Polymerase chain reaction (PCR) primers derived from a variable region of the 16S rRNA gene sequence were used to amplify DNA specifically from Ehrlichia chaffeensis (the recently proposed name for the etiologic agent of human ehrlichiosis). The 389-bp product defined by the specific primers was not detected when DNA samples from any of the other recognized species of Ehrlichia were used as amplification templates. When the PCR was applied to five suitable blood specimens obtained from patients subsequently shown to be serologically positive for E. chaffeensis, all five were positive. The same technique was applied to a total of six control blood specimens, three from febrile patients who had no serologic evidence of infection with Ehrlichia or Rickettsia species and three from patients diagnosed with Rocky Mountain spotted fever, and all six were negative. A chemiluminescent, group-specific oligonucleotide probe was shown to hybridize only with the PCR products obtained upon amplification of the five blood specimens from patients serologically diagnosed as having human ehrlichiosis. The results indicate that PCR, coupled with a nonisotopic method of confirming the identity of the PCR product, is a highly specific and efficient method of detecting the agent of human ehrlichiosis in blood. The results also suggest that E. chaffeensis is the sole etiologic agent of human ehrlichiosis in the United States. The technique was also applied to four ticks that were positive by direct immunofluorescence for Ehrlichia species, and one tick was PCR positive, indicating that E. chaffeensis DNA can be detected in ticks harboring this organism, although the sensitivity may be low.
Q fever is usually acquired by contact with aerosols generated during parturition of domestic ungulates (e.g., sheep, cows, goats). In the maritime provinces of Canada, parturient cats have also been implicated in its transmission. A 66-year-old woman from eastern Maine developed high fever, rigors, headache, myalgias, pulmonary infiltrates, and elevated hepatocellular enzymes, and the diagnosis of acute Q fever was confirmed serologically. She and 14 other family members had attended a family reunion in Maine 2 weeks earlier, when they were exposed to a parturient cat. All 11 adults and older children attending the reunion developed symptoms consistent with acute Q fever. Serum samples were obtained from 10 who attended the reunion and 8 who did not attend. Titers greater than or equal to 1:64 to Coxiella burnetii were present in all who attended the reunion but in none of those who did not. Cat-associated Q fever should be considered when sporadic cases of the disease occur in the United States.
During the spring of 1989, 86 members of a military unit from the state of Maryland, USA, participated in two-week-long training manoeuvres in the states of Arkansas (location FC) and Virginia (location FAPH). Acute febrile illnesses due to infections with two tick-borne pathogens, Rickettsia rickettsii and Ehrlichia sp., were confirmed serologically in 2 initial cases who were admitted to the hospital. A seroepidemiological investigation among unit members found an additional 17 of 109 individuals (16%) with elevated post-exposure indirect immunofluorescent antibody (IFA) titres to R. rickettsii (16 cases) and/or E. canis (2 cases). The seropositivity rate of personnel who trained at FC was 38% (15 of 40), compared to only 13% (4 of 31) and 8% (3 of 38) of personnel who trained at FAPH or who did not train in the field, respectively (P < 0.001). Seropositivity was associated with symptoms suggestive of a tick-borne illness. Only 4 (22%) and 6 (33%) of the 18 personnel seropositive for R. rickettsii reported an erythematous or petechial type of rash or a febrile illness, respectively, within 4 weeks of exposure; 5 of 18 (28%) personnel infected with R. rickettsii reported no symptoms and only 8 of 18 (44%) received medical treatment. Mild infections with R. rickettsii, or a closely related spotted fever group agent, may have accounted for the high infection rate experienced by this group.
Two chimpanzees, one (C-499) infected with the acquired immunodeficiency syndrome-associated retrovirus type 2 (ARV-2) strain of human immunodeficiency virus (HIV) and one (C-560) infected with the lymphadenopathy-associated virus type 1 (LAV-1) strain of HIV, were inoculated with approximately 104 tissue culture infective doses of the reciprocal strain. At the time of the second inoculation, both chimpanzees had high titers of HIV-specific antibodies, including antibodies that neutralized both virus strains. After inoculation of the second strain of HIV, the antibody titers in both chimpanzees increased 4to 10-fold, and in one chimpanzee (C-499), the numbers of infectious peripheral blood mononuclear cells (PBMC) increased 1,000-fold to levels that are comparable with those observed after primary HIV infections. By restriction enzyme analysis of virus recovered from PBMC, both ARV-2 and LAV-1 were identified in C-499, thus demonstrating that superinfection had occurred.
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