Meningitis: a rare but dangerous disease for students

Meningococcal meningitis is an uncommon disease, yet it affects college students at seven times the national average, and dorm residents are encouraged to be immunized.

Photo by Trung Le. Jean Haulman, associate medical director of public health and immunization at Hall Health, holds a meningococcal vaccine called “menactra”.

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The infection, which causes inflammation of the brain, can be deadly. Of those who contract it, there is a 10 to 15 percent mortality rate. Otherwise, serious debilitation is a possibility.
“Out of all the people in the United States who get meningitis and live, about 25 percent lose an arm or leg, become mentally retarded, or experience seizures,” said Jean Haulman, associate medical director of public health and immunization at Hall Health.
About one in every 100,000 people contracts the disease.
“There haven’t been any cases at UW in the four years I’ve been at Hall Health immunization — but if you get it, it has a high mortality rate and is dangerous,” she said.
The vaccine available in the United States is effective against four of the five types of meningitis. Among them, the B-strain is the most rare. Cuba has a vaccine for it, available since the 1980s, according to the BBC, yet no such vaccine is available in the United States because of the Cuban embargo, a ban on trade with the country.
Hall Health has Menactra, a vaccine available since 2005, which protects against the disease for up to 10 years, Haulman said.
Another vaccine, Menomune, is effective for five years. Both vaccines protect about 90 percent of those immunized and are made available to most young people through a federal program called Vaccines for Children (VFC). The program provides certain vaccines, including the one for meningitis, for free for all children up to age 19. Established in 1993, VFC is funded by both the Centers for Disease Control and Prevention and the state.
“The longevity of the new vaccine, along with the Vaccines for Children Program are … [leading to] more students coming to college already immunized,” Haulman said.
There is also heightened awareness about meningitis, said Jill Appel, nurse manager at Hall Health.
“The media hype around meningitis has also contributed to [getting] vaccines done [at an] earlier age. It’s also becoming standard among pediatric immunizations,” she said.
Thirty-five vaccinations have been given at Hall Health to people 19 and older in the past six months, Appel said. Most immunizations are provided during fall quarter, though students can take advantage of the program before the fall, Haulman said.
If a student is infected, Haulman must inform the campus community.
“We usually send out campus-wide e-mails,” she said. “With something like this, however, we would probably focus on students who were in close proximity to, or intimately involved with, the person infected.”
Symptoms may seem innocuous at first: a stiff neck, rash and high fever. However, Haulman said, “People can feel ok, but can get really sick quickly.”
If someone has these symptoms and starts feeling confused, they should immediately seek medical attention, she said.

Leucoderma

Leucoderma is a chronic disorder of the skin where the skin stops producing pigments that color the skin. As a result white patches appear randomly at different locations on the skin. These patches are white in color and as time passes may increase in number and size. Leucoderma is not a medical term. It is only a substitute name for vitiligo. Vitiligo is a more common name for this disease in the west where as in Asia leucoderma is used more.

The Skin is colored in different shades of brown due to a pigment called melanin.Special cells called melanocytes are responsible for the production of melanin. Sometimes, for reasons dubious, the melanocytes stop producing melanin which results in white skin patches.

There are many explanations as to why this happens but none of these explanations has been proven to be the right one. This also explains why there is no confirmed cure for leucoderma. Even after extensive scientific research, the treatments of leucoderma are still very scarce and have not been proven to work for a majority of people. The best patients can do is hide these marks with colored creams but it is to be noted, this only hides these marks and doesn't stop more patches of white skin from appearing. There is no explanation as to the location of these patches of skin. Also, a question that may rise is why only patches appear and not the whole body is affected. For this too there is no proven explanation.

About 0.5% to 2% of the worlds population currently suffer from leucoderma. Leucoderma is not a contagiuos disease so there is no way a person can have leucoderma just by being around another person having it. Even though this is a proven fact, patients suffering from leucoderma often aren't accepted well in the social world. This often results in the patients suffering from depressive disorders.

Causes
As mentioned above, the reason for leucoderma is still not very clear. However some theories are present and are as follows The first and most supported theory is autoimmune. In this case, the bodies self defense mechanism mistakes the melanocytes as foreign particles and destroys them thus putting melanin production to a halt. There is evidence that points towards this theory and tests are being carried out to determine if this is accurate and how to stop this.

The second theory suggests that the oxidant-antioxidant system of the body is, for an unknown reason, disturbed resulting in loss of melanocytes. A third theory is more based on statistical data than research. Statistics suggest that if a parent has leucoderma, his/her child will have a higher risk of having leucoderma than the rest of the population. So this theory suggests that a genetic factor is present in the causes of this disease. A fourth theory suggests that leucoderma is a direct cause of nerve damage. This can also be true as in a type of leucoderma called as segmental vitiligo, the areas of skin affected are often the areas in contact with the dorsal root of the spinal chord.

Treatments
Its very hard to find a proper cure for a disease, the reason to which is still unknown. There are many treatmets suggested for leucoderma but none of them are proven 100% successful.
Using colored creams and tanning creams to hide the patches of skin is a more common method. This hides the patches but requires a lot of time to apply the creams and the drawback is it doesnt prevent more spots from appearing.

Steroid creams are also very commonly used. Steroid affects the immune system of the body by weakening it. So when a steroid cream is applied to the skin, the antibodies in the skin are weakened and they stop attacking the melanocytes and melanin production is resumed. It is to be noted that this treatment does not guarantee that the patches will not appear again. Also, steroid creams can not be used continuously for as long as one wishes to use them. Steroids have serious side-affects which include permanent thinning of the skin and appearance of stretch marks on area of application, which are also permanent. Steroid creams also make the skin less resistant to infections.

A more advanced but complicated method is giving specific medicinal drugs and expose patient to ultra violet light in special UV radiation chambers. This causes serious sunburns and skin freckling. Also it is very time consuming and once again, doesn't guarantee results.

Whatever the reason maybe, patients who are dismayed and have lost hope as to the cure of leucoderma need not worry. Herbal medicine has been helping mankind to get rid of the worst diseases for a very very long time. In this case, we present a special oil that cures leucoderma and you can easily regain your skin color in no time. This oil has been proven to work and if you don't believe us, we offer you 100% money-back guarantee. If your scars do not disappear we will return you your money back.

What is leprosy?

Leprosy is a disease caused by the bacteria Mycobacterium leprae, which causes damage to the skin and the peripheral nervous system. The disease develops slowly (from six months to 40 years!) and results in skin lesions and deformities, most often affecting the cooler places on the body (for example, eyes, nose, earlobes, hands, feet, and testicles). The skin lesions and deformities can be very disfiguring and are the reason that infected individuals historically were considered outcasts in many cultures. Although human-to-human transmission is the primary source of infection, three other species can carry and (rarely) transfer M. leprae to humans: chimpanzees, mangabey monkeys, and nine-banded armadillos. The disease is termed a chronic granulomatous disease, similar to tuberculosis, because it produces inflammatory nodules (granulomas) in the skin and nerves over time.

What is the history of leprosy (Hansen's disease)?

Unfortunately, the history of leprosy and its interaction with man is one of suffering and misunderstanding. The newest research suggests that at least as early as 4000 B.C. individuals had been infected with M. leprae, while the first known written reference to the disease was found on Egyptian papyrus in about 1550 B.C. The disease was well recognized in ancient China, Egypt, and India, and there are several references to the disease in the Bible. Because the disease was poorly understood, very disfiguring, slow to show symptoms, and had no known treatment, many cultures thought the disease was a curse or punishment from the gods. Consequently, leprosy was left to be "treated" by priests or holy men, not physicians.

Picture of a person with leprosy (Hansen's disease)

Since the disease often appeared in family members, some people thought it was hereditary; other people noted that if there was little or no contact with infected individuals, the disease did not infect others. Consequently, some cultures considered infected people (and occasionally their close relatives) as "unclean" or as "lepers" and ruled they could not associate with uninfected people. Often infected people had to wear special clothing and ring bells so uninfected people could avoid them.
The Romans and the Crusaders brought the disease to Europe, and the Europeans brought it to the Americas. In 1873, Dr. Hansen discovered bacteria in leprosy lesions, suggesting leprosy was an infectious disease, not a hereditary disease or a punishment from the gods. However, patients with the disease were still ostracized by many societies and cared for only at missions by religious personnel. Patients with leprosy were encouraged or forced to live in seclusion up to the 1940s, even in the U.S. (for example, the leper colony on Molokai, Hawaii, and at Carville, La.), often because no effective treatments were available.
Because of Hansen's discovery of M. leprae, efforts were made to find treatments that would stop or eliminate M. leprae; in the early 1900s to about 1940, oil from Chaulmoogra nuts was used with questionable efficacy by injecting it into patients' skin. At Carville in 1941, promin, a sulfone drug, showed efficacy but required many painful injections. Dapsone pills were found to be effective in the 1950s, but soon (1960s-1970s), M. leprae developed resistance to dapsone. Fortunately, drug trials on the island of Malta in the 1970s showed that a three-drug combination (dapsone, rifampicin [Rifadin], and clofazimine [Lamprene]) was very effective in killing M. leprae. This multi-drug treatment (MDT) was recommended by the WHO in 1981 and remains, with minor changes, the therapy of choice. MDT, however, does not alter the damage done to an individual by M. leprae before MDT is started.
Currently, there are several areas (India, East Timor) of the world where the WHO and other agencies (for example, the Leprosy Mission) are working to decrease the number of clinical cases of leprosy and other diseases such as rabies and schistosomiasis that occur in remote regions. Although researchers hope to eliminate leprosy like smallpox, endemic (meaning prevalent or embedded in a region) leprosy makes complete eradication unlikely. In the U.S., leprosy has occurred infrequently but is considered endemic in Texas, Louisiana, Hawaii, and the U.S. Virgin Islands by some investigators.
Leprosy is often termed "Hansen's disease" by many clinicians in an attempt to have patients forgo the stigmas attached to being diagnosed with leprosy.

Insomnia Treatment

What Are Some  of the Treatments for Insomnia?

Generally, treatment of insomnia entails both non-pharmacologic (non-medical) and pharmacologic (medical) aspects. It is best to tailor treatment for individual person based on the potential cause. Studies have shown that combining medical and non-medical treatments typically is more successful in treating insomnia than either one alone.
Non-medical treatment and behavioral therapy include:

• sleep hygiene,
• relaxation therapy,
• stimulus control, and/or
• sleep restriction.

Examples of prescription and OTC sleep aids are:

• benzodiazepine sedatives,
• nonbenzodiazepine sedatives,
• antidepressants,
• and others.

Read more information about the OTC and prescription treatments for insomnia »

Insomnia Overview

Most adults have experienced insomnia or sleeplessness at one time or another in their lives. An estimated 30%-50% of the general population are affected by insomnia, and 10% have chronic insomnia.
Insomnia is a symptom, not a stand-alone diagnosis or a disease. By definition, insomnia is "difficulty initiating or maintaining sleep, or both" or the perception of poor quality sleep. Insomnia may therefore be due to inadequate quality or quantity of sleep. Insomnia is not defined by a specific number of hours of sleep that one gets, since individuals vary widely in their sleep needs and practices. Although most of us know what insomnia is and how we feel and perform after one or more sleepless nights, few seek medical advice. Many people remain unaware of the behavioral and medical options available to treat insomnia.
Insomnia is generally classified based on the duration of the problem. Not everyone agrees on one definition, but generally:

• symptoms lasting less than one week are classified as transient insomnia,
  
• symptoms between one to three weeks are classified as short-term insomnia, and
  
• those longer than three weeks are classified as chronic insomnia.

Statistics on Insomnia
Insomnia affects all age groups. Among adults, insomnia affects women more often than men. The incidence tends to increase with age. It is typically more common in people in lower socioeconomic (income) groups, chronic alcoholics, and mental health patients. Stress most commonly triggers short-term or acute insomnia. If you do not address your insomnia, however, it may develop into chronic insomnia.
Some surveys have shown that 30% to 35% of Americans reported difficulty falling asleep during the previous year and about 10% reported problems with long standing insomnia. There also seems to be an association between depression, anxiety, and insomnia. Although the nature of this association is unknown, people with depression or anxiety were significantly more likely to develop insomnia.

Rickets

Rickets is a disease of growing bone that is unique to children and adolescents. It is caused by a failure of osteoid to calcify in a growing person. Failure of osteoid to calcify in adults is called osteomalacia. Vitamin D deficiency rickets occurs when the metabolites of vitamin D are deficient. Less commonly, a dietary deficiency of calcium or phosphorus may also produce rickets. Vitamin D-3 (cholecalciferol) is formed in the skin from a derivative of cholesterol under the stimulus of ultraviolet-B light. Ultraviolet light or cod liver oil was the only significant source of vitamin D until early in the 20th century when ergosterol (vitamin D-2) was synthesized from irradiated plant steroids.
During the Industrial Revolution, rickets appeared in epidemic form in temperate zones where the pollution from factories blocked the sun’s ultraviolet rays. Thus, rickets was probably the first childhood disease caused by environmental pollution.
Natural nutritional sources of vitamin D are limited primarily to fatty, ocean-going fish. In the United States, dairy milk is fortified with vitamin D (400 IU/L) Human milk contains little vitamin D, generally less than 20-40 IU/L. Therefore, infants who are breastfed are at risk for rickets, especially those who receive no oral supplementation and those who have darkly pigmented skin, which blocks penetration of ultraviolet light.
Findings in rickets are illustrated in the image below.
Findings in patients with rickets.

Next Section: Pathophysiology

Pathophysiology

Cholecalciferol (ie, vitamin D-3) is formed in the skin from 5-dihydrotachysterol. This steroid undergoes hydroxylation in 2 steps. The first hydroxylation occurs at position 25 in the liver, producing calcidiol (25-hydroxycholecalciferol), which circulates in the plasma as the most abundant of the vitamin D metabolites and is thought to be a good indicator of overall vitamin D status. The second hydroxylation step occurs in the kidney at the 1 position, where it undergoes hydroxylation to the active metabolite calcitriol (1,25-dihydroxycholecalciferol). This cholecalciferol is not technically a vitamin but a hormone.
Calcitriol acts at 3 known sites to tightly regulate calcium metabolism. Calcitriol promotes absorption of calcium and phosphorus from the intestine, increases reabsorption of phosphate in the kidney, and acts on bone to release calcium and phosphate. Calcitriol may also directly facilitate calcification. These actions increase the concentrations of calcium and phosphorus in extracellular fluid. The increase of calcium and phosphorus in extracellular fluid, in turn, leads to the calcification of osteoid, primarily at the metaphyseal growing ends of bones but also throughout all osteoid in the skeleton. Parathyroid hormone facilitates the 1-hydroxylation step in vitamin D metabolism.

In the vitamin D deficiency state, hypocalcemia develops, which stimulates excess parathyroid hormone, which stimulates renal phosphorus loss, further reducing deposition of calcium in the bone. Excess parathyroid hormone also produces changes in the bone similar to those occurring in hyperparathyroidism. Early in the course of rickets, the calcium concentration in the serum decreases. After the parathyroid response, the calcium concentration usually returns to the reference range, though phosphorus levels remain low. Alkaline phosphatase, which is produced by overactive osteoblast cells, leaks to the extracellular fluids so that its concentration rises to anywhere from moderate elevation to very high levels.

Intestinal malabsorption of fat and diseases of the liver or kidney may produce the clinical and secondary biochemical picture of nutritional rickets. Anticonvulsant drugs (eg, phenobarbital, phenytoin) accelerate metabolism of calcidiol, which may lead to insufficiency and rickets, particularly in children who are kept indoors in institutions.

Calcium and vitamin D intakes are low in infants who are fed vegan diets, particularly lactovegans, and monitoring of their vitamin D status is essential.^[1]

Studies have noted that disorders of increased fibroblast growth factor 23 (FGF-23) function are associated with rickets.^[2]

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Next Section: Pathophysiology

Epidemiology

Frequency

United States

In the United States, vitamin D deficiency rickets does not occur in formula-fed infants because formula and milk sold in the United States contains 400 IU of vitamin D per liter. Except in pediatric patients with chronic malabsorption syndromes or end-stage renal disease, nearly all cases of rickets occur in breastfed infants who have dark skin and receive no vitamin D supplementation.

International

Incidence in Europe is similar to that in the United States. In sunny areas, such as in the Middle East, rickets may occur when infants are bundled in clothing and are not exposed to sunlight. In some parts of Africa, deficiency of calcium, phosphorus, or both in the diet may also lead to rickets, especially in societies were corn is predominant in the diet.

Mortality/Morbidity

Skeletal deformity and short stature may occur. Severe rickets has been associated with respiratory failure in children, and resulting pelvic distortion in females may lead to problems with vaginal delivery later in life.

Race

Individuals with dark skin are at increased risk for vitamin D deficiency rickets.

Sex

No sexual predilection is noted.

Age

By definition, rickets is observed only in growing children, although the effects may be observed later in life.

Glaucoma

Glaucoma is a disease caused by increased intraocular pressure (IOP) resulting either from a malformation or malfunction of the eye's drainage structures. Left untreated, an elevated IOP causes irreversible damage the optic nerve and retinal fibers resulting in a progressive, permanent loss of vision. However, early detection and treatment can slow, or even halt the progression of the disease.
What causes glaucoma?
The eye constantly produces aqueous, the clear fluid that fills the anterior chamber (the space between the cornea and iris). The aqueous filters out of the anterior chamber through a complex drainage system. The delicate balance between the production and drainage of aqueous determines the eye's intraocular pressure (IOP). Most people's IOPs fall between 8 and 21.  However, some eyes can tolerate higher pressures than others. That's why it may be normal for one person to have a higher pressure than another.
Common types of glaucoma
Open Angle
Open angle (also called chronic open angle or primary open angle) is the most common type of glaucoma. With this type, even though the anterior structures of the eye appear normal, aqueous fluid builds within the anterior chamber, causing the IOP to become elevated. Left untreated, this may result in permanent damage of the optic nerve and retina. Eye drops are generally prescribed to lower the eye pressure. In some cases, surgery is performed if the IOP cannot be adequately controlled with medical therapy. 
Acute Angle Closure
Only about 10% of the population with glaucoma has this type. Acute angle closure occurs because of an abnormality of the structures in the front of the eye. In most of these cases, the space between the iris and cornea is more narrow than normal, leaving a smaller channel for the aqueous to pass through. If the flow of aqueous becomes completely blocked, the IOP rises sharply, causing a sudden angle closure attack.
While patients with open angle glaucoma don’t typically have symptoms, those with angle closure glaucoma may experience severe eye pain accompanied by nausea, blurred vision, rainbows around lights, and a red eye. This problem is an emergency and should be treated by an ophthalmologist immediately. If left untreated, severe and permanent loss of vision will occur in a matter of days.
Secondary Glaucoma
This type occurs as a result of another disease or problem within the eye such as: inflammation, trauma, previous surgery, diabetes, tumor, and certain medications. For this type, both the glaucoma and the underlying problem must be treated.
Congenital
This is a rare type of glaucoma that is generally seen in infants. In most cases, surgery is required.

Signs and Symptoms
Glaucoma is an insidious disease because it rarely causes symptoms.  Detection and prevention are only possible with routine eye examinations.  However, certain types, such as angle closure and congenital, do cause symptoms.
Angle Closure (emergency)

• Sudden decrease of vision
• Extreme eye pain
• Headache
• Nausea and vomiting
• Glare and light sensitivity

Congenital

• Tearing
• Light sensitivity
• Enlargement of the cornea

DETECTION AND DIAGNOSIS

Because glaucoma does not cause symptoms in most cases, those who are 40 or older should have an annual examination including a measurement of the intraocular pressure. Those who are glaucoma suspects may need additional testing. 
The glaucoma evaluation has several components. In addition to measuring the intraocular pressure, the doctor will also evaluate the health of the optic nerve (ophthalmoscopy), test the peripheral vision (visual field test), and examine the structures in the front of the eye with a special lens (gonioscopy) before making a diagnosis.

The above photos show progressive optic nerve damage (indicated by the cup to disc ratio) caused by glaucoma. Notice the pale appearance of the nerve with the 0.9 cup as compared to the nerve with the 0.3 cup.
The doctor evaluates the optic nerve and grades its health by noting the cup to disc ratio. This is simply a comparison of the cup (the depressed area in the center of the nerve) to the entire diameter of the optic nerve. As glaucoma progresses, the area of cupping, or depression, increases.  Therefore, a patient with a higher ratio has more damage.
The progression of glaucoma is monitored with a visual field test. This test maps the peripheral vision, allowing the doctor to determine the extent of vision loss from glaucoma and a measure of the effectiveness of the treatment. The visual field test is periodically repeated to verify that the intraocular pressure is being adequately controlled.
The structures in the front of the eye are normally difficult to see without the help of a special gonioscopy lens. This special mirrored contact lens allows the doctor to examine the anterior chamber and the eye's drainage system. 
At St. Luke's, another test called the Arden Screening Test is used to confirm the diagnosis of glaucoma. This color test may show vision changes that occur before problems appear on the visual field test.

TREATMENT

Most patients with glaucoma require only medication to control the eye pressure. Sometimes, several medications that complement each other are necessary to reduce the pressure adequately. Surgery is indicated when medical treatment fails to lower the pressure satisfactorily. There are several types of procedures, some involve laser and can be done in the office, others must be performed in the operating room. The objective of any glaucoma operation is to allow fluid to drain from the eye more efficiently.
Should you be treated for glaucoma?  Click here to learn more.
St. Luke's Cataract & Laser Institute provides this on-line information for educational and communication purposes only and it should not be construed as personal medical advice.  Information published on this St. Luke's website is not intended to replace, supplant, or augment a consultation with an eye care professional regarding the viewer/user's own medical care.  St. Luke's disclaims any and all liability for injury or other damages that could result from use of the information obtained from this site.

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Typhoid fever and paratyphoid fever

Typhoid fever is an infectious feverish disease, with severe symptoms in the digestive system in the second phase of the illness. The French used to call the disease a 'boil of the intestine'.
Classic typhoid fever is a serious disease. It can be life-threatening, but antibiotics are an effective treatment.
The disease lasts several weeks and convalescence takes some time.
The disease is transmitted from human to human via food or drinking water, and it's therefore mainly hygiene and sanitary conditions that determine its spread.
It's rarely seen in Europe, and 94 per cent of imported cases are from the Indian subcontinent.
In the UK, the Health Protection Agency (HPA) data indicates sources of infection as: India, Spain, Egypt, Turkey, Tunisia, Portugal and Morocco.

What causes typhoid fever and paratyphoid fever?

Typhoid fever is caused by an infection with a bacterium.
This bacterium has different names in different places (UK experts prefer the name Salmonella enteritica serovar Typhi, but the US may still call it Salmonella typhi). It's only found in humans and may lead to serious illness.
When the bacterium passes down to the bowel, it penetrates through the intestinal mucosa (lining) to the underlying tissue.
If the immune system is unable to stop the infection here, the bacterium will multiply and then spread to the bloodstream, after which the first signs of disease are observed in the form of fever.
The bacterium penetrates further to the bone marrow, liver and bile ducts, from which bacteria are excreted into the bowel contents.
In the second phase of the disease the bacterium penetrates the immune tissue of the small intestine, and the often violent small-bowel symptoms begin.
Paratyphoid fever is caused by Salmonella paratyphi, a similar and generally milder disease.
Salmonella enteriditis and Salmonella typhimurium are other salmonella bacteria, which are unfortunately quite familiar within the UK and cause food poisoning and diarrhoea.
The term 'murine typhus' is used for salmonella in animals.

How is typhoid fever spread?

Salmonella typhi can only attack humans. So, the infection always comes from another human, either an ill person or a healthy carrier of the bacterium.
The bacterium is passed on with water and foods and can withstand both drying and refrigeration.
As it's necessary for someone to be exposed to a certain quantity of bacteria before symptoms occur, the storage of foods is also of great significance.
They must be kept refrigerated and prepared correctly, as required by general hygiene, so that any bacteria present are not able to multiply significantly.

Where does typhoid fever occur?

Typhoid fever is not a tropical disease and is related to hygiene and sanitary conditions rather than the climate itself.
Typhoid fever is found in large parts of Asia, Africa, Central and South America, where it occasionally causes epidemics.
The WHO estimates that there are approximately 16 million cases a year, which result in 600,000 deaths. Many of those infected get the disease in Asian countries.

What are the symptoms of the disease?

The incubation period is 10 to 20 days and depends on, among other things, how large a dose of bacteria has been taken in.
In the mild disease, the bacterium is eliminated very early in the course of the disease and there are perhaps only mild symptoms. It's possible to become a healthy carrier of infection.
There are two phases of classic typhoid fever:

• 1st phase: the patient's temperature rises gradually to 40ºC, and the general condition becomes very poor with bouts of sweating, no appetite, coughing and headache. Constipation and skin symptoms may be the clearest symptoms. Children often vomit and have diarrhoea. The first phase lasts a week and towards the end the patient shows increasing listlessness and clouding of consciousness.
• 2nd phase: in the second to third weeks of the disease, symptoms of intestinal infection are manifested and the fever remains very high and the pulse becomes weak and rapid. In the third week, the constipation is replaced by severe pea-soup-like diarrhoea. The faeces may also contain blood. It's not until the fourth or fifth week that the fever drops and the general condition slowly improves.

Complications

Intestinal perforation or profuse bleeding from the intestinal mucosa may occur if typhoid fever is left untreated.

Outlook

There are good prospects of cure with antibiotics, and the patient can be discharged from hospital when the general condition is stable.
But good general hygiene (as always) should be maintained in the home because bacteria may continue to be excreted for several more weeks.
If the patient is a food handler, they'll need to stay off work until at least two stool samples show absence of the infection.

What can you do yourself?

• There are several forms of vaccine that protect against Salmonella typhi. Most UK travel clinics use the injectable form (Typherix or Typhim Vi), rather than the oral form preferred in the USA (Vivotif). The injectable vaccine is easier to administer, since it only requires one dose and has less side-effects. It should be administered at least two weeks prior to potential typhoid exposure and is effective for three years.
• The routes of infection depend on hygiene conditions, and general kitchen hygiene should be maintained to prevent infection. For travel, the same precautions can be taken as described under cholera.

How is the disease diagnosed?

The clinical picture together with information on travel may be a good pointer for the doctor in moderate to severe cases. For the final diagnosis to be established, the bacteria have to be detected in samples from the stool, blood or other tissue. A serology test (Widal) not much used in the UK can be very useful overseas in areas where the infection is more common.
Malaria also needs to be considered as another possible explanation for the symptoms of the disease when the patient has been travelling in a malarial area.

How is typhoid fever treated?

Treatment may require admission to hospital, and loss of fluid and salt is treated with fluid therapy as appropriate.
The bacterium is controlled with antibiotics, and in rare cases steroid medicines are also included in the treatment.