The etiology of typhoid fever is Salmonella typhi and Salmonella enteritidis

The etiology of typhoid fever is Salmonella typhi and Salmonella enteritidis paratyphi A and B. bioserotip

Pathogenesis

The entry of Salmonella typhi (S.typhi) and Salmonella paratyphi (S.paratyphi) into the human body occurs through contaminated food germs. Some germs were destroyed in the stomach, partly escape into the intestine proliferate further. When the intestinal humoral immune response is less then the bacteria will multiply penetrate epithelial cells, especially cell-M and then to the lamina propria. In the lamina propria and breed germs difagosit by phagocyte cells mainly by macrophages. Germs can live and multiply in macrophages and subsequently taken to the plaque painful distal ileum and then to the mesenteric lymph nodes. Furthermore, through the duct torasikus germs contained in the blood circulation (resulting in the first asymptomatic bacteremia) and mnybar k sluruh retikulondotelial body organs especially the liver and spleen. In these organs the bacteria leave the phagocyte cells and proliferate outside the cell or room sinusoids and subsequent entry into the blood circulation again a second time resulting in bacteremia accompanied by signs and symptoms of systemic infection.

In the liver, the bacteria get into the gall bladder, multiply, and common bile excreted by "intermittent" into the intestinal lumen. Some germs excreted through feces and some came back into circulation after penetrating the intestine. The same process is repeated again, since macrophages have been teraktivasi and hyperactive then occur during phagocytosis of Salmonella bacteria release several inflammatory mediators which in turn will cause symptoms of systemic inflammatory reaction to a case of fever, malaise, myalgia, mental disorders, and coagulation.

In the Plaque painful hyperactive macrophage hyperplasia reaction network (intra S.typhi macrophages induce delayed type hypersensitivity reactions, tissue hyperplasia, and necrosis of organs). Salruan gastrointestinal bleeding can occur due to erosion of blood vessels around the plaque that is experiencing nkrosis painful and hyperplasia due to accumulation of mononuclear cells in the intestinal wall. Lymphoid tissue pathological process can be developed until the muscle layer, serosa intestine, and result in perforation.

Endotoxin can be attached to the capillary endothelial cell receptor with the consequent incidence of complications such as disruption nueropsikiatrik, cardiovascular, breathing, and other organ disorders.


CLINIC manifestations

The period of typhoid fever shoots last between 10-14 days. Clinical symptoms that arise are very varied from light served until severe, asymptomatic until the disease is typically accompanied by a picture of complications up to death.

In the first week of clinical symptoms was found disease complaints and symptoms similar to acute infectious diseases in general are fever, headache, dizziness, muscle pain, anorexia, nausea, vomiting, or diarrhea obstipasi, uncomfortable feeling in stomach, cough, and epistaxis. On physical examination found only body temperature to rise. The nature of the fever is rising slowly and mainly in the afternoon until the evening. In the second week of the symptoms become more obvious in the form of fever, relative bradycardia (relative bradycardia is an increase in temperature of 10C is not followed by increase in pulse rate 8 times per minute) are webbed tongue (gross in the middle, the edge of the red tip and tremor), hepatomegaly, splenomegaly, meteorismus, somnolen form of mental disorder, stupor, coma, delirium or psikosis. Roseolae rarely found rarely found in people in Indonesia.


DIAGNOSIS

There are three methods for diagnosing typhoid fever are:

1. Diagnosis mikrobiologik / breeding germs.

2. Serologic diagnosis.

3. Clinical diagnosis.

Mikrobiologik diagnosis method is the most specific method and more than 90% of untreated patients, positive blood cultures within the first week. This result is decreased drastically after the use of antibiotic drugs, where a positive result to 40%. Nonetheless bone marrow cultures still show a high yield of 90% positive. In the weeks subsequent decrease of blood culture results, but the culture of feces and urine culture increased 85% and 25% positive respectively in the week the 3rd and 4th. Organisms in the feces can still be found for 3 months from 90% of patients and approximately 3% of patients remained out S.typhi germs in stool in the long term. It can happen that a chronic carrier of germs S.typhi issue in the stool in his life, and the carrier is more common in adults than children and more often on women than men.

Diagnosis depends on serologic antibodies arising against O and H antigens, which can be detected by agglutination reaction (Widal test). Antibodies against the O antigen of group D occur within the first week of illness and reached its peak in the third and fourth weeks will decrease after 9 months to 1 year. Agglutinin titer of 1 / 200 or an increase in titer of more than 4 times the mean positive Widal test, this indicates an acute infection S.typhi.

But agglutinin O titer elevation can also be caused by germs like salmonella O antigens other than D group with a commonality factor 9 and 12 as in S.typhi. There is an increasing titer of antibody against D antigen derived from the flagellum S.typhi add specificity of Widal test results. Antibodies against flagella antigen titer escalate after the first week and peaked at week 4 to-6, and titer remain high for years. The discovery of a high titer antibody flagellum does not mean there is an acute infection. Factors to consider that affect the results of Widal test were: stage of disease, vaccination, anamnestik reaction, the endemic areas and treatment ..
MANAGEMENT

Until now, still embraced the management of typhoid fever trilogy, namely:

1. Giving antibiotics; to stop and destroy the spread of germs. Antibiotics are used:
Chloramphenicol; dose first hi 4x250 mg, 4x500 mg the second day, given during fever continued until 2 days free of fever, then the dose was reduced to 4x250 mg for 5 days later.
Ampicillin / Amoxicillin; dose of 50-150 mg / kg given for 2 weeks.
Kotrimokzasol; 2x2 tablet (1 tablet containing 400 mg sulfametokzasol-80 mg trimethoprim) was given for 2 weeks also
II and III generation cephalosporins.
Rest and treatment professionals, aims to prevent complications and speed healing. Patients should be an absolute bed rest until at least 7 days free of fever or approximately 14 days. Mobilization done gradually, in accordance with the recovery of the strength of the patient.
Diet and supporting therapy (symptomatic and supportive)

Several studies have shown Ahwa early solid feeding, which is rice with side dishes low cellulose (patang vegetables with coarse fibers) can be given safely. Also required the provision of vitamins and minerals sufficient to support the patient's general condition.