Avian influenza overview

Avian influenza Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Avian influenza from other Diseases
Epidemiology and Demographics
Risk Factors
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Chest X Ray
Other Diagnostic Studies
Treatment
Medical Therapy
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Avian influenza overview On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Avian influenza overview All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Avian influenza overview
CDC on Avian influenza overview
Avian influenza overview in the news
Blogs on Avian influenza overview
Directions to Hospitals Treating Avian influenza
Risk calculators and risk factors for Avian influenza overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D., Serge Korjian M.D., Gerald Chi, M.D.

Historical Perspective

Avian influenza was first described by Perroncito in 1878 in northern Italy following an outbreak of contagious disease of poultry. In 1918, the avian-descended influenza A H1N1 caused the first major human influenza pandemic. The first avian influenza A H5N1 virus infection in humans was described in 1997 in Hong Kong, where 18 cases were documented (including 6 deaths). The first human-to-human transmission of avian influenza infection was described in 2003 during the outbreaks in Southeast and Central Asia.

Pathophysiology

All reported cases of avian influenza are caused by influenza A virus. The genome of influenza A consists of 8 RNA gene segments, which encode 11 proteins, including hemagglutinin, neuraminidase, non-structural proteins, matrix proteins, polymerase proteins, and nucleoprotein). Influenza virus is transmitted in aerosols of respiratory secretions. The HA protein on the viral surface functions as a receptor binding site and binds to host receptors that contain sialic acid to allow viral fusion to the host cell in the respiratory tract. Following fusion, viral replication typically takes place within 1 day, and polymerase proteins and nucleoproteins are involved in viral replication, whereas the matrix protein is responsible for viral assembly prior to viral release via cytolytic or apoptotic mechanisms. Viral proteins are, at least in part, responsible for down-regulation of cytotoxic T-cell activity, evasion of immune responses, and activation of cytokines and pro-inflammatory mechanisms that contribute to host tissue injury. Avian influenza undergoes antigenic drifts and shifts that ultimately result in genetic reassortment and capacity to reinfect the same host.

Classification

To date, only influenza type A has been associated with avian influenza. Neither influenza B nor influenza C is associated with avian influenza. Classification of avian influenza may be based on either the pathogenicity of the virus (low pathogenicity vs. high pathogenicity) or the viral genetic subtypes (H5 vs. H7 vs. H9).

Cause

Avian influenza is caused by influenza A virus. Neither influenza B nor influenza C causes avian influenza. Influenza belongs to the Orthomyxoviridae family. Influenza is an enveloped, pleomorphic (spherical and filamentous forms) virus that contains a linear, segmented (8 segments), negative-sense, single-stranded RNA genome. The genome is composed of 8 segmented genes that encode 11 proteins.

Differential Diagnosis

Avian influenza should be differentiated from the following diseases or pathogens that cause upper or lower respiratory tract infection or flu-like illness, such as other influenza viruses, such as human or swine influenza, other viral, bacterial, fungal, and parasitic agents that are typically associated with nasopharyngeal and respiratory tract infections, and non-infectious causes, such as asthma, chronic obstructive pulmonary disease (COPD), drug adverse effects, and cardiac causes.

Epidemiology and Demographics

The World Health Organization (WHO) reports an incidence of 3 to 5 million cases of severe influenza disease annually, including 250,000 to 500,000 deaths every year. The case fatality rate per outbreak is highly variable and may range from less than 1 to more than 200 per 100,000 cases. Influenza may infect patients of all age groups, but elderly patients > 65 years, young children (especially patients < 2 years of age), and adolescents are at high risk of developing complications and death. There is no racial or gender predilection for avian influenza infection.

Risk Factors

The majority of cases of avian influenza infection in humans have resulted from contact with infected poultry, or contaminated environments. Human to human transmission is still rare and inefficient.

Natural History, Complications, and Prognosis

Following exposure to the avian influenza virus, an incubation period of 2 to 3 days for H5N1 and 2 to 8 days for H7N9 delays the onset of symptoms. The majority of patients present with with a high grade fever, cough, headache, sore throat, vomiting, diarrhea, and abdominal pain. Approximately 50% of patients with avian influenza develop severe complications such as acute respiratory distress syndrome, renal failure, sepsis, and multiple organ dysfunction syndrome. Of the reported cases, about 60% of patients have died, particularly those who develop early complications. Patients without complicated disease usually recover within 3 to 5 days with no sequelae.

Diagnosis

History and Symptoms

Avian influenza virus infection is associated with a wide range of illness from conjunctivitis only, to influenza-like illness, to severe respiratory illness (e.g. dyspnea, pneumonia, acute respiratory distress, viral pneumonia, respiratory failure) with multi-organ disease, sometimes accompanied by nausea, abdominal pain, diarrhea, vomiting, and occasionally neurologic impairment (altered mental status or seizures).

Treatment

Medical Therapy

Neuraminidase inhibitors can reduce the duration of viral replication and improve survival among patients with avian influenza. In cases of suspected avian influenza, oseltamivir, zanamivir, or peramivir should be administered as soon possible, preferably within 48 hours of symptom onset.