Typhoid Fever, Causes, Signs and Symptoms and Prevention

 Typhoid Fever, Causes, Signs and Symptoms and Prevention:

Typhoid fever, also known as enteric fever, is a potentially fatal multi systemic illness caused primarily by salmonella typhi and to a lesser extent by salmonella para typhi with proper treatment. Enteric fever yields a high cure rate but untreated typhoid fever may progress to delirium which is an abrupt change in the brain that causes mental confusion and emotional disruption, intestinal obstruction, intestinal hemorrhage, bowel perforation and death within one month of onset of the disease.

Most common transmission method of typhoid fever is oral transmission via ingestion of contaminated food and beverages these food handlers are often asymptomatic. They chronically shed the bacteria through feces or less commonly urine due to poor personal hygiene of these people. Food is often contaminated with bacteria. Bacteria can also be transmitted by drinking sewage contaminated water and eating shellfish and neglecting hand hygiene after using a contaminated toilet is another method of transmission. Typhoid fever occurs worldwide primarily in developing nations whose sanitary conditions are poor.

Typhoid fever is endemic in Asia, Africa and Latin America. People who are travelling to these endemic countries are at high risk of developing typhoid fever. Typhoid LaSalle monalee are able to survive a stomach pH as low as 1.5 reduction in gastric acidity may increase the risk of developing typhoid fever. Antacids proton pump inhibitors h2 receptor blockers gastrectomy and conditions like a chlorhydris can cause reduction in gastric acidity and facilitate bacterial growth. Some people may possess genetic polymorphisms which dampen the macrophage activity and facilitate bacterial growth.

Now let's discuss about the pathophysiology of typhoid fever. All pathogenic Salmonella species when present in the gut are engulfed by phagocytic cells which then passed through the mucosa and present them to the macrophages in limine appropriate. Non typhoid will Salman Olli are fergus oddest throughout the distal ileum and colon with toll-like receptors. Macrophages recognized pathogen associated molecular patterns such as flagella and lipopolysaccharides macrophages and intestinal epithelial cells then attract t-cells and neutrophils with interleukin 8 ccausin inflammation and suppressing the infection in contrast to non typhoid 'el Salmonella. Salmonella typhi and parrot I fee enter the host system primarily through the distal ileum. They adhere to the epithelium over clusters of lymphoid tissue in the iliam also known as payer patches. They have specialized fin brie to adhere to the epithelial cells the bacteria are then focus oddest by the macrophages located in payer patches the bacteria. Then induced their host macrophages to attract more macrophages. Salman le containing macrophages then reach the mesenteric lymph nodes, thoracic duct and reticuloendothelial system which consists of liver spleen bone marrow. It associated lymph nodes while traveling bacteria used the macrophage cellular mechanisms for their own reproduction. Once a critical density of organisms reached they induce macrophage apoptosis breaking out into the bloodstream to invade rest of the body. The bacteria then infect the gall bladder via either bacteremia or direct extension of infected bile. The result is that the organism re-enters the gastrointestinal tract and bile and reinfect. Speyer patches bacteria that do not reinfect the hosts are typically shed in the stools and are then available to infect other hosts.

Now I want to discuss about the signs and symptoms of classic typhoid fever. The clinical syndromes associated with salmonella typhi and para typhi are indistinguishable. Thus both organisms generate a similar type of clinical presentation signs and symptoms usually appear after seven to fourteen days of ingestion of the bacterial fever. Pattern is stepwise characterized by rising temperature over the course of each day that drops by the subsequent morning the peaks and troughs rise progressively over time. The notorious gastrointestinal manifestations develop these, include diffuse abdominal pain and tenderness and in some cases fierce right upper quadrant pain. Monocytic infiltration causes inflammation of payer patches. This may lead to narrowing of bowel lumen causing constipation that lasts the duration of the illness. In addition the patient may present with a dry cough, dull frontal headache delirium and malice . At the end of the first week of illness, fever plateaus at around 39 to 40 degrees Celsius. The patient develops rose spots which are salmon-colored and 1 to 4 centimeters in size. These generally resolved within two to five days during the second week of illness.

Chronic pulse may develop in the third week. The individual grows more toxic and anorexic with significant weight loss. The conjunctiva are infected. Some patients experience fowl green yellow liquid diarrhea also known as pea soup diarrhea. Inflammation due to the necrosis of payer patches may cause bowel perforation and peritonitis at this point overwhelming toxemia myocarditis or intestinal hemorrhage may cause death. If the individual survives to the fourth week of fever, mental confusion and abdominal distension increases over the next few days. Intestinal and neurologic manifestations may still occur weight loss and weakness increases some survivors become asymptomatic Salmonella Carriers. It have the potential to transmit the disease to other people. The clinical course of a given individual may deviate from the above description of classic disease. The signs and symptoms may vary depending on the geographic region race factors in the infecting bacterial species. The stepladder fever pattern that was once the hallmark of typhoid fever now occurs only about 12% of all cases. In most recent cases, the fever has a steady insidious onset young children individuals with AIDS and one-third of immuno competent adults with typhoid fever develop diarrhea rather than constipation.

Complications Of Typhoid Fever:

It is a multi systemic illness. It affects almost all the organ systems in the body. potential neuropsychiatric manifestations include the following a toxic confusional state characterized by disorientation delirium and restlessness. Facial twitching and coma indicates severe disease in rare cases transverse myelitis. Clinical neuropathy and polyneuropathy may occur paraplegia peripheral.

Respiratory complications may include acute low burn ammonia, an ulceration of the posterior pharynx. Cardiovascular complications may include toxic myocarditis in about one to five percent of patients. This is the leading cause of death in endemic areas. Rarely the patient may develop pericarditis hepatobiliary complications may include jaundice pancreatitis and hepatomegaly. Intestinal manifestations include intestinal hemorrhage and perforation.

The diagnosis of typhoid fever is primarily clinical based on history and signs and symptoms. The doctor should obtain a travel history from the patient. In addition culture of the organism should perform to confirm the diagnosis and test antibiotic sensitivity. Culture of the organism is considered 100%. Specific blood intestinal secretions and feces can be used to isolate the organism.

Prevention Of Typhoid Fever:

Maintaining of good personal hygiene is a good way of prevention of typhoid fever. Vaccination is recommended for travelers to parts of the world where typhoid fever is common. People who live in endemic areas and laboratory workers who work with Salmonella Typhi bacteria. There are two vaccines are available for typhoid fever, inactivated one and live attenuated one. Inactivated vaccine is given as an intravenous injection and given to people of two years and older. A single dose vaccine given two weeks before travel. Repeated doses are recommended every two years for people who remain at risk. Live Attenuated vaccine is given orally as a capsule and given to people of six years and older.