Psychodynamic therapy for adolescents suffering from co-morbid disorders of conduct and emotions in an in-patient setting: a randomized controlled trial.

BACKGROUND: Co-morbid disorders of conduct and emotions can be regarded as childhood antecedents of further negative developments (e.g. manifestation of personality disorders in adulthood). We evaluated a manualized psychodynamic therapy (PDT) for adolescents with these co-morbid disorders. METHOD: In a randomized controlled trial (RCT), 66 adolescents diagnosed with mixed disorders of conduct and emotions (F92 in ICD-10) were randomly assigned to a manualized in-patient PDT group or a waiting list/treatment-as-usual (WL/TAU) control condition. Diagnoses according to DSM-IV were also documented. Patients were compared using rates of remission as the primary outcome. The Global Severity Index (GSI) and the Strengths and Difficulties Questionnaire (SDQ) were used as secondary measures. Assessments were performed at baseline, post-treatment and at the 6-month follow-up. RESULTS: The sample consisted of severely impaired adolescents with high rates of further co-morbid disorders and academic failure. Patients in the treatment group had a significantly higher rate of remission [odds ratio (OR) 26.41, 95% confidence interval (CI) 6.42-108.55, p < 0.001]. Compared with the control group, the PDT group resulted in significantly better outcomes on the SDQ (p = 0.04) but not the GSI (p = 0.18), with small between-group effect sizes (SDQ: d = 0.38, GSI: d = 0.18). However, the scores of patients treated with PDT were post-treatment no longer significantly different from normative data on the GSI and within the normal range on the SDQ. The effects in the treatment group were stable at follow-up. Furthermore, most patients were reintegrated into educational processes. CONCLUSION: PDT led to remarkable improvement and furthered necessary preconditions for long-term stabilization. In future, PDT should be compared to other strong active treatments.

Antibody to dengue 1 detected more than 60 years after infection.

We investigated the duration of humoral responses to dengue virus infection in individuals who recalled experiencing dengue fever-like illnesses at the time of the Second World War, when dengue fever epidemics occurred throughout the Pacific and Southeast Asia. In July 1943 dengue fever reappeared in Hawaii following an interval of 31 years. Over the next 12 months a total of 1498 locally transmitted cases were reported, and at least 46 imported cases were identified, most of which were among members of the military returning from the Pacific Theatre of the war. Serum samples collected in 2005, more than 60 years after onset of symptoms, were tested for the presence of dengue-specific antibodies using a rapid ELISA test, and by plaque reduction neutralization test. Four of seven samples were positive for dengue-specific IgG and demonstrated neutralization titers >or=160 to dengue 1. We describe the existence of dengue-specific antibodies in the serum of people infected more than 60 years earlier.

Candidate target genes for loss of heterozygosity on human chromosome 17q21.

Loss of heterozygosity (LOH) on chromosome 17q21 has been detected in 30% of primary human breast tumours. The smallest common region deleted occurred in an interval between the D17S746 and D17S846 polymorphic sequences tagged sites that are located on two recombinant P1-bacteriophage clones of chromosome 17q21: 122F4 and 50H1, respectively. To identify the target gene for LOH, we defined a map of this chromosomal region. We found the following genes: JUP, FK506BP10, SC65, Gastrin (GAS) and HAP1. Of the genes that have been identified in this study, only JUP is located between D17S746 and D17S846. This was of interest since earlier studies have shown that JUP expression is altered in breast, lung and thyroid tumours as well as cell lines having LOH in chromosome 17q21. However, no mutations were detected in JUP using single-strand conformation polymorphism analysis of primary breast tumour DNAs having LOH at 17q21. We could find no evidence that the transcription promoter for JUP is methylated in tumour DNAs having LOH at 17q21. We suspect that the target gene for LOH in primary human breast tumours on chromosome 17q21 is either JUP and results in a haploinsufficiency for expression or may be an unidentified gene located in the interval between D17S846 and JUP.

Experimental infection of horses with West Nile virus.

A total of 12 horses of different breeds and ages were infected with West Nile virus (WNV) via the bites of infected Aedes albopictus mosquitoes. Half the horses were infected with a viral isolate from the brain of a horse (BC787), and half were infected with an isolate from crow brain (NY99-6625); both were NY99 isolates. Postinfection, uninfected female Ae. albopictus fed on eight of the infected horses. In the first trial, Nt antibody titers reached >1:320, 1:20, 1:160, and 1:80 for horses 1 to 4, respectively. In the second trial, the seven horses with subclinical infections developed Nt antibody titers >1:10 between days 7 and 11 post infection. The highest viremia level in horses fed upon by the recipient mosquitoes was approximately 460 Vero cell PFU/mL. All mosquitoes that fed upon viremic horses were negative for the virus. Horses infected with the NY99 strain of WNV develop low viremia levels of short duration; therefore, infected horses are unlikely to serve as important amplifying hosts for WNV in nature.

A recombinant particulate antigen of Japanese encephalitis virus produced in stably-transformed cells is an effective noninfectious antigen and subunit immunogen.

A COS-1 cell line, stably transformed by a plasmid encoding the premembrane and envelope glycoproteins of Japanese encephalitis virus, produced a noninfectious recombinant antigen expressed as extracellular particles. Extracellular particles purified by equilibrium density centrifugation in sucrose gradients followed by electron microscopy were characterized as spherical particles with an average diameter of approximately 30 nm and a buoyant density of 1.15 g/cc. Purified extracellular particles were shown by western blot to contain premembrane, membrane and envelope proteins. The gradient-purified particles exhibited hemagglutination activity at the same pH optimum (6.6) as Japanese encephalitis virus. Recombinant antigen from cell culture fluid was concentrated by precipitation with polyethylene glycol and evaluated for immunogenicity in 8-10-week-old ICR mice. Groups of five mice received only one immunization of recombinant antigen with or without Freund's incomplete adjuvant. Mice immunized with recombinant antigen plus Freund's incomplete adjuvant elicited the highest anti-viral titers as determined by both enzyme-linked immunosorbent assay (ELISA) and plaque-reduction neutralization tests. The polyethylene glycol-concentrated recombinant antigen was also evaluated for use in IgM antibody-capture ELISA and indirect IgG ELISA. The IgM-capture ELISA results using recombinant antigen correlated well with the results of a similar test using Japanese encephalitis virus-infected mouse brain antigen for the analysis of serum samples from patients with symptoms of acute encephalitis. Similar IgG titers were observed in an indirect ELISA comparing recombinant antigen and purified Japanese encephalitis virus as plate-bound antigens. Based on these studies, this entirely safe, easily produced antigen that expresses authentic Japanese encephalitis virus envelope glycoprotein would provide an excellent alternative to standard viral antigens used in various ELISA formats.

Common occurrence of concurrent infections by multiple dengue virus serotypes.

The co-circulation of all 4 dengue virus serotypes in the same community, common since the 1950s in Southeast Asia, has now become a frequent occurrence in many Caribbean Islands, Mexico, and Central and South America in the past 20 years. As a consequence, the frequency of concurrent infections would be expected to increase in these areas. To assess this, using state of the art technology, we screened viremic serum samples and mosquitoes inoculated with serum samples collected during epidemics involving multiple dengue virus serotypes in Indonesia, Mexico, and Puerto Rico for virus isolation. Of 292 samples tested, 16 (5.5%) were found to contain 2 or more dengue viruses by an indirect immunofluorescence test and/or the reverse transcriptase-polymerase chain reaction.

Origin of the West Nile virus responsible for an outbreak of encephalitis in the northeastern United States.

In late summer 1999, an outbreak of human encephalitis occurred in the northeastern United States that was concurrent with extensive mortality in crows (Corvus species) as well as the deaths of several exotic birds at a zoological park in the same area. Complete genome sequencing of a flavivirus isolated from the brain of a dead Chilean flamingo (Phoenicopterus chilensis), together with partial sequence analysis of envelope glycoprotein (E-glycoprotein) genes amplified from several other species including mosquitoes and two fatal human cases, revealed that West Nile (WN) virus circulated in natural transmission cycles and was responsible for the human disease. Antigenic mapping with E-glycoprotein-specific monoclonal antibodies and E-glycoprotein phylogenetic analysis confirmed these viruses as WN. This North American WN virus was most closely related to a WN virus isolated from a dead goose in Israel in 1998.

O'nyong-nyong fever in south-central Uganda, 1996-1997: clinical features and validation of a clinical case definition for surveillance purposes.

O'nyong-nyong (ONN) fever, caused by infection with a mosquito-borne central African alphavirus, is an acute, nonfatal illness characterized by polyarthralgia. During 1996-1997, south-central Uganda experienced the second ONN fever epidemic ever recognized. Among 391 persons interviewed and sampled, 40 cases of confirmed and 21 of presumptive, well-characterized acute, recent, or previous ONN fever were identified through active case-finding efforts or during a household serosurvey and by the application of clinical and laboratory criteria. Among confirmed cases, the knees and ankles were the joints most commonly affected. The median duration of arthralgia was 6 days (range, 2-21 days) and of immobilization was 4 days (range, 1-14 days). In the majority, generalized skin rash was reported, and nearly half had lymphadenopathy, mainly of the cervical region. Viremia was documented in 16 cases, primarily during the first 3 days of illness, and in some of these, body temperature was normal. During this epidemic, the combination of fever, arthralgia, and lymphadenopathy had a specificity of 83% and a sensitivity of 61% in the identification of cases of ONN fever and thus could be useful for surveillance purposes.

Evaluation of an IgM immunoblot kit for dengue diagnosis.

A commercial IgM immunoblot kit was evaluated for dengue diagnosis with a panel of serum specimens collected from patients in a dengue endemic area. The kit is not recommended for use in its present form because of its undesirable rate of false-positive results. However, by substituting internal controls with the reference positive and negative controls that are more representative of those seen in endemic areas and by modifying the positive and negative scoring criteria, sensitivity and specificity of 80.3% and 94.5%, respectively, were obtained. These results are comparable with those obtained with the IgM ELISA on specimens, most of which were obtained from outpatient health care facilities. With further technical modifications, inclusion of a visual guide to ensure scoring standardization, and a more complete elaboration of the limitations of the test, wide application of the kit in diagnostic laboratories should be possible.

First recorded outbreak of yellow fever in Kenya, 1992-1993. I. Epidemiologic investigations.

Outbreaks of yellow fever (YF) have never been recorded in Kenya. However, in September 1992, cases of hemorrhagic fever (HF) were reported in the Kerio Valley to the Kenya Ministry of Health. Early in 1993, the disease was confirmed as YF and a mass vaccination campaign was initiated. Cases of suspected YF were identified through medical record review and hospital-based disease surveillance by using a clinical case definition. Case-patients were confirmed serologically and virologically. We documented 55 persons with HF from three districts of the Rift Valley Province in the period of September 10, 1992 through March 11, 1993 (attack rate = 27.4/100,000 population). Twenty-six (47%) of the 55 persons had serologic evidence of recent YF infection, and three of these persons were also confirmed by YF virus isolation. No serum was available from the other 29 HF cases. In addition, YF virus was isolated from a person from the epidemic area who had a nonspecific febrile illness but did not meet the case definition. Five patients with confirmed cases of YF died, a case-fatality rate of 19%. Women with confirmed cases of YF were 10.9 times more likely to die than men (P = 0.010, by Fisher's exact test). Of the 26 patients with serologic or virologic evidence of YF, and for whom definite age was known, 21 (81%) were between 10 and 39 years of age, and 19 (73%) were males. All patients with confirmed YF infection lived in rural areas. There was only one instance of multiple cases within a single family, and this was associated with bush-clearing activity. This was the first documented outbreak of YF in Kenya, a classic example of a sylvatic transmission cycle. Surveillance in rural and urban areas outside the vaccination area should be intensified.

First recorded outbreak of yellow fever in Kenya, 1992-1993. II. Entomologic investigations.

The first recorded outbreak of yellow fever in Kenya occurred from mid-1992 through March 1993 in the south Kerio Valley, Rift Valley Province. We conducted entomologic studies in February-March 1993 to identify the likely vectors and determine the potential for transmission in the surrounding rural and urban areas. Mosquitoes were collected by landing capture and processed for virus isolation. Container surveys were conducted around human habitation. Transmission was mainly in woodland of varying density, at altitudes of 1,300-1,800 m. The abundance of Aedes africanus in this biotope, and two isolations of virus from pools of this species, suggest that it was the principal vector in the main period of the outbreak. A third isolate was made from a pool of Ae. keniensis, a little-known species that was collected in the same biotope. Other known yellow fever vectors that were collected in the arid parts of the valley may have been involved at an earlier stage of the epidemic. Vervet monkeys and baboons were present in the outbreak area. Peridomestic mosquito species were absent but abundant at urban sites outside the outbreak area. The entomologic and epidemiologic evidence indicate that this was a sylvatic outbreak in which human cases were directly linked to the epizootic and were independent of other human cases. The region of the Kerio Valley is probably subject to recurrent wandering epizootics of yellow fever, although previous episodes of scattered human infection have gone unrecorded. The risk that the disease could emerge as an urban problem in Kenya should not be ignored.

Clinical pharmacokinetics in the 21st century. Does the evidence support definitive outcomes?

Clinical pharmacokinetics emerged as a clinical discipline in the late 1960s and early 1970s. Clinical pharmacokinetic monitoring (CPM) helped many pharmacists to enter the clinical arena, but the focus was more on the pharmacists and tools. With the widespread acceptance of pharmaceutical care and patient-focused pharmacy, we now must take a sobering look at how clinical pharmacokinetics fits into the pharmaceutical care process. The existing literature is laden with articles that evaluate the effect of CPM on surrogate end-points. Many pharmacists have also had personal experiences that attest to the usefulness of CPM. Decreased mortality, decreased length of treatment, decreased length of hospital stay, decreased morbidity, and decreased adverse effects from drug therapy have been examined in an effort to measure and evaluate the impact of CPM on patient outcomes. While many of these studies demonstrated significant positive outcomes, several showed that CPM did not have a significant impact on specific patient outcomes. A few studies even found a negative impact on specific patient outcomes. Ultimately, there is good evidence in only a few specific patient groups to support the benefit of CPM. Despite the limitations of data supporting the routine use of CPM in managing drug therapy in diverse populations, many pharmacists continue to expend considerable time and effort in this activity. We need to define those patients who are most likely to benefit from CPM and incorporate this into our provision of pharmaceutical care, while minimising the time and money spent on CPM that provides no value. In redefining the patients who will benefit from CPM, we need to critically re-evaluate clinical studies on the relationship between drug concentration and response. Similarly, we need to pay special attention to recent studies evaluating the impact of CPM on outcomes in specific subpopulations. In the absence of specific studies demonstrating the value of CPM in particular patients, we propose that a more comprehensive decision-making process be undertaken that culminates in the quintessential question: 'Will the results of the drug assay make a significant difference in the clinical decision-making process and provide more information than sound clinical judgement alone?' We also need to consider opportunities to expand the use of CPM for new drugs and where new evidence suggests benefit. Even when there is strong evidence that CPM is useful in managing therapy in particular patient groups, clinicians need to remember that the therapeutic range is no more than a confidence interval and, therefore, we need to 'treat the patient and not the level'. We need to incorporate the patient-specific and outcome-oriented principles of pharmaceutical care into our CPM, even as we utilise CPM as an essential tool in pharmaceutical care.

Validation of the Hartford nomogram in trauma surgery patients.

OBJECTIVE: To validate the Hartford nomogram for once-daily aminoglycoside dosing in trauma surgery patients. METHODS: A chart review was performed in trauma surgery patients who were started on once-daily aminoglycoside therapy. A peak aminoglycoside concentration was drawn 30 minutes after the end of the first or second infusion, and a random concentration was drawn approximately 10 hours after the dose. The 10-hour random concentration was used to validate the Hartford nomogram by predicting the actual dosing interval (determined by extrapolating the peak and random concentrations to achieve a trough concentration <1 mg/L). The percentage of intervals accurately predicted by the nomogram was determined. RESULTS: Forty-nine patients (34 men and 15 women), age 43.0+/-15.9 y, total body weight 81.3+/-24.5 kg, ideal body weight 68.1+/-10.7 kg, dosing body weight (DBW) 72.0+/-14.4 kg, and estimated creatinine clearance [Cl(cr)] 89.5+/-20.6 mL/min/1.73 m2 were evaluated. Patients received 505+/-105 mg (7.0+/-0.4 mg/kg) of either gentamicin or tobramycin per dose. The concentration 30 minutes after the infusion was 22.4+/-5.9 mg/L, the concentration at the end of the dosing interval was 0.20+/-0.46 mg/L, the 10-hour random concentration was 2.6+/-1.8 mg/L, the elimination rate constant was 0.26+/-0.08 h(-1), the elimination half-life was 3.0+/-1.2 hours, and the volume of distribution was 19.9+/-7.9 L (0.28+/-0.09 L/kg of DBW). Ninety-eight percent (48/49) of the intervals were accurately predicted by the nomogram. CONCLUSIONS: In trauma surgery patients with Cl(cr) of more than 60 mL/min/1.73 m2, the Hartford nomogram using a single random aminoglycoside concentration accurately predicted the same once-daily aminoglycoside intervals as determined by two concentrations. Less aggressive therapeutic drug monitoring in this patient subpopulation can lead to significant cost savings.

Japanese encephalitis among hospitalized pediatric and adult patients with acute encephalitis syndrome in Hanoi, Vietnam 1995.

The etiologic spectrum of acute encephalitis syndrome (AES) has not been well defined in Vietnam. Cohort and case-control studies were performed on all adult and pediatric AES patients admitted to the Neurology Service of Bach Mai Hospital between June 5 and August 3, 1995. Among pediatric AES patients, 31 (67%) of 46 had acute Japanese encephalitis (JE), compared with only two (6%) of 33 adult AES patients (P < 0.0001). For confirmed JE cases, serum specimens obtained 15-21 days after symptom onset had the highest mean anti-JE IgM signal-to-noise (P/N) ratios (8.08 + 1.09 SE). A serosurvey of adult household members did not reveal any cases of recent subclinical JE infection, although 26% had evidence of past JE infection. The use of bed netting was nearly universal but did not appear to reduce the risk of AES or JE. Given the high incidence of JE, particularly among children, Vietnam seems well suited for the development of a targeted JE vaccination strategy.

Evaluation of aminoglycoside pharmacokinetics in postpartum patients using Bayesian forecasting.

Many postpartum women have suboptimal serum concentrations after standard doses of aminoglycosides. The purpose of this study was to characterize the pharmacokinetics of aminoglycosides in postpartum patients through the use of Bayesian forecasting and to test the ability of these subpopulation parameters to predict actual aminoglycoside serum concentrations. In phase I, 28 postpartum patients who received empiric gentamicin therapy were identified and Bayesian subpopulation parameters generated. In phase II, additional gentamicin concentrations (peaks and troughs) were evaluated to test bias and precision of Bayesian subpopulation versus traditional estimates in predicting actual aminoglycoside serum concentrations. In phase I, 56 gentamicin serum concentrations in 28 patients, (age, 26 +/- 7 years; actual body weight [ABW], 84.3 +/- 18.4 kg; ideal body weight [IBW], 54.6 +/- 5.1 kg; dosing weight [DW], 66.3 +/- 9.4 kg; creatinine clearance [Clcr], 140.4 +/- 34.0 ml/min / 1.73 m2), were evaluated to calculate subpopulation pharmacokinetic parameters of volume of distribution (Vd) 0.29 +/- 0.07 l/kg (DW); elimination rate constant (ke) 0.29 +/- 0.05 h-1 and half-life (t1/2) 2.5 +/- 0.5 hours. In phase II, 50 gentamicin serum concentrations in 25 patients (age, 23 +/- 4 years; ABW 79.4 +/- 17.5 kg; IBW 55.0 +/- 7.3 kg; DW 64.8 +/- 9.6 kg; Clcr 139.7 +/- 29.3 ml/min/1.73 m2) were evaluated to calculate subpopulation pharmacokinetic parameters of Vd 0.30 +/- 0.04 l/kg (DW); ke 0.27 +/- 0.06 h-1; and t1/2 2.9 +/- 0.8 hours. Predictive performance tests (95% confidence intervals) demonstrate that subpopulation postpartum Bayesian parameters show greater precision for peak concentrations and less bias for trough concentrations than do traditional population estimates (p < 0.05). Definition of the Bayesian subpopulation parameters will allow us to dose aminoglycosides optimally in postpartum patients who have fragmented data.

Venezuelan equine encephalitis febrile cases among humans in the Peruvian Amazon River region.

A survey was conducted from October 1, 1993 to June 30, 1995 to determine the arboviral etiologies of febrile illnesses in the city of Iquitos in the Amazon River Basin of Peru. The study subjects were patients who were enrolled at medical care clinics or in their homes by Peruvian Ministry of Health (MOH) workers as part of the passive and active disease surveillance program of the MOH. The clinical criterion for enrollment was the diagnosis of a suspected viral-associated, acute, undifferentiated febrile illness of < or = 5 days duration. A total of 598 patients were enrolled in the study. Demographic information, medical history, clinical data, and blood samples were obtained from each patient. The more common clinical features were fever, headache, myalgia, arthralgia, retro-ocular pain, and chills. Sera were tested for virus by the newborn mouse and cell culture assays. Viral isolates were identified initially by immunofluorescence using polyclonal antibody. An ELISA using viral-specific monoclonal antibodies and nucleotide sequence analysis were used to determine the specific variety of the viruses. In addition, thin and thick blood smears were observed for malaria parasites. Venezuelan equine encephalitis (VEE) virus subtype I, variety ID virus was isolated from 10 cases, including three cases in October, November, and December 1993, five cases in January and February 1994, and two cases in June 1995. The ELISA for IgM and IgG antibody indicated that VEE virus was the cause of an additional four confirmed and four presumptive cases, including five from January through March 1994 and three in August 1994. Sixteen cases were positive for malaria. The 18 cases of VEE occurred among military recruits (n = 7), agriculture workers (n = 3), students (n = 3), and general laborers (n = 5). These data indicated that an enzootic strain of VEE virus was the cause of at least 3% (18 of 598) of the cases of febrile illnesses studied in the city of Iquitos in the Amazon Basin region of Peru.

Phylogeny of the genus Flavivirus.

We undertook a comprehensive phylogenetic study to establish the genetic relationship among the viruses of the genus Flavivirus and to compare the classification based on molecular phylogeny with the existing serologic method. By using a combination of quantitative definitions (bootstrap support level and the pairwise nucleotide sequence identity), the viruses could be classified into clusters, clades, and species. Our phylogenetic study revealed for the first time that from the putative ancestor two branches, non-vector and vector-borne virus clusters, evolved and from the latter cluster emerged tick-borne and mosquito-borne virus clusters. Provided that the theory of arthropod association being an acquired trait was correct, pairwise nucleotide sequence identity among these three clusters provided supporting data for a possibility that the non-vector cluster evolved first, followed by the separation of tick-borne and mosquito-borne virus clusters in that order. Clades established in our study correlated significantly with existing antigenic complexes. We also resolved many of the past taxonomic problems by establishing phylogenetic relationships of the antigenically unclassified viruses with the well-established viruses and by identifying synonymous viruses.

Venezuelan equine encephalitis and Oropouche virus infections among Peruvian army troops in the Amazon region of Peru.

An outbreak of a febrile illness characterized by headache, ocular pain, myalgia, and arthralgia occurred during June 1994 among Peruvian army troops in Northern Peru. On June 14-16, 1994, clinical data and blood samples were obtained from eight soldiers with a febrile illness, and from 26 others who had a history of febrile illness during the past three months. A follow-up blood sample was obtained 107 days later from four of the febrile and seven of the afebrile soldiers. Serum samples were tested for dengue (DEN), Oropouche (ORO), and Venezuelan equine encephalitis (VEE) IgM and IgG antibodies by an enzyme-linked immunosorbent assay (ELISA). Virus isolation was performed by inoculation of newborn mice and Vero cell cultures. Viral isolates were identified by immunofluorescence, ELISA, and nucleotide sequencing. A VEE virus infection was confirmed in three of the eight febrile soldiers, two by virus isolation, and one by serology. Antigenic analysis indicated that one of the virus isolates was similar to VEE subtype I, variety ID, viruses previously isolated in Colombia and Venezuela. Nucleotide sequence data showed that both viral isolates were identical to one another and closely related to VEE ID viruses previously isolated in Peru, Colombia, and Venezuela. Serologic results showed that two of 26 afebrile soldiers had IgM antibody to VEE and four had IgG antibody to VEE; two febrile soldiers had IgG antibody in their first serum samples. Oropouche-specific IgM antibody was detected in one of the eight febrile and five of the afebrile soldiers, and 18 of the 34 soldiers had low titers of ORO IgG antibody titers, which did not meet the diagnostic criteria for confirmed cases. All soldiers were negative for DEN IgM antibody, and 10 had flavivirus IgG antibody that reacted with DEN antigens. These data indicated that VEE ID virus was one of the causes of illness among Peruvians soldiers and that this was the first association of this VEE subtype with human disease in Peru.