Definition. Typhoid fever is an acute, often severe illness caused by S. typhosa and characterized by fever, headache, apathy, cough, prostration, splenomegaly, maculopapular rash, and leukopenia. Typhoid fever is a classic example of enteric fever caused by salmonellae. Incidence and Prevalence. Typhoid fever is a disease of major importance in areas of the world that have not attained high standards of public health. A progressive decrease in the incidence of typhoid fever has occurred in the United States since 1900, but sporadic cases and limited outbreaks continue to occur. About 400 to 500 cases per year have been reported in recent years. Some of these infections were acquired in other areas of the world, but many were acquired in the United States from food contaminated by chronic typhoid carriers.

In the United States, more than 3000 chronic typhoid carriers are under super-vision by health departments, but the actual number of chronic carriers is probably considerably higher. Typhoid fever will continue to occur on a limited scale in countries with high standards of public health because of the frequency of typhoid in other areas of the world, the magnitude of intercontinental travel, and the existence of reservoirs of chronic carriers. Epidemiology. The ultimate source of infection with S. typhosa is a patient with typhoid fever or a typhoid carrier. Patients with typhoid fever excrete large numbers of S. typhosa in feces or urine, and viable bacilli may also be present in vomitus, respiratory secretions, or pus. Chronic enteric carriers, the most important source of infection, often excrete 106 or more viable bacilli per gram of feces.


The typhoid bacillus can survive for weeks in water, ice, dust, and dried sewage. Water containing typhoid bacilli has been responsible for many outbreaks in the past; it may be contaminated directly by excreta containing S. typos or by excreta washed down from remote sites by rain or introduced by faulty sanitation or plumbing. Foods may be contaminated directly from typhoid fever and that vascular hyper-reactivity by excreta, by water containing S. typhosa, and to epinephrine or norepinephrine appears during occasionally by contaminated dust. Flies also have the £6riAe phase oi the disease ana persists into been implicated as mechanical vectors in the convalescence.

Oysters and another shell deN eloquent d toke7t16.M% and \IMAM k1.)WC.- fish may be infected in polluted tidal waters. Inactivity is considered to be indicators of endo-areas where typhoid fever is common in the antitoxin activity. However, volunteers made their dece of the disease increases during the summer an‘, to the engine prior to challenge with S. Tryphosa Pathogenesis. The portal of entry, of S. typhosa develop typical typhoid fever, an observation is almost always the gastrointestinal tract. The apparently in conflict with the hypothesis that initial invasion is not associated with marked endotoxin released during infection is responsible multiplication of S. typhosa in the intestine, for the fever and other manifestations. although organisms are occasionally detected in Pathology.

The proliferation of large mononuclear stools for several days during .this period: Bacilli cells derived from reticuloendothelial tissue is apparently gain access to the blood through lymph the most prominent feature of the pathology of physics in the small intestine and produce a typhoid fever.

Involvement of lymphoid tissue in initial transient bacteremia that is rapidly the intestinal tract, principally Peyer’s patches terminated as organisms are removed from the in the terminal ileum, leads to necrosis and ulcers-blood by reticuloendothelial cells in the liver, spleen, too. Erosion of blood vessels may give rise to bone marrow, and lymph nodes. The incubation period of typhoid fever may correspond to the phase of invasion from the intestine and intracellular multiplication in phagocytes; clinical manifestations of the disease may become evident as bacteria begin to re-enter the blood.

The applicability of these results in volunteers to naturally occurring typhoid infection is unknown. Variation in pathogenicity among different strains of S. types is known to exist, and changes related to cultivation on artificial media cannot be excluded. It has been suggested but not definitely established that the endOtoxins of S. typhosa are responsible for some of the clinical manifestations of typhoid fever. This concept is based on the similarities of certain manifestations of typhoid fever and the events observed after the injection of bacterial endotoxin. For example, both typhoid fever and injection of endotoxin are associated with headache, chills, fever, polymorphonuclear leukopenia, thrombocytopenia, and reticuloendothelial cell hyperplasia.

The liver is enlarged and often shows cloudy swelling and focal areas of necrosis. The spleen and mesenteric lymph nodes are enlarged and show hyperplasia of reticuloendothelial cells. Bronchitis is common, and pneumonia is not unusual. Microscopic examination of the maculopapular skin lesions reveals round cell infiltration and vascular congestion. Clinical Manifestations. The incubation period usually is 8 to 14 days but varies from five days to five weeks. The duration of illness in the case of average severity is about four weeks. The onset is usually gradual and associated with anorexia, lethargy, malaise, headache, general aches and pains, and fever.


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