hantavirus cardiopulmonary syndrome viruses

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  • Feb 18, 2020

CDC - Hantavirus Pulmonary Syndrome (HPS) - Hantavirus
CDC – Hantavirus Pulmonary Syndrome (HPS) – Hantavirus

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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-.

Sami M. Akram; Ben Huang

Last update: May 14, 2019 ..

Hantaviruses is a genus of, negative sense single-stranded RNA virus in Bunyaviridae family. Usually infect mice. Hantavirus causing pulmonary syndrome (HVPS) in the United States and causes hemorrhagic fever with renal syndrome (HFRS) in other parts of the world, especially Europe and East Asia (China, Russia, and Korea).

Hantaan is a river in Korea where the virus was first identified in this genus in 1976. This virus causes hemorrhagic fever Korea American troops fought in the Korean war in the 1950s. The first outbreak was reported on US soil from the four corners region of the native Indian tribes in 1993. In this the four corners of the southwestern United States, Arizona, New Mexico, Colorado, and Utah come together. The first patient was a woman, who presented with acute onset of dyspnea and was found to have diffuse bilateral infiltrates. He autopsy showed that the lungs are twice the weight of a normal lung for her age. During the evaluation of the outbreak, all the victims were found to have exposure to deer mice. There is no transmission from person to person during this outbreak. Health care workers who resuscitated the patient is not infected. American species of hantavirus, which causes outbreaks in the four corners was eventually named Sin Nombre hantavirus.

Hantaviruses enveloped RNA virus is 80 nm to 120 nm. This genome is divided into three segments. Large segments (L) coding for viral transcriptase, medium (M) segment coding for the glycoprotein of capsules and small segments (S) coding for a protein of the virus nucleocapsid.

There are several species of hantavirus causes hantavirus pulmonary syndrome (HPS) is also known as hantavirus cardiopulmonary syndrome (HCP). The host for Sin Nombre hantavirus are deer mice (Peromyscus maniculatus) was found in a rural area along the Mississippi River. New York virus associated with white foot mouse (Peromyscus leucopus). The other hantaviruses are Black Creek Canal virus, Bayou virus with the main host of the wild rat rat family.

Since 1995, hantavirus pulmonary syndrome is a disease were reported, and in 2015 the non hantavirus pulmonary disease made are reported as well. In the United States, most cases occur west of the Mississippi River, but overall 36 countries have reported cases of hantavirus pulmonary syndrome. In 2001, there were 255 cases reported by the United States. Brazil has the highest number of cases. The cases of South America exceeds the number of cases in North America. The countries with the most cases are Brazil, Argentina, and Chile.

In the United States, most cases of hantavirus infection have occurred as a pandemic, most recently in Yosemite National Park among the visitors to the park during the months of July August 2012.

transmission occurs with exposure to dirt dry aerosol and urine of rodents from the family of mice, which are the main reservoir in nature.

transmission from person to person has noted in outbreaks in Argentina due to the Andes virus in 1996. The health care workers, including five doctors got infected during an outbreak of Andes virus. A review of cases with well-defined exposure of the registry indicates that the incubation period of hantavirus pulmonary syndrome was 9 to 33 days (median 14 to 17 days). Such as person-to-person transmission has not been reported with Sin Nombre or other species of Hanta virus.

In the whole world, hantaviruses infect humans about 30,000 per year and causes hemorrhagic fever with renal syndrome (HFRS).

There is no ideal model for the study of hantavirus infections that lead to hantavirus pulmonary syndrome. In the rhesus monkey model of recently described, Sin Nombre virus causes hantavirus pulmonary syndrome as a disease characterized by low platelets, leukocytosis, and a rapid onset of respiratory distress due to interstitial pneumonia. The first clinical picture of infection in this model is coughing, tachypnea and respiratory crackles. The initial onset of symptoms occurred on day six, but the overall range is 14 to 16 dayss. Within 72 hours of the onset of respiratory symptoms, there are acute respiratory failure with severe multilobar right ventricle pulmonary infiltrates and pleural effusion due to heart failure. Nasal, oral, and rectal swabs were consistently negative for viral RNA even at peak infection. This suggests that unlike the Andean species, Sin Nombre virus is not transmitted from person to person. While swabs to negative, viremia is shown in the model infected before the onset of respiratory symptoms with an average of two days.

The virus causes cytokines dominated by pro-inflammatory (Th1 / Th2 cytokines, IFN-g, IL-1beta, IL-6, IL-18 and IL-13) release in the model ape and recorded around 12 days post-infection. Release anti-inflammatory cytokines (IL-1 receptor antagonist, IL-15 and GM-CSF) occurs when the respiratory symptoms are present. Neutrophilia with a left shift present in the model are infected, which is like an infection hantavirus pulmonary syndrome in humans. In humans, neutrophilia with a left shift support the diagnosis of hantavirus pulmonary syndrome. Interestingly, one can see a mixed pattern (viruses and bacteria) in the complete blood count (CBC) with an increase in atypical lymphocytes and increased band, and overall normal white blood cells (WBC). polymorphonuclear cells may or may not increase.

There was no increase in D-dimer in monkey models. In human infections, however, are usually normal prothrombin time; Studies in humans have shown that infection of tissue plasminogen activator (tPA) lifted

host response :. Immunoglobulin M (IgM) produced by the host initially followed by immunoglobulin G (IgG) antibodies. Immunoglobulin E (IgE) antibodies were also found and foremost, contribute to host defense against infection Hanta virus.

Immune complexes lining the red blood cells and platelets. Thrombocytopenia is often recorded on CBC human hantavirus pulmonary syndrome infection.

The test becomes abnormal liver injury late in the disease and reflect the final stage in the natural history of the disease.

While there is an infection of endothelial spread of various tested in this model organs (heart, kidney, spleen, and liver), cytokine responses were dominant in the lungs that is suggestive of the compartmentalization of the immune response is recorded in hantavirus man syndrome lungs. The hantaviruses capable of preferentially enters endothelial cells, and immunohistochemical studies showed hantavirus nucleic acids in lung endothelial cells and macrophages. Recently decay accelerating factor, and CD55 receptors on endothelial cells has been identified as a co-factor required for attachment and entry of hantavirus in human endothelial cells. Differences co-factors may explain the different clinical manifestations (hantavirus pulmonary syndrome and hemorrhagic fever with renal syndrome of hantaviruses). Hanta virus is able to multiply in the endothelial cells without causing visible cytopathic effects and injury in in-vitro models.

There is a functional disorder of the vascular endothelium to dilate the capillaries. Direct mechanism for vascular endothelial injury needs further explanation.

In the early stages, lung histology showed multifocal thickening of the alveolar septa by edema, macrophages, fibrin, and some neutrophils. There is very little debris cellular, membrane thickness, and some type II pneumocytes reparative. Type I pneumocyte whole process in its early stages, and there is minimal external injury to the endothelium. This is in contrast with the histologic findings of diffuse alveolar damage, where there is extensive cellular debris, demolition of type 1 pneumocytes, prominent neutrophilic infiltrate with fibrosing alveolitis.

In the final stage, or congratulations, histology is like that of the exudative and proliferative phase of diffuse alveolar damage. There is distortion of lung architecture and reparative proliferation of the type 2 pneumocytes.

vascular changes are also seen in other organs, especially the spleen. In the liver, there are scattered coagulative necrosis. There is no single pathognomonic features on histology. early histological features of lung tissue obtained by biopsy can provide guidance but seldom attained in clinical practice.

Bring up the history of exposure to detail critical. Activities that dust raise and have the potential to aerosolize rodent feces, saliva, or feces can cause inhalation of viral particles, which fall into the lower lobe and establish an infection. Healthy and immunocompetent patients could be infected as well. There is no history of an upper respiratory infection.

There are five clinical stage or phase of hantavirus infection caused hepatopulmonary syndrome. The incubation phase (4-33 days); febrile phase, the phase of cardiopulmonary, diuretic phase and recovery phase. Sudden onset of fever and associated with flu-like symptoms and rash erythematous. Cough heralds the onset of cardiopulmonary phase. This phase occurs about three days after the fever phase. Hypotension, respiratory failure, and oliguria during this phase. petechial rash was also noted. Most deaths occurred during cardiopulmonary this phase. The rapid development of this fever, flu-like illness severe cardiopulmonary failure is one of the characteristics of the syndrome hepatopulmonary.

If the patient survives for two weeks or more, diuretic phase sets in. Patients relatively hipervolemi during this period. Recovery phase started late and may require up to four months. Because the fluid shifts frequently, electrolyte abnormalities often through phases 2-4.

The diagnosis should include a condition that causes a fever with a rash, fever with thrombocytopenia such as dengue fever, fever with atypical pneumonia, gram negative sepsis, and acute respiratory distress syndrome (ARDS).

Abnormalities noted in the complete blood count (CBC) as well as in the chemical because the liquid electrolyte imbalance. Interestingly CBC image may have a left shift with and without neutrophilia, which is more typical of a bacterial infection, atypical lymphocytosis present showed a viral etiology. There thrombocytopenia in the prodromal phase, which also supports the diagnosis hepatopulmonary syndrome. Generally, the prothrombin time within normal limits.

Serology is the most common approach to confirm hanta virus infection. This test indirect ELISA IgG and IgM, and M antibody-capture ELISA. Specific hantavirus immunoglobulin M (IgM) was detected early in the disease. Documenting increased titers of specific hantavirus immunoglobulin G (IgG) is another method to make a diagnosis. This is an ELISA test, which is used by the Centers for Disease Control and Prevention (CDC) also. The IgM antibodies last for months after infection hantavirus. Serologic tests do not differentiate between different types of hantavirus.

immunoblot and neutralization tests have also been used to diagnose hantavirus infection. These tests are cumbersome to perform and does not distinguish between the various species of hantavirus.

There is a clear need for rapid tests in this disease because of its rapid development and its predictable after the fever phase sets in. A one-hour enzyme immune assay has been developed. There is a wide range of rapid tests each identify certain species of hantavirus. The sensitivity of rapid tests mostly are in the range of 96% to 100%.

a very specific molecular tests (100%) and sensitivity (94%). Polymerase chain reaction (PCR) tests detect other related species of hantavirus, which can cause hepatopulmonary syndrome or hemorrhagic fever with renal syndrome as Puumala virus or virus Dobrava. PCR tests can be performed on clinical specimens obtained from a biopsy. Sin Nombre virus was not shed in feces, urine or saliva swabs from these areas may not detect the virus. Hantavirus antigens can be detected by immunohistochemistry in clinical specimens such as blood and tissue. The real-time PCR (RT-PCR) test allows for the quantitative detection of viral antigen using S segment of the viral genome.

Overall, using molecular tests and superior antigen detection tests in the early phases of the disease. Since IgM stay alive for months, tests to detect specific IgM antibodies can be used in the healing phase of the disease.

Therefore, the combination of serological assays (ELISA) and molecular testing (RT-PCR) appears to be the optimal approach today.

imaging in stage shows interstitial edema fever, and physical exam during this phase may reveal crackles on auscultation of the lungs. interstiti ThePatterns al changing rapidly multi-lobar disease bilateral alveolar space. Disease is more central alveolar space or in the lower lobes and therefore not as peripheral infiltrates acute respiratory distress syndrome (ARDS). ARDS has no previous pattern of interstitial infiltrates and peripheral alveolar disease patterns.

There are no approved antiviral therapies for treating hantavirus infection. Supportive care is the primary therapy. early admission to the intensive care unit are justified as the disease tends to progress. Consider early intubation and supplemental oxygen to save the physiological reserves during periods of respiratory support. While hantavirus infection is systemic and viral nucleic acids are found in other organs in immunohistochemistry, the clinical picture is dominated by pathology in the lungs. Due to rapid fluid shifts, attention should be paid to fluid and electrolyte balance in intensive care units.

death in severe cases with evidence of bilateral infiltrates on chest x-ray (CXR) is high, in the range of 30% to 50%. mild cases are not fatal. Upon the occurrence of febrile phase, if the disease is not growing rapidly to cardiopulmonary phase within three to five days of impossible to progress afterwards. In this case, the results are much better, and death are possible.

Rodent control in and around human habitation in the main method of hantavirus infection prevention. There is no limit on the trip.

hantavirus cardiopulmonary syndrome is a deadly disease and the best managed by interprofessional team which includes ICU nurses. There is no specific treatment for the infection and aggressive support and mechanical ventilation is required in most patients. Even with optimal therapy, the mortality rate exceeded 40%. Patients who sustain a chest x-ray which obviously tend to have good results.

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