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<B><font size=+1 color=brown><center>Bird flu: a new dread - II</font>
November 30 2005
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Bird flu is in news making a common health conscious human so concerned about what he should or he should not do, Mehnaaz Sultan Khuroo explains in detail all about the diseases, preventions and the reality behind
Human-to-human transmission of influenza A (H5N1) has been suggested in several household clusters and in one case of apparent child-to-mother transmission. Intimate contact without the use of precautions was implicated, and so far no case of human-to-human transmission by small-particle aerosols has been identified. </b>
In 1997, human-to-human transmission did not apparently occur through social contact, and serologic studies of exposed health care workers indicated that transmission was inefficient. Serologic surveys in Vietnam and Thailand have not found evidence of asymptomatic infections among contacts. Recently, intensified surveillance of contacts of patients by reverse-transcriptase–polymerase-chain-reaction (RT-PCR) assay has led to the detection of mild cases, more infections in older adults, and an increased number and duration of clusters in families in northern Vietnam, findings suggesting that the local virus strains may be adapting to humans. However, epidemiologic and virologic studies are needed to confirm these findings. To date, the risk of nosocomial transmission to health care workers has been low, even when appropriate isolation measures were not used. However, one case of severe illness was reported in a nurse exposed to an infected patient in Vietnam.
Given the survival of influenza A (H5N1) in the environment, several other modes of transmission are theoretically possible. Oral ingestion of contaminated water during swimming and direct intranasal or conjunctival inoculation during exposure to water are other potential modes, as is contamination of hands from infected fomites and subsequent self-inoculation. The widespread use of untreated poultry feces as fertilizer is another possible risk factor.
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.
The incubation period of avian influenza A (H5N1) may be longer than for other known human influenza. In 1997, most cases occurred within two to four days after exposure; recent reports 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.
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.
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.
Diagnosis
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.
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, 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.
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.
The diagnostic yield of different types of samples and virologic assays is not well defined. In contrast to infections with human influenza virus, throat samples may have better yields than nasal samples. Rapid antigen assays may help provide support for a diagnosis of influenza A infection, but they have poor negative predictive value and lack specificity for influenza A (H5N1). The detection of viral RNA in respiratory samples appears to offer the greatest sensitivity for early identification, but the sensitivity depends heavily on the primers and assay method used. Laboratory confirmation of influenza A (H5N1) requires one or more of the following: a positive viral culture, a positive PCR assay for influenza A (H5N1) RNA, a positive immunofluorescence test for antigen with the use of monoclonal antibody against H5, and at least a fourfold rise in H5-specific antibody titer in paired serum samples.
--To be concluded
(Author is MD, Department of Pathology, Shree Ramachandran Medical College and Research Institute, Porur, Chennai, India.)