Are We Safe From Bird Flu ?

[jigSAW]

Further findings (in continuation to my last post)

Characterization of Virus
Studies of isolates of avian influenza A (H5N1) from patients in 1997 revealed that virulence factors included the highly cleavable hemagglutinin that can be activated by multiple cellular proteases, a specific substitution in the polymerase basic protein 2 (Glu627Lys) that enhances replication, and a substitution in nonstructural protein 1 (Asp92Glu) that confers increased resistance to inhibition by interferons and tumor necrosis factor {alpha} (TNF-{alpha}) in vitro and prolonged replication in swine, as well as greater elaboration of cytokines, particularly TNF-{alpha}, in human macrophages exposed to the virus Since 1997, studies of influenza A (H5N1) indicate that these viruses continue to evolve, with changes in antigenicity and internal gene constellations; an expanded host range in avian species and the ability to infect felids; enhanced pathogenicity in experimentally infected mice and ferrets, in which they cause systemic infections; and increased environmental stability.
Phylogenetic analyses indicate that the Z genotype has become dominant33 and that the virus has evolved into two distinct clades, one encompassing isolates from Cambodia, Laos, Malaysia, Thailand, and Vietnam and the other isolates from China, Indonesia, Japan, and South Korea. Recently, a separate cluster of isolates has appeared in northern Vietnam and Thailand, which includes variable changes near the receptor-binding site and one fewer arginine residue in the polybasic cleavage site of the hemagglutinin. However, the importance of these genetic and biologic changes with respect to human epidemiology or virulence is uncertain.
Patterns of Viral Replication
The virologic course of human influenza A (H5N1) is incompletely characterized, but studies of hospitalized patients indicate that viral replication is prolonged. In 1997, virus could be detected in nasopharyngeal isolates for a median of 6.5 days (range, 1 to 16), and in Thailand, the interval from the onset of illness to the first positive culture ranged from 3 to 16 days. Nasopharyngeal replication is less than in human influenza, and studies of lower respiratory tract replication are needed. The majority of fecal samples tested have been positive for viral RNA (seven of nine), whereas urine samples were negative. The high frequency of diarrhea among affected patients and the detection of viral RNA in fecal samples, including infectious virus in one case, suggest that the virus replicates in the gastrointestinal tract. The findings in one autopsy confirmed this observation.
Highly pathogenic influenza A (H5N1) viruses possess the polybasic amino acid sequence at the hemagglutinin-cleavage site that is associated with visceral dissemination in avian species. Invasive infection has been documented in mammals,and in humans, six of six serum specimens were positive for viral RNA four to nine days after the onset of illness. Infectious virus and RNA were detected in blood, cerebrospinal fluid, and feces in one patient.Whether feces or blood serves to transmit infection under some circumstances is unknown.

[jigSAW]

Conclusion....

Clinical Features

The clinical spectrum of influenza A (H5N1) in humans is based on descriptions of hospitalized patients. The frequencies of milder illnesses, subclinical infections, and atypical presentations (e.g., encephalopathy and gastroenteritis) have not been determined, but case reports indicate that each occurs. Most patients have been previously healthy young children or adults.
Incubation
The incubation period of avian influenza A (H5N1) may be longer than for other known human influenzas. In 1997, most cases occurred within two to four days after exposure; recent reports1 indicate similar intervals but with ranges of up to eight days. The case-to-case intervals in household clusters have generally been 2 to 5 days, but the upper limit has been 8 to 17 days, possibly owing to unrecognized exposure to infected animals or environmental sources.
Initial Symptoms
Most patients have initial symptoms of high fever (typically a temperature of more than 38°C) and an influenza-like illness with lower respiratory tract symptoms. Upper respiratory tract symptoms are present only sometimes. Unlike patients with infections caused by avian influenza A (H7) viruses, patients with avian influenza A (H5N1) rarely have conjunctivitis. Diarrhea, vomiting, abdominal pain, pleuritic pain, and bleeding from the nose and gums have also been reported early in the course of illness in some patients. Watery diarrhea without blood or inflammatory changes appears to be more common than in influenza due to human viruses and may precede respiratory manifestations by up to one week. One report described two patients who presented with an encephalopathic illness and diarrhea without apparent respiratory symptoms.
Clinical Course
Lower respiratory tract manifestations develop early in the course of illness and are usually found at presentation. In one series, dyspnea developed a median of 5 days after the onset of illness (range, 1 to 16). Respiratory distress, tachypnea, and inspiratory crackles are common. Sputum production is variable and sometimes bloody. Almost all patients have clinically apparent pneumonia; radiographic changes include diffuse, multifocal, or patchy infiltrates; interstitial infiltrates; and segmental or lobular consolidation with air bronchograms. Radiographic abnormalities were present a median of 7 days after the onset of fever in one study (range, 3 to 17). In Ho Chi Minh City, Vietnam, multifocal consolidation involving at least two zones was the most common abnormality among patients at the time of admission. Pleural effusions are uncommon. Limited microbiologic data indicate that this process is a primary viral pneumonia, usually without bacterial suprainfection at the time of hospitalization.
Progression to respiratory failure has been associated with diffuse, bilateral, ground-glass infiltrates and manifestations of the acute respiratory distress syndrome (ARDS). In Thailand, the median time from the onset of illness to ARDS was 6 days (range, 4 to 13). Multiorgan failure with signs of renal dysfunction and sometimes cardiac compromise, including cardiac dilatation and supraventricular tachyarrhythmias, has been common.Other complications have included ventilator-associated pneumonia, pulmonary hemorrhage, pneumothorax, pancytopenia, Reye's syndrome, and sepsis syndrome without documented bacteremia.
Mortality
The fatality rate among hospitalized patients has been high, although the overall rate is probably much lower. In contrast to 1997, when most deaths occurred among patients older than 13 years of age, recent avian influenza A (H5N1) infections have caused high rates of death among infants and young children. The case fatality rate was 89 percent among those younger than 15 years of age in Thailand. Death has occurred an average of 9 or 10 days after the onset of illness (range, 6 to 30), and most patients have died of progressive respiratory failure.
Laboratory Findings
Common laboratory findings have been leukopenia, particularly lymphopenia; mild-to-moderate thrombocytopenia; and slightly or moderately elevated aminotransferase levels. Marked hyperglycemia, perhaps related to corticosteroid use, and elevated creatinine levels also occur. In Thailand, an increased risk of death was associated with decreased leukocyte, platelet, and particularly, lymphocyte counts at the time of admission.
Virologic Diagnosis
Antemortem diagnosis of influenza A (H5N1) has been confirmed by viral isolation, the detection of H5-specific RNA, or both methods. Unlike human influenza A infection,26 avian influenza A (H5N1) infection may be associated with a higher frequency of virus detection and higher viral RNA levels in pharyngeal than in nasal samples. In Vietnam, the interval from the onset of illness to the detection of viral RNA in throat-swab samples ranged from 2 to 15 days (median, 5.5), and the viral loads in pharyngeal swabs 4 to 8 days after the onset of illness were at least 10 times as high among patients with influenza A (H5N1) as among those with influenza A (H3N2) or (H1N1). Earlier studies in Hong Kong also found low viral loads in nasopharyngeal samples. Commercial rapid antigen tests are less sensitive in detecting influenza A (H5N1) infections than are RT-PCR assays. In Thailand, the results of rapid antigen testing were positive in only 4 of 11 patients with culture-positive influenza A (H5N1) (36 percent) 4 to 18 days after the onset of illness.
Management
Most hospitalized patients with avian influenza A (H5N1) have required ventilatory support within 48 hours after admission,15,16 as well as intensive care for multiorgan failure and sometimes hypotension. In addition to empirical treatment with broad-spectrum antibiotics, antiviral agents, alone or with corticosteroids, have been used in most patients (Table 3), although their effects have not been rigorously assessed. The institution of these interventions late in the course of the disease has not been associated with an apparent decrease in the overall mortality rate, although early initiation of antiviral agents appears to be beneficial.1,15,16 Cultivable virus generally disappears within two or three days after the initiation of oseltamivir among survivors, but clinical progression despite early therapy with oseltamivir and a lack of reductions in pharyngeal viral load have been described in patients who have died.
Pathogenesis
Host Immune Responses
The relatively low frequencies of influenza A (H5N1) illness in humans despite widespread exposure to infected poultry indicate that the species barrier to acquisition of this avian virus is substantial. Clusters of cases in family members may be caused by common exposures, although the genetic factors that may affect a host's susceptibility to disease warrant study.
The innate immune responses to influenza A (H5N1) may contribute to disease pathogenesis. In the 1997 outbreaks, elevated blood levels of interleukin-6, TNF-{alpha}, interferon-{gamma}, and soluble interleukin-2 receptor were observed in individual patients, and in the patients in 2003, elevated levels of the chemokines interferon-inducible protein, monocyte chemoattractant protein, and monokine induced by interferon-{gamma} were found three to eight days after the onset of illness. Recently, plasma levels of inflammatory mediators (interleukin-6, interleukin-8, interleukin-1{beta}, and monocyte chemoattractant protein 1) were found to be higher among patients who died than among those who survived (Simmons C: personal communication), and the average levels of plasma interferon-{alpha} were about three times as high among patients with avian influenza A who died as among healthy controls. Such responses may be responsible in part for the sepsis syndrome, ARDS, and multiorgan failure observed in many patients.
Among survivors, specific humoral immune responses to influenza A (H5N1) are detectable by microneutralization assay 10 to 14 days after the onset of illness. Corticosteroid use may delay or blunt these responses.
Pathological Findings
Limited postmortem analyses have documented severe pulmonary injury with histopathological changes of diffuse alveolar damage, consistent with findings in other reports of pneumonia due to human influenza virus.43 Changes include filling of the alveolar spaces with fibrinous exudates and red cells, hyaline-membrane formation, vascular congestion, infiltration of lymphocytes into the interstitial areas, and the proliferation of reactive fibroblasts. Infection of type II pneumocytes occurs. Antemortem biopsy of bone marrow specimens has shown reactive histiocytosis with hemophagocytosis in several patients, and lymphoid depletion and atypical lymphocytes have been noted in spleen and lymphoid tissues at autopsy. Centrilobular hepatic necrosis and acute tubular necrosis have been noted in several instances.
Case Detection and Management
The possibility of influenza A (H5N1) should be considered in all patients with severe acute respiratory illness in countries or territories with animal influenza A (H5N1), particularly in patients who have been exposed to poultry. However, some outbreaks in poultry were recognized only after sentinel cases occurred in humans. Early recognition of cases is confounded by the nonspecificity of the initial clinical manifestations and high background rates of acute respiratory illnesses from other causes. In addition, the possibility of influenza A (H5N1) warrants consideration in patients presenting with serious unexplained illness (e.g., encephalopathy or diarrhea) in areas with known influenza A (H5N1) activity in humans or animals.

[darkcrunk]

I see .. . .

well, after reading what all you had to say, i think it is very uncertain if we are safe or not ! . . Most of us eat chicken - farm chickens basically. Once it starts to spread, it would be a disaster ! ..

n Saba, i find it hard to believe you have no idea what "bird flu" is . . if its true, then i am sorry to say . . but tumi ekta BOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOKA :P

[mritticool]

ok..um in pune nw where bird flu is rulin..as long as birds r dre bird flu wil b dre..hehe..i still hav chicken eggs..

[ami_tiptip_bristi]

bird flu...shunle aktu voy pai....kintu khaoyar somoy thik e khai...

[jigSAW]

Originally Posted by mritticool

ok..um in pune nw where bird flu is rulin..as long as birds r dre bird flu wil b dre..hehe..i still hav chicken eggs..

you are right!
and we are not in Danger Zone yet.

there are some immediate preventives suggested for people of Bangladesh:

1) Prepare your chicken in traditional well cooked process. Properly boiled chicken ensures germs to perish

2) Don't eat / or get in contact with Migratory birds

3) When you go to Market place, where, chickens and other birds are sold, make sure your mouth is covered / closed, since it's airborne

take look at this global map for zones effected by Bird Flu!

[amar pritibi]

Thread maker er ta jani na..........
But ami........ free........

[Severus]

bird flu is actually a conspiracy created by international Beef meet seller assoc.

[jigSAW]

Originally Posted by Severus

bird flu is actually a conspiracy created by international Beef meet seller assoc.

hahahahahaha!!!!!!