hantavirus pulmonary syndrome while pregnant

  • 16 min read
  • Feb 19, 2020

Why a hantavirus pandemic is unlikely to happen
Why a hantavirus pandemic is unlikely to happen

Michael J. Howard, Timothy J. Doyle, Frederick T. Koster, Sherif R. Zaki, Ali S. Khan, A. Eskild Petersen, Clarence J. Peters, Ralph T. Bryan, Hantavirus Pulmonary Syndrome in Pregnancy, Clinical infectious diseases, Volume 29, Issue 6, December 1999 Pages 1538-1544,

The comprehensive review hantavirus pulmonary syndrome (HPS) during pregnancy in 5 women characterize the impact of Sin Nombre virus infection on maternal and fetal outcomes. Histopathology, serology, and clinical information is evaluated for evidence of vertical transmission. mother’s age ranged from 20 to 34 years and gestational age 13-29 weeks. Symptoms, physical findings, and laboratory values ​​other than those associated with pregnancy is not noticeably different from nonpregnant patients with HPS, although somewhat lower fever. One of maternal mortality and fetal loss occurred 2. Gross, microscopic and immunohistochemical examination for hantavirus antigens second autopsy performed on the fetus and placenta 3 showed no evidence of transmission of hantavirus transplacental. There is no serological evidence of conversion in three children who are still alive. Maternal and fetal outcome of HPS HPS patients appeared similar to non-pregnant and pregnant patients with other causes of acute respiratory distress syndrome. There is no evidence of vertical transmission of Sin Nombre virus is found.

Hantaviruses are lipid-enveloped, trisegmented, negative-sense RNA virus belonging to the family Bunyaviridae. The genus name, hantavirus, derived from Hantaan River in Korea, where the prototype Hantaan virus was first isolated from the striped field mouse (Apodemus agrarius) in 1976 []. Additional hantavirus species found mainly outside the Western Hemisphere, including Seoul, Dobrava and Puumala viruses; This virus, together with Hantaan virus, is responsible for a spectrum of diseases known as hemorrhagic fever with renal syndrome []. All hantaviruses associated with primary rat reservoirs, and their transmission to humans is thought to involve inhaling an aerosol of virus excreted in rat urine and feces.

hantavirus disease in the Western Hemisphere first emerged as a public health threat in the southwestern United States in 1993 [,]. The newly recognized disease called hantavirus pulmonary syndrome (HPS), and the etiologic agent was found to be a previously undescribed hantavirus, Sin Nombre virus (SNV) []. HPS is characterized by severe pulmonary edema noncardiogenic that cause breathing problems often resemble acute respiratory distress syndrome (ARDS). Case-fatality rate of HPS is ~ 45% [,].

In October 1999, a total of 229 cases of HPS have been confirmed in the United States. Five of the patients were women who were pregnant at the time of their illness. Although much is currently known about the causes of ARDS during pregnancy than other [], the effects of HPS on maternal and fetal outcomes only briefly presented [].

In addition, this series of cases of pregnant women with HPS 5 provides a unique opportunity to assess the likelihood of hantavirus vertical transmission from mother to child. Experience with other members of the family Bunyaviridae indicate that vertical transmission probability [].

Here we summarize the presentation, clinical, and pregnancy outcome of five pregnant women with HPS and assess the available evidence on the possibility of vertical transmission of hantavirus from women to their fetuses.

HPS is a disease were reported in most of the states in the United States. the state health department doing early testing for antibodies to SNV and advanced to the Center for Disease Control and Prevention (CDC) case report forms and specimens from people who test positive. suspected cases must meet the CDC definition of the following: fever (temperature> 38.3 ° C) occurred in previously healthy people characterized by bilateral, diffuse interstitial pulmonary edema that may radiographically resemble ARDS develops within 72 hours of hospital, with compromises requiring breathing supplemental oxygen; or respiratory diseases is described lead to death by autopsy examination showed noncardiogenic pulmonary edema without an identifiable cause. People with underlying medical conditions such as malignancy or immunodeficiency, or those with acute tha conditiont provide a possible explanation for respiratory disorders, such as recent trauma, burn, or aspiration, were excluded from consideration. case report forms provide demographic and limited epidemiological and clinical data for each patient suspected cases; These data, along with laboratory results noted below, inserted into the HPS National CDC Surveillance Database. In addition to compatible clinical disease, confirmed cases should have good serological evidence of hantavirus infection, positive results of reverse transcriptase-PCR (RT-PCR) testing for hantavirus RNA, or positive results of immunohistochemistry test for hantavirus antigens in tissue.

pregnant case patients with HPS is ensured by including all the female patients were found in CDC’s National Surveillance HPS database who meet the CDC definition for HPS and has had a positive pregnancy test at some point during their illness. A thorough abstraction of medical records is done for each woman meets these criteria.

When possible, the autopsy of the fetus and placenta tissue analysis carried out at the hospital involved and at the CDC. Gross examination standards have been equipped with formalin-fixed and paraffin-embedded sections microscopically, immunohistochemistry and RT-PCR on RNA SNV. These techniques have been described in detail elsewhere [,].

In October 1999, 5 (2.2%) of the 229 confirmed cases of HPS in the United States have occurred in pregnant women. Of these 5 patients, two are American Indian, 2 non-Hispanic whites, and one was Hispanic. They ranged in age from 20-34 years (), previously healthy, and taking a prenatal vitamin only when their disease. None of the patients reported alcohol or drug use, and only 2 patients were smokers. All patients had at least one prenatal visit and had no complications in their pregnancy before being diagnosed with HPS. gestational age at diagnosis ranges from 13-29 weeks. None of the women had evidence of abnormal development of fetal distress, or pregnancy complications them before the presentation.

demographic characteristics of pregnant women with hantavirus pulmonary syndrome.

demographic characteristics of pregnant women with hantavirus pulmonary syndrome.

frequency of signs and symptoms present for 5 confirmed pregnant HPS patients was similar to that seen in non-pregnant patients () [,,]. important differences in the presentation, including the lack of documented fever for 3 of the 5 patients, although all give the history of subjective fever. Further differences noted in the description of the case below. prodromal period ranging from 1 to 5 days, and hospitalized survivors ranged from 6 to 11 days. 1 maternal deaths occur within 24 hours of admission, for the case-fatality rate of 20%. Two out of five pregnancies resulted in fetal death in utero. One baby was born prematurely with brain and lung complications significantly and died after discharge from the hospital. clinical findings at the time of hospital admission and laboratory research results are summarized in during their stay.

clinical and laboratory findings on admission and during hospitalization for 5 pregnant women with hantavirus pulmonary syndrome.

clinical and laboratory findings as they enter and for hospitalized for 5 pregnant women with hantavirus pulmonary syndrome.

1 patient presented among patients with HPS was first seen during the spring of 1993, before special diagnostic reagents for SNV developed. He is an American Indian 25 years, pregnant women 6, paragraph 5, at 29 weeks gestation. He admitted the diagnosis was pneumonia and ARDS. He came to the hospital to visit her husband, who is in the medical intensive care unit with the same diagnosis. Her husband was later confirmed to also have the HPS. The main complaints include fever, nausea, back pain, cough, vomiting, and myalgia for 1 day prior to admission, and he experienced a syncopal episode in the emergency department.

On examination, he had a tympanic temperature of 38.2 ° C and recorded into tachypneic, tachycardia, and hypoxia. Rales present on lung auscultation, and recorded diffuse pain on palpation of the abdomen. Physical examination also revealed a clear drainage from the nose and eyes. Her respiratory status deteriorated rapidly, and he was intubated and placed on mechanical ventilation. The follolaboratory values ​​entered wings note: WBC count, elevated by a left shift; hematocrit, 35%; and platelet count, 155,000 (). Analysis of serum showed a mild metabolic acidosis, hyponatremia, and hypokalemia. Studies of coagulation and liver function tests within normal limits. pressure pulmonary artery occlusion consistent with pulmonary edema noncardiogenic. positive pressure mechanical ventilation and inverse ratio effective in maintaining adequate oxygen delivery. Despite these efforts, the fetal heart tones lost on the fourth hospital day, and vaginal delivery of a baby boy steep ensued.

During the following days, these patients showed a dramatic recovery. its oxygen requirements decreased and he was weaned off the ventilator, she was extubated 3 days after giving birth, and she proceeded to the gradual resolution of her symptoms of lung disease. She was released from the hospital receiving oxygen outpatient treatment discontinued one week later.

The course of perinatal infant son complicated by severe respiratory distress syndrome. A patent ductus arteriosus was recorded, and the child had pulmonary hemorrhage and brain with continuous seizure activity. He remained ventilator dependent for 5 months; then he was extubated, out of the hospital, and later died at home. There is no further information available for this child, and an autopsy was not performed. placental tissue were consistent with spontaneous preterm birth and are not tested for the virus antigen or nucleic acid. The results of serologic studies for hantavirus in negative child birth.

Patient 2 was a 34 years old white woman, pregnant 3, paragraph 2, at 13 weeks of pregnancy who do not have a past medical history significant apart from tobacco use light. He was seen in the emergency department of a community hospital complaining of shortness of breath and cough productive with 5-day history of fever, chills, headache, myalgia, weakness, and anorexia. He also noted watery eyes, runny nose and sore throat. At this time, the patient was found fever, hypoxia, tachycardia, and hypotension. He had a syncopal episode in the emergency department and hospitalized. Physical examination showed “congested nasal mucosa with red throat and tympanic membrane and coryza,” bilateral rales and crackles, tachycardia without murmurs, and no rash. Her diagnosis entry including hypovolemia, dehydration, and pneumonia bronchopulmonary. The doctors admit worried that she developed HELLP (hemolytic anemia, elevated liver enzymes, and low platelets) syndrome. He was transferred by air ambulance to a tertiary care center and was admitted to the medical intensive care unit. Admission laboratory values ​​showed his little elevation WBC count with a left shift, hemoconcentration, and thrombocytopenia were significantly (). mild coagulopathy and slightly elevated liver transaminase levels was also noted. Her serum bicarbonate levels dropped to 11 mEq / L and its arterial pH fell to 7:12 as his respiratory status deteriorated.

Her condition quickly deteriorated, necessitating intubation and pulmonary artery catheterization. Although pharmacological inotropic support and the maximum and successful cardioversion for ventricular tachycardia and fibrillation, he died within 20 hours from the time of admission. The diagnosis of HPS was made at autopsy. Lung and kidney tissue from these patients both SNV positive by immunohistochemistry. fetal tissue (lung, kidney, heart, liver, adrenals, intestines, and spleen) negative for SNV by immunohistochemistry in CDC laboratories.

Patient 3 is an American Indian woman of 20 years, pregnant women 2, paragraph 1, which contracted mild cases of HPS in November 1993 during the 20th week of pregnancy. Her main complaint including productive cough, fever, and pain. He noted a few days diffuse abdominal pain, diarrhea, and urinary frequency with burning on urination. Her initial diagnosis was pneumonia and urinary tract infections as possible. Due to an increased oxygen demand, he was transferred to the intensive care unit and treated in hospital for 8 days in moderate respiratory distress. He never intubated. HPS diagnosis was confirmed by serology at the fourth hospital day. These patients continued to have an uncomplicated vaginal delivery of a healthy, seven-pound 9 ounces, the full-term girl, No abnormal noted on gross examination of the placenta, and it was not tested further. Kids tested negative for IgG antibodies to SNV at the age of 12 months and appeared to be healthy.

Patient 4, a 27 years old Hispanic woman, presented in September 1994 in the first 17 weeks of pregnancy. His main complaint included two days of dry cough, back pain, vomiting, fever, and chills, and burning on urination. Physical examination reveals an ill-appearing pregnant female with bilateral periorbital mild “swelling,” voices, and tachycardia. He was admitted with a diagnosis of pyelo-nephritis in pregnancy and “viral syndrome.” Due to the rapidly deteriorating respiratory compromise, he was transferred to the intensive care unit where a confirmed serological diagnosis of HPS. Her respiratory status is stable under treatment with high-flow oxygen, and he did not require intubation. He was discharged after five days and went on to have a spontaneous vaginal delivery without complications a healthy 7-pound, full-term children.

placental tissue was tested and did not have any evidence SNV infection by the gross, microscopic and immunohistochemical analysis. Cord blood and serial serum samples from children negative for IgM antibodies to SNV and exhibited the expected loss of titratable maternal IgG antibodies to SNV. This child seems healthy without apparent sequelae of maternal infection.

Patient 5 was a white woman 28 years at 16 weeks of pregnancy were presented in January 1998 complaining of fever, chills, headache, sore throat, cough, dyspnea, epigastric pain, and vomiting. She visited a doctor primarily on the fourth day of illness and was diagnosed with influenza might. She was given a recommendation to reduce the symptoms and called her obstetrician that same day, which stipulates that the pregnancy seemed normal. The next day she presented to the emergency department of respiratory disorders and intubated and transferred to a tertiary care facility with a diagnosis of ARDS, sepsis, and abdominal pain. On admission, her WBC count 43,100 (with 36 shape ribbon% and 12% atypical lymphocytes), her platelet count was reduced to 47,000, and the hematocrit is 51% (). elevated liver enzymes and low albumin levels were also noted. Abdominal ultrasound showed gallbladder wall thickening, but no rocks or evidence of biliary obstruction.

On transfer, the patient was noted to have a small amount of bleeding vagina and cervix closed on examination. fetal heart tones can not be found. Pelvic ultrasound performed on the second hospital noted that there are fetal heart motion. That night, the patient delivered nonviable 93-g male fetus and placenta delivered later by curettage. Negative amniotic fluid culture. fetal tissue (lung, kidney, heart, liver) and negative for SNV placenta by immunohistochemical analysis in the CDC laboratory.

The patient experienced a moderate increase in her status of cardiovascular and pulmonary after giving birth to him. She remained intubated for a total of 9 days and did not have a need oxygen when discharged from the hospital two days after extubation.

The presentation of the pregnant woman with noncardiogenic pulmonary edema is a rare and serious scenario with a wide differential diagnosis which now includes the HPS. This 5 cases represent only our experience with HPS in pregnancy. Mother and various physiological changes of pregnancy-related complications that may cause or lead to ARDS make generalizations about the effects of HPS is difficult in this small subgroup of patients.

ARDS on a new pregnancy has been checked []. Deaths due to ARDS during pregnancy did not differ significantly from that patient is not pregnant (43% -44%) and is associated with marked high level of perinatal morbidity and fetal loss (23%) [,,]. infectious diseases remain the most prominent among known etiologic factors that lead to ARDS during pregnancy, although the conditions associated with pregnancy, including preeclampsia, eclampsia and hemorrhage, also plays an important role. In one series of cases studied 16 pregnant women with ARDS, Mabie et al. [] Take note of communicable diseases as the main etiology in half of the cases, four of which are due to viral pneumonia. One patient with influenza A survived but had a spontaneous labor at 22 weeks. Two of the 3 patients with pneumonia because varicella-zoster virus survived and had a normal uncomplicated delivery. The third patient died after giving birth to a baby 30 weeks spontaneously. The child survived but has a complicated course, including prolonged mechanical ventilation for respiratory distress syndrome, intraventricular hemorrhage, and patent ductus arteriosus is not like the case 1 described above.

It is not clear what physiological changes of pregnancy may have contributed to the clinical results of five women with HPS. Although the numbers are small limit useful comparison with nonpregnant patients with HPS, it is clear that the changes associated with pregnancy can change the parameters believed to be important in screening for patients with HPS and manage patients with ARDS. Physiological anemia due to intravascular volume expanded to affect the delivery of oxygen and can cover hemokonsentrasi commonly seen in HPS. Only 2 of the 5 patients in this study developed a hematocrit value of 50% []. Increasing the volume of intra-abdominal pregnancy effectively reduce pulmonary compliance, thereby lowering the functional residual capacity and positive pressure ventilation may be complicated. In addition, there may be com-pe-ti-tion because the blood is driven into the bed of blood vessels in the placenta, thereby increasing the overall oxygen requirement.

These factors may contribute to the benefit should be obtained from the delivery for pregnant patients with ARDS [,,,]. Currently, there is no clear evidence to support the delivery of therapeutic or induced to pregnant patients with ARDS due to hantavirus infection. Obviously, the pregnancy must be considered, since it limits the viability of the fetus. Most authors recommend an individualized treatment with vaginal delivery attempts, if necessary, ordering a cesarean section for obstetric indications standard [,].

physiological and anatomical changes of pregnancy can explain signs and symptoms seen unexpected in this case series. For example, urinary complaints and sinusitis are the two most common reasons for women to seek medical help during pregnancy. This may be why two patients in the study presented with urinary tract complaints mainly. Watery eyes and sinus drainage is not seen in the initial clinical characterization of HPS but may represent what is otherwise a common complaint among pregnant women. Two of 5 patients also complain of a sore throat, which had been suggested earlier to a negative predictor for HPS []. The significance of this finding is unclear.

Especially important in this group of patients are considered differential diagnosis for one patient who died of HPS. He is considered to have preeclampsia variant known as HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome. Common pathogenesis leading to multiple organ system failure that define HELLP syndrome appears to be an insult to the blood vessel endothelium capillary level that has not been described [,]. Similarly, SNV infection appears to exert its effect on the level of vascular endothelium leading to increased capillary leakage, may make the initial presentation of two difficult to distinguish. The striking differences between HELLP syndrome and HPS is that SNV hantavirus infection usually has a pathological effect on the organs of the chest (lungs and heart) without causing significant liver, kidney, or blood vessel injury elsewhere. Several studies have demonstrated marked accumulation of hantavirus antigens and genetic material is mainly distributed in the pulmonary capillary endothelium [,,]. Do insult is a direct result of viral infection or occur as a consequence of the activity of immune cells or mediators released actions of a systemic immune response is not clear, and further studies are needed.

List of viruses known to be transmitted through the placenta is long and includes some of the well-known adverse effects on fetal growth and development [,]. Rubella, a classic example, causing only mild illness in mothers not lead to growth retardation, malformations, and sometimes death of the fetus. On the other hand, cytomegalovirus infection may go completely unnoticed in the fetus after the mother had mild or subclinical primary infection in pregnancy. Some viruses (eg, influenza virus) known to have never spread vertically to the fetus, and others may vary cause fetal infections (hepatitis B virus, HIV, lymphocytic chorio-meningitis virus) [,]. Although there is no evidence of transmission of laboratory or field in the vertical hantavirus reservoir rodent species [], another group of rodent-borne virus, which arenaviruses, did show evidence of vertical transmission. In rodents, these viruses infect the fetus on a regular basis and the results of chronic fetal infection, viremik to mostly non-pathogenic (lymphocytic choriomeningitis virus and Lassa virus) or severely affect the puppy (Machupo and Junin virus). In humans, arenaviruses can also infect the placenta and fetus and can cause damage to the fetus and abortion []. Thus, the lack of evidence for vertical transmission of hantaviruses in humans or rodents are important contrast of vertical transmission observed for arenaviruses.

Transplacental (in the womb) infection generally implies that the virus is able to infect placental trophoblast tissue and passes directly into the fetal circulation. indirect mode of transmission in the absence of a clear placental infection have been proposed and could occur at HPS. There is a possibility that, small vascular lesions induced viral allow diapedesis of leukocytes infected mothers or coated red blood cells into the fetal circulation, as has been proposed in other viral diseases such as HIV []. placental samples submitted for pathologic examination in this study showed no gross or microscopic evidence of infection. All available tissue samples were negative by immunohistochemistry. Likewise, the placenta and fetal tissues from 2 cases with fetal death (patients 2 and 5) revealed no evidence of infection hantavirus. These data argue route transplacental vertical transmission.

2 women with mild cases of HPS (patients 3 and 4) in this study continue to have full-term vaginal delivery complicated without further evidence of hantavirus infection. Although acute infection, patients 1 deliver 29 week old baby with some great possibilities perinatal complications of prematurity and / or maternal hypoxemia and hypotension. So far, these children have had serologic evidence of infection. This provides evidence against a vertical route perinatal transmission in patients with acute infection or healing HPS.

It should also be noted that the definition of vertical transmission can include perinatal transmission in breast milk. This example is no other viruses (mumps, HIV, and cytomegalovirus) [,]. When there is no conclusive evidence of the type of transmission in any reported cases of human or animal models involving hantaviruses that cause HPS. Our case series showed that both transplacental or perinatal transmission occurs in HPS in North America.

Review of human cases of hantavirus infection during pregnancy only found 14 reports in the literature [,]. Four of these quotes show the mother-to-fetus transmission of hantavirus Transplacental. Three are in pregnant women with hemorrhagic fever with renal syndrome caused by viruses Hantaan [], but only one is clearly documented by serological testing of the fetus []. The first of these reported cases of transmission occurs in a Korean woman acute Hantaan virus infection (documented by “serology”) []. She had a spontaneous abortion after maternal hypotension episode at ~ 7 months of pregnancy. Systemic fetal autopsy showed bleeding around the lungs, kidneys, and adrenal glands that are considered consistent with Korean hemorrhagic fever. There is no mention of serological testing of the fetus and there is no conclusive evidence of transplacental infection. The authors did note that the fetal death can result from hypotension or other complications of systemic infection of the mother. In fact, the fetal autopsy findings consistent with those seen in pregnant women who suffer from other diseases that cause severe hypotension [,].

The most convincing case in the literature reported by Lee [] in 1989. He describes a 28-year old Korean woman in the eighth month of pregnancy who develop hemorrhagic fever with renal syndrome due to primary Hantaan virus infection documented. On the 28th day of his hospitalization, well after she acute renal insult start determination, he spontaneously delivered 3.3 kg fetus that survived only 11 h. Then, serological testing showed IgM in titer of 1: 256 in fetal cord blood. Fetal autopsy showed hemorrhagic lungs, kidneys and adrenal tissue similar to that recorded in the previous cases.

It is interesting to note that some reports of human cases of the virus Hantaan [,], Puumala virus [,], and SNV [,] the infection has found no evidence of vertical transmission in pregnant women they studied. The fact that transmission occurs inconsistently on Hantaan virus infection and does not appear to occur with closely related viruses such as Puumala virus and SNV indicated that this is a heterogeneous group of viruses with low and variable levels of transplacental transmission.

The fifth patient was the only woman known to be infected with SNV during pregnancy. These cases demonstrate the features of epidemiology and mortality similar to that observed for nonpregnant patients with HPS. There is currently no evidence of these cases to support the vertical transmission of SNV to the fetus in the uterus or womb.

The diagnosis of ARDS in pregnancy, although complications are rare, continues to grow in complexity, and HPS should be considered in patients from areas of endemicity have a history of possible exposure. It should be reiterated that the physiology and immunology of pregnancy can cause variations in the typical presentation and course of the infection HPS. there is still no evidence to support the initial, delivery is induced in patients with HPS or other pregnant patients with ARDS. clinical management should be individualized, with the decisions about the management of maternal-fetal made jointly between critical care and obstetrician.

We thank Joni Young to help in preparing the manuscript.

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