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The role of corticosteroids in treatment of septic shock is still quite controversial Clinical data have suggested an association between mortality in patients with septic shock and poor adrenal reserve to cosyntropin (Cortrosyn) stimulation testing Administration of stress doses of hydrocortisone, for example 100 mg intravenously three times a day for 5 days followed by a 6-day tapering-dose regimen, to patients with relative adrenal insufficiency and pressor-dependent septic shock may reduce mortality However, the usefulness of cosyntropin stimulation testing and use of stress-dose hydrocortisone in patients with septic shock are not so well defined as to be standard of care
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Salmonellosis includes infection by any of approximately 2000 serotypes of salmonellae The taxonomy of Salmonella species has been confusing All salmonella serotypes are members of a single species, Salmonella enterica Human infections are caused almost exclusively by S enterica subsp enterica, of which three serotypes typhi, typhimurium, and choleraesuis are predominantly isolated Three clinical patterns of infection are recognized: (1) enteric fever, the best example of which is typhoid fever, due to serotype typhi; (2) acute enterocolitis, caused by serotype typhimurium, among others; and (3) the septicemic type, characterized by bacteremia and focal lesions, exemplified by infection with serotype choleraesuis All types are transmitted by ingestion of the organism, usually from contaminated food or drink
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Expanded knowledge of the pathophysiology of sepsis and septic shock and recognition that cytokines play a critical role suggest novel approaches to therapy Strategies include blocking the effects of endotoxin with anti-endotoxin monoclonal antibodies; blockade of TNF- , a potent cytokine mediator of septic shock, with anti-TNF monoclonal antibody or soluble TNF receptor; use of IL-1 receptor antagonists to inhibit the proinflammatory effects of IL-1 binding to its receptor; use of corticosteroids; and blocking platelet or thrombin activation None of these strategies have been met with improved survival However, a single randomized placebo-controlled trial showed that recombinant human activated protein C (drotrecogin alfa) reduced mortality of septic patients with APACHE II scores 25, but the benefits of this agent remain controversial This drug should be used cautiously because of the risk of bleeding Drotrecogin alfa is not beneficial for
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1 Enteric Fever (Typhoid Fever)
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Gradual onset of malaise, headache, nausea, vomiting, abdominal pain Rose spots, relative bradycardia, splenomegaly, and abdominal distention and tenderness Slow (stepladder) rise of fever to maximum and then slow return to normal
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Leukopenia; blood, stool, and urine culture positive for salmonella
CMDT 2008
Differential Diagnosis
Enteric fever must be distinguished from other gastrointestinal illnesses and from other infections that have few localizing findings Examples include tuberculosis, infective endocarditis, brucellosis, lymphoma, and Q fever Often there is a history of recent travel to endemic areas, and viral hepatitis, malaria, or amebiasis may be in the differential as well
General Considerations
Enteric fever is a clinical syndrome characterized by constitutional and gastrointestinal symptoms and by headache It can be caused by any Salmonella species The term typhoid fever applies when serotype typhi is the cause Infection is transmitted by consumption of contaminated food or drink The incubation period is 5 14 days Salmonella is an intracellular pathogen Infection begins when organisms breach the mucosal epithelium of the intestines by transcytosis, an organismmediated transport process through the cell via an endocytic vesicle Having crossed the epithelial barrier, organisms invade and replicate in macrophages in Peyer s patches, mesenteric lymph nodes, and the spleen Serotypes other than typhi usually do not cause invasive disease, presumably because they lack the necessary human-specific virulence factors Bacteremia occurs, and the infection then localizes principally in the lymphoid tissue of the small intestine (particularly within 60 cm of the ileocecal valve) Peyer s patches become inflamed and may ulcerate, with involvement greatest during the third week of disease The organism may disseminate to the lungs, gallbladder, kidneys, or central nervous system
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