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Hantaviruses, members of the Bunyaviridae family, can cause two patterns of disease in humans, hantavirus hemorrhagic fever with renal syndrome (HFRS) and cardiopulmonary syndrome (HCPS), being the latter hegemonic on the American continent. Andesvirus is one of the strains that can cause HCPS and is endemic in Chile. Its transmission occurs through direct or indirect contact with infected rodents' urine, saliva, or feces and inhalation of aerosol particles containing the virus. HCPS rapidly evolves into acute but reversible multiorgan dysfunction. The hemodynamic pattern of HCPS is not identical to that of cardiogenic or septic shock, being characterized by hypovolemia, systolic dysfunction, and pulmonary edema secondary to increased permeability. Given the lack of specific effective therapies to treat this viral infection, the focus of treatment lies in the timely provision of intensive care, specifically hemodynamic and respiratory support, which often requires veno-arterial extracorporeal membrane oxygenation (VA-ECMO). This narrative review aims to provide insights into specific ICU management of HCPS based on the available evidence and gathered experience in Chile and South America including perspectives of pathophysiology, organ dysfunction kinetics, timely life support provision, safe patient transportation, and key challenges for the future., Competing Interests: Declaration of competing interest The authors declare that they have no competing interests., (Copyright © 2024 Elsevier Inc. All rights reserved.)

In 1993, the Southwest found itself staring down a disease then known as "unexplained adult respiratory syndrome." During the outbreak, 12 of 23 known patients died. What we now recognize as hantavirus cardiopulmonary syndrome still remains a rare and deadly disease. Although no cure exists, modern supportive techniques such as extracorporeal membrane oxygenation have increased survival among these patients. Early diagnosis has become the primary factor in patient survival. The initial presentation of hantavirus is similar to acute respiratory distress syndrome, necessitating a high index of suspicion to afford the patient the best chance of survival. Diagnosis is further complicated by prolonged and nonspecific incubation periods making it difficult to pinpoint an exposure. Familiarizing oneself with common clinical presentations, diagnostic strategies, and testing is the best way to increase patient survival. Because hantavirus has a predilection for rural areas, transport to a tertiary facility is paramount to provide the resources necessary to care for these complex patients. Rapid sequence intubation, although common in airway-compromised patients, could prove fatal in the setting of the severe hemodynamic instability found in hantavirus cardiopulmonary syndrome. Anticipation of significant pressor use and fluid administration could likely mean the difference in patient mortality during transport., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Published by Elsevier Inc.)

Hantaviruses are tri-segmented lipid-enveloped RNA viruses belonging to the Bunyaviridae family. Human infection corresponds to a zoonosis associated with two different clinical syndromes: hemorrhagic fever with renal syndrome that occurs in Asia and Europe and hantavirus cardiopulmonary syndrome (HCPS) that occurs in the North America, Central America and South America. The major pathogenic mechanisms in HCPS include (1) direct microvascular endothelial injury leading to increased capillary permeability and the development of noncardiogenic pulmonary edema and acute respiratory distress syndrome, and (2) exaggerated host immune response leading to secondary organ damage. The incubation period for this disease is quite long (6-39 days, median: 18 days); however, rapid progression to respiratory failure and shock can occur highlighting the importance of high index of clinical suspicion. Management revolves around high-quality supportive care. Various management and preventative strategies are currently being explored and warrant further examination to improve the overall outlook following infection with hantavirus., Competing Interests: None declared., (Thieme. All rights reserved.)

Two related hyperinflammatory syndromes are distinguished following infection of humans with hantaviruses: haemorrhagic fever with renal syndrome (HFRS) seen in Eurasia and hantavirus pulmonary syndrome (HPS) seen in the Americas. Fatality rates are high, up to 10% for HFRS and around 35%-40% for HPS. Puumala virus (PUUV) is the most common HFRS-causing hantavirus in Europe. Here, we describe recent insights into the generation of innate and adaptive cell-mediated immune responses following clinical infection with PUUV. First described are studies demonstrating a marked redistribution of peripheral blood mononuclear phagocytes (MNP) to the airways, a process that may underlie local immune activation at the site of primary infection. We then describe observations of an excessive natural killer (NK) cell activation and the persistence of highly elevated numbers of NK cells in peripheral blood following PUUV infection. A similar vigorous CD8 Tcell response is also described, though Tcell responses decline with viraemia. Like MNPs, many NK cells and CD8 T cells also localize to the lung upon acute PUUV infection. Following this, findings demonstrating the ability of hantaviruses, including PUUV, to cause apoptosis resistance in infected target cells, are described. These observations, and associated inflammatory cytokine responses, may provide new insights into HFRS and HPS disease pathogenesis. Based on similarities between inflammatory responses in severe hantavirus infections and other hyperinflammatory disease syndromes, we speculate whether some therapeutic interventions that have been successful in the latter conditions may also be applicable in severe hantavirus infections., (© 2019 The Authors. Journal of Internal Medicine published by John Wiley & Sons Ltd on behalf of Association for Publication of The Journal of Internal Medicine.)

Hantavirus cardiopulmonary syndrome is characterized by pulmonary capillary leakage and alveolar flooding, resulting in 50% mortality due to fulminant hypoxic respiratory failure. In addition, depression of cardiac function ensues, which complicates the picture with cardiogenic shock. Early diagnosis and appropriate use of extracorporeal membrane oxygenation (ECMO) are amongst the lifesaving interventions in this fatal illness. However, a recent case report demonstrates that implementation of high volume continuous hemofilteration along with protective ventilation reverses the cardiogenic shock within few hours in hantavirus infected patients. This review article is focused on the recent advances in clinical features, diagnosis, management, epidemiology, and pathogenesis of hantavirus induced cardiopulmonary syndrome. It provides information for clinicians to help in correct diagnosis during the early stages of viral infection that could improve the prognosis of this viral illness., (© 2018 Wiley Periodicals, Inc.)

In Germany Puumala virus (PUUV), known to cause mild forms of hemorrhagic fever with renal syndrome (HFRS), is the predominating endemic hantavirus. We herein describe an unusually severe case of a PUUV infection that occurred in summer 2015 in South Eastern Germany in a region known to be endemic for PUUV since over ten years. A 54-year-old female gardener was admitted to hospital with fever, cough and dyspnea. Within 48hours the patient developed a rapid progressive adult respiratory distress syndrome (ARDS) with circulatory failure and required ECMO (extracorporeal membrane oxygenation) treatment. Serological and molecular biological examinations of serum samples confirmed an infection with PUUV. Partial sequences of the S- and M-segment clustered to a strain previously described in South Eastern Germany. Our reported case highlights, that in rare incidents PUUV can cause hantavirus cardiopulmonary syndrome, a syndrome that is usually found after infections with New World hantaviruses, and neurological symptoms., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Hantavirus cardiopulmonary syndrome has a high mortality rate, and early connection to extracorporeal membrane oxygenation has been suggested to improve outcomes. We report the case of a patient with demonstrated Hantavirus cardiopulmonary syndrome and refractory shock who fulfilled the criteria for extracorporeal membrane oxygenation and responded successfully to high volume continuous hemofiltration. The implementation of high volume continuous hemofiltration along with protective ventilation reversed the shock within a few hours and may have prompted recovery. In patients with Hantavirus cardiopulmonary syndrome, a short course of high volume continuous hemofiltration may help differentiate patients who can be treated with conventional intensive care unit management from those who will require more complex therapies, such as extracorporeal membrane oxygenation.

Objectives: To review the literature on extracorporeal life support (ECLS) during pregnancy to determine its efficacy and safety for the mother and fetus., Methods: A comprehensive literature search was obtained from MEDLINE via PubMed.gov and from ScienceDirect.com using the following search queries: ECLS and pregnancy, extracorporeal membrane oxygenation (ECMO) and pregnancy, ECMO and H1N1 influenza, acute respiratory distress syndrome (ARDS) and pregnancy, pregnancy and H1N1 influenza, and Extracorporeal Life Support Organization registry., Results: Our literature search produced 332 articles for review. A total of 45 patients treated with ECLS or ECMO during pregnancy were reported in 26 publications. Postpartum patients were not included. Indications for ECLS were severe H1N1 influenza with ARDS (n = 33), other ARDS (n = 8), cardiogenic shock (n = 3), and cardiac arrest (n = 1). The mean gestational age was 26.5 weeks (range, 12-38 weeks), and the median duration of ECLS was 12.2 days (range, 1-57 days). The survival rate was 77.8% (35 of 45) for mothers and 65.1% (28 of 43) for fetuses. In addition, we report a 25-year-old pregnant patient with hantavirus cardiopulmonary syndrome unresponsive to pressors and inotropes. The patient was placed on venoarterial ECMO for 72 hours, recovered without complications, and delivered a healthy infant. The mother and son remain asymptomatic 6 years later., Conclusions: ECLS during pregnancy is effective and relatively safe for the mother and fetus. The first successful use of ECLS in a pregnant patient with life-threatening hantavirus cardiopulmonary syndrome is being reported together with this review., (Copyright © 2016 The American Association for Thoracic Surgery. Published by Elsevier Inc. All rights reserved.)

Objective: The aim of the study was to evaluate the outcome of extracorporeal membrane oxygenation (ECMO) support in Hantavirus cardiopulmonary syndrome (HCPS) patients with a predicted mortality of 100%, and the complications associated with this treatment modality and different cannulation techniques., Methods: A total of 51 patients with refractory HCPS were supported with ECMO between April 1994 and June 2010. They were divided into group A consisting of the 26 patients treated between 1994 and 2000 and group B consisting of 25 patients treated between 2003 and 2010. No patients were treated between September 2000 and December 2003. Patients in group A were intubated when they became hypoxic and placed on ECMO when they became hemodynamically unstable, whereas patients in group B had elective insertion of vascular sheaths and were almost concurrently intubated and placed on ECMO when they decompensated. Cannulation of the femoral vessels was performed percutaneously in 18 (35.3%) patients and with an open technique in 33 (64.7%) patients., Results: Complications from percutaneous cannulation occurred in 4/18 (22.27%) patients: retroperitoneal hematoma in 2/18 (11.1%) and lower-extremity ischemia in 2/18 (11.1%) patients. Complications from open femoral cannulation occurred in 12/33 (36.3%) patients: bleeding in 10/33 (30.3%) patients and ischemia in 2/33 (6.1%) patients. The overall survival was 66.6% (34 of 51 patients); 56% (14/26) for group A and 80% (20/25) for group B (p = 0.048). There was no difference in mortality regarding the method of cannulation. A trend toward increased mortality in patients with cannulation complications was recognized, but it was not statistically significant. Mortality was not associated with ECMO duration (average 121.7h, range: 5-276h). All survivors recovered and were discharged from the hospital after a mean hospital stay of 19.8 days (range: 10-39 days)., Conclusions: Two-thirds of 51 HCPS patients with a predicted mortality of 100%, who were supported with ECMO, survived and recovered completely. Survival was significantly higher in the second half of the study. Complications associated with both types of femoral cannulation were associated with a trend toward decreased survival, which was not significant., (Copyright © 2011 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.)

On April 25, 2011, the Maine Center for Disease Control and Prevention was notified of a suspected case of hantavirus pulmonary syndrome (HPS) in a man aged 70 years with no recent out-of-state travel. The Maine resident went to a community hospital in early April with a 5-day history of fatigue, decreased appetite, weakness, chills, myalgias, and progressive shortness of breath. On examination, he was hypoxic and tachypneic. The patient was admitted with laboratory evidence of acute renal insufficiency, leukocytosis and thrombocytopenia, and appearance of diffuse bilateral infiltrates on chest radiograph. Two days later, he was transferred to a tertiary-care facility for management of respiratory failure with hypoxemia and worsening renal insufficiency. The next day, he was intubated and mechanically ventilated. Serum specimens demonstrated high titers of hantavirus reactive immunoglobulin M (1:6,400) and immunoglobulin G (1:1,600) antibodies. Hantavirus RNA was detected in the patient's blood. The patient was discharged to a skilled nursing facility 1 month after admission and is recovering with extensive rehabilitation.

Hantavirus pulmonary syndrome, also known as hantavirus cardiopulmonary syndrome, is a recently described infectious syndrome found throughout the Americas. Although infection is sporadic and uncommon compared with other atypical pneumonia syndromes, its high mortality rate warrants the maintenance of a high index of suspicion in rural settings. Because no specific therapies are available for the disease, prevention and early recognition play an important role in reducing mortality from the disease. This article reviews the nature of the viruses that cause hantavirus pulmonary syndrome, the epidemiology and ecology of disease transmission, and disease recognition, treatment, and prevention., (Copyright 2010 Elsevier Inc. All rights reserved.)

In 1978, hantaviruses were first described as the etiological agent of hemorrhagic fever with renal syndrome (HFRS) in Korea. Since then, numerous related, enveloped, negative-stranded RNA viruses have been identified, forming the genus Hantavirus within the family Bunyaviridae. These pathogens are distributed worldwide and thus can be classified, on the basis of phylogenetic origins, into Old World viruses or New World viruses (ie North, Central, and South America). Similarly, these viruses cause two major types of syndromes, corresponding respectively to their phylogenies: the original HFRS or the more recently described hantavirus pulmonary syndrome (HPS). As the hantavirus pulmonary syndrome is the primary hantaviral disease in North America, it will thus be the focus of this review.

The ability to diagnose and treat infectious diseases and handle infectious disease outbreaks continues to improve. For the most part, the major plagues of antiquity remain historical footnotes, yet, despite many advances, there is clear evidence that major pandemic illness is always just one outbreak away. In addition to the HIV pandemic, the smaller epidemic outbreaks of Legionnaire's disease, hantavirus pulmonary syndrome, and severe acute respiratory syndrome, among many others, points out the potential risk associated with a lack of preplanning and preparedness. Although pandemic influenza is at the top of the list when discussing possible future major infectious disease outbreaks, the truth is that the identity of the next major pandemic pathogen cannot be predicted with any accuracy. We can only hope that general preparedness and the lessons learned from previous outbreaks suffice.

Introduction: A 14-year-old boy with cardiorespiratory failure was referred for air medical transport. The complexity of care during air medical transport and subsequent diagnosis of hantavirus warranted a post hoc review of the literature to establish optimal transport management criteria., Methods: This is a case report and literature review, defining epidemiology, presentation, cause of pulmonary edema and cardiac failure, management, and outcome., Results: Hantavirus cardiopulmonary syndrome is rare in children. Severe cases have manifestations similar to those seen in adults: atypical pneumonia progresses to respiratory failure with severe pulmonary edema and associated circulatory compromise. Mechanical ventilation, judicious fluid replacement, and early inotropic therapy are central to transport management. Critical care may require extracorporeal membrane oxygenation (ECMO). Mortality remains high, although it appears to be lower in children younger than 14 years., Conclusion: Hantavirus infection commonly progresses to a cardiopulmonary syndrome, in which mortality is high. Optimal management includes: early suspicion/recognition based on characteristic clinical course and history; provision of oxygen and comprehensive ventilatory support; judicious fluid replacement; early and intensive inotropic therapy; prompt referral to an appropriate level of care; skillful interfacility transport. Definitive care can involve ECMO.

Viruses in the genus Hantavirus can cause one of two serious illnesses when transmitted from rodents to humans: hemorrhagic fever with renal syndrome (HFRS) or hantavirus pulmonary syndrome (HPS). Of the two diseases, HPS is more severe with an approximate 40% mortality across the Americas. The high rate of mortality could be reduced if effective therapeutics could be discovered for treatment of this illness. Herein we review approaches being explored for the discovery of therapeutics for HPS and how they could be employed in treatment and prevention of disease.

Objective: The purposes of this study are to evaluate the outcome of extracorporeal membrane oxygenation support in a subgroup of patients with Hantavirus cardiopulmonary syndrome who had a predicted mortality of 100% and to assess the complications associated with this treatment modality and with different cannulation techniques., Methods: Thirty-eight patients with severe Hantavirus cardiopulmonary syndrome were supported with extracorporeal membrane oxygenation between April 1994 and June 2006. Cannulation of the femoral vessels was performed on an emergency basis by a percutaneous approach in 15 (39.5%) and by an open technique in 23 (60.5%) patients. Duration of extracorporeal membrane oxygenation averaged 132 hours (range: 5-276 hours)., Results: Complications from percutaneous cannulation occurred in 4 (26.6%) of 15 patients: retroperitoneal hematoma in 2 (13.3%) and lower extremity ischemia in 2 (13.3%) patients, which resolved after insertion of a distal perfusion cannula. Complications from open femoral cannulation occurred in 8 (34.8%) of 23 patients: severe bleeding in 7 (30.4%) patients and lower extremity ischemia in 1 (4.3%) patient who required a leg amputation. The overall survival was 60.5% (23/38 patients). Six (40%) of the 15 patients cannulated percutaneously and 9 (39.1%) of 23 patients who had open cannulation died. All survivors recovered completely and were discharged from the hospital after a mean hospital stay of 20.8 days (range: 10-39 days)., Conclusions: Almost two thirds of the patients with severe Hantavirus cardiopulmonary syndrome who were supported with extracorporeal circulation survived and recovered completely. The complications associated with both types of femoral cannulation may be attributed to the fact that all patients were in shock or in full cardiac arrest, and the procedure had to be done expeditiously. Earlier institution of extracorporeal membrane oxygenation may decrease the complication rates and improve the overall survival.

Hantavirus cardiopulmonary syndrome (HCPS) is caused by infection with multiple types of hantaviruses throughout the Americas. All strains induce a pulmonary capillary leak syndrome with cardiogenic shock in severe cases, and almost all strains have an overall mortality rate of 35%. Some strains in South America are commonly associated with either mild disease without pulmonary edema or severe disease with pulmonary hemorrhage. Early recognition during the thrombocytopenic prodrome phase and transport to intensive care improve survival, due to very rapid progression of respiratory failure and shock in some patients. Limited fluid replacement, early inotropic therapy, and mechanical ventilation also improve survival. Extracorporeal membrane oxygenation (ECMO) has been life saving for patients with refractory shock. Ribavirin does not appear to reduce mortality, but hyperimmune serum offers a promising future therapy because survival is correlated with higher neutralizing antibody titers at admission.

Hantavirus cardiopulmonary syndrome (HCPS) is associated with rapid cardiopulmonary collapse from endothelial injury, resulting in massive capillary leak, shock and severe hypoxemic respiratory failure. To date, treatment remains supportive and includes mechanical ventilation, vasopressors and extracorporeal membrane oxygenation, with mortality approaching 50%. Two HCPS survivors initially given drotrecogin alpha (activated) (DAA) for presumed bacterial septic shock are described. Vasoactive medications were required for a maximum of 52 h, whereas creatinine levels and platelet counts normalized within seven to nine days. Given the similar presentations of HCPS and bacterial septic shock, empirical DAA therapy will likely be initiated before a definitive diagnosis of HCPS is made. Further observations of DAA in HCPS seem warranted.

The medical records of 27 patients with hantavirus pulmonary syndrome were analyzed according to the need for invasive mechanical ventilation in relation to the following data up on hospital admission: age, gender, fever, cough, dyspnea, systolic arterial blood pressure, heart rate, levels of hemoglobin, hematocrit, leukocytes, lymphocytes, platelets, creatinine and arterial blood gases. The volume infused during the first 24 hours after admission, the use of inotropic agents, the use of corticosteroids and the patient outcomes were also evaluated. A favorable outcome was related to systolic blood pressure(3) 100 mmHg, heart rate lower than 100 beats per minute, creatinine below 1.6 mg/dl, arterial blood pH(3) 7.35, bicarbonate higher than 15 mEq/dl, oxygen saturation higher than 84.1%, lower rehydration volume in the first 24 hours of hospitalization and no use of inotropic agents. Absence of clinical and laboratory signs of circulatory shock up on admission was associated with a favorable outcome of the patients.

Reported here are two cases of hantavirus pulmonary syndrome caused by Puumala virus infection, which rapidly resolved after initiation of corticosteroid treatment combined with continuous veno-venous hemodiafiltration. These cases emphasize the role of the inflammatory response in the pathogenesis of hantavirus pulmonary syndrome.

Sin Nombre virus (SNV), an emerging pathogen in the United States, was identified in 1993. This hantavirus, a member of the Bunyaviridae family of RNA viruses, is transmitted by its reservoir host Peromyscus maniculatus, the deer mouse. Transmission is by inhalation of aerosolized feces, urine, or saliva from the infected mice. The illness that pursues, hantavirus pulmonary syndrome (HPS), is characterized initially by mild flu-like symptoms, followed by rapid progression to respiratory distress. There is no established therapeutic regimen and treatment is only supportive. Preventive methods include attempts to minimize contact with the rodents since elimination of the virus is not realistic.

Infectious febrile nephropathies, initially described as epidemics during military campaigns in Europe and Asia at the turn of the 20(th) century, were eventually all unified under the rubric of hemorrhagic fever with renal syndrome (HFRS) and ascribed to infection from rodent-borne hantaviruses. At the end of the century, hantavirus pulmonary syndrome (HPS) was described throughout the Americas as a consequence of infection with the New World hantaviruses. The epidemiology and clinical manifestations of these diseases are linked to the ecology of their associated rodent hosts. Murine rodents (Old World mice and rats) are associated with the severe forms of HFRS in Asia and the Balkans due to Hantaan, Dobrava, and Seoul viruses. Hantaan virus causes an estimated 50-100,000 infections a year in China alone. Arvicoline rodents (voles) are associated with a mild form of HFRS in Europe called nephropathia epidemica due to Puumala virus. Sigmodontine rodents (New World rats and mice) are associated with approximately 200 HPS cases per year throughout the Americas caused by over a dozen viruses. The viruses are mainly transmitted as small-particle aerosols of rodent excreta, and the subsequent infections share cardiovascular shock as a prominent feature, although HFRS causes predominantly renal disease, while HPS causes a predominantly non-cardiogenic pulmonary edema - hemorrhage involvement varies in the syndromes on the basis of virus subtypes. Efforts are underway to refine prevention strategies, understand the pathogenesis of the shock, and identify therapeutic modalities.

Hantavirus pulmonary syndrome (HPS) is a severe cardiopulmonary illness most often caused by the Sin Nombre virus, which is transmitted to humans by inhalation of aerosolized particles of rodent excreta or direct rodent contact. Although HPS is more common in the western United States, cases have been identified in 31 states. The illness begins as a nonspecific febrile prodrome, sharing many of its initial symptoms with other more common viral infections. Patients then quickly develop noncardiogenic pulmonary edema, respiratory failure, and shock. Characteristic laboratory findings include thrombocytopenia, a left-shifted leukocytosis, hemoconcentration, and presence of immunoblasts. The overall case fatality rate of HPS is approximately 40 percent. Diagnosis is confirmed by serologic identification of IgM and IgG antibodies to Sin Nombre virus. There is no specific therapy, but early recognition of HPS during the prodromal phase can expedite initiating cardiopulmonary support in an intensive care unit, which is associated with improved survival rates. Prevention of HPS involves avoiding contact with rodents and rodent habitats.

Study Objectives: To describe the clinical features and laboratory abnormalities of 16 adults with confirmed Hantavirus pulmonary syndrome (HPS) due to Andes virus in Temuco, Chile., Design: A retrospective chart review abstracting clinical, radiologic, laboratory, and epidemiologic data., Setting: ICU of the university teaching hospital in Temuco, Chile., Patients: Sixteen patients with HPS treated between 1997 and 1999., Results: Patients were aged from 19 to 45 years, 82% were men, and 88% were farm or timber workers with occupational acquisition of HPS. After an incubation period ranging from 5 to 25 days, a prodromal influenza-like phase frequently was accompanied by abdominal symptoms. From 1 to 7 days later, respiratory insufficiency and hemodynamic instability suddenly appeared. In 81%, hemorrhage was evident; in 63%, moderate-to-severe bleeding occurred. The most prominent laboratory abnormalities were hemoconcentration, leukocytosis, thrombocytopenia, altered partial thromboplastin time (PTT), creatine kinase, transaminases, and hyponatremia. Creatinine elevation was common, with clinical importance in two patients. All patients had severe hypoxemia and pulmonary edema. Fifteen patients received supportive treatment, and 5 patients were treated with corticosteroids. The mortality rate was 43.8%., Conclusions: Bad prognostic factors appeared to be severe hypotension, lower PaO(2)/fraction of inspired oxygen values, prolonged PTT, hemorrhage, greater volume load, and profuse bronchorrhea. The effects of treatment with corticosteroids could not be determined. Hemorrhage and renal involvement were common in our patients, features not often described in the North American literature of Sin Nombre virus HPS.

Objective: Sin Nombre hantavirus (SNV) is the leading causative agent of hantavirus cardiopulmonary syndrome (HCPS) in the United States and Canada. Relatively few cases of HCPS have involved children. This report describes the clinical characteristics of a series of pediatric cases of SNV infection in the United States and Canada from 1993 through March 2000., Methods: We analyzed clinical and laboratory data on 13 patients who were 85% of patients had elevated levels of serum aspartate aminotransferase, alanine aminotransferase, and hypoalbuminemia. Leukocytosis and hemoconcentration were seen in less than one third of patients at admission. HCPS developed in 12 of the 13 patients (92%), and 4 of those 12 died (33% case-fatality ratio). The majority of HCPS patients (8 of 12 [67%]) were critically ill and required mechanical ventilation. Extracorporeal membrane oxygenation was used in 2 patients, 1 of whom survived. An elevated prothrombin time (>/=14 seconds) at admission was predictive of mortality., Conclusions: Infection with SNV in children and adolescents causes HCPS with a clinical course and mortality rate similar to that described in adults. We believe that early recognition of HCPS in children and adolescents and appropriate referral to tertiary care centers that are experienced with HCPS are important in reducing mortality.

Invasive disease due to group A beta-hemolytic streptococci (GABHS) can be divided into 3 categories of disease: streptococcal toxic shock syndrome (strepTSS), necrotizing fasciitis, and other invasive GABHS disease. Patients with strepTSS may have multiorgan failure within hours of presentation. Clindamycin and penicillin G should be used in combination for treatment of invasive GABHS disease. The mortality rate for menstrual staphylococcal toxic shock syndrome has decreased with early recognition and treatment, and removal of hyperabsorbent tampons from the market. Kawasaki syndrome (KS) is the most common cause of acquired heart disease in children in the U. S., and atypical forms have a higher mortality rate than typical KS. Hantavirus pulmonary syndrome is a zoonosis with an 80% mortality rate if the diagnosis is not made on first presentation and patients return to the hospital in shock. Children and adolescents with Lyme disease have an excellent prognosis and respond well to antimicrobial therapy. Cat scratch disease (CSD) is caused by Bartonella henselae and is transmitted by flea-infested kittens. CSD lymphadenopathy typically resolves spontaneously in 2ñ3 months; however, there is a 50% likelihood of resolution in 1 month if patients receive a 5-day treatment course with azithromycin.

Objective: To describe our experience with the use of extracorporeal membrane oxygenation (ECMO) as a rescue therapy in adult patients with severe cardiopulmonary failure from Hantavirus pulmonary syndrome., Design: Case series., Setting: Tertiary referral center., Patients: Patients with confirmed Hantavirus infection, who developed severe cardiopulmonary failure in which conventional therapy was assessed as being unsuccessful., Interventions: Records of previous patients treated for Hantavirus pulmonary syndrome were reviewed and findings consistent with 100% mortality were found., Measurements and Main Results: Findings associated with a 100% mortality rate were a) cardiac index of <2.5 L/min/m2; b) serum lactate concentration of >4.0 mmol/L (normal range 0.0 to 2.2); c) pulseless electrical activity or ventricular fibrillation or ventricular tachycardia; and d) refractory shock despite fluid resuscitation, and vasoactive medications. From 1994 to 1996, seven patients were admitted with confirmed Hantavirus pulmonary syndrome and severe cardiopulmonary failure. Three of the seven patients had at least two of the four criteria for a 100% mortality rate listed above, and appeared to be failing optimal conventional therapy. These three patients received support with venoarterial ECMO. The first patient was placed on ECMO during cardiac arrest and died. The next two patients who received ECMO for Hantavirus pulmonary syndrome survived after relatively short, uncomplicated ECMO runs, and were discharged without complications., Conclusions: ECMO successfully provided cardiopulmonary support in two patients with severe Hantavirus pulmonary syndrome who survived with a good outcome. Our experience suggests that ECMO is a beneficial therapy for patients critically ill with Hantavirus pulmonary syndrome.

Hantavirus pulmonary syndrome is an acute, often fatal, febrile illness causing rapid pulmonary failure and cardiovascular instability. Since first described in 1993, considerable progress has been made in identifying the hantaviruses responsible for the disease and in defining its epidemiologic and diagnostic features.

The term atypical pathogens has been applied in recent years to Chlamydia pneumoniae, Mycoplasma pneumoniae, and the various species of Legionella. The incidence of pneumonia caused by these pathogens has increased with the development of specific diagnostic techniques. Atypical pathogen community-acquired pneumonia demonstrates a broad spectrum of severity from a mild disease not requiring hospitalization to adult respiratory distress syndrome necessitating mechanical ventilation. The clinical, radiological, and laboratory manifestations of the disease are similar to those of community-acquired pneumonia caused by other pathogens, and reliable etiological differentiation cannot be based on these factors alone. The possibility of shortening treatment time, at least in some patients, by antibiotic therapy with the new macrolides has been added to standard therapeutic regimens with erythromycin, tetracyclines, or quinolones.

The objective of this report is to summarize the medical literature relevant to the epidemiology, diagnosis, treatment, and control of hantavirus pulmonary syndrome (HPS). The English language literature was searched from January 1993 through March 1995, manually and using Medline, including conference proceedings and reference lists. We selected relevant articles on clinical aspects of HPS. HPS is a newly described illness that progresses through three phases: prodromal, cardiopulmonary, and convalescent. Its hallmark is the rapid progression from nonspecific prodromal symptoms to respiratory insufficiency caused by noncardiogenic pulmonary edema. Unlike other hantavirus infections, renal involvement and hemorrhagic manifestations are not dominant features in HPS. Treatment is based on close intensive care monitoring, oxygen, and cardiovascular support with inotropic and vasopressor drugs. Preventive measures include avoiding contact with rodents and their excrement. Peromyscus maniculatus is the primary rodent vector for the Sin Nombre virus, which caused the epidemic of HPS in the southwest United States in May 1993. HPS has a unique set of clinical findings and is caused by a genetically distinct hantavirus. Physicians and other health professionals should consider this disease when evaluating patients with unexplained respiratory insufficiency after a febrile prodrome, especially when history suggests possible rodent contact. Sporadic cases and possibly epidemics of HPS are likely in the future, particularly when ecological changes increase the population of infected rodent vectors in an area.

Hantavirus pulmonary syndrome (HPS) is a viral infection from a new strain of Hantavirus. The Hantavirus was first discovered in North America in 1993 after an outbreak of fatal illness on a Navajo Indian reservation in New Mexico. Since then, 122 cases of HPS (with a high mortality rate of more than 50%) have been reported in 23 states, with the highest prevalence in the Four Corners area. The reservoir for Hantavirus is small rodents, mostly field mice, vole, and chipmunks. It is transmitted through inhalation of airborne virus from dry rodent excreta and saliva. A North American strain of Hantavirus, named ain nombre virus (SNV), primarily affects the lungs, causing rapid accumulation of fluids and leading to noncardiogenic pulmonary edema, pleural effusion, and acute respiratory distress syndrome (ARDS). In the prodromal stage, HPS presents with flu-like symptoms, nausea, vomiting, and gastrointestinal pain and is often mistaken on the first visit for other infectious diseases or gastroenteritis. In the second acute stage, rapid respiratory deterioration begins: HPS is often misdiagnosed for pneumonia, idiopathic ARDS, and pulmonary edema. HPS treatment with an experimental antiviral intravenous drug, ribavirin, is under investigation. Practitioners must possess through clinical knowledge on the diagnoses, pathology, treatment, and course of the disease to reduce the mortality and morbidity rate of this rare but serious infection. A case report based on a recent HPS death in New York State on Long island in April 1995 is presented.

Emerging infections are defined as infections that are newly identified or recognized, or those whose incidence in humans has significantly increased over the past 20 years. The interaction of several factors contributes to the emergence of infectious disease, including changes in human behavior, technological advances, economic development, increased international travel, microbial adaptation and lapses in public health measures. Biomedical research has allowed us to identify and classify previously uncultured pathogens, characterize microbial virulence factors, create new diagnostic tests and develop vaccines. Here, we highlight a few emerging infections and illustrate the role that molecular medicine has played in furthering our understanding of these diseases.

Only months after the first report of a brief prodromal illness followed by rapidly progressive noncardiogenic pulmonary edema and death, the causative agent was tentatively identified as a previously unknown hantavirus. Although hantaviral infections are well known in Asia, none had ever been reported in the United States. A collaborative effort between local, state, regional, and federal authorities allowed rapid identification of a new set of clinical and laboratory findings, now known as the hantavirus pulmonary syndrome. Inclusion, exclusion, and confirmatory criteria have been established to help identify potential cases. However, tests for the infection are still experimental, so physicians should send samples to the Centers for Disease Control and Prevention for testing in suspected cases. Ribavirin (Virazole) may be beneficial early in the course of hantavirus pulmonary syndrome, and supportive care is essential. Rodents, particularly the deer mouse in the Southwest, are the natural hosts for the hantaviruses. Prevention of this new syndrome centers on avoidance of contact with and inhalation of saliva, urine, and feces of infected rodents.