Hantavirus pulmonary syndrome (HPS) is caused by multiple closely related hantaviruses that have been identified in the western United States and, sporadically, in the eastern United States, Canada and several South American countries. SPH is characterized by a feverish prodrome that leads to the rapid onset of non-cardiogenic pulmonary edema and hypotension or shock. Sporadic cases in the United States caused by related viruses may present renal involvement. In Argentina and Chile, the picture sometimes consists of digestive hemorrhage. Nosocomial transmission has only been documented in this geographic region.
Hantaviruses are a genus of the Bunyaviridae family, consisting of lipid-enveloped viruses and a single-stranded RNA genome consisting of three unique segments. Several pathogenic viruses have been identified within the genus, such as the Hantaan virus , which causes the most severe variant of haemorrhagic fever with renal syndrome (FHSR), present mainly in continental Asia; The Dobrava virus ,
Which also produces a very severe form of FHSR, observed mainly in the Balkans; The Puumala virus responsible for an
A who can affect the pulmonary syndrome
People with pulmonary syndrome usually have a history of recent outdoor stays, or of residence in an area with large populations of field mice. Groups of cases have occurred among people who have cleaned houses infested by rodents. P. maniculatus is one of the most common mammals in North America and, wherever it is found, is usually the dominant member of the rodent community.
About half the cases appear between May and July. The patients belong almost exclusively to the age group of 12-70 years; 60% of them are 20-39 years old. Sporadic cases have been reported in children younger than 12 years. Two-thirds of those affected are males, which probably reflects more outdoor activities. It is not known whether the almost complete absence of disease in young children reflects an innate resistance or simply a lack of exposure. Evidence of human-to-human transmission has been obtained in Argentinean epidemics.
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Hantaviruses do not cause a symptomatic disease in their reservoir hosts, which remain infected and have no symptoms throughout life. These infected rodents disseminate the virus with saliva, urine and feces for many weeks, although the duration of this process and the period of greatest capacity for infection are unknown. The presence of infectious virus in the saliva, the sensitivity of these animals to parenteral inoculation of hantavirus, and observations of infected rodents field indicate that the bite is significant in transmission between these animals.
Infectious aerosols with saliva or rodent excreta have been implicated in the transmission of hantavirus to humans. Some visitors from areas with infected rodents have been infected after an exposure of only 5 minutes. Hantaviruses may spread through contaminated food and fissures in the skin or mucous membranes; Human contagion has occurred due to rodent bites . Transmission between people is very rare, but has been documented in Argentina.
Pulmonary syndromes are characterized by abrupt and very severe pulmonary edema, with anoxia and acute heart failure. The virus is present in the pulmonary capillaries, suggesting that pulmonary edema is a consequence of the attack of the T lymphocytes to capillaries infected by the. The severity of the disease is directly related to the titer of viremia during the acute phase.
The pulmonary syndrome is characterized by a prodrome and cardiopulmonary phase. The mean duration from the onset of prodromal symptoms to hospitalization is 5.4 days, and from the onset of symptoms to death is 8 days (median 7 days, with a range of 2-16 days). The prodromal symptoms most common are fever and myalgias (100%), cough and / or ladisnea (76%), gastrointestinal symptoms such as vomiting, diarrhea and periumbilical pain (76%) and headache (71%).
The cardiopulmonary phase begins with progressive cough and dyspnea. The most frequent initial physical signs are tachypnea (100%), tachycardia (94%) and hypotension (50%). In the most severe cases, acute progressive pulmonary edema occurs rapidly, Hypoxia and shock. Pulmonary vascular permeability is complicated by cardiogenic shock, associated with an increase in vascular resistance.
Clinical evolution in patients who die is characterized by pulmonary edema accompanied by marked hypotension, which usually ends with sinus bradycardia, electromechanical dissociation and tachycardia or fibrillation. Diagnosis
The diagnosis of pulmonary syndrome should be considered in a previously healthy patient. Presents with a prodrome febri
And acute respiratory distress. The combination of thrombocytopenia, febrile prodrome and exposure to the open air during the spring and summer months is very suggestive of HPS. The specific diagnosis of this disorder is established by serological tests that detect IgM antibodies against hantavirus. The hantavirus antigen can be detected in the tissues by immunohistochemistry and by amplification of the hantavirus nucleotide sequences, detected by the reverse transcriptase-polymerase chain reaction. Consult with the state health department or the Centers for Disease Control and Prevention for assistance in diagnosis, epidemiological research, and epidemic control.
They consist of leukocytosis (median, 26. 000 cells / μl), increased hematocrit (as a consequence of hemoconcentration), thrombocytopenia (median, 64,000 / ìl), prolongation of prothrombin and partial thromboplastin times, increased serum concentrations of lactate dehydrogenase, decreased protein Proteinuria and microscopic hematuria. Patients who die usually have disseminated intravascular coagulation, with frank hemorrhage and, exceptionally, leukocytosis.
The differential diagnosis of pulmonary syndrome should take into account adult respiratory distress syndrome, pneumonic plague, psittacosis, severe mycoplasma pneumonia , influenza, leptospirosis, inhalation anthrax, rickettsial infections, pulmonary tularemia, Atypical viral and bacterial pneumonia, legionellosis, meningococcemia and other sepsis syndromes. The key factor for the diagnosis of HPS is thrombocytopenia.
Patients with hantavirus infection need maintenance of adequate oxygenation, along with careful monitoring and support of cardiovascular function. The pathophysiology of HPS resembles that of the dengue shock syndrome (see Chapter 266). Inferential or inotropic drugs (such as dobutamine) should be administered in combination with adequate volume replacement to treat symptomatic hypotension or shock but without aggravating pulmonary edema.
Intravenous ribavirin has been shown to be of no utility in HPS, Although it may be helpful if administered in the early stages of FHSR.
Further information and advice on the treatment of pulmonary syndrome, control measures,
Diagnosis and collection of biohazardous samples from the Centers for Disease Control and Prevention, National Center for Infectious Diseases, Special Pathogens Branch, Atlanta, Forecasts.
In some geographic areas, mortality is about 50%. Severe hematocrit anomalies, leukocyte count, lactate dehydrogenase, partial thromboplastin time, and elevated viral load predict mortality with high specificity and sensitivity.
The avoidance of contact with rodents is the only preventive strategy, and its control in the home and its surroundings is fundamental. Prevention of barriers to health care as well as level 3 biosecurity centers and practices are recommended for laboratory manipulation of blood,