Dr. H. L. Niman, Phd. - NYC Toddler Death Raises Concerns

[Extrapolation]

Suspect Swine H1N1 Toddler Death in NY Raises Concerns


Dr. Henry L. Niman, Phd
May 19, 2009 - 17:02
Recombinomics

Commentary


"A medical examiner will determine if the 16-month-old boy who died shortly after arriving at Elmhurst Hospital in Queens is the second death from swine flu in New York City.

Family members say the boy was turning blue as they rushed him to the hospital."
______________

The above comments on a suspect swine flu fatality in Queens, New York raise additional pandemic concerns. The number of confirmed and suspect cases in Queens has been high (see updated map), leading to more than a dozen school closings, due in part to the high number of students with flu like symptoms, as well as the confirmed swine H1N1 death of an assistant principal.

Yesterday, the suspect toddler developed a fever in the morning, was eating in the afternoon, and was unresponsive by evening, when he was rushed to the hospital and died. The sudden death, coupled with rapid development of cyanosis, are classic symptoms associated with fatal influenza cases in 1918.

In 1918 an H1N1 swine flu recombined with an H1N1 seasonal flu that led to 20-50 million fatalities, as the virus spread world wide and affected approximately 1/3 of the population. That outbreak began as mild disease in the spring and most of the fatalities were associated with outbreaks in the fall of 1918 and 1919. There were multiple waves during the outbreak, raising concerns of a similar scenario in 2009.

An efficiently transmitted swine H1N1 in the human population has not been reported since 1918. Although WHO has not yet raised the pandemic phase from 5 to 6, the sustained transmission in North America, combined with reports of community spread in Europe and Asia leaves little doubt that the 2009 pandemic has begun.

The evolution of the H1N1 is being closely monitored by sequencing labs across the world, and most isolates to date are closely related. However, the presence of avian PB2 raises concerns that the frequency of cases will not decline in the summer in the northern hemisphere, because the avian PB2 is optimal at 41 C, which would lead to efficient transmission in the summer.

Moreover, the seasonal flu has the mammalian version of PB2, which has optimal activity at 34 C. However, the swine H1N1 transmitting in the summer hemisphere may acquire E627K, leading to a virus efficiently transmitting in the winter also.

Similarly, swine H1N1 in the southern hemisphere may acquire H274Y, leading to Tamflu resistance, which could complicate treatment of the more severe cases, which may involve previously healthy young adults. Another H1N1 death (44M) was just reported in St. Louis, MO.

-end

 

[Extrapolation]

Re: Dr. H. L. Niman, Phd. - NYC Toddler Death Raises Concerns

Epidemiology, Clinical Manifestations, and Diagnosis of Swine H1N1 Influenza A

Authors:

Anna R Thorner, MD
Section Editor

Martin S Hirsch, MD
Deputy Editor

Barbara H McGovern, MD



Last literature review version 17.1: January 2009 | This topic last updated: May 18, 2009


INTRODUCTION — Swine influenza viruses usually infect pigs but occasionally can cross species barriers to infect humans. In the past, cases of person-to-person transmission have been reported but have been confined to small outbreaks [1,2].

In late March and early April 2009, an outbreak of H1N1 influenza A virus infection was detected in Mexico, with subsequent cases observed in several other countries including the United States [1,3].

The epidemiology, clinical manifestations, and diagnosis of H1N1 influenza A virus infection will be reviewed here. The treatment and prevention of H1N1 influenza A virus infection are discussed separately; the epidemiology, clinical manifestations, and diagnosis of seasonal and avian (H5N1) influenza virus infections are also reviewed elsewhere. (See "Treatment and prevention of swine H1N1 influenza" and see "Epidemiology of influenza" and see "Epidemiology; transmission; and pathogenesis of avian influenza" and see "Clinical manifestations and diagnosis of influenza in adults" and see "Clinical features and diagnosis of influenza in children" and see "Clinical manifestations and diagnosis of avian influenza").

EPIDEMIOLOGY

Historical perspective — Illness with influenza in pigs was first recognized during the influenza pandemic of 1918 to 1919, and a swine influenza virus was first isolated from a human in 1974 [2,4]. Between 1958 and 2005, 37 cases of swine influenza among civilians were reported [2]. Six cases (17 percent) resulted in death. Forty-four percent of infected individuals had known exposure to pigs. Cases were reported in the United States, former Czechoslovakia, the Netherlands, Russia, Switzerland, and Hong Kong.

In 1976, swine influenza virus caused a respiratory illness with one fatality among 13 soldiers in Fort Dix, New Jersey [5]. No exposure to pigs was found. A subsequent epidemiologic study showed that up to 230 soldiers had been infected with the virus [2,6].

2009 outbreak — In March and April 2009, an outbreak of respiratory illnesses was first noted in Mexico, which was eventually identified as being related to H1N1 influenza A [7].

As of May 18, 2009, there have been over 8800 laboratory-confirmed cases in 40 countries [3]. Over 3100 laboratory-confirmed cases of H1N1 influenza A infection have been reported in Mexico, with 68 deaths [3]. In the United States, over 5100 confirmed cases have been reported from 48 states [8]. The majority of cases in the US have been mild, although some patients have required hospitalization [8,9]. A few fatal cases have occurred outside of Mexico [3]. (See "Mortality" below).

Updated information on the number of confirmed cases can be found at the websites of the United States Centers for Disease Control and Prevention (http://www.cdc.gov/swineflu) and the World Health Organization (http://www.who.int/csr/disease/swineflu/en/index.html).

In one report, among 532 cases of H1N1 influenza A in the United States, 318 (60 percent) occurred in individuals 18 years of age or younger (range 3 months to 81 years), which is similar to the age distribution that occurs with seasonal influenza [10,11].

On April 29, 2009, the World Health Organization raised its pandemic alert level to phase 5, indicating that there is sustained person-to-person spread in at least two countries [8]. This designation implies that a pandemic is imminent and that the time to finalize the organization, communication, and implementation of the planned mitigation measures is short.

SNIP

VIROLOGY Influenza subtypes — Clinical influenza can be caused by several different influenza A subtypes, although H1N1 is the most common subtype implicated in both swine and human infections [12]. Human cases of swine H3N2 influenza virus infection have been reported rarely [2]. Other subtypes that have circulated in pigs include H1N2, H3N1, and H3N2.

Role of pigs — Pigs may play an important role in interspecies transmission of influenza virus. Susceptible pig cells possess receptors for both avian and human influenza strains, which allow for the reassortment of influenza virus genes from different species if a pig cell is infected with more than one strain [2,13,14].

Since the late 1990s, triple reassortant swine influenza A viruses containing genes from swine, human, and avian strains of influenza have been detected among swine herds in North America [15-17]. Eleven sporadic cases of triple reassortant swine H1 influenza A viruses were detected in the United States between December, 2005, and February, 2009 [15]. Nine patients had exposure to pigs.

The outbreak that began in March 2009 was caused by an H1N1 virus that had not been recognized previously in pigs or humans, although six of its eight gene segments were similar to ones previously detected in triple reassortant swine influenza viruses in pigs in North America [18]. This strain represents a quadruple reassortment of two swine strains, one human strain, and one avian strain of influenza [10]. The largest proportion of genes comes from swine influenza viruses (30.6 percent from North American swine influenza strains, 17.5 percent from Eurasian swine influenza strains), followed by North American avian influenza strains (34.4 percent) and human influenza strains (17.5 percent) [19].

It is not clear yet how this virus arose or was initially transmitted to humans. On May 2, 2009, the Canadian government reported the identification of H1N1 influenza A from a swine herd in Alberta, Canada [3]. It is suspected that the pigs became infected following exposure to a farm worker who had recently visited Mexico and had developed an influenza-like illness.

SNIP

Person-to-person transmission — Influenza virus is present in respiratory secretions of infected persons. As a result, influenza virus can be transmitted through sneezing and coughing via large-particle droplets [1,20]. Transmission via contact with surfaces that have been contaminated with respiratory droplets or by aerosolized small-particle droplets may also occur, although these modes of transmission have not been proven [1]. In addition to respiratory secretions, other bodily fluids (eg, diarrheal stool) should also be considered infectious [1]. (See "Clinical manifestations and diagnosis of influenza in adults", section on Transmission).

In contrast to previous outbreaks described above, the outbreak of H1N1 influenza A infection that began in March 2009 appears to involve sustained human-to-human transmission, as suggested by the large numbers of patients with respiratory illnesses identified within a short period of time at various locations around the world [21].

Transmissibility appears substantially higher compared with seasonal influenza [22]. The secondary attack rate of the strain causing this outbreak is estimated to be 22 to 33 percent, compared with 5 to 15 percent for seasonal influenza [23]. Several of the isolates causing disease in the United States have been found to be nearly genetically identical to isolates in Mexico, supportive of person-to-person transmission [18,24].

Infection control and social distancing measures are discussed separately. (See "Treatment and prevention of swine H1N1 influenza", section on Social distancing measures and section on Infection control).

Shedding — Since the duration of shedding of H1N1 influenza A virus is currently unclear, the estimated duration of shedding is based upon what is known for seasonal influenza virus [25].

Patients with H1N1 influenza A virus infection are considered to be infectious from one day prior to the development of signs and symptoms until resolution of fever [25]. Individuals should be considered contagious until seven days after illness onset. Longer periods of shedding may occur in children (especially young infants), elderly adults, patients with chronic illnesses, and immunocompromised hosts. (See "Clinical manifestations and diagnosis of influenza in adults", section on Transmission and see "Clinical features and diagnosis of influenza in children", section on Transmission).

Incubation period — Although the precise incubation period has not been established for H1N1 influenza A infection, it could range from one to seven days, and most likely from one to four days [20].

CLINICAL MANIFESTATIONS — The signs and symptoms of influenza caused by H1N1 influenza A virus are similar to those of seasonal influenza [1]. The severity appears to be less than what was observed during the influenza pandemic of 1918 to 1919 [22]. (See "Epidemiology of influenza").

Signs and symptoms — The most common clinical findings of the 2009 H1N1 influenza outbreak in patients in the United States have been fever, chills, headache, upper respiratory tract symptoms, myalgias, arthralgias, and fatigue; vomiting and diarrhea have also been common, both of which are unusual features of seasonal influenza [10,20]. In New York City, 95 percent of patients with H1N1 influenza A have met the case definition for influenza-like illness (subjective fever plus cough and/or sore throat) [20]. In contrast, approximately one third of patients seen at two hospitals in Mexico had no fever at presentation [26]. (See "Clinical manifestations and diagnosis of influenza in adults").

Certain groups, such as infants, elderly individuals, and immunocompromised hosts, may have atypical presentations.

The full range of complications of infection with the current strain of H1N1 influenza A is not yet known, although fatal and non-fatal cases of pneumonia have occurred. (See "Complications" below).

Children — Young children are less likely to have the usual influenza signs and symptoms, such as fever and cough [27]. Infants may present with fever and lethargy, and may not have cough or other respiratory symptoms. Symptoms of severe disease in infants and young children may include apnea, tachypnea, dyspnea, cyanosis, dehydration, altered mental status, and extreme irritability. (See "Clinical features and diagnosis of influenza in children").

Complications — During the 2009 outbreak, rapidly progressive pneumonia, respiratory failure, and acute respiratory distress syndrome have been reported in some cases in Mexico [28]. In the United States, most described cases to date have been mild. In one report, among 399 patients in the US whose hospitalization status was known, 36 (9 percent) required hospitalization. Among 22 hospitalized patients with available data, 12 had risk factors for influenza complications, 11 had pneumonia, eight required intensive care unit admission, four had respiratory failure, and two died [10]. (See "Treatment and prevention of swine H1N1 influenza", section on Definition of high risk.

SNIP

http://utdonline.net/home/content/topic.do?topicKey=pulm_inf/18836