06 September 2009
GEMPA PANGALENGAN, 2 SEPTEMBER 2009
ALLAHU AKBAR ................ !
Pangalengan pun terguncang, kuasa Mu maha besar. Kami hanya bisa ber Takbir, ber Tasbih, ber Tahmid. Laa ilaha illalloh.
Sesaat setelah kami beranjak dari tempat kerja kami (Pkm Pangalengan DTP), jam 14.55 wib bumi Pangalengan pun tak luput dari guncangan gempa dengan kekuatan yang baru pertama kali dirasakan sebesar ini (7,3 SR)dalam beberapa puluh atau ratus tahun terakhir.
Beberapa saat kemudian sekitar jam 15.30 wib. petugas/piket jaga pkm kami yng berjumlah 2 orang pun dibuat panik, sibuk dst karena korban mulai berdatangan tiada henti. Baik yang mengalami luka ringan, sedang dan berat, bahkan yang telah meniggal dunia.
Selanjutnya....
21 Mei 2009
Sosial Budaya Provinsi Jawa Barat
04-01-2008 | |
Silih Asah Silih Asih Silih Asuh Kata-kata puitis diatas bukan sembarangan puisi, melainkan sebagai filsafat hidup yang dianut mayoritas penduduk Jawa Barat. Filosofi ini mengajarkan manusia untuk saling mengasuh dengan landasan saling mengasihi dan saling berbagi pengetahuan dan pengalaman. Sejatinya, inilah suatu konsep kehidupan demokratis yang berakar pada kesadaran dan keluhuran akal budi, yang akar filsafatnya menusuk jauh ke dalam bumi dalam pengertian hafiah. Berbeda dengan peradaban masyarakat lain di Nusantara, peradaban masyarakat Jawa Barat yang berpenduduk asli dan berbahasa Sunda sangat dipengaruhi oleh alam yang subur dan alami. Itulah sebabnya, dalam interaksi sosial, masyarakat di sana menganut falsafah seperti di kutip di atas. Selain akrab dengan alam lingkungan dan sesama manusia, manusia Sunda juga dekat dengan Tuhan yang menciptakan mereka dan menciptakan alam semesta tempat mereka berkehidupan (Triangle of life). Keakraban masyarakat Sunda dengan lingkungan tampak dari bagaimana masyarakat Jawa Barat, khususnya di pedesaan, memelihara kelestarian lingkungan. Di provinsi ini banyak muncul anggota masyarakat yang atas inisiatif sendiri memelihara lingkungan alam mereka. Keakraban masyarakat Jawa Barat dengan Tuhan, menyebabkan masyarakat di sana relatif dikenal sebagai masyarakat yang agamis, relijius, yang memegang teguh nilai-nilai ajaran agama yang mereka anut yakni agama Islam sebagai agama dengan penganut terbesar, kemudian Kristen (Katolik dan Protestan), Hindu, Budha, dan lainnya. Kendati demikian, dalam proses kehidupan sehari-hari, masyarakat Jawa Barat relatif terbuka saat berinteraksi dengan nilai-nilai baru yang cenderung sekuler dalam suatu proses interaksi dinamis dan harmonis. Peningkatan kualitas kehidupan dan kerukunan umat beragama tergambarkan dengan meningkatnya sarana peribadatan. Jumlah Mesjid meningkat dari 43.005 buah pada tahun 2004 menjadi 50.339 buah pada tahun 2005, Gereja Kristen dari 1.536 buah menjadi 1.629 buah, Gereja Katolik/Kapel dari 50 buah menjadi 110 buah, Pura/Kuil/Sanggah dari 24 buah menjadi 25 buah dan Vihara/Cetya/Klenteng dari 171 menjadi 181 buah. Budaya Jawa Barat didominasi Sunda. Adat tradisionalnya yang penuh khasanah Bumi Pasundan menjadi cermin kebudayaan di sana. Perda Kebudayaan Jawa Barat bahkan mencantumkan pemeliharaan bahasa, sastra, dan aksara daerah, kesenian, kepurbakalaan dan sejarahnya, nilai-nilai tradisional dan juga museum sebagai bagian dari pengelolaan kebudayaan. Pariwisata berbasis kebudayaan yang menampilkan seni budaya Jawa Barat, siap ditampilkan dan bernilai ekonomi. Untuk melestarikan budaya Jawa Barat, pemerintah daerah menetapkan 12 desa budaya, yakni desa khas yang di tata untuk kepentingan melestarikan budaya dalam bentuk adat atau rumah adat. Desa budaya tersebut adalah sebagai beikut:
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13 Mei 2009
FILARIASI (KAKI GAJAH)
Filariasis
From Wikipedia, the free encyclopedia
Filariasis Classification and external resources | |
ICD-10 | B74. |
---|---|
ICD-9 | 125.0-125.9 |
MeSH | D005368 |
-
- See special page for Filariasis in domestic animals
Filariasis (Philariasis) is a parasitic and infectious tropical disease, that is caused by thread-like filarial nematode worms. There are 9 known filarial nematodes which use humans as the definitive host. These are divided into 3 groups according to the niche within the body that they occupy: Lymphatic Filariasis, Subcutaneous Filariasis, and Serous Cavity Filariasis. Lymphatic Filariasis is caused by the worms Wuchereria bancrofti, Brugia malayi, and Brugia timori. These worms occupy the lymphatic system, including the lymph nodes, and in chronic cases these worms lead to the disease Elephantiasis. Subcutaneous Filariasis is caused by Loa loa (the African eye worm), Mansonella streptocerca, Onchocerca volvulus, and Dracunculus medinensis (the guinea worm). These worms occupy the subcutaneous layer of the skin, the fat layer. Serous Cavity Filariasis is caused by the worms Mansonella perstans and Mansonella ozzardi, which occupy the serous cavity of the abdomen. In all cases, the transmitting vectors are either blood sucking insects (fly or mosquito) or Copepod crustaceans in the case of Dracunculus medinensis.
Human filarial nematode worms have a complicated life cycle, which primarily consists of five stages. After the male and female worm mate, the female gives birth to live microfilariae by the thousands. The microfilariae are taken up by the vector insect (intermediate host) during a blood meal. In the intermediate host, the microfilariae molt and develop into 3rd stage (infective) larvae. Upon taking another blood meal the vector insect injects the infectious larvae into the dermis layer of our skin. After approximately one year the larvae molt through 2 more stages, maturing into to the adult worm.
Individuals infected by filarial worms may be described as either "microfilaraemic" or "amicrofilaraemic," depending on whether or not microfilaria are found in their peripheral blood. Filariasis is diagnosed in microfilaraemic cases primarily through direct observation of microfilaria in the peripheral blood. Occult filariasis is diagnosed in amicrofilaraemic cases based on clinical observations and, in some cases, by finding a circulating antigen in the blood.
Presentation
The most spectacular symptom of lymphatic filariasis is elephantiasis—thickening of the skin and underlying tissues—which was the first disease discovered to be transmitted by a mosquito bite. Elephantiasis results when the parasites lodge in the lymphatic system.
Elephantiasis affects mainly the lower extremities, while the ears, mucus membranes, and amputation stumps are affected less frequently. However, different species of filarial worms tend to affect different parts of the body: Wuchereria bancrofti can affect the legs, arms, vulva, and breasts, while Brugia timori rarely affects the genitals. Interestingly, those who develop the chronic stages of elephantiasis are usually amicrofilaraemic, and often have adverse immunlogical reactions to the microfilaria as well as the adult worm.
The subcutaneous worms present with skin rashes, urticarial papules, and arthritis, as well as hyper- and hypopigmentation macules. Onchocerca volvulus manifests itself in the eyes causing "river blindness" (onchocerciasis), the 2nd leading cause of blindness in the world. Serous cavity filariasis presents with symptoms similar to subcutaneous filariasis, in addition to abdominal pain because these worms are also deep tissue dwellers.
Incidence/prevalence
Filariasis is endemic in tropical regions of Asia, Africa, Central and South America, with more than 120 million people infected and one billion people at risk for infection.[1]
In communities where lymphatic filariasis is endemic, as many as 10 percent of women can be afflicted with swollen limbs, and 50 percent of men can suffer from mutilating genital symptoms.[2]
History
Lymphatic Filariasis is thought to have affected humans since approximately 4000 years ago [3]. Artifacts from ancient Egypt (2000 BC) and the Nok civilization in West Africa (500 BC) show possible elephantiasis symptoms. The first clear reference to the disease occurs in ancient Greek literature, where scholars differentiated the often similar symptoms of lymphatic filariasis from those of leprosy.
The first documentation of symptoms occurred in the 16th century, when Jan Huyghen van Linschoten wrote about the disease during the exploration of Goa. Similar symptoms were reported by subsequent explorers in areas of Asia and Africa, though an understanding of the disease did not began to develop until centuries later.
In 1866, Timothy Lewis, building on the work of Jean-Nicolas Demarquay and Otto Henry Wucherer, made the connection between microfilariae and elephantiasis, establishing the course of research that would ultimately explain the disease. In 1876, Joseph Bancroft discovered the adult form of the worm. In 1877, the life cycle involving an arthropod vector was theorized by Patrick Manson, who proceeded to demonstrate the presence of the worms in mosquitoes. Manson incorrectly hypothesized that the disease was transmitted through skin contact with water in which the mosquitoes had laid eggs. In 1900, George Carmichael Low determined the actual transmission method by discovering the presence of the worm in the proboscis of the mosquito vector.[3]
Diagnosis
Filariasis is usually diagnosed by identifying microfilariae on a Giemsa stained thick blood film. Blood must be drawn at night, since the microfilaria circulate at night(nocturnal periodicity), when their mosquito vector is most likely to bite. Also,decreased peripheral temperature may attract more microfilariae. Various concentration methods are also applied- i.Membrane filter ii.Knott's concentration method iii.Sedimentation technique
Polymerase chain reaction (PCR) and antigenic assays are also available for making the diagnosis. The latter are particularly useful in amicrofilaraemic cases. Lymph Node aspirrate,Chylus fluid may also yield Microfilriae. Imaging like CT,MRI may reveal "Filarial Dance Sign" in Chylus fluid. X-ray can show calcified adult worm in lymphatics. DEC provokation test is performed to obtain satisfying number of parasite in day-time samples. Circulating Filarial Antgen (CFA) may be detected by PCR. Xenodiagnosis is now obsolete EOsinophilia is a non-specific primary sign.
Treatment
The recommended treatment for killing adult filarial worms in patients outside the United States is albendazole (a broad spectrum anthelmintic) combined with ivermectin.[4][2] A combination of diethylcarbamazine (DEC) and albendazole is also effective.[2]
In 2003 the common antibiotic doxycycline was suggested for treating elephantiasis.[5] Filarial parasites have symbiotic bacteria in the genus Wolbachia, which live inside the worm. When the symbiotic bacteria are killed by the antibiotic, the worms themselves also die. Clinical trials in June 2005 by the Liverpool School of Tropical Medicine reported that an 8 week course almost completely eliminated microfilaraemia.[6][7]
Eradication efforts
In 1993, the International Task Force for Disease Eradication declared lymphatic filariaisis to be one of six potentially eradicable diseases.[2] Studies have demonstrated that transmission of the infection can be broken when a single dose of combined oral medicines is consistently maintained annually for approximately seven years.[8] With consistent treatment, the reduction of microfilariae means the disease will not be transmitted, the adult worms will die out, and the cycle will be broken.[8]
The strategy for eliminating transmission of lymphatic filariasis is mass distribution of medicines that kill the microfilariae and stop transmission of the parasite by mosquitoes in endemic communities.[8] In sub-Saharan Africa, albendazole (donated by GlaxoSmithKline) is being used with ivermectin (donated by Merck & Co.) to treat the disease, whereas elsewhere in the world albendazole is used with diethylcarbamazine.[2] Using a combination of treatments better reduces the number of microfilariae in blood.[8] The use of insecticide-treated mosquito bed nets also reduces the transmission of lymphatic filariasis as well as malaria, which is prevalent in many of the same communities in Africa.[8][9]
The efforts of the Global Programme to Eliminate LF are estimated to have already prevented 6.6 million new filariasis cases from developing in children, and to have stopped the progression of the disease in another 9.5 million people who have already contracted it. Dr Mwele Malecela, who chairs the programme, said: "We are on track to accomplish our goal of elimination by 2020."[10]
FLU BABI
Swine influenza
From Wikipedia, the free encyclopedia
Swine influenza (also called swine flu, hog flu, Mexican flu and pig flu) refers to influenza caused by those strains of influenza virus, called swine influenza virus (SIV), that usually infect (is endemic in) pigs.[2] As of 2009 these strains are all found in Influenza C virus and the subtypes of Influenza A virus known as H1N1, H1N2, H3N1, H3N2, and H2N3. Swine influenza is common in pigs in the midwestern United States (and occasionally in other states), Mexico, Canada, South America, Europe (including the United Kingdom, Sweden, and Italy), Kenya, Mainland China, Taiwan, Japan and other parts of eastern Asia.[2]
Transmission of swine influenza virus from pigs to humans is not common and properly cooked pork poses no risk of infection. When transmitted, the virus does not always cause human influenza and often the only sign of infection is the presence of antibodies in the blood, detectable only by laboratory tests. When transmission results in influenza in a human, it is called zoonotic swine flu. People who work with pigs, especially people with intense exposures, are at risk of catching swine flu. However, only about fifty such transmissions have been recorded since the mid-20th century, when identification of influenza subtypes became possible. Rarely, these strains of swine flu can pass from human to human. In humans, the symptoms of swine flu are similar to those of influenza and of influenza-like illness in general, namely chills, fever, sore throat, muscle pains, severe headache, coughing, weakness and general discomfort.
Electron microscope image of the reassorted H1N1 influenza virus photographed at the CDC Influenza Laboratory. The viruses are 80–120 nanometres in diameter.[1]
The 2009 flu outbreak in humans, known as "swine flu", is due to a new strain of influenza A virus subtype H1N1 that contained genes most closely related to swine influenza.[3] The origin of this new strain is unknown. However, the World Organization for Animal Health (OIE) reports that this strain has not been isolated in pigs.[4] This strain can be transmitted from human to human,[5] and causes the normal symptoms of influenza.[6]
Swine influenza is endemic in pigs
Pigs can become infected with human influenza, and this appears to have happened during the 1918 flu pandemic and the 2009 flu outbreak.
Classification
Of the three genera of influenza viruses that cause human flu, two also cause influenza in pigs, with Influenzavirus A being common in pigs and Influenzavirus C being rare.[7] Influenzavirus B has not been reported in pigs. Within Influenzavirus A and Influenzavirus C, the strains found in pigs and humans are largely distinct, although due to reassortment there have been transfers of genes among strains crossing swine, avian, and human species boundaries.
Influenza C
Influenza C viruses infect both humans and pigs, but do not infect birds.[8] Transmission between pigs and humans have occurred in the past.[9] For example, influenza C caused small outbreaks of a mild form of influenza amongst children in Japan,[10] and California.[10] Due to its limited host range and the lack of genetic diversity in influenza C, this form of influenza does not cause pandemics in humans.[11]
Influenza A
Swine influenza is known to be caused by influenza A subtypes H1N1,[12] H1N2,[12] H3N1,[13] H3N2,[12] and H2N3.[14] In pigs, three influenza A virus subtypes (H1N1, H3N2, and H1N2) are the most common strains worldwide.[15] In the United States, the H1N1 subtype was exclusively prevalent among swine populations before 1998; however, since late August 1998, H3N2 subtypes have been isolated from pigs. As of 2004, H3N2 virus isolates in US swine and turkey stocks were triple reassortants, containing genes from human (HA, NA, and PB1), swine (NS, NP, and M), and avian (PB2 and PA) lineages.[16]
Surveillance
Please help improve this article or section by expanding it. Further information might be found on the talk page. (May 2009) |
Although there is no formal national surveillance system in the United States to determine what viruses are circulating in pigs,[17] there is an informal surveillance network in the United States that is part of a world surveillance network.
History
Swine influenza was first proposed to be a disease related to human influenza during the 1918 flu pandemic, when pigs became sick at the same time as humans.[18] The first identification of an influenza virus as a cause of disease in pigs occurred about ten years later, in 1930.[19] For the following 60 years, swine influenza strains were almost exclusively H1N1. Then, between 1997 and 2002, new strains of three different subtypes and five different genotypes emerged as causes of influenza among pigs in North America. In 1997-1998, H3N2 strains emerged. These strains, which include genes derived by reassortment from human, swine and avian viruses, have become a major cause of swine influenza in North America. Reassortment between H1N1 and H3N2 produced H1N2. In 1999 in Canada, a strain of H4N6 crossed the species barrier from birds to pigs, but was contained on a single farm.[19]
The H1N1 form of swine flu is one of the descendants of the strain that caused the 1918 flu pandemic.[20][21] As well as persisting in pigs, the descendants of the 1918 virus have also circulated in humans through the 20th century, contributing to the normal seasonal epidemics of influenza.[21] However, direct transmission from pigs to humans is rare, with only 12 cases in the U.S. since 2005.[22] Nevertheless, the retention of influenza strains in pigs after these strains have disappeared from the human population might make pigs a reservoir where influenza viruses could persist, later emerging to reinfect humans once human immunity to these strains has waned.[23]
Swine flu has been reported numerous times as a zoonosis in humans, usually with limited distribution, rarely with a widespread distribution. Outbreaks in swine are common and cause significant economic losses in industry, primarily by causing stunting and extended time to market. For example, this disease costs the British meat industry about £65 million every year.[24]
1918 pandemic in humans
The 1918 flu pandemic in humans was associated with H1N1 and influenza appearing in pigs,[21] this may reflect a zoonosis either from swine to humans, or from humans to swine. Although it is not certain in which direction the virus was transferred, some evidence suggests that, in this case, pigs caught the disease from humans.[18] For instance, swine influenza was only noted as a new disease of pigs in 1918, after the first large outbreaks of influenza amongst people.[18] Although a recent phylogenetic analysis of more recent strains of influenza in humans, birds, and swine suggests that the 1918 outbreak in humans followed a reassortment event within a mammal,[25] the exact origin of the 1918 strain remains elusive.Cite error:Closing missing for tag.
This new strain appeared to be closely related to the strain involved in the 1918 flu pandemic. Moreover, the ensuing increased surveillance uncovered another strain in circulation in the U.S.: A/Victoria/75 (H3N2) spread simultaneously, also caused illness, and persisted until March.[26] Alarmed public-health officials decided action must be taken to head off another major pandemic, and urged President Gerald Ford that every person in the U.S. be vaccinated for the disease.[27]
The vaccination program was plagued by delays and public relations problems.[28] On October 1, 1976, the immunization program began and by October 11, approximately 40 million people, or about 24% of the population, had received swine flu immunizations. That same day, three senior citizens died soon after receiving their swine flu shots and there was a media outcry linking the deaths to the immunizations, despite the lack of positive proof. According to science writer Patrick Di Justo, however, by the time the truth was known — that the deaths were not proven to be related to the vaccine — it was too late. "The government had long feared mass panic about swine flu — now they feared mass panic about the swine flu vaccinations." This became a strong setback to the program.[29]
There were reports of Guillain-Barré syndrome, a paralyzing neuromuscular disorder, affecting some people who had received swine flu immunizations. This syndrome is a rare side-effect of modern influenza vaccines, with an incidence of about one case per million vaccinations.[30] As a result, Di Justo writes that "the public refused to trust a government-operated health program that killed old people and crippled young people." In total, less than 33% of the population had been immunized by the end of 1976. The National Influenza Immunization Program was effectively halted on Dec. 16.
Overall, there were about 500 cases of Guillain-Barré syndrome (GBS), resulting in death from severe pulmonary complications for 25 people, which, according to Dr. P. Haber, were probably caused by an immunopathological reaction to the 1976 vaccine. Other influenza vaccines have not been linked to GBS, though caution is advised for certain individuals, particularly those with a history of GBS.[31][32] Still, as observed by a participant in the immunization program, the vaccine killed more Americans than the disease did.[33]
1988 zoonosis
In September 1988, a swine flu virus killed one woman and infected others. 32-year old Barbara Ann Wieners was eight months pregnant when she and her husband, Ed, became ill after visiting the hog barn at a county fair in Walworth County, Wisconsin. Barbara died eight days later, after developing pneumonia.[34] The only pathogen identified was an H1N1 strain of swine influenza virus.[35] Doctors were able to induce labor and deliver a healthy daughter before she died. Her husband recovered from his symptoms.
ILI was reportedly widespread among the pigs exhibited at the fair. 76% of 25 swine exhibitors aged 9 to 19 tested positive for antibody to SIV, but no serious illnesses were detected among this group. Additional studies suggested between one and three health care personnel who had contact with the patient developed mild influenza-like illnesses with antibody evidence of swine flu infection. However, there was no community outbreak.[36][37]
1998 US outbreak in swine
In 1998, swine flu was found in pigs in four U.S. states. Within a year, it had spread through pig populations across the United States. Scientists found that this virus had originated in pigs as a recombinant form of flu strains from birds and humans. This outbreak confirmed that pigs can serve as a crucible where novel influenza viruses emerge as a result of the reassortment of genes from different strains.[38][39][40]
2007 Philippine outbreak in swine
Please help improve this article or section by expanding it. Further information might be found on the talk page. (April 2009) |
On August 20, 2007 Department of Agriculture officers investigated the outbreak (epizootic) of swine flu in Nueva Ecija and Central Luzon, Philippines. The mortality rate is less than 10% for swine flu, unless there are complications like hog cholera. On July 27, 2007, the Philippine National Meat Inspection Service (NMIS) raised a hog cholera "red alert" warning over Metro Manila and 5 regions of Luzon after the disease spread to backyard pig farms in Bulacan and Pampanga, even if these tested negative for the swine flu virus.[41][42]
2009 outbreak in humans
The 2009 flu outbreak is due to a new strain of subtype H1N1 not previously reported in pigs.[4] Following the outbreak, on May 2, 2009, it was reported in pigs at a farm in Alberta, Canada, with a link to the outbreak in Mexico. The pigs are suspected to have caught this new strain of virus from a farm worker who recently returned from Mexico, then showed symptoms of an influenza-like illness.[43] These are probable cases, pending confirmation by laboratory testing.
The new strain was initially described as apparent reassortment of at least four strains of influenza A virus subtype H1N1, including one strain endemic in humans, one endemic in birds, and two endemic in swine.[44] Subsequent analysis suggested it was a reassortment of just two strains, both found in swine.[3] Although initial reports identified the new strain as swine influenza (ie, a zoonosis originating in swine), its origin is unknown. Several countries took precautionary measures to reduce the chances for a global pandemic of the disease.[45]
Transmission
Transmission between pigs
Influenza is quite common in pigs, with about half of breeding pigs having been exposed to the virus in the US.[46] Antibodies to the virus are also common in pigs in other countries.[46]
The main route of transmission is through direct contact between infected and uninfected animals.[15] These close contacts are particularly common during animal transport. Intensive farming may also increase the risk of transmission, as the pigs are raised in very close proximity to each other.[47][48] The direct transfer of the virus probably occurs either by pigs touching noses, or through dried mucus. Airborne transmission through the aerosols produced by pigs coughing or sneezing are also an important means of infection.[15] The virus usually spreads quickly through a herd, infecting all the pigs within just a few days.[2] Transmission may also occur through wild animals, such as wild boar, which can spread the disease between farms.[49]
Transmission to humans
People who work with poultry and swine, especially people with intense exposures, are at increased risk of zoonotic infection with influenza virus endemic in these animals, and constitute a population of human hosts in which zoonosis and reassortment can co-occur.[50] Vaccination of these workers against influenza and surveillance for new influenza strains among this population may therefore be an important public health measure.[51] Transmission of influenza from swine to humans who work with swine was documented in a small surveillance study performed in 2004 at the University of Iowa.[52] This study among others forms the basis of a recommendation that people whose jobs involve handling poultry and swine be the focus of increased public health surveillance.[50] Other professions at particular risk of infection are veterinarians and meat processing workers, although the risk of infection for both of these groups is lower than that of farm workers.[53]
Interaction with avian H5N1 in pigs
Pigs are unusual as they can be infected with influenza strains that usually infect three different species: pigs, birds and humans.[54] This makes pigs a host where influenza viruses might exchange genes, producing new and dangerous strains.[54] Avian influenza virus H3N2 is endemic in pigs in China and has been detected in pigs in Vietnam, increasing fears of the emergence of new variant strains.[55] H3N2 evolved from H2N2 by antigenic shift.[56] In August 2004, researchers in China found H5N1 in pigs.[57]
These H5N1 infections may be quite common: in a survey of 10 apparently healthy pigs housed near poultry farms in West Java, where avian flu had broken out, five of the pig samples contained the H5N1 virus. The Indonesian government has since found similar results in the same region. Additional tests of 150 pigs outside the area were negative.[58][59]
Signs and symptoms
[edit] In swine
In pigs influenza infection produces fever, lethargy, sneezing, coughing, difficulty breathing and decreased appetite.[15] In some cases the infection can cause abortion. Although mortality is usually low (around 1-4%),[2] the virus can produce weight loss and poor growth, causing economic loss to farmers.[15] Infected pigs can lose up to 12 pounds of body weight over a 3 to 4 week period.[15]
In humans
Direct transmission of a swine flu virus from pigs to humans is occasionally possible (called zoonotic swine flu). In all, 50 cases are known to have occurred since the first report in medical literature in 1958, which have resulted in a total of six deaths.[61] Of these six people, one was pregnant, one had leukemia, one had Hodgkin disease and two were known to be previously healthy.[61] Despite these apparently low numbers of infections, the true rate of infection may be higher, since most cases only cause a very mild disease, and will probably never be reported or diagnosed.[61]
According to the Centers for Disease Control and Prevention (CDC), in humans the symptoms of the 2009 "swine flu" H1N1 virus are similar to those of influenza and of influenza-like illness in general. Symptoms include fever, cough, sore throat, body aches, headache, chills and fatigue. The 2009 outbreak has shown an increased percentage of patients reporting diarrhea and vomiting.[62] The 2009 H1N1 virus is not zoonotic swine flu, as it is not transmitted from pigs to humans, but from person to person.
Because these symptoms are not specific to swine flu, a differential diagnosis of probable swine flu requires not only symptoms but also a high likelihood of swine flu due to the person's recent history. For example, during the 2009 swine flu outbreak in the United States, CDC advised physicians to "consider swine influenza infection in the differential diagnosis of patients with acute febrile respiratory illness who have either been in contact with persons with confirmed swine flu, or who were in one of the five U.S. states that have reported swine flu cases or in Mexico during the 7 days preceding their illness onset."[63] A diagnosis of confirmed swine flu requires laboratory testing of a respiratory sample (a simple nose and throat swab).[63]
Prevention
Prevention of swine influenza has three components: prevention in swine, prevention of transmission to humans, and prevention of its spread among humans.
Prevention in swine
Methods of preventing the spread of influenza among swine include facility management, herd management, and vaccination. Because much of the illness and death associated with swine flu involves secondary infection by other pathogens, control strategies that rely on vaccination may be insufficient.
Control of swine influenza by vaccination has become more difficult in recent decades, as the evolution of the virus has resulted in inconsistent responses to traditional vaccines. Standard commercial swine flu vaccines are effective in controlling the infection when the virus strains match enough to have significant cross-protection, and custom (autogenous) vaccines made from the specific viruses isolated are created and used in the more difficult cases.[64][65] Present vaccination strategies for SIV control and prevention in swine farms typically include the use of one of several bivalent SIV vaccines commercially available in the United States. Of the 97 recent H3N2 isolates examined, only 41 isolates had strong serologic cross-reactions with antiserum to three commercial SIV vaccines. Since the protective ability of influenza vaccines depends primarily on the closeness of the match between the vaccine virus and the epidemic virus, the presence of nonreactive H3N2 SIV variants suggests that current commercial vaccines might not effectively protect pigs from infection with a majority of H3N2 viruses.[66][67] The United States Department of Agriculture researchers say that while pig vaccination keeps pigs from getting sick, it does not block infection or shedding of the virus.[68]
Facility management includes using disinfectants and ambient temperature to control virus in the environment. The virus is unlikely to survive outside living cells for more than two weeks, except in cold (but above freezing) conditions, and it is readily inactivated by disinfectants.[2] Herd management includes not adding pigs carrying influenza to herds that have not been exposed to the virus. The virus survives in healthy carrier pigs for up to 3 months and can be recovered from them between outbreaks. Carrier pigs are usually responsible for the introduction of SIV into previously uninfected herds and countries, so new animals should be quarantined.[46] After an outbreak, as immunity in exposed pigs wanes, new outbreaks of the same strain can occur.[2]
Prevention in humans
- Prevention of pig to human transmission
The transmission from swine to human is believed to occur mainly in swine farms where farmers are in close contact with live pigs. Although strains of swine influenza are usually not able to infect humans this may occasionally happen, so farmers and veterinarians are encouraged to use a face mask when dealing with infected animals. The use of vaccines on swine to prevent their infection is a major method of limiting swine to human transmission. Risk factors that may contribute to swine-to-human transmission include smoking and not wearing gloves when working with sick animals.[69]
- Prevention of human to human transmission
Influenza spreads between humans through coughing or sneezing and people touching something with the virus on it and then touching their own nose or mouth.[70] Swine flu cannot be spread by pork products, since the virus is not transmitted through food.[70] The swine flu in humans is most contagious during the first five days of the illness although some people, most commonly children, can remain contagious for up to ten days. Diagnosis can be made by sending a specimen, collected during the first five days for analysis.[71]
Recommendations to prevent spread of the virus among humans include using standard infection control against influenza. This includes frequent washing of hands with soap and water or with alcohol-based hand sanitizers, especially after being out in public.[72] Chance of transmission is also reduced by disinfecting household surfaces, which can be done effectively with a diluted chlorine bleach solution.[73] Although the current trivalent influenza vaccine is unlikely to provide protection against the new 2009 H1N1 strain,[74] vaccines against the new strain are being developed and could be ready as early as June 2009.[75]
Experts agree that hand-washing can help prevent viral infections, including ordinary influenza and the swine flu virus. Influenza can spread in coughs or sneezes, but an increasing body of evidence shows small droplets containing the virus can linger on tabletops, telephones and other surfaces and be transferred via the fingers to the mouth, nose or eyes. Alcohol-based gel or foam hand sanitizers work well to destroy viruses and bacteria. Anyone with flu-like symptoms such as a sudden fever, cough or muscle aches should stay away from work or public transportation and should contact a doctor to be tested.
Social distancing is another tactic. It means staying away from other people who might be infected and can include avoiding large gatherings, spreading out a little at work, or perhaps staying home and lying low if an infection is spreading in a community. Public health and other responsible authorities have action plans which may request or require social distancing actions depending on the severity of the outbreak.
Treatment
In swine
As swine influenza is rarely fatal to pigs, little treatment beyond rest and supportive care is required.[46] Instead veterinary efforts are focused on preventing the spread of the virus throughout the farm, or to other farms.[15] Vaccination and animal management techniques are most important in these efforts. Antibiotics are also used to treat this disease, which although they have no effect against the influenza virus, do help prevent bacterial pneumonia and other secondary infections in influenza-weakened herds.[46]
In humans
If a person becomes sick with swine flu, antiviral drugs can make the illness milder and make the patient feel better faster. They may also prevent serious flu complications. For treatment, antiviral drugs work best if started soon after getting sick (within 2 days of symptoms). Beside antivirals, palliative care, at home or in hospital, focuses on controlling fevers and maintaining fluid balance. The U.S. Centers for Disease Control and Prevention recommends the use of Tamiflu (oseltamivir) or Relenza (zanamivir) for the treatment and/or prevention of infection with swine influenza viruses, however, the majority of people infected with the virus make a full recovery without requiring medical attention or antiviral drugs.[76] The virus isolates in the 2009 outbreak have been found resistant to amantadine and rimantadine.[77]
In the U.S., on April 27, 2009, the FDA issued Emergency Use Authorizations to make available Relenza and Tamiflu antiviral drugs to treat the swine influenza virus in cases for which they are currently unapproved. The agency issued these EUAs to allow treatment of patients younger than the current approval allows and to allow the widespread distribution of the drugs, including by non-licensed volunteers.[78]