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Interaction of acute feline herpesvirus-1 and chronic feline immunodeficiency virus infections in experimentally infected specific pathogen free cats.

Cats with or without chronic feline immunodeficiency virus (FIV) infection were exposed to feline herpesvirus, type 1 (FHV-1). FIV infected cats became sicker than non-FIV infected cats and required more supportive treatment. However, there were no differences in the length of their illness or in the levels and duration of FHV-1 shedding. FHV-1 infection caused a transient neutrophilia at Day 7 with a rapid return to preinfection levels. The neutrophilia coincided with a transient lymphopenia that was accompanied by a decline in both CD4+ and CD8+ T-lymphocytes. A brief decrease in the CD4+/CD8+ T-lymphocyte ratio occurred at Day 14 in both FIV infected and non-infected cats. This decrease was mainly the result of an absolute and transient increase in CD8+ T-lymphocytes. CD4+ and CD8+ T-lymphocyte numbers and CD4+/CD8+ T-lymphocyte ratios returned to baseline within 4-8 weeks in both FIV infected and non-infected cats. FIV infected cats produced less FHV-1 neutralizing antibodies during the first 3 weeks of infection than non-FIV infected animals. The IgM FHV-1 antibody response was depressed in FIV infected cats whereas the IgG antibody response was unaffected. FHV-1 infection evoked a comparable transient loss of lymphocyte blastogenic responses to concanavalin A and pokeweed mitogen in both FIV infected and non-infected cats. However, response to pokeweed mitogen took longer to return to normal in FIV infected animals. Lymphocytes from FIV infected cats had a greater and more sustained proliferative response to FHV-1 antigen than non-FIV infected cats. The ongoing IgG antibody response to FIV was not affected by FHV-1 infection.

Acute Disease↗

Pre-infection frequencies of equine herpesvirus-1 specific, cytotoxic T lymphocytes correlate with protection against abortion following experimental infection of pregnant mares.

In general, vaccines containing inactivated equine herpesvirus-1 (EHV-1) fail to prevent abortion in pregnant mares following infection with a virulent strain of EHV-1. We have tested the hypothesis that resistance to EHV-1-induced abortion in pregnant mares is associated with high frequencies of EHV-1 specific, major histocompatibility complex (MHC) class I-restricted, cytotoxic T lymphocytes (CTL) in the circulation. To test this theory, three groups of pregnant mares were assembled with varying backgrounds of infection or vaccination in an attempt to mimic the immune status of the general population. Group 1 mares (n=9) were untreated controls selected at random. Group 2 mares (n=5) were vaccinated three times intramuscularly with inactivated EHV-1. Group 3 mares (n=3) had been infected with EHV-1 on four previous occasions. The frequency of CTL in blood leucocytes was measured by limiting dilution analysis at three time points; at the beginning of pregnancy (approximately 28 weeks before infection) in the Group 2 and Group 3 mares (4-7 weeks of gestation) (Group 1 was unavailable for sampling) and then 2 weeks before (30-40 weeks of gestation) and 3 weeks after experimental infection in all the mares. Serum samples were collected to monitor complement fixing (CF) antibody titres. Mares in all three groups were infected experimentally with EHV-1 strain Ab4/8 by the intranasal route after which they were monitored clinically to determine the outcome of pregnancy and samples were collected to determine the duration of nasopharyngeal shedding and cell-associated viraemia. The untreated control mares showed low pre-infection CTL. After experimental infection, they all seroconverted, aborted and demonstrated expected clinical and virological signs. Some vaccinated mares (3/5) had elevated titres of CF antibody prior to their first vaccination. All the vaccinated mares seroconverted after vaccination and exhibited higher CTL frequencies than controls before infection. Four of the five foaled normally. The multiply infected mares had low CF antibody titres prior to infection and showed neither seroconversion nor clinical or virological signs after infection. All multiply infected mares exhibited high frequencies of CTL before infection and they all foaled normally. The CTL frequencies observed differed significantly from the expected frequencies in the control and multiply infected groups at 2 weeks pre-infection (P=0.034) and between the foaling and aborting mares at 2 weeks pre-infection (P=0.005) and 3 weeks post-infection (P=0.015). The results show a positive correlation between the number of virus-specific CTL in the peripheral blood of pregnant mares and their protection against abortion induced by EHV-1 infection. Therefore, as indicated by this study, rational approaches to the development of new vaccines for EHV-1 should stimulate cytotoxic immune responses and develop virus-specific CTL as pre-requisites for protection against abortion.

Abortion, Veterinary↗

Feline leukemia virus infection as a potentiating cofactor for the primary and secondary stages of experimentally induced feline immunodeficiency virus infection.

Preexistent feline leukemia virus (FeLV) infection greatly potentiated the severity of the transient primary and chronic secondary stages of feline immunodeficiency virus (FIV) infection. Of 10 FeLV-FIV carrier cats, 5 died of experimentally induced FIV infection, compared with 2 deaths in 10 cats infected only with FeLV and 1 death in 7 cats infected only with FIV. FIV-infected cats with preexistent FeLV infections developed severe depression, anorexia, fever, diarrhea, dehydration, weight loss, and leukopenia 4 to 6 weeks after infection and were moribund within 2 weeks of the onset of signs, whereas cats infected only with FIV developed much milder self-limiting gross and hematologic abnormalities. Pathologic findings in dually infected cats that died were similar to those observed previously in cats dying from uncomplicated primary FIV infection but were much more widespread and severe. Coinfection of asymptomatic FeLV carrier cats with FIV did not increase the levels of FeLV p27 antigen present in their blood over that seen in cats infected with FeLV alone. The amount of proviral FIV DNA was much higher, however, in dually infected cats than in cats infected only with FIV; there was a greater expression of FIV DNA in lymphoid tissues, where the genome was normally detected, and in nonlymphoid tissues, where FIV DNA was not usually found. Dually infedted cats that recovered from the primary stage of FIV infection remained more leukopenic than cats infected with FIV or FeLV alone, and their CD4+/CD8+ T-lymphocyte ratios were inverted. One of these cats developed what was considered to be an opportunistic infection. It was concluded, therefore, that a preexistent FeLV infection in some way enhanced the expression and spread of FIV in the body and increased the severity of both the resulting transient primary and chronic secondary stages of FIV infection. This study also demonstrated the usefulness of the FIV model in studying the role of incidental infectious diseases as cofactors for immunodeficiency-causing lentiviruses.

Animals↗

Pseudomonas aeruginosa infection in human immunodeficiency virus infected patients.

OBJECTIVES: (1) To determine the incidence and outcome of Pseudomonas aeruginosa infection in HIV-infected patients. (2) To study the antimicrobial susceptibility of P. aeruginosa isolates in this particular population. (3) To identify risk factors for these infections. PATIENTS AND METHODS: A retrospective case-control study performed in a 28-bed infectious-diseases unit in a 940-bed university hospital. All cases were defined as HIV-infected patients with severe infections due to P. aeruginosa, including bacteremia, lower or upper respiratory tract infections, infections related to a central venous catheter, and cutaneous/muscular infection. Each case was matched with an HIV-seropositive control not infected by P. aeruginosa and hospitalized on the same dates as the cases. RESULTS: One thousand and thirty-five HIV-infected patients were hospitalized during the study period. A first severe P. aeruginosa infection was documented in 41 patients, giving an overall annual incidence note of 2.51 episodes per 100 admissions. Forty of the 41 case notes were available for analysis. They consisted of 17 cases of bacteraemia, four upper respiratory tract infections, 10 lower respiratory tract infections, three catheter-related infections, and six cutaneous/muscular infections. Of these 40 cases, 60% were nosocomial and the remainder were community-acquired. The overall mortality rate was 22% (47% in bacteraemic forms). Twenty five percent of patients relapsed after an average of 37 days. The case-control comparison showed that AIDS was more frequent among the cases (92% vs. 74%, P = 0.04), who also had a lower PN count (P = 0.005), and a lower CD4 cell count (15.7 +/- 18.8/mm3 vs. 118 +/- 211/mm3; P = 0.0007). The number of days spent in hospital in the previous 3 months (29.3 +/- 20.7 vs. 19.7 +/- 14, P = 0.04) was significantly higher among the cases. In a multivariate analysis, examining treatments received in the previous month, only co-trimoxazole [OR = 5.5 (1.1-26.9)], penicillins [OR = 5.2 (1.1-25.3)], steroids [OR = 5.5, (1.2-25.5)] and a CD4 cell count below 50/mm3 [OR = 13.2 (1.4-129.4)] were identified as risk factors. CONCLUSION: P. aeruginosa infection is a not frequent bacterial disease in highly immunodeficient HIV-infected patients. It is frequently fatal and must be borne in mind in the advanced stages of HIV disease, especially when patients have received co-trimoxazole (trianthoprim-sulphamethoxazole), penicillins or steroids.

AIDS-Related Opportunistic Infections↗

Nosocomial infection rates in adult and pediatric intensive care units in the United States. National Nosocomial Infections Surveillance System.

To determine which intensive care unit (ICU) infection rate may be best for interhospital and intrahospital comparisons and to assess the influence of invasive devices and type of ICU on infection rates, we analyzed data from the National Nosocomial Infections Surveillance System. From October 1986 to December 1990, 79 hospitals reported 2,334 hospital-months of data from 196 hospital units. The median overall infection rate was 9.2 infections per 100 patients. However, this infection rate had a strong positive correlation with average length of ICU stay (r = 0.60, p less than 0.0001). When patient-days was used in the denominator, the median overall nosocomial infection rate was 23.7 infections per 1,000 patient-days. Although there was a marked reduction in the correlation with average length of stay, this rate had a strong positive correlation with device utilization (r = 0.59, p less than 0.0001). To attempt to control for average length of stay and device utilization, we examined device-associated nosocomial infection rates. Central line-associated bloodstream infection rates, catheter-associated urinary tract infection rates, and ventilator-associated pneumonia rates varied by ICU type. The distributions of device-associated infection rates were different between some ICU types and were not different between others (coronary and medical ICUs or medical-surgical and surgical ICUs). Comparison of device-associated infection rates and overall device utilization identified hospital units with outlier infection rates or device utilization. These data show that: (1) choice of denominator is critical when calculating ICU infection rates; (2) device-associated infection rates vary by ICU type; and (3) intrahospital and interhospital comparison of ICU infection rates may best be made by comparing ICU-type specific, device-associated infection rates.

Adult↗

Effect of a comprehensive infection control program on the incidence of infections in long-term care facilities.

BACKGROUND: Control of infection within the long-term care facility is a daunting problem. Elderly patients are at high risk for contracting infection because of reduced innate immunity, malnutrition, and the presence of chronic medical conditions. This small study tested the effect of developing and implementing a comprehensive preventive infection control program in the long-term care setting and examined the resultant incidence of infections. METHODS: Eight private, freestanding, long-term care facilities in urban and suburban settings were selected for the study. The 4 test sites had a total of 443 beds; there were 447 beds in 4 matched control sites. Data on infection rates were accrued in both preintervention and intervention years. The control homes maintained their existing infection control policies and procedures. The test homes were provided with an infection control educational program and replaced all currently used germicidal products with single-branded products for a 12-month period. A criteria-based standardized infection control surveillance system was used to monitor and report infections in all facilities. RESULTS: In the preintervention year, the test sites experienced 743 infections (incidence density rate, 6.33) and the control homes experienced 614 infections (incidence density rate, 3.39). In the intervention year, the test homes reported 621 infections, a decrease of 122 infections (incidence density rate, 4.15); in the control homes, the number of infections increased slightly, to 626 (incidence density rate, 3.15). The greatest reduction in infections in the test homes was in upper respiratory infections (P =.06). CONCLUSIONS: This study provides additional evidence that a comprehensive infection control program that includes handwashing and environmental cleaning and disinfecting may help reduce infections among the elderly residing in long-term care settings.

Age Distribution↗

Congenital cytomegalovirus infection in infants infected with human immunodeficiency virus type 1.

OBJECTIVES: To determine the rate of in utero transmission of cytomegalovirus (CMV) in perinatally HIV-exposed infants and to determine whether coinfection with CMV in early life affects outcome. METHODS: Infants born to HIV-infected women between March, 1988, and March, 1995, were evaluated (n = 206). Congenital or in utero CMV infection was defined as a positive CMV culture or shell vial assay on urine obtained in the first 3 weeks of life. HIV-infected infants either had positive serology beyond 18 months of age or, for an infant younger than 18 months, had a positive HIV PCR or HIV culture on at least two separate occasions. RESULTS: There were 30 HIV-infected and 171 uninfected infants (144 who seroreverted and 27 infants with at least 2 negative HIV PCR or culture results and normal immunologic studies during the first 6 months of age). Urine culture for CMV was obtained during the first 3 weeks of life on 154 infants: 24 of 30 (80%) HIV-infected infants; and 130 of 171 (76%) HIV-uninfected infants. Overall 10 of 154 (6.5%) infants were infected with CMV: 5 of 24 (21%) HIV-infected and 5 of 130 (3.8%) HIV-uninfected infants. The rate of in utero CMV infection was significantly higher in HIV-infected infants (P = 0.008). Dually infected infants were more immunosuppressed than their CMV-negative counterparts. At 3 months of age the percentage of CD4+ T lymphocytes (P = 0.0021) and CD4:CD8 ratios (P = 0.0018) were significantly lower in the CMV-infected infants than in the CMV-uninfected infants. At 6 months of age the absolute CD4+ T lymphocyte counts (P = 0.0038), percentage of CD4+ T lymphocytes (P = 0.044) and CD4:CD8 ratios (P = 0.037) were significantly lower in the CMV-infected infants. The mean survival of HIV-infected infants who were coinfected with CMV in early life (5 in utero and 1 perinatally infected infant identified at 7 weeks) was 24.77 months. Kaplan-Meier survival analysis indicated a trend toward decreased survival in the infants who were coinfected with CMV in early life (P = 0.088). CONCLUSIONS: Congenital CMV infection is more common in HIV-infected infants than in HIV-uninfected infants. Infection with CMV in early life is associated with greater immunosuppression and may be associated with a more rapid progression of HIV infection in infants.

AIDS-Related Opportunistic Infections↗

Nasal carriage of and infection with Staphylococcus aureus in HIV-infected patients.

BACKGROUND: Staphylococcus aureus is a common cause of serious infection in patients infected with HIV. OBJECTIVES: To evaluate risk factors for and quantitative effect of S. aureus infection in HIV-infected patients, with special attention to nasal carriage. DESIGN: Prospective, multihospital cohort study. SETTING: Three tertiary care Veterans Affairs Medical Centers. PARTICIPANTS: 231 ambulatory HIV-infected patients. RESULTS: Thirty-four percent of patients were nasal carriers of S. aureus. Of these patients, 38% were persistent carriers and 62% were intermittent carriers. Twenty-one episodes of infection occurred in 13 patients: Ten were bacteremias (including 2 cases of endocarditis), 1 was pneumonia, and 10 were cutaneous or subcutaneous infections. Seventeen (85%) of these episodes occurred in patients with CD4 counts less than 100 cells/mm3. Recurrent infections occurred in 3 of 7 patients who survived an initial S. aureus infection. The mortality rate was higher among patients with S. aureus infection than among those without infection (P = 0.03). Factors significantly associated with S. aureus infection were nasal carriage, presence of a vascular catheter, low CD4 count, and neutropenia. Molecular strain typing indicated that for 6 of 7 infected patients, the strain of S. aureus isolated from the infected sites was the same as that previously cultured from the nares. CONCLUSION: Nasal carriage is an important risk factor for S. aureus infection in HIV-infected patients. Controlled studies are indicated to determine whether eradication of nasal carriage in a selected subset of patients (for example, those with a low CD4 cell count) might prevent invasive S. aureus infection in patients with HIV infection.

AIDS-Related Opportunistic Infections↗

A dual role for endothelial cells in cytomegalovirus infection? A study of cytomegalovirus infection in a series of rat endothelial cell lines.

Several clinical findings point to the involvement of microvascular endothelial cells in cytomegalovirus-related pathology. In this study the interactions of cytomegalovirus (CMV) with microvascular endothelial cells was investigated in an in vitro rat model. A series of rat endothelial cell lines, considered representative for the heterogeneity of heart microvascular endothelium in vivo, were infected with rat CMV (RCMV). The course of infection and production of infectious virus were examined using immunofluorescence staining and plaque titration assays, and was compared with infection of fully permissive rat fibroblasts. These endothelial cell lines displayed differences in susceptibility to CMV infection. Two endothelial cell lines (RHEC 50 and 191) were practically non-permissive, while four endothelial cell lines (RHEC 3, 10, 11 and 116) were partly permissive for CMV infection. In contrast to CMV infection in fibroblasts, only limited infection of the permissive endothelial cell lines was observed without spreading of CMV infection through the monolayer, although infectious virus was produced. Detachment of infected endothelial cells and recovery of the monolayer with time was observed. The detached endothelial cells were able to transmit CMV infection to fibroblast monolayers, but not to endothelial monolayers. Our in vitro results demonstrate differences in permissiveness for RCMV between the series of rat endothelial cell lines, which is suggestive for endothelial heterogeneity to CMV infection in vivo. Our findings indicate that endothelial cells are relatively resistant to CMV infection and that, upon infection, the endothelial monolayer may dispose of the virus via detachment of the infected cells. This points to a dual role for the endothelium in CMV infection in vivo: a barrier for CMV infection (by the endothelial monolayer) on the one hand and spreading of CMV infection (by detached infected cells) on the other hand.

Animals↗

The effect of different infection levels on acquired resistance to gastrointestinal nematodes in artificially infected cattle.

The objective of this study was to evaluate the effect of different infection levels of Ostertagia ostertagi and Cooperia oncophora in a simulated 'first grazing season' on the resistance of calves to an artificial challenge infection. The infection levels were determined by the infection schedules and the chemoprophylaxis used. Thirty six 7-11-month old Holstein-Friesian bull calves were randomly divided into four groups. The animals of group B received an ivermectin sustained release bolus (ISRB) on day 0. The calves of group D were treated on days 0 and 56 with a subcutaneous injection of doramectin (0.2 mg kg(-1) BW). Group C was the untreated control group. The calves of group N were used as helminth-naive controls, while the animals of groups B, C and D were trickle infected for 24 weeks. The infection schedules were designed to simulate the expected infection pattern for each treatment group under set-stocked conditions in temperate climate areas. After the last infection, all animals were treated with oxfendazole. One week later, all animals received a challenge infection of 50,000 O. ostertagi L3 and 100,000 C. oncophora L3, spread over 10 consecutive days. During the primary infection period the faecal egg output and the serum pepsinogen and antibody levels reflected the different levels of host-parasite contact between the groups (group C > group D > group B > group N). After the challenge infection, faecal egg counts, total Ostertagia burden, size of the adult worms and abomasal globule leucocyte counts all indicated a positive relationship between the level of Ostertagia infection during the primary infection period and the level of acquired resistance. A reduction of host-parasite contact during the primary infection period, as a consequence of the infection schedule and the chemoprophylaxis used, resulted in a diminished level of resistance to the artificial challenge infection with O. ostertagi. Faecal cultures and small intestine worm counts indicated that all previously infected groups had acquired a high degree of resistance to the Cooperia challenge infection.

Animal Husbandry↗

Effects of infection of Eimeria tenella, E. acervulina, and E. maxima upon Salmonella typhimurium infection in chickens.

Three experiments were conducted to examine whether Salmonella typhimurium infection is enhanced by concurrent infection with Eimeria tenella, E. acervulina, or E. maxima. There were two groups in each experiment: birds infected with a daily oral dose of approximately 1 X 10(4) cfu of S. typhimurium for 5 days after coccidial infection and birds infected with S. typhimurium alone with the similar exposure schedule. Chickens were necropsied 7, 10, and 14 days after coccidial infection. The numbers of S. typhimurium in the contents of ceca and small intestine were counted, and numbers of chickens positive for S. typhimurium in the liver and bile were examined. In E. tenella infection, the S. typhimurium counts in the ceca and small intestine of concurrently infected chickens were significantly greater than those of birds infected with S. typhimurium alone. In E. acervulina infection, the S. typhimurium counts in the ceca of chickens killed 14 days after E. acervulina infection and the numbers of birds positive for S. typhimurium in the ceca of chickens killed 10 and 14 days after E. acervulina infection were significantly greater than those of chickens infected with S. typhimurium alone. In E. maxima infection, the numbers of birds positive for S. typhimurium in the ceca and liver of chickens killed 7 days after E. maxima infection were significantly greater than those of birds infected with S. typhimurium alone. Results of this study indicate that infection with E. acervulina or E. maxima is able to enhance S. typhimurium infection in chickens.

Animals↗

Plasmodium cynomolgi: serum-mediated blocking and enhancement of infectivity to mosquitoes during infections in the natural host, Macaca sinica.

The infectivity of Plasmodium cynomolgi in its natural host, the toque monkey, Macaca sinica, to Anopheles tessellatus mosquitoes was studied in relation to the evolution of anti-sexual-stage immunity in the host during the course of a blood-induced infection. The effects of serum on the infectivity of gametocytes and the intrinsic infectivity of gametocytes to mosquitoes on each day were assessed in membrane feeding experiments. Mosquitoes were also directly fed on the animal on each day. Our results demonstrate that during the very early patent period, before the peak of gametocytemia, the infection serum enhanced the infectivity of gametocytes up to two to three times above their infectivity in normal monkey serum. Subsequently, serum drawn post-peak of parasitemia ceased to enhance, and began to suppress, infectivity. After 2-3 months, long after parasitemias ceased patency, the serum no longer suppressed and between 3 and 4 months the serum again tended to enhance gamete infectivity before losing any significant effect. Serum infectivity enhancing effects were consistent with low indirect immunofluorescence test antibody titers against blood stage parasites first during the very early days of a blood infection before reaching blocking levels, and again during convalescence when antibodies were declining. The serum infectivity blocking effects on gametocytes were seen at the peak of antibody titers from about Days 9 to 23 of an infection. From 78 to 95% of the total infectivity of the parasite to mosquitoes during an infection occurred when infectivity enhancing activity was present in the serum. Hence, the infectivity of the parasite to mosquitoes was largely dependent on infectivity enhancing antibodies in host serum.

Animals↗

Experimental vesicular stomatitis virus infection of swine: extent of infection and immunological response.

Swine, a natural host species for infection by vesicular stomatitis virus (VSV), were infected with VSV-New Jersey (VSV-NJ) serotype virus obtained from a recent field isolate. Tissues collected from the infected pigs were examined for the presence of infective virus, for viral antigens, and/or for viral nucleic acid. Infective virus could be recovered from tissues near the site of infection for as long as 6 days after the primary infection with VSV. However, no infective virus was recovered following hypothermia induced 11 weeks after infection, or following a secondary challenge with virus 22 weeks after initial infection. Immunofluorescence tests for viral antigens and nucleic acid hybridization assays failed to detect viral antigens or nucleic acids in tissues from which no infective virus could be recovered. Titers of serum-neutralizing antibody peaked 3-5 weeks after infection and then fell slightly until the secondary infection which caused a rapid anamnestic response. Peripheral blood mononuclear cells (PBM) tested 3, 5, 8 or 18 weeks after primary infection all produced readily detectable antigen-specific proliferative responses when cultured with VSV. Thus, although direct tests failed to demonstrate persistence of virus after infection, the humoral and cellular immune response remained elevated for months. Infective VSV was not required to stimulate the proliferative response since UV-inactivated VSV was immunogenic in these in vitro tests. Following primary infection, antigen-specific proliferative responses could be stimulated by several strains of VSV-NJ, but not by VSV-Indiana (VSV-Ind) serotype virus. Secondary infection had relatively little effect on the proliferative response to VSV-NJ strains, but it did cause the PBM to gain responsiveness to VSV-Ind.

Animals↗

Aleutian mink disease parvovirus infection of mink macrophages and human macrophage cell line U937: demonstration of antibody-dependent enhancement of infection.

Aleutian mink disease parvovirus (ADV) infects macrophages in adult mink. The virulent ADV-Utah I strain, but not the cell culture-adapted ADV-G strain, infects mink peritoneal macrophage cultures and the human macrophage cell line U937 in vitro. However, preincubation of ADV-G with ADV-infected mink serum enhanced its infectivity for U937 cells. the enhancing activity was present in the protein A-binding immunoglobulin G fraction in the serum, but F(ab')2 fragments failed to enhance the infection. On the other hand, the same sera inhibited ADV-G infection of Crandell feline kidney (CRFK) cells. Although U937 cells were not fully permissive for antibody-enhanced ADV-G infection, ADV mRNA expression, genome amplification, and protein expression were identical to those found previously for ADV-Utah I infection of U937 cells. Preincubation of ADV-Utah I with soluble protein A partly inhibited the infection of U937 cells but did not affect infection of CRFK cells. In mink peritoneal macrophages, preincubation with the infected mink serum did not make ADV-G infectious. However, the infectivity for mink macrophages of antibody-free ADV-Utah I prepared from the lungs of infected newborn mink kits was enhanced by ADV-infected mink serum. Moreover, protein A partly blocked ADV-Utah I infection of mink macrophage cultures. These results suggested that ADV-Utah I enters mink macrophages and U937 cells via an Fc receptor-mediated mechanism. This mechanism, antibody-dependent enhancement, may also contribute to ADV infection in vivo. Furthermore, since ADV infection in mink is characterized by overproduction of anti-ADV immunoglobulins, antibody-dependent enhancement may play a critical role in the establishment of persistent infection with ADV in vivo.

Aleutian Mink Disease Virus↗

Visceral leishmaniasis in human immunodeficiency virus (HIV)-infected and non-HIV-infected patients. A comparative study.

Visceral leishmaniasis is an endemic infection in Mediterranean countries, where it has become a frequent complication of acquired immunodeficiency syndrome (AIDS). The incidence of visceral leishmaniasis is increasing in Spain due to human immunodeficiency virus (HIV)-related cases, but some aspects of its epidemiology, clinical features, and management remain unknown. In addition, no comparative clinical studies about the disease in HIV-infected and non-HIV-infected patients have been reported. During a 24-year period, 120 cases of visceral leishmaniasis were diagnosed at our institution and 80 (66%) were associated with HIV infection. The mean age at diagnosis was higher in HIV-infected that in non-HIV-infected patients (33.2 versus 23.2 yr; p = 0.002), but the male/female ratio was similar in both groups. The main risk factor for HIV infection was intravenous drug abuse (78.7%). The clinical presentation of leishmaniasis was similar in both groups, but HIV-infected patients had a lower frequency of splenomegaly than HIV-negative individuals (80.8% versus 97.4%; p = 0.02). HIV-infected patients had a greater frequency and degree of leukopenia, lymphocytopenia, and thrombocytopenia. Most of them were profoundly immunosuppressed (mean CD4+ lymphocyte count, 90 cells/mm3) at the time of diagnosis of leishmaniasis, and 53.7% had AIDS. The sensitivity of serologic studies for Leishmania was significantly lower in HIV-infected than in non-HIV-infected patients (50% versus 80%; p < 0.001), but the diagnostic yield of bone marrow aspirate (67.1% versus 79.4%) and bone marrow culture (62.9% versus 66.6%) was similar in both groups. After initial treatment, the response rate was significantly lower in HIV-infected than in non-HIV-infected individuals (54.8% versus 89.7%; p = 0.001). The relapse rate was 46.2% and 7.5%, respectively (p < 0.001). Secondary prophylaxis with antimonial compounds or amphotericin B seems to be useful in preventing relapses in HIV-infected patients. The mortality rate was higher (53.7% versus 7.5%; p < 0.001) and the median survival time shorter (25 versus > 160 mo; p < 0.001) in AIDS patients than in HIV-negative individuals. Although leishmaniasis could contribute to death in a significant number of HIV-infected patients, it was the main cause of death in only a few of them. The CD4+ lymphocyte count and the use of highly active antiretroviral therapy and secondary prophylaxis for leishmaniasis were the most significant prognostic factors for survival in AIDS patients. Visceral leishmaniasis behaves as an opportunistic infection in HIV-infected individuals and should be considered as an AIDS-defining disease.

AIDS-Related Opportunistic Infections↗

[Chlamydia pneumoniae infection and Mycoplasma pneumoniae infection in pediatric patients].

We evaluated a total of 1104 pediatric patients with acute lower respiratory tract infection for C. pneumoniae infection and M. pneumoniae infection by serology during July 1995 to December 1998. A microimmunofluorescence test was used for diagnosis of C. pneumoniae infection and a high density particle agglutination test for that of M. pneumoniae infection. Acute C. pneumoniae infection was found in 149 patients (13.5%), acute M. pneumoniae infection in 118 patients (10.7%), and dual infection in 27 patients (2.4%). Among 305 patients with pneumonia, M. pneumoniae infection (83 patients, 27.2%) was more common than C. pneumoniae infection (47 patients, 15.4%). However among 799 patients with bronchitis. C. pneumoniae infection (102 patients, 12.8%) was more common than M. pneumoniae infection (35 patients, 4.4%). Patients with C. pneumoniae infection were more younger and more frequently wheezing than patients with M. pneumoniae infection. These findings demonstrate that C. pneumoniae infection in very common pathogen of pediatric lower respiratory tract infection as M. pneumoniae infection in Japan.

Acute Disease↗

Treatments for symptomatic urinary tract infections during pregnancy.

BACKGROUND: Urinary tract infections, including pyelonephritis, are serious complications that can result in significant maternal and neonatal morbidity and mortality. There is a large number of drugs, and combination of them, available to treat urinary tract infections, most of them tested in non-pregnant women. Attempts to define the optimal antibiotic regimen for pregnancy has, therefore, been problematic. OBJECTIVES: The objective of this review was to try to determine, from the best available evidence from randomized control trials, which agent is most effective for the treatment of symptomatic urinary tract infections during pregnancy in terms of cure rates, recurrent infection, incidence of preterm delivery and premature rupture of membranes, admission to neonatal intensive care unit, need for change of antibiotic, and incidence of prolonged pyrexia. SEARCH STRATEGY: The Cochrane Pregnancy and Childbirth Group trials register, the Cochrane Controlled Trials Register and reference lists of articles were searched. SELECTION CRITERIA: All trials were considered where the intention was to allocate participants randomly to one of at least two alternative treatments for any symptomatic urinary tract infection. DATA COLLECTION AND ANALYSIS: Trial quality assessment and data extraction were performed by the two reviewers. MAIN RESULTS: Five studies were included. There were no significant differences between studied treatments with regard to cure rates, recurrent infection, incidence of preterm delivery and premature rupture of membranes, admission to neonatal intensive care unit, need for change antibiotic and incidence of incidence of prolonged pyrexia. REVIEWER'S CONCLUSIONS: Although antibiotic treatment is effective for the cure of urinary tract infections, there are insufficient data to recommend any specific treatment regimen for symptomatic urinary tract infections during pregnancy. All of the antibiotics studied were shown to be very effective in decreasing the incidence of outcomes measured. Complications were very rare. All included trials had very small sample sizes to try to detect important differences between treatments. Future studies should evaluate the most promising antibiotics, in terms of class, timing, dose, acceptability, maternal and neonatal outcomes and costs.

Anti-Infective Agents, Urinary↗

The epidemiology of 2056 remote site infections and 1966 surgical wound infections occurring in 1865 patients: a four year study of 40,923 operations at Rush-Presbyterian-St. Luke's Hospital, Chicago.

Over a 4-year period 40,923 operations and 44,716 surgical admissions were monitored for both community and hospital onset infections. One thousand eight hundred sixty-five patients had 1966 surgical wound infections and 2056 remote infections including 1652 hospital onset and 404 community onset infections. One thousand one hudnred forty-four patients with multiple infections averaged 40 days in the hospital contrasted with 24 days for 721 patients with a single wound infection. The total excess cost of hospitalization for these patients was $951,150. A statistically significant reduction occurred for urinary tract infections, lower respiratory infections and clean and contaminated surgical wound infections. It is suggested that these are all inter-related and a significant reduction in surgical wound infections can be achieved through control of infections at remote sites, particularly those associated with medical devices. The coagulase positive staphylococcus is still the most important single bacterial species in the primary etiology of surgical wound infections. When the gastrointestinal tract is entered or "supra" infecting organisms appear, gram negative bacteria and mixed gram negative and gram positive infections are dominant. Reduction in remote site infections occurring in surgical patients is necessary to reduce the incidence of surgical wound infections, suggest preventive and control measures, and document the effectiveness of such measures.

Adolescent↗