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. 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. 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. world, the magnitude of intercontinental travel, and the existence of reservoirs of chronic carriers. Epidemiology.
The ultimate source of infection with Patients with typhoid fever excrete large numbers of Chronic enteric carriers, the most important source of infection, often excrete 106 or more viable bacilli per gram of feces. 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
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.
In the United States, more than 3000 chronic typhoid carriers are under supervision by health departments, but the actual number of chronic carriers is probably considerably higher. world, the magnitude of intercontinental travel, and the existence of reservoirs of chronic carriers. Epidemiology. The ultimate source of infection with S. 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. Tryphosa or by excreta washed down from remote sites by rain or introduced by faulty sanitation or plumbing. Foods may be contaminated directly by typhoid fever and that vascular hyper-reactivity by excreta, by water containing S. typhosa, and to epinephrine or norepinephrine appears occasionally by contaminated dust. Flies also have the £6riAe phase of the disease and persist into being implicated as mechanical vectors in the convalescence. Both of these phenomena the transmission of infection.
Oysters and another shell deN eloquent d toke7t16.M% and IMAM k1.)WC.- fish may be infected in polluted tidal waters. Inactivity — are considered to be indicators of endo-areas where typhoid fever is common the antitoxin activity. However, volunteers made tolerance of the disease increases during the summer and, to India unit pilot to challenge with S. Tryphosa Pathogenesis. The portal of entry of S. Tryphosa develops typical typhoid fever, an observation almost always in 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, on. Erosion of blood vessels may give rise to bone marrow, and lymph nodes. Organisms multi- intestinal hemorrhage. Intestinal lesions are ply at these intracellular sites and are discharged into the blood for a period of days. 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. During the phase of bacteremia, infection of the biliary tract regularly occurs, and multiplication of organisms in bile leads to seeding of the intestinal tract with millions of bacilli.
The entry of infected bile into the intestine is responsible for the increase in the number of organisms in stools during the second and third weeks of disease. Infection of the gall-bladder is usually asymptomatic, although symptoms of cholecystitis occasionally develop. The infective dose of S. typhosa for men is influenced by many factors. It has been assumed that a small number of bacilli, possibly 10 or 100, could initiate infection. This view is supported by studies of certain laboratory accidents and the occurrence of typhoid fever after exposure to water containing a small number of bacilli. Observations on volunteers infected orally with several strains of S. typhosa indicate that a dose of about 106 viable units is required to infect 50 percent of a group.
The applicability of these results in volunteers to naturally occurring typhoid infection is unknown. Variation in pathogenicity among different strains of S. typhosa 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 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. It has been demonstrated in volunteers that tolerance to the pyrogenic action of endotoxin is present during the convalescent phase usually confined to autos and st mucosa but occasionally penetrate muscular and serosal layers and produce intestinal perforation. Healing of intestinal lesions does not give rise to appreciable scarring or stricture formation.
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. During the first week, there is a gradually increasing remittent fever. Dull, continuous headache is a prominent symptom in almost all cases. About two-thirds of the patients have a nonproductive cough, and epistaxis occurs in about 10 percent. The majority of patients have vague abdominal pain or discomfort.
Constipation is frequent and more common than diarrhea, which occurs in only about 20 percent of the patients. During the second week of illness, the temperature shows less of a tendency to remit and is often sustained at around 40° C.. During this phase patients are often severely ill with marked weak-ness, abdominal discomfort, and distention. Mental dullness is prominent, and delirium may occur. Diarrhea is more common during the second week than during the first, and stools may contain blood. As the illness extends into the third week, the patient continues to be febrile and becomes increasingly exhausted and weak. Patients without complications usually begin to improve during the third and fourth weeks. The temperature gradual-ly begins to decline and maybe normal by the end of the fourth week. The physical signs vary with the stage of the disease. During the first week, fever and slight abdominal tenderness may be the only findings.