An analysis of forty-two cases of laboratory-acquired tularemia: Treatment with broad spectrum antibiotics

Abstract

Forty-one vaccinated and one unvaccinated laboratory personnel acquired typhoidal tularemia as a result of probable aerosol exposure. The resulting disease was characterized by non-specific grippal and respiratory symptoms of varying severity, the majority being mildly to moderately ill. Phenolized and acetone-extracted vaccines were ineffective in preventing clinical disease but probably modified the course of illness. Among the thirty-four hospitalized patients, twenty had abnormal findings on chest roentgenograms. Fifteen had oval, bronchopneumonic lesions, one had diffuse bronchopneumonia, one had lobar pneumonia. Pleural effusion occurred in five patients, in two as an isolated finding. Hilar adenopathy occurred in nine patients. Such findings should prompt consideration of tularemia in the differential diagnosis. Agglutinin and hemagglutinin serum levels were not useful in the early recognition of disease. Results of skin tests were positive in seventeen of thirty-one patients when first seen; however, this was useful in suggesting the diagnosis in only thirteen since four were known to have had positive reactions to skin tests prior to onset of illness. P. tularensis was regularly isolated during the first few days of hospitalization from sputum when available (fourteen of sixteen patients), and frequently from gastric aspirates (twenty-two of thirty-one patients) and pharyngeal washings (eighteen of thirty-two patients), and as late as the third week of untreated illness by guinea pig inoculation or plating on appropriate culture media. The illness of approximately 75 per cent of the hospitalized patients resulted from laboratory strains resistant to streptomycin, the remainder from streptomycin-sensitive strains. Two of the hospitalized and seven of the non-hospitalized patients with minimal symptoms were untreated. Thirty-one of the hospitalized group were treated with broad spectrum antibiotics given in four equally divided doses; in the majority of patients 2 gm. were given daily for seven to fourteen days. Following initiation of therapy the mean duration of any fever was approximately three days; there was corresponding improvement of symptoms within forty-eight hours and with the exception of the critically ill patient all patients were fully ambulatory within one week. With treatment there was prompt regression of pulmonary lesions and gradual clearing over the following four to six weeks. P. tularensis could be isolated from sputum samples, pharyngeal washings or gastric aspirates throughout the first week of therapy. Among fifteen of the patients so treated during the first week of disease, five suffered relapses whereas in sixteen patients with similar therapy instituted after the first week of disease no relapses occurred. It is apparent that this group of drugs are bacteriostatic and fail to eradicate the organism from the host. When such therapy is started early in illness the host's immune status often is incapable of preventing relapses. Retreatment during relapse with the same antibiotic is effective. Mild residual and unexplained symptoms following control of the acute phase of disease were observed in only two patients, a much lower incidence than usually cited. This low occurrence of residual complaints is attributed to the continuing physician-patient relationship with appropriate reassurance during the twelve-month follow-up.