Hantavirus pulmonary syndrome (HPS) is an infectious disease that is acquired through exposure to rodents carrying the causative virus, the Hantavirus. A few cases have been documented, where the infection was acquired through human to human contact [1] [2].

HPS usually occurs in specific geographical locations, such as north and south America. The disease appears to affect all individuals equally, although men may have a higher incidence rate due to more recurrent exposure to the vector. For the same reason, HPS typically does not present in young children or the elderly.

HPS is one of many syndromes that can arise from Hantavirus infection [3] [4]. The affected organ systems depend on the specific type of Hantavirus an individual has come in contact with. The severity of illness varies greatly between cases, ranging from mild to severe. Furthermore, it demonstrates significantly high case mortality rates, estimated at up to 50%. This syndrome is characterized by severe respiratory compromise. The illness has several stages entailing a prodromal phase, respiratory phase, and convalescent phase. The disease has an incubation period of one week to one month, after which prodromal symptoms manifest.

Prodromal symptoms are often nonspecific and may involve gastrointestinal discomfort, vomiting, headache, and muscle pain [5]. These individuals also experience pyrexia. The typical signs usually last up to 5 days.

Subsequently, the host immune system attacks endothelial cells lining the lungs, displaying viral antigens. This process leads to increased permeability of the endothelium and thus pulmonary edema. The cardiopulmonary phase lasts up to 48 hours and is characterized by the emergence of respiratory findings such as coughing, tachypnea, crepitations, and dyspnea. Patients frequently require mechanical ventilation during this time. Some individuals may develop hypotension and circulatory collapse due to cardiogenic shock, the latter being the main cause of death in HPS [6] [7] [8]. Oliguria is not an uncommon observation during this phase, and in a few cases, may lead to renal failure.

The third stage is preceded by an episode of diuresis and is made evident by the resolution of cardiopulmonary features.

Upon presentation, baseline blood tests, as well as more specific laboratory testing should be carried out. Often requested laboratory studies include:

• Complete blood count (CBC), urea and electrolytes, peripheral smear, and arterial blood gas analysis (ABGA).
• Immunochemistry.
• Serology.
• PCR (polymerase chain reaction).

CBC may reveal low platelets and elevated white blood cells, with an unusually high proportion of immature cells [9]. Serum lactate dehydrogenase (LDH) is also high. Other parameters may reflect the distributive shock experienced in Hantavirus pulmonary syndrome [6] [7]. One such finding is hemoconcentration. A peripheral blood smear, in addition to the above, may reveal the presence of atypical immune cells, as well as immunoblasts [9]. Once these findings are observed, HPS can be diagnosed.

Imaging studies are usually carried out in the form of a chest radiograph. Signs of pulmonary edema that may be visualized include increased hilar markings, diffuse bilateral infiltrates, Kerley B lines, and peribronchial thickening. The cardiac silhouette is of normal size, and pleural effusions might also be present.

There is no specific antiviral treatment for HPS. Management focuses on supportive care, which may include oxygen therapy and mechanical ventilation to assist with breathing. Early recognition and hospitalization are crucial for improving outcomes. In some cases, patients may require intensive care support.

The prognosis for HPS varies. While the disease can be severe and life-threatening, early diagnosis and supportive care can improve survival rates. The mortality rate for HPS is approximately 30-40%, but this can vary depending on the timeliness of treatment and the patient's overall health.

HPS is caused by hantaviruses, a group of viruses carried by certain rodent species. In North America, the primary carrier is the deer mouse. Humans can become infected through inhalation of aerosolized virus particles from rodent urine, droppings, or nesting materials. Direct contact with rodents or their excreta can also lead to infection.

HPS is relatively rare but can occur in rural and semi-rural areas where humans come into contact with infected rodents. Cases have been reported in the United States, Canada, and parts of Central and South America. The disease is more common in spring and summer when people are more likely to encounter rodents.

Once inhaled, hantaviruses enter the body and target the endothelial cells lining the blood vessels, particularly in the lungs. This leads to increased vascular permeability, causing fluid to leak into the lung tissues and air spaces, resulting in pulmonary edema (fluid accumulation) and respiratory distress.

Preventing HPS involves minimizing exposure to rodents and their habitats. This can be achieved by sealing homes to prevent rodent entry, keeping food in rodent-proof containers, and maintaining clean living environments. When cleaning areas with potential rodent exposure, use protective gear and disinfectants to reduce the risk of inhaling virus particles.

Hantavirus Pulmonary Syndrome is a serious respiratory illness caused by hantaviruses transmitted from rodents. It presents with flu-like symptoms that can quickly progress to severe respiratory distress. While there is no specific treatment, early supportive care can improve outcomes. Preventive measures focus on reducing rodent exposure.

If you suspect you have been exposed to rodents and are experiencing symptoms such as fever, muscle aches, and difficulty breathing, it is important to seek medical attention promptly. Inform your healthcare provider about any potential rodent exposure, as this information can aid in diagnosis and management. Remember, prevention is key, so take steps to avoid contact with rodents and their droppings.

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