhoid fever a number of complications can occur:

· Intestinal hemorrhage due to bleeding in congested Peyer's patches; this can be very serious but is usually non-fatal.
· Intestinal perforation in distal ileum: this is a very serious complication and is frequently fatal. It may occur without alarming symptoms until septicemia or diffuse peritonitis sets in.
· Encephalitis
· Metastatic abscesses, cholecystitis, endocarditis and osteitis

The fever is still very high and oscillates very little over 24 hours. Dehydration ensues and the patient is delirious (typhoid state). By the end of third week defervescence commences that prolongs itself in the fourth week.

Causative Agents

Salmonella typhi, and Salmonella paratyphi, which are subspecies of Salmonella enterica

Mode of Transmission

Fecal-oral route


Diagnosis is made by blood, bone marrow or stool cultures, urine sample, and with the Widal test (demonstration of salmonella antibodies against antigens O-somatic and H-flagellar). In epidemics and less wealthy countries, after excluding malaria, dysentery or pneumonia, a therapeutic trial time with chloramphenicol is generally undertaken while awaiting the results of Widal test and blood cultures.

Incubation Period

The incubation period of typhoid fever varies with the size of the infecting dose and averages 7-14 (range, 3-60) days.


Salmonella organisms penetrate the mucosa of both small and large bowel, coming to lie intracellularly where they proliferate. There is not the same tendency to mucosal damage as occurs with Shigella infections but ulceration of lymphoid follicles may occur. The evolution of typhoid is fascinating. Initially S. typhi proliferates in the second part of the Payer’s patches of the lower small intestine from where systemic dissemination occurs, to the liver, spleen, and reticuloendothelial system. For a period varying from 1 to 3 weeks the organism multiplies within these organs.

Rupture of infected cell occurs, liberating organisms into the bile and for a second time cause infection of the lymphoid tissue of the small intestine paticularly in the ileum. It is this phase of heavy infection that brings the classical bowel pathology of typhoid in its train. Invasion of the mucosa causes the epithelial cells to synthesize and release various proinflammatory cytokines including IL-1, IL-6, IL-8, TNF-β, INF, GM-CSF etc.


After ingestion by the host, S. typhi invades through the gut and multiplies within the mononuclear phagocytic cells in the liver, spleen, lymph nodes, and Peyer patches of the ileum.

In studies of healthy, previously unvaccinated men, ingestion of 107 S. typhi bacilli caused disease in 50% of volunteers. Investigations of outbreaks seem to indicate that an inoculum of as few as 200 organisms may lead to the disease. Perhaps such a discrepancy exists because many who ingest S. typhi are not healthy men and have any one of a number of risk factors* (see below). As the number of organisms increases, the incubation period decreases. The number of bacilli ingested does not change the subsequent clinical syndrome.

After successfully passing through the stomach, any Salmonella subspecies may be phagocytized by the gut's intraluminal dendritic cells, causing inflammation that leads to diarrhea. Only the subspecies S. enterica causes severe disease in the rest of the body. Its specialized fimbriae adhere to the epithelium that overlies Peyer patches. Peyer patches are grossly visible aggregates of 5-100 lymphoid follicles in the small bowel submucosa; these patches are larger and more numerous distally. They are the primary mechanism for sampling antigens in the gut and initiating response. S. enterica enters them via 1 of 3 pathways.

Intraluminal dendritic cells may infiltrate through the gut epithelium while carrying the bacterium. M cells may transport it as well. Immobile and interspersed among regular enterocytes in Peyer patches, M cells are epithelial cells that mature into professional phagocytes. They phagocytize bacteria such as S. enterica and present them to macrophages and T cells in the lamina propria. Most interestingly, S. enterica may convert normally nonphagocytic epithelial cells into bacterially-mediated endocytosis (BME).

In BME, Salmonella uses a type III secretion system—macromolecular channels that gram-negative bacteria such as Salmonella insert into eukaryotic cells and intracellular membranes to inject virulence proteins—to inject proteins SipA and SipC into the epithelial cell. These disrupt the normal brush border and force the cell to form membrane ruffles. The ruffles engulf the bacilli and create vesicles that carry them across the epithelial cell cytoplasm and the basolateral membrane. Salmonella pathogenicity island 1 (SPI-1) in the genome encodes the elements of BME.

In the submucosa, Salmonella enters macrophages via bacteria-triggered pinocytosis or via macrophage receptor–mediated phagocytosis. The intravacuolar environment activates the PhoP/PhoQ regulon, leading to modification of protein and lipopolysaccharide elements of the bacterial inner and outer membranes. Thus, Salmonella resists lysis and decreases host proinflammatory signaling. The bacterium also produces homocysteine to inactivate nitric oxide and enzymes against other microbicides. Finally, with the Vi antigen, a polysaccharide capsule, S. typhi and S. paratyphi further protect themselves from lysis within the macrophage and from neutrophils and complement without.

The newly described Salmonella pathogenicity island 2 (SPI-2) encodes a type III secretion system that carries bacterial proteins across the vacuole membrane and into the cytosol. Other virulence factors from SPI-2 prevent or alter fusion of the Salmonella-containing vacuole with other intracellular compartments, rearrange the actin cytoskeleton around the vacuole, and may prevent the implantation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and nitric oxide synthase into the vacuole membrane.

The infected macrophage provides Salmonella a vehicle safe from other elements of the immune system and in which it can multiply and travel. It passes through the mesenteric lymph nodes into the thoracic duct and the lymphatics beyond to seed the reticuloendothelial tissues—liver, spleen, bone marrow, and lymph nodes. In these havens, it multiplies until some critical density is reached. It causes the apoptosis in the macrophages and enters the bloodstream to attack the rest of the body. At this stage, the Vi antigen comes into play. It forms a capsule to protect the bacterium from complement and from phagocytic immune cells.

From blood or from the liver via bile ducts, it infects the gallbladder and reenters the gastrointestinal tract in the bile, spreading to other hosts via stool. In addition, it occasionally invades the urinary tract and spreads via urine.

After primary intestinal infection, further seeding of the Peyer patches occurs through infected bile. They may become hyperplastic and necrotic with infiltration of mononuclear cells and neutrophils, forming ulcers that may hemorrhage through eroded blood vessels or perforate the bowel wall, causing peritonitis.

The host recognizes the invader with toll-like receptors 2, 4, and 5. These induce cytokines such as interferon alpha, interleukin (IL)–12, and tumor necrosis factor-alpha, which recruit macrophages and cause the high fevers of the disease. Macrophages and neutrophils suppress the active infection. Later, humoral and CD4 T-cell–mediated immunity clears it.

*Risk Factors

Salmonella has mechanisms against acidic environments, but a pH level of 1.5 or less kills most of the bacilli. People who continually ingest antacids, histamine-2 receptor antagonists (H2 blockers), or proton pump inhibitors; who have undergone gastrectomy; or who have achlorhydria due to aging or other factors require fewer bacilli to produce clinical disease. Acquired immune deficiencies or hereditary deficiencies in immune modulars such as IL-12 and IL-23 increase risk for infection, complications, and death.


Travelers to endemic countries should avoid raw unpeeled fruits or vegetables since they may have been prepared with contaminated water; in addition, they should drink only boiled water.

In endemic countries, the most cost-effective strategy for reducing the incidence of typhoid fever is the institution of public health measures to ensure safe drinking water and sanitary disposal of excreta. The effects of these measures are long-term and reduce the incidence of other enteric infections, which are a major cause of morbidity and mortality in those areas. In the absence of such a strategy, mass immunization with typhoid vaccines at regular intervals also considerably reduces the incidence of infections.

Routine typhoid vaccination is not recommended in the United States. Vaccination is indicated for travelers to endemic areas, persons with intimate exposure (eg, household contact) to a documented S. typhi carrier, and microbiology laboratory personnel who frequently work with S. typhi.

Travelers should be vaccinated at least 1 week prior to departing for an endemic area. Because typhoid vaccines lose effectiveness after several years, consultation with a specialist in travel medicine is advised if the individual is traveling several years after vaccination.

The only absolute contraindication to vaccination is a history of severe local or systemic reactions following a previous dose. No data have been reported on pregnant women who receive any of the typhoid vaccines available in the United States.

The following 3 typhoid vaccines are used:

o Vi capsular polysaccharide (ViCPS) antigen vaccine (Typhim Vi, Pasteur Merieux) is composed of purified Vi antigen, the capsular polysaccharide elaborated by S. typhi isolated from blood cultures. In recent studies, one 25-mg injection of purified ViCPS produced seroconversion (ie, at least a 4-fold rise in antibody titers) in 93% of healthy US adults. Similar results were observed in Europe. Two field trials in disease-endemic areas showed overall protection rates of 72% in Nepal and 50-64% in South Africa.

· + The efficacy of vaccination with ViCPS has not been studied among persons from areas without endemic disease who travel to endemic regions or among children younger than 5 years. ViCPS has not been given to children younger than 1 year.

· + Primary vaccination with ViCPS consists of a single parenteral dose of 0.5 mL (25 mg IM) one week before travel. The vaccine manufacturer does not recommend the vaccine for children younger than 2 years. Booster doses are needed every 2 years to maintain protection if continued or renewed exposure is expected.

· + Adverse effects include fever, headache, erythema, or induration greater than or equal to 1 cm. In a study conducted in Nepal, the ViCPS vaccine produced fewer local and systemic reactions than the control (the 23-valent pneumococcal vaccine). Among school children in South Africa, ViCPS produced less erythema and induration than the control bivalent vaccine.

o Ty21a (Vivotif Berna, Swiss Serum and Vaccine Institute) is an oral vaccine that contains live attenuated S. typhi Ty21a strains in an enteric-coated capsule. The vaccine elicits both serum and intestinal antibodies and cell-mediated immune responses.

· + No prospective randomized trials have been performed in the United States. Several field trials were conducted among school children in Chile. Using 3 doses on alternate days, investigators produced a 66% protection rate that lasted for 5 years (95% CI, 50-77%). In another trial in Chile, the incidence of clinical typhoid fever significantly decreased among persons who received 4 doses of vaccine compared with persons who received 2 doses (P <.001) or 3 doses (P = .002). However, an efficacy rate of only 42% was recorded in Indonesia, suggesting that the vaccine may not be effective in areas where exposure is intense. The efficacy of vaccination with Ty21a has not been studied among persons from areas without endemic disease who travel to disease-endemic regions. · + In the United States, primary vaccination with Ty21a consists of one enteric-coated capsule taken on alternate days to a total of 4 capsules. The capsules must be refrigerated (not frozen), and all 4 doses must be taken to achieve maximum efficacy.

· + The optimal booster schedule has not been determined; however, the longest reported follow-up study of vaccine trial subjects indicated that efficacy continued for 5 years after vaccination. The manufacturer recommends revaccination with the entire 4-dose series every 5 years if continued or renewed exposure to S. typhi is expected.

· + Adverse effects are rare. They include abdominal discomfort, nausea, vomiting, fever, headache, and rash or urticaria.

· + The vaccine manufacturer recommends that Ty21a not be administered to children younger than 6 years. It should not be used among immunocompromised persons. The parenteral vaccines present theoretically safer alternatives for this group.

o Acetone-inactivated parenteral vaccine is currently available only to members of the US Armed Forces. Efficacy rates for this vaccine range from 75-94%. Booster doses should be administered every 3 years if continued or renewed exposure is expected.

o Of note, the parenteral heat-phenol–inactivated vaccine (Wyeth-Ayerst) has been discontinued. No information has been reported concerning the use of one vaccine as a booster after primary vaccination with a different vaccine. However, using either the series of 4 doses of Ty21a or 1 dose of ViCPS for persons previously vaccinated with parenteral vaccine is a reasonable alternative to administration of a booster dose of parenteral inactivated vaccine.


Typhoid fever in most cases is not fatal. Antibiotics, such as ampicillin, chloramphenicol, trimethoprim-sulfamethoxazole, and ciprofloxacin, have been commonly used to treat typhoid fever in developed countries. Prompt treatment of the disease with antibiotics reduces the case-fatality rate to approximately 1%.

When untreated, typhoid fever persists for three weeks to a month. Death occurs in between 10% and 30% of untreated cases. Vaccines for typhoid fever are available and are advised for persons traveling in regions where the disease is common (especially Asia, Africa and Latin America). Typhim Vi is an intramuscular killed-bacteria vaccination and Vivotif is an oral live bacteria vaccination, both of which protect against typhoid fever. Neither vaccine is 100% effective against typhoid fever and neither protects against unrelated typhus.


Resistance to ampicillin, chloramphenicol, trimethoprim-sulfamethoxazole and streptomycin is now common, and these agents have not been used as first line treatment now for almost 20 years. Typhoid that is resistant to these agents is known as multidrug-resistant typhoid (MDR typhoid).

Ciprofloxacin resistance is an increasing problem, especially in the Indian subcontinent and Southeast Asia. Many centers are therefore moving away from using ciprofloxacin as first line for treating suspected typhoid originating in India, Pakistan, Bangladesh, Thailand or Vietnam. For these patients, the recommended first line treatment is ceftriaxone.

There is a separate problem with laboratory testing for reduced susceptibility to ciprofloxacin: current recommendations are that isolates should be tested simultaneously against ciprofloxacin (CIP) and against nalidixic acid (NAL), and that isolates that are sensitive to both CIP and NAL should be reported as "sensitive to ciprofloxacin", but that isolates testing sensitive to CIP but not to NAL should be reported as "reduced sensitivity to ciprofloxacin". However, an analysis of 271 isolates showed that around 18% of isolates with a reduced susceptibility to ciprofloxacin (MIC 0.125–1.0 mg/l) would not be picked up by this method. It not certain how this problem can be solved, because most laboratories around the world (including the West) are dependent disc testing and cannot test for MICs.


Intestinal manifestations

o The 2 most common complications of enteric fever are intestinal hemorrhage (12% in one British series) and perforation (3-4.6% of hospitalized patients).

o From 1884-1909 (ie, preantibiotic era), the mortality rate in patients with intestinal perforation in typhoid fever was 66-90% but now is significantly lower. Approximately 75% of patients have guarding, rebound tenderness, and rigidity, particularly in the right lower quadrant.

o Diagnosis is particularly difficult in the approximately 25% of patients with perforation and peritonitis who do not have the classic physical findings. Often, the discovery of free intra-abdominal fluid may be the only sign of perforation.

Hepatobiliary manifestations

o Mild elevation of transaminases without symptoms is common in persons with typhoid fever.

o Jaundice may occur in persons with enteric fever and may be due to hepatitis, cholangitis, cholecystitis, or hemolysis.

o Pancreatitis and simultaneous acute renal failure and hepatitis with hepatomegaly have been reported.

Cardiopulmonary manifestations

o Nonspecific electrocardiographic changes occur in 10-15% of patients with typhoid. Toxic myocarditis occurs in 1-5% of persons with typhoid and is a significant cause of death in disease-endemic countries.

o Toxic myocarditis occurs in patients who are severely ill and toxemic and is characterized by tachycardia, weak pulse and heart sounds, hypotension, and electrocardiographic abnormalities.

o Pericarditis rarely occurs, but peripheral vascular collapse without other cardiac findings is increasingly described. Pulmonary manifestations have also been reported in patients with typhoid fever.

Neuropsychiatric manifestations

o In the past 2 decades, reports from the disease-endemic areas have documented a wide spectrum of neuropsychiatric manifestations of typhoid fever.

o A toxic confusional state, characterized by disorientation, delirium, and restlessness, is characteristic of late-stage typhoid. Occasionally, these and other neuropsychiatric features may dominate the clinical picture at an early stage.

o Facial twitching or convulsions may be the presenting feature; sometimes, paranoid psychosis or catatonia may develop during convalescence. Meningismus is not uncommon, but frank meningitis is rare. Encephalomyelitis may develop, and the underlying pathology may be that of demyelinating leukoencephalopathy. Rarely, transverse myelitis, polyneuropathy, or cranial mononeuropathy may develop.

o Other less commonly reported events are spastic paraplegia, peripheral or cranial neuritis, Guillain-Barré syndrome, schizophrenia-like illness, mania, and depression.

Hematologic manifestations

o Subclinical disseminated intravascular coagulation occurs commonly in persons with typhoid fever.

o Hemolytic-uremic syndrome is rare.

o Hemolysis may also be associated with glucose-6-phosphate dehydrogenase deficiency.

Genitourinary manifestations

o Approximately 25% of patients excrete S. typhi in their urine at some point during their illness.

o Immune complex glomerulitis and proteinuria have been reported, and IgM, C3 antigen, and S. typhi antigen can be demonstrated in the glomerular capillary wall.

o Nephritic syndrome may complicate chronic S. typhi bacteremia associated with urinary schistosomiasis.

Musculoskeletal manifestations

o Skeletal muscle characteristically shows Zenker degeneration, particularly affecting the abdominal wall and thigh muscles.

o Clinically evident polymyositis may occur.

CNS manifestations

o Focal intracranial infections are uncommon.

o Recently, multiple brain abscesses have been reported.


Served as Primary Source. Typhoid Fever by John L Brusch, MD, FACP, Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

Served as Secondary Source.

Provided information on Pathogenesis.

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