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 enteriditis—are predominantly isolated. Three clinical patterns of infection are recognized: (1) enteric fever, for example, 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. All types are transmitted by ingestion of the organism, usually from tainted food or drink.
1. ENTERIC FEVER (TYPHOID FEVER)
ESSENTIALS OF DIAGNOSIS
Gradual onset of headache, 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.
Leukopenia; blood, stool, and urine cultures positive for Salmonella.
Enteric fever is a clinical syndrome characterized by GI symptoms as well as constitutional symptoms such as fever, malaise, and headache. It may have a long incubation period (6–30 days), and the GI symptoms may resolve but then recur. Progressive infection often evolves with delirium. Enteric fever is caused by typhoidal strains of Salmonella, S typhi (typhoid fever) and to a lesser extent S paratyphi (subtypes A, B and C). Unlike other strains of Salmonella, the S typhi and S paratyphi subtypes A and B are restricted to human hosts. Salmonella is an intracellular pathogen. Infection begins when organisms breach the mucosal epithelium of the intestines by transcytosis, an organism-mediated transport process through the cell via an endocytic vesicle. Having crossed the epithelial barrier, organisms invade and replicate in macrophages in Peyer 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 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 CNS.
During the prodromal stage, there is increasing malaise, headache, cough, and sore throat, often with abdominal pain and constipation, while the fever ascends in a stepwise fashion. After about 7–10 days, it reaches a plateau and the patient is much more ill, appearing exhausted and often prostrated. There may be marked constipation, especially early, or “pea soup” diarrhea; marked abdominal distention occurs as well. If there are no complications, the patient’s condition will gradually improve over 7–10 days. However, relapse may occur for up to 2 weeks after defervescence.