In 1997, ticks removed from humans and received alive by the Tick-Borne Disease Laboratory of the U.S. Army Center for Health Promotion and Preventive Medicine (USACHPPM) were tested for pathogens by polymerase chain reaction (PCR). Thirty-three of 222 (15%) Amblyomma americanum (L.) DNAs produced amplicons of the expected size of Ehrlichia chaffeensis Anderson, Dawson & Wilson and 26/222 (12%) produced amplicons indicating Borrelia burgdorferi Johnson, Schmid, Hyde, Steigalt & Brenner. Five (2%) appeared to be co-infected with both organisms. Thirteen of 308 (4%) Dermacentor variabilis (Say) were PCR-positive for spotted fever group rickettsiae. Restriction fragment-length polymorphism analysis indicated all were Rickettsia montana. One hundred twenty-seven D. variabilis from Monroe County, WI, were tested for B. burgdorferi and 14 (11%) were positive. Five of 24 (21%) Ixodes scapularis Say were positive for B. burgdorferi and one (2%) was positive for the agent of human granulocytic ehrlichiosis. Different species of ticks transmit different pathogens, and most tick-borne diseases have similar early symptoms, therefore knowing the species and infection status of the tick enhances the physician's ability to consider tick-borne agents as a potential cause of disease and recommend appropriate therapy. Ongoing surveillance of the vector species of human diseases provides an additional estimate of human encounters with infected ticks, and testing ticks removed from humans may increase our knowledge of the vector status of tick species for transmitting tick-borne pathogens.

Abstract.A study was conducted in northern California to estimate the prevalence and distribution in ixodid ticks of the rickettsial agents of human monocytic (HME) and human granulocytic (HGE) ehrlichioses. More than 650 ixodid ticks were collected from 17 sites in six California counties over a 15-month period. Ehrlichia chaffeensis, the causative agent of HME, was detected by a nested polymerase chain reaction (PCR) in Ixodes pacificus (minimum infection rate [MIR] ϭ 13.3%) and Dermacentor variabilis (infection rateϭ20.

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Human monocytic ehrlichiosis (HME) is a sometimes fatal, emerging tick-borne disease caused by the bacterium Ehrlichia chaffeensis. It is frequently misdiagnosed because its symptoms mimic those of the flu. Current evidence indicates that Amblyomma americanum (L.), the lone star tick, is the major vector of HME. To determine if E. chaffeensis is present in ticks at Aberdeen Proving Ground, MD, questing A. americanum ticks were collected from 33 sites. Nucleic acid was extracted from 34 adult and 81 nymphal pools. Sequences diagnostic for E. chaffeensis from three different loci (16S rRNA, 120-kDa protein, and a variable-length polymerase chain reaction [PCR] target, or VLPT) were targeted for amplification by the PCR. Fifty-two percent of the collection sites yielded pools infected with E. chaffeensis, confirming the presence and widespread distribution of E. chaffeensis at Aberdeen Proving Ground. Analysis with the both the 120-kDa protein primers and the VLPT primers showed that genetic variance exists. A novel combination of variance for the two loci was detected in two tick pools. The pathogenic implications of genetic variation in E. chaffeensis are as yet unknown.

Using a heterologous rat cDNA probe, we have identified a 14.7 kbp Drosop hila melanogas ter ge nomic clone containing the X-linked gene Pgd+, which encodes the enzyme 6-phosphogluconate dehydrogenase (6PGD). We used in situ hybridization to larval polytene chromosomes, a somatic transient expression assay for enzyme activity, and the rescue of the lethal Pgd-phenotype by germline transformation to verify the identity of the gene. A 7.4 kbp fragment including the gene and approximately 1.2 kbp of upstream and 1.8 kbp of downstream sequences was relocated to autosomal ectopic sites by germline transformation; this transduced gene exhibits levels of enhanced activity in males comparable to those of the indigenous gene at its normal X chromosome locus. We conclude that the sequences responsible for dosage compensation of Pgd+ are included in this fragment.