Nipah virus and bird flu
- 1. NIPAH VIRUS Dr. Rajesh K. Mandal MD Resident,Internal Medicine,PG 2
- 2. • Nipah virus (NiV) infection is a newly emerging zoonosis that causes severe disease in both animals and humans. The natural host of the virus are fruit bats (flying foxes) of the Pteropodidae Family, Pteropus genus. • Nipah virus (NiV) is a member of the family Paramyxoviridae, genus Henipavirus. • RNA viruses,order Mononegavirales containing five established species. • Barking Pig Syndrome • Porcine Respiratory and Encephalitis Syndrome • Porcine Respiratory and Neurologic Syndrome
- 3. • Nipah virus was identified in April 1999, when it caused an outbreak of neurological ( Encephalitis) and respiratory disease on pig farms in peninsular Malaysia. • Its name originated from Sungai Nipah, a village in the Malaysian Peninsula where otbreaks took place.
- 4. Structure • Henipa virions are pleomorphic (variably shaped), ranging in size from 40 to 600 nm in diameter. • They possess a lipid membrane overlying a shell of viral matrix protein. • At the core is a single helical strand of genomic RNA tightly bound to N (nucleocapsid) protein and associated with the L (large) and P (phosphoprotein) proteins, which provide RNA polymerase activity during replication.
- 5. • Hendra virus and Nipah virus genomes are non-segmented, single-stranded negative-sense RNA. • Both genomes are 18.2 kb in length and contain six genes corresponding to six structural proteins.
- 6. Out Breaks • In the 1999 outbreak, Nipah virus caused a relatively mild disease in pigs, but nearly 300 human cases with over 100 deaths were reported. • In order to stop the outbreak, more than a million pigs were euthanized, causing tremendous trade loss for Malaysia. Since this outbreak, no subsequent cases (in neither swine nor human) have been reported in either Malaysia or Singapore. • In 2001, NiV was again identified as the causative agent in an outbreak of human disease occurring in Bangladesh. Genetic sequencing confirmed this virus as Nipah virus, but a strain different from the one identified in 1999. • In the same year, another outbreak was identified retrospectively in Siliguri, India with reports of person-to-person transmission in hospital settings (nosocomial transmission). Unlike the Malaysian NiV outbreak, outbreaks occur almost annually in Bangladesh and have been reported several times in India.
- 7. Locations of henipavirus outbreaks (red stars–Hendra virus; blue stars– Nipah virus) and distribution of henipavirus flying fox reservoirs (red shading–Hendra virus ; blue shading–Nipah virus)
- 9. • The recent outbreak in Kerala is thought to have been caused by dead bats found in a well of a family's home in the village of Changaroth. • The infection reportedly spread among family members and was passed on to others who had been in contact with the family.
- 10. • The Nipah virus has already claimed 10 lives in the Indian state of Kerala, including a 31 year-old nurse who was treating the infected. • Some 40 people have been quarantined in a bid to halt its spread. But the world is watching, nervously.
- 11. Transmisson and Reservoirs • In Malaysia and Singapore, humans were apparently infected with Nipah virus only through close contact with infected pigs. • The NiV strain identified in this outbreak appeared to have been transmitted initially from bats to pigs, with subsequent spread within pig populations. • The transmission in pigs was through direct contacts with infected fluids such as urine,saliva,bronchial secretions. • Virus was isolated from urine of Bats of Pteropus hypomelanus roosting in the East coast of malaysia.
- 14. • Nipah virus infection has beeen seen in23 species from 10 genera of bats in resion as widely spread as Yunan and Hainan island of China,Cambodia, Thailand,India,Madagascar,Ghana in West Africa. • Person-to-person transmission of Nipah virus in Bangladesh and India is regularly reported since 2001. This is most commonly seen in the family and caregivers of Nipah virus- infected patients. • Domestic animals such as cats and Dogs have also shown positive for Nipah virus.
- 15. Transmission to Humans • In malaysian outbreaks human infections occurred through direct contact with respiratory secretions and urine from infected pigs. • Occupational contacts in abattoir workers,pork sellers • In Bangladesh Nipah virus infection in human resulted from consumption of raw date palm sap contaminated by Bat saliva and human to human transmission. • In philippines, there was evidence of horse to human and human to human transmission.
- 16. Mechanism of infection • The virion binds and fuses to the surface of a host cell via the F and G proteins. • The lipid bi-layers are then melted and the viral nucleocapsid is released into the host cell. • The negative sense viral RNA is transcribed to mRNA which acts as a template for more negative sense viral RNA. • The viral RNA is used to make the necessary proteins (N,P,M,F,G,L,C,V,W) which congregate near the cell membrane. • Once all the necessary proteins are assembled a new viral cell will bud off and infect other host cells. • The new viral cells are able to fuse together and create a huge multinucleated cell called syncytia.
- 18. sign and Symptoms • Infection with Nipah virus is associated with encephalitis. After exposure and an incubation period of 5 to 14 days,illness presents with 3-14 days of fever and headache,nausea,vomiting,mailase followed by drowsiness, disorientation and mental confusion. • Meningismus is seen in about one third of patients although marked nuchal rigidity and photophobia is uncommon. • These signs and symptoms can progress to coma within 24-48 hours. Some patients have a respiratory illness during the early part of their infections, and half of the patients showing severe neurological signs showed also pulmonary signs. • seizures occur in 20% individuals
- 19. • Other neurological menifestations are segmental myoclonus including predominantly diaphragm,upper limb and neck musculature, cerebellar dysfunction,tremors, areflexia. • Brain stem involvement characterized by pinpoint pupil,un reactive pupil,abnormal Dolls eye reflex,tachycardia and hypertension occurs in more severe cases and protends poorer prognosis. • Patients may show features of atypical pneumonia with diffuse interstitial infiltrates in radiograph.
- 20. • During the Nipah virus disease outbreak in 1998-99 in Malaysia and singapore, 265 patients were infected with the virus. About 40% of those patients who entered hospitals with serious nervous disease died from the illness. • Mortality rate was greater than 70% in Bangladesh outbreaks. • Long-term sequelae following Nipah virus infection have been noted, including persistent convulsions and personality changes. • Latent infections with subsequent reactivation of Nipah virus and death have also been reported months and even years after exposure.
- 21. Diagnosis • Laboratory diagnosis of a patient with a clinical history of NiV can be made during the acute and convalescent phases of the disease by using a combination of tests. • Virus isolation attempts and real time polymerase chain reaction (RT-PCR) from throat and nasal swabs, cerebrospinal fluid, urine, and blood should be performed in the early stages of disease. • Antibody detection by ELISA (IgG and IgM) can be used later on. IgM capture ELISA, indirect IgG ELISA have high speceficity for diagnosis. • CSF Analysis : WBC count 10 to 800 cells/mm3 with lymphocyte predominance and elevated protein 50 to 250 mg/dl. Glucose is normal and RBC is usually not present.
- 22. • Blood leucocyte count is normal,moderate thrombocytopenia can occur. liver transaminases may be mild to moderately elevated but clinical jaundice is not the feature of the illness. • In fatal cases, immunohistochemistry on tissues collected during autopsy may be the only way to confirm a diagnosis. • MRI : Multiple,small ,asymmetric focal lesions ( <5mm) in subcortical and deep white matter without surrounding edema. • EEG : continous slow waves with or without periodic bitemporal independent sharp wave charges.
- 23. Differential Diagnosis • Classical swine fever, • PRRS (porcine reproductive and respiratory syndrome), • Aujeszky’s disease (pseudorabies), • Swine enzootic pneumonia (Mycoplasma hyopneumoniae), • Porcine pleuropneumonia (Actinobacillus pleuropneumoniae).
- 25. Suspected Case • A person fulfilling both of the following criteria is defined as a suspected case: 1. Features of acute encephalitis as demonstrated by a. Acute onset of fever AND b. Evidence of acute brain dysfunction as manifested by i. Altered mental status OR ii. New onset of seizure OR iii. Any other neurological deficit 2. Epidemiological linkage a. Drinking raw date palm sap OR b. Occurring during Nipah season OR c. Patient from Nipah endemic area
- 26. Probable Case • A person with features of acute encephalitis during a Nipah outbreak in the area OR with history of contact with confirmed Nipah patient . • In both suspected and probable cases, the patient might present with respiratory features with or without encephalitis. • The respiratory features are ; -Illness < 7 days duration AND - Acute onset of fever AND -Severe shortness of breath, cough AND -Chest radiograph showing diffuse infiltrates.
- 27. Conformed Case • suspected or probable case with laboratory confirmation of Nipah virus infection either by: -IgM antibody against Nipah virus by ELISA in serum or cerebrospinal fluid -Nipah virus RNA identified by PCR from respiratory secretions, urine, or cerebrospinal fluid.
- 28. Cluster • Two or more suspect cases living within a 30 minute walk of each other who develop symptoms within 21 days of each other.
- 29. Complications • Septicemia, • Bleeding from the gastrointestinal tract, • Renal impairment, • Relapse or late-onset encephalitis • Residual neurological deficit
- 30. Treatment • Treatment is limited to supportive care. May require intensive care monitoring • Mechanical ventilation for air way protection should be initiated with onset of neurological deterioration. • Because Nipah virus encephalitis can be transmitted person-to-person, standard infection control practices and proper barrier nursing techniques are important in preventing hospital-acquired infections (nosocomial transmission). • The drug Ribavirin has been shown to be effective against the viruses in vitro, but human investigations to date have been inconclusive and the clinical usefulness of ribavirin remains uncertain.
- 31. • Animal studies showed Ribavirin as well as chloroquine were ineffective. • Asprin and pentoxyfylline were used in Malaysian outbreaks in view of atrerial thrombosis,but not studied for evaluation of effecacy. • Passive immunization using a human monoclonal antibody targeting the Nipah G glycoprotein has been evaluated in the post-exposure therapy in the ferret model and found to be of benefit.
- 32. Prevention • Nipah virus infection can be prevented by avoiding exposure to sick pigs and bats in endemic areas and not drinking raw date palm sap. • Additional efforts focused on surveillance and awareness will help prevent future outbreaks. Research is needed to better understand the ecology of bats and Nipah virus, investigating questions such as the seasonality of disease within reproductive cycles of bats. • Surveillance tools should include reliable laboratory assays for early detection of disease in communities and livestock, and raising awareness of transmission and symptoms is important in reinforcing standard infection control practices to avoid human-to-human infections in hospital settings (nosocomial infection). • A subunit vaccine, using the Hendra G protein, produces cross-protective antibodies against HENV and NIPV has been recently used in Australia to protect horses against Hendra virus. This vaccine offers great potential for henipavirus protection in humans as well.
- 35. Recent Activities in kerela • To prevent infection, people in affected areas should In Kerala, authorities are currently on high alert and have set up medical camps to control the situation and prevent a further spreading of the virus. • They are also educating the public and giving specific instructions about general infection control practices,avoiding exposure and contact with sick people, as well as domestic animals also avoid consuming raw date palm sap or other raw fruits.
- 38. References • 1. Heymann, D. L. (2015). Control of Communicable Diseases Manual, 20th Edition. Nipah and Hendra Viral Diseases. American Public Health Association. 2015: 428-431. • 2. Centers for Disease Control and Prevention. Nipah Virus. www.cdc.gov/vhf/nipah/. • 3. World Health Organization. www.who.int/csr/disease/nipah/en/. • 4. uptodate • 5.https://www.ncbi.nlm.nih.gov/pubmed/26981928# • 6.https://www.ncbi.nlm.nih.gov/pubmed/10482278# • 7.National Guideline for Management, Prevention and Controlof Nipah Virus Infection including Encephalitis-Bangaldesh
- 39. •Thank you
- 40. Avian Influenza/ Bird Flu
- 41. Avian Influenza • Avian influenza—known informally as avian flu or bird flu is a variety of influenza caused by viruses adapted to birds.The type with the greatest risk is highly pathogenic avian influenza (HPAI). • Out of the three types of influenza viruses (A, B, and C), influenza A virus is a zoonotic infection with a natural reservoir almost entirely in birds.Avian influenza, for most purposes, refers to the influenza A virus.
- 42. Virology • Influenza A virus • Virus classification • Group: Group V ((−)ssRNA) • Order: Unassigned • Family: Orthomyxoviridae • Genus: Influenzavirus A • Species: Influenza A virus
- 43. • a pleiomorphic (non-uniform) envelope with a diameter of 50–120 nm • Influenza type A viruses are categorized into subtypes based on the type of two proteins on the surface of the viral envelope • H = hemagglutinin, a protein that causes red blood cells to agglutinate. • N = neuraminidase, an enzyme that cleaves the glycosidic bonds of the monosaccharide sialic acid (previously called neuraminic acid) • There are 18 different known H antigens (H1 to H18) and 11 different known N antigens (N1 to N11). • All known subtypes of influenza A viruses can infect birds, except subtypes H17N10 and H18N11, which have only been found in bats.
- 44. • Genetic factors in distinguishing between "human flu viruses" and "avian influenza viruses" include: • PB2: (RNA polymerase): Amino acid (or residue) position 627 in the PB2 protein encoded by the PB2 RNA gene. Until H5N1, all known avian influenza viruses had a Glu at position 627, while all human influenza viruses had a lysine. • HA: (hemagglutinin): Avian influenza HA binds alpha 2–3 sialic acid receptors, while human influenza HA binds alpha 2–6 sialic acid receptors. Swine influenza viruses have the ability to bind both types of sialic acid receptors.
- 45. • The influenza A virus subtypes that have been confirmed in humans, ordered by the number of known human pandemic deaths, are: • H1N1 caused "Spanish flu" in 1918 and the 2009 swine flu outbreak • H2N2 caused "Asian flu" in the late 1950s • H3N2 caused "Hong Kong flu" in the late 1960s • H5N1 considered a global influenza pandemic threat through its spread in the mid-2000s • H7N7 has unusual zoonotic potential • H1N2 is currently endemic in humans and pigs • H9N2, H7N2, H7N3, H5N2, and H10N7. • H1N1,H2N2,H3N2 have been incorporated into any human adapted or pandemic influenza strain • H7N9 potential of causing pandemic remains unknown.
- 46. Antigenic Shift and Drifts • Major changes in the envelope glycoproteins, the hemagglutinin and the neuraminidase, are referred to as antigenic shifts, and minor changes are called antigenic drifts. • Antigenic shifts are associated with epidemics and pandemics of influenza A, whereas antigenic drifts are associated with more localized outbreaks of varying extent.
- 47. • Avian influenza strains are divided into two types based on their pathogenicity: high pathogenicity (HP) or low pathogenicity (LP). • The most well-known HPAI strain, H5N1, appeared in China in 1996, and also has low pathogenic strains found in North America. • Companion birds in captivity are unlikely to contract the virus and there has been no report of a companion bird with avian influenza since 2003. Pigeons do not contract or spread the virus
- 48. Epidemiology • The most widely quoted date for the beginning of recorded history of avian influenza (initially known as fowl plague) was in 1878 when it was differentiated from other diseases that caused high mortality rates in birds. • Fowl plague, however, also included Newcastle disease until as recently as the 1950s. Between 1959 and 1995, there were 15 recorded occasions of the emergence of HPAI viruses in poultry, but losses were minimal. • Between 1996 and 2008 however, HPAI outbreaks in poultry have occurred at least 11 times and 4 of these outbreaks have involved millions of birds • Influenza A/H5N1 was first isolated from a goose in China in 1996. Human infections were first reported in 1997 in Hong Kong. • Since 2003, more than 700 human cases of Asian HPAI H5N1 have been reported to the WHO, primarily from 15 countries in Asia, Africa, the Pacific, Europe, and the Middle East, though over 60 countries have been affected • Majority reported in main land china,additional cases reported in Hongkong,Macau,Taiwan,Malaysia and canada
- 49. • Between early 2013 to early 2017, 916 lab-confirmed human cases of H7N9 were reported to the World Health Organization (WHO). • On 9 January 2017, the National Health and Family Planning Commission of China reported to WHO 106 cases of H7N9 which occurred from late November through late December, including 35 deaths, 2 potential cases of human-to-human transmission, and 80 of these 106 persons stating that they have visited live poultry markets. •
- 50. • There are many subtypes of avian influenza viruses, but only some strains of five subtypes have been known to infect humans: H5N1, H7N3, H7N7, H7N9, and H9N2. • At least one person, an elderly woman in Jiangxi Province, China, died of pneumonia in December 2013 from the H10N8 strain, the first human fatality confirmed to be caused by that strain.
- 51. • Lineages of Influenza A Viruses • Avian influenza (AI) viruses – influenza viruses which infect birds – have evolved into distinct genetic lineages in different geographic locations. • AI viruses circulating in birds in Asia, called Asian lineage AI viruses, can be recognized as genetically different from AI viruses that circulate among birds in North America (called North American lineage AI viruses). • These broad lineage classifications can be further narrowed by genetic comparisons,the North American lineage of H7N9 viruses could be further broken down into the North American ‘wild bird’ lineage versus the North American ‘poultry’ lineage.
- 52. • Highly Pathogenic and Low Pathogenic Avian Influenza A Viruses • Avian influenza A viruses are designated as highly pathogenic avian influenza (HPAI) or low pathogenicity avian influenza (LPAI) based on molecular characteristics of the virus and the ability of the virus to cause disease and mortality in chickens in a laboratory setting. • HPAI and LPAI designations do not refer to the severity of illness in cases of human infection with these viruses; both LPAI and HPAI viruses have caused severe illness in humans
- 53. Influenza A H5 • There are nine known subtypes of H5 viruses (H5N1, H5N2, H5N3, H5N4, H5N5, H5N6, H5N7, H5N8, and H5N9). • Most H5 viruses identified worldwide in wild birds and poultry are LPAI, but occasionally HPAI viruses have been detected. Sporadic H5 virus infection of humans has occurred, such as with Asian lineage HPAI H5N1 viruses currently circulating among poultry in Asia and the Middle East. • Human infection of H5N1 virus infections have been reported in 16 countries, often resulting in severe pneumonia and greater than 50% mortality.
- 54. Influenza A H7 • There are nine known subtypes of H7 viruses (H7N1, H7N2, H7N3, H7N4, H7N5, H7N6, H7N7, H7N8, and H7N9). • Most H7 viruses identified worldwide in wild birds and poultry are LPAI viruses. H7 virus infection in humans is uncommon. The most frequently identified H7 viruses associated with human infection are Asian lineage avian influenza A(H7N9) viruses, which were first detected in China in 2013. • While human infections are rare, these have commonly resulted in severe respiratory illness and death. In addition to Asian lineage H7N9 viruses, H7N2, H7N3, H7N7 virus infections have been reported. These viruses have primarily caused mild to moderate illness in people, with symptoms that include conjunctivitis and/or upper respiratory tract symptoms.
- 55. Influenza A H9 • There are nine known subtypes of H9 viruses (H9N1, H9N2, H9N3, H9N4, H9N5, H9N6, H9N7, H9N8, and H9N9); all H9 viruses identified worldwide in wild birds and poultry are LPAI viruses. • H9N2 virus has been detected in bird populations in Asia, Europe, the Middle East and Africa. Rare, sporadic H9N2 virus infections in people have been reported to generally cause mild upper respiratory tract illness; one infection has results in death
- 56. • Only two influenza A virus subtypes (i.e., H1N1, and H3N2) are currently in general circulation among people. • Some subtypes are found in other infected animal species. For example, H7N7 and H3N8 virus infections can cause illness in horses, and H3N8 virus infection cause illness in horses and dogs.
- 57. Avian Influenza in Poultry (Domesticated Birds) • Domesticated birds (chickens, turkeys, etc.) may become infected with avian influenza A viruses through direct contact with infected waterfowl or other infected poultry, or through contact with surfaces that have been contaminated with the viruses. • Infection of poultry with LPAI viruses may cause no disease or mild illness and may only cause mild signs (such as ruffled feathers and a drop in egg production) and may not be detected. • Infection of poultry with HPAI viruses can cause severe disease with high mortality. Both HPAI and LPAI viruses can spread rapidly through flocks of poultry. HPAI virus infection in poultry (with HPAI H5 or HPAI H7 viruses) can cause disease that affects multiple internal organs with mortality up to 90% to 100%, often within 48 hours. Some ducks can be infected without any signs of illness.
- 58. • Avian influenza outbreaks are of concern in domesticated birds for several reasons: • the potential for low pathogenic H5 and H7 viruses to evolve into highly pathogenic viruses • the potential for rapid spread and significant illness and death among poultry during outbreaks of highly pathogenic avian influenza • the economic impact and trade restrictions from a highly pathogenic avian influenza outbreak • the possibility that avian influenza A viruses could be transmitted to humans
- 59. Transmissson in Humans • Although avian influenza A viruses usually do not infect people, rare cases of human infection with these viruses have been reported. Infected birds shed avian influenza virus in their saliva, mucous and feces. • Human infections with virus occurs through air droplets or possibly dust inhalation or infected materials with virus on it and then touches their mouth, eyes or nose. • Rare human infections with some avian viruses have occurred most often after unprotected contact with infected birds or surfaces contaminated with avian influenza viruses.
- 60. Signs and Symptoms • Incubation period : 3 to 7 days but as long as 10 days • Influenza is most frequently described as a respiratory illness characterized by systemic symptoms, such as headache, feverishness, chills,myalgia, and malaise, as well as accompanying respiratory tract signs and symptoms, particularly cough and sore throat. • The patient has a fever, with temperatures of 38°–41°C (100.4°– 105.8°F). A rapid temperature rise within the first 24 h of illness is generally followed by gradual defervescence over 2–3 days.
- 61. • In uncomplicated influenza, the acute illness generally resolves over 2–5 days, and most patients have largely recovered in 1 week,although cough may persist 1–2 weeks longer. • Severe Disease : Fulminant pneumonia, acute respiratory distress, respiratory failure,seizures,septic shock, multi organ failure, Rhabdomyolysis, DIC, encephalopathy. • Reye’s syndrome is a serious complication in children that is associated with influenza B and—to a lesser extent—influenza A virus infection as well as with varicella-zoster virus and other viral infections. An epidemiologic association between Reye’s syndrome and aspirin therapy for the antecedent viral infection has been noted.
- 62. Case defination • Confirmed case : Avian influenza A H7N9 virus infection in patients conformed by CDC`s lab or CDC certified public lab or Lab using USFDA authorized test. • Probable case : Illness compatable with influenza, lab diagnostic positive for Influenza A, negative for H1 ,Negative for H1pdm09 and negative for H3 in Real time reverse PCR ( rRT-PCR ) • Case under investigation : illness compatable with influenza,meeting exposure criteria,lab conformation not known patient rnt travel < 10 days of illness onset,to a area where human cases of Avian influenza A H7N9 have been detected or area where H7N9 viruses are known to be circulating in animals or patient having contact with conformed cases of H7N9 within 10 days.
- 63. • Close contacts : involves coming within 6 feets/2meters or within room or care area of conformed casesr having direct contact with respiratory secretions • Patients are likely to be infectious one day prior to illness and continues untill resolution of illness.
- 64. Diferential Diagnosis • influenza may be difficult to differentiate on clinical grounds alone from an acute respiratory illness caused by any of a variety of respiratory viruses or by Mycoplasma pneumoniae. • Severe streptococcal pharyngitis or early bacterial pneumonia may mimic acute influenza, although bacterial pneumonias generally do not run a self-limited course. • Purulent sputum in which a bacterial pathogen can be detected by Gram’s staining is an important diagnostic feature in bacterial pneumonia.
- 65. Diagnosis • Influenza A virus infection in people cannot be diagnosed by clinical signs and symptoms alone; laboratory testing is needed. • Avian influenza A virus infection is usually diagnosed by collecting a swab from the upper respiratory tract (nose or throat) of the sick person. (Testing is more accurate when the swab is collected during the first few days of illness.) • The laboratory looks for avian influenza A virus either by using a Real Time reverse PCR ( r RT-PCR). Culture is usually not recommended.
- 66. • Lab : WBC normal or slightly decreased, Elevated AST,ALT,LDH,CRP,creatine kinase • Imaging: On radiograph multilobar patchy consolidations and ground glass opacity. Other CT findings of airbronchogram,interlobular septal thickening,centrilobular nodules,reticular opacities,cic changes,bronchial dilatation,subpleural linear opacities. • Postmortem Histopathology : Intraalveolar hemorrrhage,hyaline formation,pneumocyte hypertrophy,interstitial fibrosis,hypoxic and fatty changes in liver,kidney • However for some patients who are no longer very sick or who have fully recovered, can show evidence of antibodies in response to the virus. It requires two blood specimens (one taken during the first week of illness and another taken 3-4 weeks later). It is done by Hemagglutination inhibition assay.
- 67. Treatment • CDC currently recommends a neuraminidase inhibitor for treatment of human infection with avian influenza A viruses. • Analyses of available avian influenza viruses circulating worldwide suggest that most viruses are susceptible to oseltamivir, peramivir, and zanamivir. However, some evidence of antiviral resistance has been reported in Asian H5N1 and Asian H7N9 viruses isolated from some human cases.
- 68. Treatment
- 69. • Zanamivir is administered via an oral inhalation device and may exacerbate bronchospasm in asthmatic patients. • Oseltamivir has been associated with nausea and vomiting, whose frequency can be reduced by administration of the drug with food. • Amantadine causes CNS side effects, primarily jitteriness, anxiety, insomnia, or difficulty concentrating. These side effects disappear promptly upon cessation of therapy. • Rimantadine appears to be equally efficacious and is associated with less frequent CNS side effects than is amantadine.
- 70. • Antibacterial drugs should be reserved for the treatment of bacterial complications of acute influenza, such as secondary bacterial pneumonia. • The choice of antibiotics should be guided by Gram’s staining and culture of appropriate specimens of respiratory secretions, such as sputum.
- 71. Prevention • The best way to prevent infection with avian influenza A viruses is to avoid sources of exposure. Most human infections with avian influenza A viruses have occurred following direct or close contact with infected poultry. • People who have had contact with infected birds may be given influenza antiviral drugs preventatively. While antiviral drugs are most often used to treat influenza, they also can be used to prevent infection in someone who has been exposed to influenza viruses. When used to prevent seasonal influenza, antiviral drugs are 70% to 90% effective.
- 72. • Chemoprophylaxis with oseltamivir or zanamivir has been 84–89% efficacious against influenza A and B. • Chemoprophylaxis with amantadine or rimantadine is no longer recommended because of widespread resistance to these drugs.
- 73. Vaccination • Since 1975, influenza vaccines have been trivalent—i.e., they have contained two influenza A subtypes (H3N2 and H1N1) and one influenza B component. However, two antigenically distinct lineages of influenza B virus have circulated since the 1980s, and a quadrivalent vaccine that includes both B lineages is now available (2013–2014) as well. Quadrivalent vaccines are available in both inactivated and liveattenuated vaccine formulations. • The United States government maintains a stockpile of vaccines to protect against some Asian avian influenza A H5N1 viruses. The stockpiled vaccine could be used if similar H5N1 viruses were to begin transmitting easily from person to person. • Since influenza viruses change, CDC continues to make new candidate vaccine viruses as needed. Creating a candidate vaccine virus is the first step in producing a vaccine.
- 74. References • 1. Harrisons principle of internal medicine.19ed • 2. Centers for Disease Control and Prevention.www.cdc.gov • 3. World Health Organization • 4. uptodate