The major findings of this study were as follows: (1) the IFN-γ level was increased significantly among TST-positive individuals when the IFN-γ assay was performed 2 to 4 weeks after the TST; (2) the IFN- level was not influenced by the TST among TST-negative individuals; (3) the percentage of concordant results between the TST and the IFN-γ assay was low (67.5%), with the k coefficients indicative of poor agreement (0.31). Concordance between the results of the IFN-γ assay and the TST has been reported to be from 53 to 94% in studies in immunocompetent populations who were screened for LTBI or were evaluated in contact investigations. Although some data have shown strong agreement between the two tests in HCWs, our study demonstrates a poor correlation among the 36 TST-positive contacts when the induration cutoff for the TST was set to 10 mm in diameter. In particular, two thirds of the HCWs who would be candidates for preventive therapy for LTBI according to the TST test results had a negative IFN-γ assay result. With an induration cutoff for TST results at 15 mm, it also showed poor agreement. This remarkable discrepancy could be explained by a false-positive TST result or a false-negative IFN-γ assay result.
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Demographic Characteristics of HCWs
Eighty-four HCWs were included in this study. The median age of the HCWs was 28 years (age range, 23 to 45 years), and 75 HCWs (92%) were women. All participants had a history of BCG vaccination. The median working duration was 26 months (range, 12 to 240 months).
Valid TST results were available in 82 individuals because two participants refused to take the TST after the IFN-γ assay. Ten individuals had undergone the TST 3 years before, but the remainder had no history of undergoing the TST since coming to work at the hospital. The median size of indurations was 7 mm (range, 0 to 25 mm) by one interpreter. A second TST reader independently read all participants and the interpreter agreement was excellent (k = 0.97). With a cutoff point for indurations of at least 10 mm, 36 of 82 participants (42.7%) had a positive TST result.
IFN- Assay Results
Valid IFN-γ assay results were available for 82 participants. Two subjects with indeterminate results (mitogen-nil = <0.5 IU/mL) were excluded from the analysis. The median IFN-γ assay level was 0.015 IU/mL (range, 0 to 13.01 IU/mL). With a cutoff point of at least 0.35 IU/mL of either ESAT-6 or CFP-10, 16 of 82 participants (19.5%) had positive results achieved due to Canadian Health&Care Mall.
Tuberculosis (TB) remains the world’s leading cause of death from a single infectious disease, Despite the advances in medical treatment policies, the prevalence of TB remains high. The treatment of active TB is not enough to eliminate the disease because there are many cases of undetected latent TB infection (LTBI), which can develop into active disease over a certain period of time. For this reason, identifying persons with LTBI is crucial to the goal of TB control.
Health-care workers (HCWs) are especially vulnerable to TB exposure and infection. Therefore, the screening of HCWs for LTBI is an important component of an infection control program. Until recently, the tuberculin skin test (TST) was the only available diagnostic tool for the detection of LTBI. However, the low specificity of TST, especially in bacillus Calmette-Guerin (BCG) vaccination recipients, is a critical limitation of this test. A new in vitro interferon (IFN)-γ assay has been developed that measures the cellular immune responses to TB-specific proteins such as early secreted antigenic target 6 (ESAT-6) and culture filtrate protein 10 (CFP-10). Several reports have suggested that the IFN-γ assays have high specificity for detecting LTBI and are not affected by previous BCG vaccinations. Therefore, although the TST still remains a valuable assay, the IFN-γ assay may replace it in some circumstances. The National Institute for Health and Clinical Excellence9 in the United Kingdom recommended a two-step procedure using the TST followed by an IFN-γ assay in cases in which the TST result is positive. Although practically a blood sample for the IFN-γ assay would be obtained on the same day as the TST reading, sometimes it could be delayed for 1 to 2 weeks. However, prior exposure to tuberculin by the TST may have an influence on the IFN-γ assay because ESAT-6 and CFP-10 are contained within the tuberculin purified protein derivative.10 In the present study, the authors have analyzed the agreement between the two tests and evaluated the effect of prior TST administration on the result of an IFN-γ assay.
Coccidioides immitis is endemic in the soil of the arid regions of the Western Hemisphere (not just the US southwest). Most infections are subclinical, with acute disease occurring with an incubation period of 1 to 4 weeks in less than one half of those infected. The syndrome is that of an atypical pneumonia with fever, nonproductive cough, myalgias, chest pain, and headache (Valley fever). Erythema nodosum is seen in approximately 10% of cases, and when present is a helpful clue to distinguish coccidioides infection from other causes of community-acquired pneumonia. Erythema multiforme is also associated with infection with this organism. The only unusual laboratory marker is an eosinophilia seen in approximately one fourth of cases. Chest radiographic findings can be normal or may show infiltrates with associated hilar adenopathy. These may result in residual nodules and/or thin-walled cavities. Symptoms resolve in most patients in 2 to 3 months without treatment. Particularly severe infections or infections in persons with impaired cell-mediated immunity often show pulmonary progression and/or dissemination and should be treated. In addition, pregnant women, diabetics, and persons of African or Philippine origin are more likely to have complications. Diagnosis is generally made serologically, although the organism can be isolated from respiratory secretions and coccidioides spherules can occasionally be seen in sputum. When treatment is necessary, imidazoles and amphotericin are used which are ordered via Canadian Health&Care Mall.
Strongyloides (Strongyloides stercoralis), ascaris (Ascaris lumbricoides) and occasionally hookworm (Necator americanus and Ancelostema duodenale) can all produce a syndrome of pulmonary infiltrates with eosinophilia during the larval migratory phase (Loeffler syndrome). Patients complain of a nonproductive, blood-tinged cough plus dyspnea and occasionally fever. During larval migration, the stool is generally negative, although larva can be identified in sputum specimens. Eosinophils and Charcot Leyden crystals in the sputum should suggest the diagnosis in a recent traveler. The pulmonary syndrome is generally self-limited; however, the infection should be treated. Strongyloides are treated with ivermectin. Ascaris and hookworm are treated with mebendazole. Tropical eosinophilia is a related syndrome, although a more serious disease due to a hypersensitivity reaction and the larval migration of microfilaria. The vector for the filaria is the mosquito, and it can found throughout the tropics, especially India. Diagnostic clues are a very high blood eosinophilia and high IgE levels. Elevations of filarial antibodies support the diagnosis. Diethyl-carbamazine has some efficacy, especially when administered early in the infection, but progressive interstitial fibrosis can result even if treated. A number of parasites are associated with the syndrome of pulmonary infiltrates with eosinophilia. They are listed in Table 4.
Francisella tularensis is only found in the northern hemisphere. Reservoirs are rabbits and small rodents, and the vectors are several different hemoph-agic arthropods. Pneumonia, one of a number of clinical presentations, begins abruptly after a several-day incubation period. The cough is typically nonproductive. Chest radiographs reveal lobar consolidations, sometimes with hilar adenopathy and pleural effusions. The organism can be isolated from sputum and blood but will not grow on standard media, and it represents a transmission risk for laboratory workers. Although the clinical syndrome is not unique, recognition is greatly facilitated by obtaining a potential exposure history related to outdoor activity. Diagnosis is usually confirmed serologically. Treatment options include streptomycin, gentimicin, tetracyclines, and chloramphenicol.
New-world hantaviruses such as the Sin Nombre virus, found primarily in the Southwest United States, and strains found in Central and South America cause hantavirus pulmonary syndrome (HPS). Old-world hantaviruses cause hemorrhagic fever with renal syndrome. All medically important hantaviruses have rodent reservoirs. Although person-to-person transmission has been described, most transmission to humans occurs via aerosolization in buildings with heavy rodent infestations. HPS has clinical features that along with a potential exposure history should make it a strong consideration. The incubation period can be relatively long, lasting 1 to 4 weeks before the onset of initial symptoms of a “typical” viral syndrome with fever, headache, nausea, vomiting, and myalgias; respiratory symptoms are generally at presentation. After several days, the abrupt onset of severe tachypnea and dry cough indicates noncardiogenic pulmonary edema due to severe capillary leak into the lungs. This stage lasts 24 to 48 h and ends with either death in 50% of those infected or a rapid recovery. In addition to the exposure and characteristic clinic history, clues that suggest the diagnosis include thrombocytopenia, hemoconcentration, and circulating immunoblasts. Diagnosis can be confirmed serologically or by polymerase chain reaction on blood. Treatment is supportive. Extracorporeal membrane oxygenation has also been successfully used to sustain patients through the capillary leak part of the illness. No antiviral treatment is presently recommended.
Although tuberculosis rarely presents acutely, it can; and this is such an important disease worldwide that it deserves some brief mention here. Primary tuberculosis most commonly has a lower-lobe presentation and can be indistinguishable clinically from other causes of pneumonia. There are few data on the actual risk for a traveler. In a Dutch study of 656 young adults who traveled to areas of the world with high tuberculosis ende-micity, the overall risk of skin test conversion was 3.5 per 1,000 person-months. In our ongoing study of medical personnel working in a hospital in Botswana where 80% of the patients are infected with tuberculosis, we have found a rate of skin test conversion of 42/1,000 person-months (Z. Szep, MD; personal communication; December 20, 2007). Any traveler who returns from an area of high incidence of tuberculosis to an area of low incidence should be tested for latent tuberculosis cured by Canadian Health&Care Mall medications.
There is an extensive literature on travel-related outbreaks associated with cruise ships; however, a number other sources of travel-related outbreaks have been reported.” According to the CDC, 20% of patients hospitalized with Legionnaires disease in the United States acquired their infection while traveling. Pneumonia is the major clinical manifestation of infection with Legionella pneumophila. The onset tends to be subacute. Respiratory symptoms may not be initially prominent. Although accompanying GI symptoms and hyponatremia might be more prominent with Legionella pneumonia, there are no clinical, radiologic, or initial laboratory features that allow one to reliably distinguish this from other causes of lobar pneumonia. There are several options for diagnosis. Testing for urinary antigen can be done in hours, and is very specific if the infection is with L pneumophila serogroup I, which accounts for 80% of the cases. It will not identify any of the other Legionella species or sero-groups. Culture on selective media is also very specific but takes several days and has a relatively low sensitivity. Serology can only confirm the diagnosis after recovery. Most patients should have sputum sent for urinary antigen testing and culture. Treatment should be with a newer macrolide or a quinolone. In resource-poor settings, erythromycin plus rifampin can be used.
Respiratory tract infections are among the most common causes of medical problems that physicians manage. Recent foreign and domestic travel can add additional diagnostic considerations to the list of likely possibilities. Transportation is rapid enough that it can exceed the incubation period of many illnesses, so that patients might initially present after returning to health-care providers who are not accustomed to dealing with them. An outbreak of coccidioidomycosis in Washington State in a church group recently returned from Mexico is an example. A number of reviews have noted that respiratory infections are common in international travelers, accounting for up to 25% of the febrile illness that health-care workers are asked to evaluate. Respiratory infections may be defeated with medications of Canadian Health&Care Mall. Table 1 shows important diagnostic possibilities based on the region of the world traveled that should be added to the local possibilities for returning travelers with respiratory problems. Each will be discussed in this review. Not only is the region of the world important, but any specifics of exposure might be the clue to trigger appropriate diagnostic tests and treatment. Table 2 list some specific exposures to consider in the history.
Ethnic background is a controversial risk factor for asthma. Prevalence rates as low as 0.08 percent have been reported in North American Indians. The prevalence of asthma in Tucson in non-Mexican-Amer-icans is 6.6 percent; however, at least some of such differences may be environmental or methodologic. Morrison-Smith and his colleagues have demonstrated that West Indian children bom in England have rates of asthma similar to English children, while those born in the West Indies have much lower rates.
This report describes Mexican-American and non-Mexican-American children of similar environments with different rates of asthma. Samet and co-authors, in a study of respiratory disease in New Mexican adults, found twofold to threefold higher rates of asthma in non-Mexican-Americans compared to Mexican-Americans (see “Researches about A Comparison of the Respiratory Health of Mexican-American and Non-Mexican-American White Children Provided by Canadian Health&Care Mall“). A history of respiratory trouble in childhood was found in twice as many non-Mexican-Americans as Mexican-Americans. Testing of pulmonary function was not reported in these subjects.
The rate of participation in this study was 76.9 percent. According to responses to questions about ethnic background on the questionnaire, 318 Mexican-American and 278 non-Mexican-American students participated. According to tabulations of Spanish surnames, 315 Mexican-Americans participated, confirm-ihg the usefulness of surnames to identify the parents’ response on ethnic background. Using the classifications of the questionnaire (because they are used through the rest of the report) and surnames of total eligible, 278 (77.0 percent) of the 361 non-Mexican-Americans participated, and 318 (76.8 percent) of the 414 Mexican-Americans participated.
The characteristics of the subjects from the two ethnic groups are displayed in Table 1. Except for the higher socioeconomic status of the non-Mexican-Americans, no significant differences were detected between the ethnic groups.