Management of Hantavirus Cardiopulmonary Syndrome in Critical Care Transport: A Review.

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.

Proteinuria in Hantavirus Cardiopulmonary Syndrome: A Frequent Finding Linked To Mortality.

OBJECTIVES: To determine the relative frequency and prognosis value of proteinuria in hantavirus cardiopulmonary syndrome (HCPS) due to Andes virus. METHODS: This observational analytical study prospectively obtained data from patients admitted to 12 health centers in nine Chilean cities between 2001 and 2018. Only patients with confirmed Andes virus HCPS and laboratory characterization that included qualitative proteinuria determination at admission were considered. RESULTS: The database involved 175 patients, 95 of them had a measurement of urine protein at the time of hospital admission. They were mainly male (71%) and the median age was 35 [22-47] years. Median duration of the febrile prodromal time was 5 [4-7] days. Hospital length of stay and hospital mortality rate were 10 [7-14] days and 21.1%, respectively. Seventy-three patients (77%) were identified with proteinuria at admission, which was associated with increased mortality rate (26% versus 5%, p=0.036) and the relative risk was 1.3 [1.1-1.6], p=0.002. CONCLUSIONS: Proteinuria is a frequent finding in patients with HCPS, which is associated with a higher mortality rate.

Hantavirus Infection with Renal Failure and Proteinuria, Colorado, USA, 2019.

In North America, hantaviruses commonly cause hantavirus pulmonary syndrome (HPS). Clinical descriptions of hantavirus-associated renal disease in the Americas are scarce. Herein, we discuss the case of a 61-year-old man whose predominant manifestations were acute kidney injury and proteinuria. Clinical recognition of renal signs in hantavirus infections can reduce risk for death.

Capillary leak-syndrome triggered by Maripa virus in French Guiana: case report and implication for pathogenesis.

BACKGROUND: We report hereby a severe case of Hantavirus Pulmonary Syndrome" (HPS) induced by Maripa virus in French Guiana and describe the mechanism of severity of the human disease. CASE PRESENTATION: A 47-year- old patient started presenting a prodromic period with fever, dyspnea, cough and head ache. This clinical presentation was followed by a rapid respiratory, hemodynamic and renal failure leading to admission in the ICU. Biological exams revealed an increased haematocrit level with a paradoxical low protein level. Echocardiographic and hemodynamic monitoring showed a normal left ventricular function with low filling pressures, an elevated extravascular lung water index and pulmonary vascular permeability index. These findings were compatible with a capillary leak-syndrome (CLS). CONCLUSIONS: The severity of HPS caused by the virus Maripa in French Guiana can be explained by the tropism of hantavirus for the microvascular endothelial cell leading to a CLS.

EVALUATING THE IMPACTS OF COINFECTION ON IMMUNE SYSTEM FUNCTION OF THE DEER MOUSE ( PEROMYSCUS MANICULATUS) USING SIN NOMBRE VIRUS AND BARTONELLA AS MODEL PATHOGEN SYSTEMS.

: Simultaneous infections with multiple pathogens can alter the function of the host's immune system, often resulting in additive or synergistic morbidity. We examined how coinfection with the common pathogens Sin Nombre virus (SNV) and Bartonella sp. affected aspects of the adaptive and innate immune responses of wild deer mice ( Peromyscus maniculatus). Adaptive immunity was assessed by measuring SNV antibody production; innate immunity was determined by measuring levels of C-reactive protein (CRP) in blood and the complement activity of plasma. Coinfected mice had reduced plasma complement activity and higher levels of CRP compared to mice infected with either SNV or Bartonella. However, antibody titers of deer mice infected with SNV were more than double those of coinfected mice. Plasma complement activity and CRP levels did not differ between uninfected deer mice and those infected with only Bartonella, suggesting that comorbid SNV and Bartonella infections act synergistically, altering the innate immune response. Collectively, our results indicated that the immune response of deer mice coinfected with both SNV and Bartonella differed substantially from individuals infected with only one of these pathogens. Results of our study provided unique, albeit preliminary, insight into the impacts of coinfection on immune system function in wild animal hosts and underscore the complexity of the immune pathways that exist in coinfected hosts.

A neuropathic pain syndrome associated with hantavirus infection.

Hantaviruses are a group of single-stranded RNA viruses of the Bunyaviridae family. "New World" hantaviruses cause hantavirus cardiopulmonary syndrome (HCPS) in North America. HCPS carries with it significant mortality and those patients who survive the disease are often left with substantial morbidity. Neurologic complications of hantavirus infections are rare, with only sparse cases of central nervous system involvement having been documented in the literature. To our knowledge, there are no reports of hantavirus infection contributing to peripheral nervous system dysfunction. Here we report a case of possible small fiber neuropathy associated with hantavirus infection, in a patient who survived HCPS. Persistent and treatment-resistant neuropathic pain may be a prominent feature in hantavirus-associated peripheral neuropathy.

A 44-Year-Old Man With Sore Throat and Fatigue After Using an Old Camper Van.

A 44-year-old man from Connecticut with no significant past medical history presented to the ED with a 2-week history of sore throat and fatigue, subsequently developing cough, dyspnea, fevers, and chills. The patient reported buying an old camper van and noticed a large infestation of rodent droppings, which he had cleaned thoroughly from the cabin. He used the camper van on several camping trips in Vermont, and symptoms started on his return.

Another case of "European hantavirus pulmonary syndrome" with severe lung, prior to kidney, involvement, and diagnosed by viral inclusions in lung macrophages.

Puumala virus (PUUV) is considered a classic Old World etiologic agent of nephropathia epidemica (NE), or hemorrhagic fever with renal syndrome (HFRS). HFRS is considered to be distinct from hantavirus (cardio-)pulmonary syndrome (HPS or HCPS), described in the New World. Here, we report a severe case, which fulfilled most, if not all, Centers for Disease Control and Prevention (CDC) criteria for HPS, needing non-invasive ventilation and subsequent acute hemodialysis. However, the etiological agent was PUUV, as proved by serological testing, real-time polymerase chain reaction (PCR), and sequencing. Viral antigen was detected by specific anti-PUUV immunostaining, showing, for the first time, greenish intracytoplasmic inclusions in bronchoalveolar lavage (BAL) macrophages. This case definitely confirms that HPS can be encountered during PUUV infections. Interestingly, special findings could render the diagnosis easier, such as greenish homogeneous cytoplasmic inclusions, surrounded by a fine clear halo in BAL macrophages. Therefore, although the diagnosis remains difficult before the onset of renal involvement, the occurrence of severe respiratory failure mimicking community-acquired pneumonia must alert the clinician for possible HPS, especially in endemic areas.

[Hantapulmonary syndrome].

Features of hantavirus pulmonary syndrome are considered in the review - zoonosis natural focal polyetiological viral infection, that is characterized by lung injury. Etiology of the disease, main characteristics of the agents, epidemiology, contagiousness, pathogenesis, clinical presentation of this pathology are examined. Laboratory diagnostics, therapy and prophylaxis ofhantavirus pulmonary syndrome are described.

Isolation of sochi virus from a fatal case of hantavirus disease with fulminant clinical course.

Sochi virus, a novel genetic variant of Dobrava-Belgrade virus, was isolated in cell culture from a fulminant lethal case of hantavirus disease presenting with shock and combined kidney and lung failure. Sochi virus is transmitted to humans from host reservoir Apodemus ponticus and must be considered a life-threatening emerging agent.

Hantavirus pulmonary syndrome.

Hantavirus pulmonary syndrome (HPS) is a severe disease characterized by a rapid onset of pulmonary edema followed by respiratory failure and cardiogenic shock. The HPS associated viruses are members of the genus Hantavirus, family Bunyaviridae. Hantaviruses have a worldwide distribution and are broadly split into the New World hantaviruses, which includes those causing HPS, and the Old World hantaviruses [including the prototype Hantaan virus (HTNV)], which are associated with a different disease, hemorrhagic fever with renal syndrome (HFRS). Sin Nombre virus (SNV) and Andes virus (ANDV) are the most common causes of HPS in North and South America, respectively. Case fatality of HPS is approximately 40%. Pathogenic New World hantaviruses infect the lung microvascular endothelium without causing any virus induced cytopathic effect. However, virus infection results in microvascular leakage, which is the hallmark of HPS. This article briefly reviews the knowledge on HPS-associated hantaviruses accumulated since their discovery, less than 20 years ago.

Hantavirus pulmonary syndrome: encephalitis caused by virus Andes.

Hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome (HPS) are rodent-borne emerging diseases caused by members of the genus Hantavirus, family Bunyaviridae. Some species of hantavirus may cause encephalitis, but this is the first report in Andes virus associated to HPS.

[Hantavirus infection associated to a staphylococcal sepsis. Report of one case]. / Hantavirus asociado a sepsis estafilocócica. Caso clínico.

We report a previously healthy 36-year-old mole who developed a pulmonary syndrome caused by Hantavirus infection. He was admitted to an intensive care unit in shock and respiratory failure and died four hours after admission. Blood cultures were positive for Staphylococcus aureus. This patient could be an index case that shows, for the first time, an association of Hantavirus Pulmonary Syndrome with Staphylococcus aureus infection similar to what happens with other viruses.

Hantavirus asociado a sepsis estafilocócica: caso clínico / Hantavirus infection associated to a staphylococcal sepsis: report of one case

We report a previously healthy 36-year-old mole who developed a pulmonary syndrome caused by Hantavirus infection. He was admitted to an intensive care unit in shock and respiratory failure and died four hours after admission. Blood cultures were positive for Staphylococcus aureus. This patient could be an index case that shows, for the first time, an association of Hantavirus Pulmonary Syndrome with Staphylococcus aureus infection similar to what happens with other viruses.

Hantavirus pulmonary syndrome coexistent with Dengue.

Dengue is an arthropod-borne disease caused by viruses of Flaviviridae family. It poses a major public health burden in tropical and sub-tropical regions. Clinical features of dengue vary from a mild flu-like disease and rash, to a potentially lethal haemorrhagic fever or shock syndrome. Hantavirus pulmonary syndrome is a rodent-born disease emerging in the American continent and is caused by viruses of the Bunyaviridae family. Potential reservoirs of these agents were described in Brazilian Central Plateau. Dengue infection is transmitted by mosquitoes, while hantaviruses are acquired by contact or inhalation of aerosolised excreta of infected rodents. Dengue and hantavirus infections have also been considered as emerging public health problems in some Indian areas; moreover, other infections mixed with dengue have been documented. The case of a Brazilian patient with hantavirus pulmonary syndrome and serologic evidence of dengue infection is described.

Hantavirus pulmonary syndrome in five pediatric patients - four states, 2009.

Hantavirus pulmonary syndrome (HPS) is a reportable infectious disease with a high case-fatality rate, transmitted to humans by exposure to rodents. Each year, 20--40 cases of HPS occur in the United States; cases in persons aged <17 years make up fewer than 7% of those cases, and cases in children aged <10 years are exceptionally rare. CDC received reports of five pediatric cases of HPS occurring during May 16--November 25, 2009, among children aged 6--14 years from Arizona, California, Colorado, and Washington. Three of the children were aged <10 years, and all five had exposure to rodents. This report summarizes the five cases, including the clinical findings and likely means of transmission of a hantavirus. Thrombocytopenia, elevated white blood cell (WBC) count, and pulmonary infiltrates were observed in all five children; elevated hematocrit was observed in three. One child died, and three of the four children who recovered required mechanical ventilation during hospitalization. Clinicians should consider HPS in the differential diagnosis for children with unexplained acute respiratory distress, especially if recent rodent exposure is noted. Public health agencies should promote preventive measures, including rodent control in housing and play areas, and children should be advised to avoid contact with rodents and areas of infestation.

Potential renal sequelae in survivors of hantavirus cardiopulmonary syndrome.

Although other hantaviruses are associated with renal manifestations, hantavirus cardiopulmonary syndrome (HCPS) has not been associated with such sequelae. The HCPS survivors were prospectively evaluated for renal complications. Subjects underwent yearly evaluation, laboratory studies, and 24-hour urine collection. Thirty subjects were evaluated after recovery from HCPS with the first follow-up at a median of 7.4 months after discharge. Subjects were a wide age range (18-51) but had an equal gender composition. Eighteen of 30 (60%) returned for > 1 evaluation. Half (15/30) had a 24-hour urine collection with > 150 mg of total protein and 6 had > 300 mg. Seven had a Cockcroft-Gault creatinine clearance (CrClCG) < 90 mL/min/1.73 m2 and 2 were < 60. Fifty-three percent met the definition of chronic kidney disease. Those treated with extracorporeal membrane oxygenation had less renal sequelae (P = 0.035). Our data suggest that renal sequelae may occur in HCPS. Further study of renal complications of New World hantavirus infections are needed.