Aug2014

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Veterinary College, Bengaluru Monthly e-Bulletin

Newsletter Date : 31 August 2014

Volume No: 3 Issue : 08

Raveendra Hegde and Rashmi K.M AICRP FMD Regional centre, Institute of Animal Health and Veterinary Biologicals, KVAFSU, Hebbal, Bangalore ( honkankereravi@yahoo.com)

Foot and mouth disease (FMD) is the most important livestock disease in the world in terms of its economic impact. FMD status of a country is an important determinant of international trade in livestock products and the existence of FMD is an effective barrier from the markets with highest prices for these products. The disease is ranked as number one priority disease to be taken up for the control and eradication globally. India is a developing nation with vast resources in Livestock sector and has very large populations of susceptible animals. Indian livestock sector is predominantly composed of small, marginal and landless farmers who keep livestock as their resource of income and livelihood. Control of FMD is relevant, for protecting the livestock industries in developed countries and for livelihoods and income generation in the developing countries like India, where FMD is endemic. Progressive risk reduction of FMD can help in progressive market access of livestock commodities from developing countries. Control of Foot and Mouth disease: Control of FMD is usually achieved by mass vaccination of all the susceptible livestock repeatedly at regular intervals till the disease incidence comes down to negligible levels. Several countries in Western Europe followed this strategy of regular coordinated mass vaccination, control of animal movements, quarantine practices and strict zoo-sanitary measures from early 1950s and successfully eradicated the disease and further from 1992 stopped vaccination altogether. At present, these countries (FMD free developed countries) follow the stamping out method in case of any fresh incursion, in which all the affected and in contact animals are killed and disposed off in order to quickly control the disease. In developing countries like India, where the disease is endemic, repeated vaccination along with other control measures such as restriction on animals movement and zoo sanitary measures will be the best option to build-up herd immunity, which in turn will eliminate the circulating virus from the population and bring down the incidence.

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FMD control programme (FMDCP) in India: The implementation of FMDCP involves the participation and execution by several agencies including the DADF, State Govts, ICAR, Vaccine manufacturers, Milk federation, Meat and other industry and more importantly livestock farmers, the beneficiaries. The action plan will define the role to be played by each of the participating agency so that the progress of the FMDCP can be monitored and assessed objectively to attain the goal of control of FMD as per the OIE guidelines. Overall objectives is to control FMD in India in a systematic fashion to achieve control and eradication of FMD in India in the next 20-30 years and take measures to maintain the status of freedom thus achieved. Specific objectives: 1. To build up a strong herd immunity in the target populations of the country by repeated mass vaccination of all cattle, buffaloes and pigs so that the disease incidence comes down and the virus circus in the population is interrupted to that extent that there is no incidence of the disease 2. All the target animals in FMDCP will be vaccinated twice a year at every six months intervals. 3. Increase the area of vaccination coverage in a defined manner so that we try to achieve freedom from clinical disease in a few defined zones of the country by 2018-20. 4. Continuous vaccination efforts to include more and more areas of the country without clinical disease so that the entire country is covered by 2030 5. Maintain the vigil to ensure that the disease is not introduced in areas of freedom from disease. 6. Follow OIE/FAO-PCP pathway to establish defined zones of freedom with vaccination initially and freedom without vaccination ultimately in the entire country. Expected results: • Period up to 2010: Gradual reduction in disease incidence with absence of clinical infection in few clearly defined zones of the country • Period 2020-2030: Absence of clinical disease in more and more areas. Defined areas of freedom with vaccination. • 2031-2035: More areas of freedom with vaccination and parts of the country free without vaccination • Beyond 2035: More areas or the entire country free without vaccination leading to eradication. Essential components of FMDCP implementation: • Disease surveillance and diagnosis: timely reporting of the disease without any delay will be an essential pre requisite for the success of the programme. All concerned stake holders especially the state AHDs and people engaged in the field should be educated fully about the importance of reporting of the incidence, collection of clinical samples and sending them to the laboratory for diagnosis and serotype identification. • Vaccine availability: the responsibility lies with vaccine manufacturers to supply the vaccine on time as per the defined schedules every six months and integral to the vaccine supply is associated logistics of cold chain maintenance at the district/taluk/dispensary level and further to the field level till the vaccine is administered. • Vaccination schedule: The vaccination as per the schedule should be carried out in a Pulse Polio like vaccination campaign so that all the target population is covered in a shortest possible time. The schedule is defined as per the epidemiology of the disease in a particular state or zone.

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Vaccination logistics: the state and district administration should be involved in fully providing the necessary logistics such as vaccinators, mobility, syringes & needles, farmers education etc. and ultimately implementation of the programme as scheduled. • Animal identification: the animals vaccinated are to be given a permanent identification (ear tags/ barcodes). • Assessment of post vaccinal immune response: since FMDCP involves several rounds of vaccination, seromonitoring is carried out from the beginning of the programme for which we already have diagnostic capabilities. The assessment will decide the frequency of vaccinations as we progress in the programme and also helps in setting up emergency measures in the event of disease incidence. • Biosecurity and zoo-sanitary measures: restriction on movement of animals have to be strictly enforced to prevent the spread of disease. As we progress in the programme, the disease incidence to be reported immediately and strict, biosecurity measures to be implemented including the isolation of affected animals, sanitation & disinfection, movement control etc. to prevent the spread of disease. • Extension activities: educating all the stake holders including field veterinarians, farmers, and all other public good is a necessity for the successful implementation of the programme. Wide media publicity is necessary to reach to the farmers about the programme and its benefits. • Economic impact analysis: is essential at regular intervals in order to assess the impact of the programme • Regional initiatives: the cooperation and coordination of all the state Govts is necessary in uniformly implementing the FMDCP which will go long way in achieving the targets in stipulated time lines. Early disease reporting, imposition of movement restriction between states, sharing information on disease incidence, simultaneous vaccination in border areas will all contribute to the success of the programme thereby elimination of the disease in the region. FMD control programme in India is envisaged as per the FAO’s PCP having following seven stages: Stage 0

FMD risk not controlled and no reliable information

Stage 1

Understanding of the epidemiology of FMD in the country and develop a risk based approach to reduce the impact of FMD

Stage 2

A strategic FMD control plan that has the aim of reducing the impact of FMD in at least one zone or sector is developed

Stage 3

Implementation of control strategy that has the aim of eliminating FMD from at least a zone of the country

Stage 4

Maintain zero circulation or incursions. It should have the evidence that FMD is not occurring endemically within the zone or country

Stage 5

Maintain zero circulation or incursions and withdraw vaccinations. Once, the OIE requirements for recognition of ‘free with vaccination’ are fulfilled, a dossier has to be submitted to OIE for recognition of this status

Stage 6

Free without vaccinations. Application to OIE for recognition of ‘‘free without vaccination’’ status (zone or whole country)

Stage 0

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FMD risk not controlled and

StageNo 1 : 3 Issue Understanding of the epidem Volume : 08 01


The control programme (FMDCP) was launched in India during 10th plan period in 2003–2004 in 54 selected districts spread over 8 states of the country covering 30 million cattle and buffalo population with an objective of creating FMD free zones and then expanding these zones to cover the entire country. The basic approach is to vaccinate all cattle and buffalo every 6 months. Due to initial success, additional 167 districts (another 80–90 million cattle and buffalo) have been included under the programme in 2010–2011. Currently, this programme includes 221 districts of the country covering states of Southern peninsula (Kerala, Tamil Nadu, Puducheri, Karnataka and Andhra Pradesh), Maharashtra, Goa, Daman and Diu, Gujarat, Punjab, Haryana, Delhi, Dadra and Nagar Haveli, Andaman & Nicobar Islands, Lakshadweep and 16 districts in Uttar Pradesh, and targeting 120 million cattle and buffalo and pigs. The target of this progressive zoning approach is that all animals are vaccinated twice a year (6 monthly) to build up strong herd immunity and certain number of random serum samples are tested in each district for pre and post vaccination SP- antibody level by a liquid phase blocking (LPB) ELISA (LPB-ELISA) and concurrent disease surveillance. There is no scope for slaughter of affected and in-contact cattle. It is expected that the FMDCP will be expanded to cover the entire country (640 districts) targeting 315 million cattle, buffalo and pigs in a phased manner before the end of 12th plan period. The FMDCP is fully funded by Govt of India and implemented by state Animal Husbandry Departments. The vaccination of livestock in non FMD areas were also being done under ASCAD programme of GOVT of India, but not carried out twice a year. Impact of vaccination: Due to implementation of the vaccinations covering large number of animals under FMDCP and ASCAD programmes, the incidence of the disease has definitely comedown compared to the period before 2003. The herd immunity in FMDCP areas has progressively increased with minor aberrations that speak for positive impact of vaccination for last 6–7 years. The severity of clinical sickness has been reduced substantially and number of FMD cases/outbreaks has dropped in different parts of the country as estimated by real-time monitoring and surveillance. The 3AB3 DIVA test shows reduced circulation of the virus in regularly vaccinated areas compared to other areas of the country. Few sporadic cases of FMD in some vaccinated populations/ districts affecting a few animals were recorded. This may be due to unrestricted animal movement from the neighbouring unvaccinated districts/states. Nevertheless, infection could not spread due to surrounding herd immunity. FMD Control programme and Seromonitoring in Karnataka state In the state of Karnataka FMD-CP is being implemented since September 2011 and so far six rounds of vaccination have been carried out. The FMD Regional centre, IAH&VB, Bangalore has been entrusted the responsibility of seromonitoring under FMD-CP for the state and the centre has screened all the serum samples up to FMD-CP phase VI. The reported vaccination coverage has increased from 58 percent in the I phase to 96 percent in VI phase. At the beginning of FMD-CP, during I phase, the protective titre against all the three serotypes (O, A, Asia-1) together was 5 percent in the prevaccination serum samples and gradually increased to 49 percent at the beginning of VI phase. The post vaccination protective titre increased from 18 percent (I Phase) to 80 percent (VI phase). The serosurveillance study of random samples indicated that the apparent percent prevalence of FMD infection as evinced by DIVA-ELISA was reduced from 48 percent to 21 percent. This indicates the systematic vaccination

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carried out under FMDCP covering large number of target animals has impact in reduction of clinical disease in the state of Karnataka during 2014. Seromonitoring of FMD vaccination under FMDCP in Karnataka Total number of animals protected against all three serotypes Species of animals

Phase I

Species of animals

Cattle Buffalo Cattle + Buffalo Total

Phase II

Pre Vacc. 161 47 208

Post Vacc. 596 161 757

Pre vaccinated 5.02 3.40 4.53

Post vacc. 2945 1321 4266 8853

Post vaccinated 20.23 12.18 17.74

759

1187

4.53% 22.15

17.74% 39.31

Buffalo

1975 5401

1612 4631

406 1155

607 1794

20.55 21.38

37.65 38.73

2461 1403

10032 1961 1114

506 275

730 435

21.38% 20.56 19.60

38.73% 37.22 39.04

Cattle + Buffalo Total

3864

3075

781

1165

20.21

37.88

Cattle

3103 1950 5053

6939 3252 1973 5225

1927 1151 3078

20.21% 45.6 41.1 44

37.88% 59.2 58.3 59

3711 2205

10278 3737 2116

1056 593

1969 1141

44% 28.45 27

59% 53 54

5916

5853

1649

3110

28

53

28%

53%

Cattle

Cattle + Buffalo Total Cattle Buffalo Cattle + Buffalo Total

Phase VI

Pre vacc. 3204 1383 4587

3019

Buffalo

Phase V

% of animals protected against all three serotypes (pre & post vaccination)

3426

Buffalo

Phase IV

Total numbers protected

Cattle

Cattle + Buffalo Total

Phase III

Total number of serum samples screened

1415 802 2217

11769

Cattle

3853

3861

1960

3181

51

82

Buffalo

2092

2124

936

1606

45

76

Cattle + Buffalo Total

5945

5985

2896

4787

49

80

49%

80%

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Raveendra Hegde, Rashmi K M, Giridhar P and M.D. Venkatesha Institute of Animal Health and Veterinary Biologicals, KVAFSU, Hebbal, Bangalore ( honkankereravi@yahoo.com) Introduction Foot-and-mouth disease (FMD) is a highly contagious viral disease which affects all cloven-hoofed domestic animals including cattle, sheep, goats, pigs, and buffalo and wildlife. The highly contagious nature of the virus and severity of economic impacts associated with the disease, determine FMD’s status as the most important disease limiting trade of animals and animal products throughout the world. The disease has high morbidity, low mortality and the adult animals generally recover. The disease has debilitating effects, including weight loss, decrease in milk production, chronic mastitis, and loss of drought power, resulting in a loss in productivity for a considerable time. Mortality, however, can be high in young animals or in some wildlife populations. Clinical signs are generally more severe in temperate breeds associated with intensive farming particularly in immunologically naive populations and most severe in high-production modern livestock breeds, particularly dairy cattle and pigs making the disease intolerable to modern farming practices, especially in developed countries. Even under subsistence farming conditions, FMD can result in serious economic losses. Wide host range, an ability to infect in small doses, a rapid rate of replication, a high level of viral excretion and multiple modes of transmission, including spread by the wind aggravate the FMD outbreak scenario. These features make FMD a difficult and expensive disease to control and eradicate, and one that is much feared disease associated with livestock production. Etiology • FMD virus (FMDV) is a member of the genus Aphthovirus in the family Picornaviridae. There are seven major viral serotypes: O, A, C, SAT 1, SAT 2, SAT 3 and Asia 1 and multiple subtypes in each serotype. The seven serotypes are immunologically distinct and immunity to one FMDV serotype does not protect an animal from other serotypes. Species Affected • FMDV mainly affects cloven-hooved mammals (order Artiodactyla) and many other species of different orders. • Cattle, pigs, sheep, goats, water buffalo, yaks, ranched or farmed cervids such as reindeer, deer and elk are susceptible to FMD. Llamas and alpacas can be infected experimentally and camels have a very low susceptibility. • The disease has been reported in at least 70 species of wild (or captive wild) artiodactyls including African buffalo, bison, moose, chamois, giraffes, wildebeest blackbuck, warthogs, kudu, impala, and several species of deer, antelopes and gazelles. African buffalo are important maintenance hosts for FMDV in Africa. • FMDV can also infect hedgehogs, armadillos, kangaroos, nutrias, and capybaras. • Several clinical cases have been reported in captive Asian elephants, but African elephants are not

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not considered susceptible under natural conditions in southern Africa. • Laboratory animal models include guinea pigs, rats and mice, but these animals are not thought to be important in transmitting FMDV in the field. Geographical Distribution • North and Central America, New Zealand, Australia, Greenland, Iceland and Western Europe are free of FMDV. • Western Europe was affected by some recent outbreaks (eradication was successful), but FMD has not been reported in North America for more than 60 years. The last U.S. outbreak occurred in 1929, while Canada and Mexico have been FMD-free since 1952-1953. The serotypes of FMDV are not distributed uniformly around the world. • The current global burden of FMDV infection is maintained within three continental reservoirs in Asia, Africa and South America. The cumulative incidence of FMDV serotypes show that six of the seven serotypes (O, A, C, SAT 1, 2, 3) have occurred in Africa, while four (O, A, C, Asia 1) in Asia and Europe and three (O, A, C) in South America, FMD virus serotype O and A are circulating in the middle East. • Currently FMDV serotypes C appear to have vanished from the globe. Serotype O is the most widely prevalent serotype in the world, including India and is the major serotype causing recent outbreaks in many disease free countries. Transmission: • FMD is usually spread by movement of infected animals. • The virus can enter the body by inhalation, ingestion or through skin abrasions and mucous membranes. • FMDV is excreted from all secretions and excretions from acutely infected animals, including expired air, saliva, milk, urine, feces and semen. • Cattle are susceptible to aerosolized virus, while pigs produce large amounts of aerosolized virus. Airborne transmission can occur under favorable climatic conditions up to 250 kms. • Mechanical transmission by fomites and living (e.g., animal) vectors is an important means of transmission of FMDV. Infected milk may be the source of infection to young calves, milk tankers and people can act as mechanical vectors for FMDV. • FMDV on an average remains viable in the environment for three months or less. Virus stability increases at lower temperatures and very cold climates, may be for six months. Survives for longer in organic material, as well as protection from sunlight. The virus may survive for 14 days in dry faeces, > 6 months in slurry and for 39 days in winter. FMDV is inactivated at pH below 6.0 or above 9.0. This virus gets inactivated by acidification of muscles during rigor mortis. However, in the bones and glands, FMDV may persist for longer time. Pathogenesis • In the cattle infected via respiratory tract, virus initially replicates in the pharynx from where it proceeds towards the epithelium of the mucosa associated lymphoid tissue of the nasopharynx, mucous membrane of oral cavity and invades the basal layer of the stratified epithelium of the tongue and produce primary lesions. • Virus also invades the lymphatics and enter into the blood stream resulting in spread of virus to other

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organs and tissues such as epithelium of mouth, dental pad, coronary band, interdigital space of hoof, mammary gland, teats (cattle) and snout (pigs) where the secondary lesions develop. • One to -two days after infection, fever and viraemia may be observed. In advanced and unaddressed cases, secondary bacterial infection may set up causing extensive damage of the tissue. Heart muscles of young animals may show acute degeneration of the myocardial fibers (tiger heart). • Sometime involvement of damaged skin in pigs may be observed that are kept on concrete. Generally, the vesicular lesions appear at these sites (parts of knees and hocks) and within 48h it ruptures. • The viremia persists for about 3 days. The virus is excreted during viraemia for somedays thereafter as serum antibody develops viraemia decreases, and the animal ceases to be infectious. Incubation Period: The incubation period for FMD can vary with the species of animal, the dose of virus, the viral strain and the route of inoculation. Two to 14 days in cattle, one to 12 days in sheep(most infection appear in 2-8 days), two days or more in pigs(even short 18-24 hours). Other reported incubation periods are 4 days in wild boar, 2 days in feral pigs, 2-3 days in elk, 2-14 days in Bactrian camels, and possibly up to 21 days in water buffalo infected by direct contact. Clinical Signs: Cattle: 0 • Initially pyrexia of 40 C lasting 1-2 days, followed by variable number of vesicles develop on tongue, hard palate, dental pad, lips, gums, muzzle, coronary band, and interdigital space and also may be on teats particularly of lactating cows. • Young calves may die before the appearance of vesicles die due to heart failure • The vesicles on the tongue often coalesce, rupture quickly, and are highly painful, and the animal becomes reluctant to eat. Infected animals salivate profusely and develop mucoid to mucopurulent nasal discharge. • Affected animals become lethargic, may lose condition rapidly, and may have gradual or sudden, severe decreases in milk production. • Hoof lesions, with pain, occur in the area of the coronary band and interdigital space, recovery resulting in under run sole and chronic lameness. • Some cattle that recover from FMD are reported to develop heat intolerance syndrome (HIS; also called ‘hairy panters’) characterized by abnormal hair growth, pronounced panting with elevated body temperature and pulse rate during hot weather, and failure to thrive. The pathogenesis of this syndrome is not known, and a definitive link with FMD has not been established, but endocrine disturbances were suspected by some early investigators. Pigs • Mouth lesions are small, less apparent than in cattle, and drooling is rare. • Fever may be seen with shorter elevation of temperature and some cases show the temperature is near normal or even below normal.

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Sometimes vesicles are found on the snout or udder, hock or elbows if the pigs are housed on rough concrete floors. Severe lesions on the feet cause lameness and blanching of the skin around the coronary bands as a first signs of FMD. The horns of the digits are sometimes sloughed. Decreased appetite, lethargic and huddle together.

Young pigs up to 14 weeks of age may die suddenly from heart failure, piglets less than 8 weeks of age are particularly susceptible. Sheep and Goats: • FMD tends to be mild in sheep and goats and a significant number of infected animals may be asymptomatic. • Common signs in small ruminants are fever, mild to severe lameness of one or more legs. • Vesicles do occur on the feet, but may rupture and be hidden by foot lesions from other causes. Mouth lesions are often not noticeable and may appear as shallow erosions. • Drop in Milk production, rams can be reluctant to mate. Significant numbers of ewes abort in some outbreaks. Young lambs and kids may die due to heart failure. The clinical signs in wildlife resemble those in domesticated livestock, with vesicles and erosions particularly on the feet and in the mouth. Diagnosis: Primary diagnosis of FMD commonly involves • Recognition of typical clinical signs in affected animals. Before an outbreak is declared it is usual to demonstrate FMD virus or antigen using laboratory tests • Diagnosis of FMD is by virus isolation or by the demonstration of FMD viral antigen or nucleic acid in samples of tissue or fluid. Detection of virus-specific antibody can also be used for diagnosis, and antibodies to viral nonstructural proteins (NSPs) can be used as indicators of infection, irrespective of vaccination status. Identification of the agent: • The demonstration of FMD viral antigen or nucleic acid is sufficient for a positive diagnosis. • Enzyme-linked immunosorbent assays (ELISA) can be used to detect FMD viral antigens and for serotyping. • Lateral flow devices (LFD) can be used to detect FMD viral antigens. • The ELISA has replaced complement fixation (CF) in most laboratories. • Reverse transcription polymerase chain reaction (RT-PCR) and/or virus isolation using susceptible cell cultures (primary bovine thyroid cells, primary pig, calf or lamb kidney cells, or BHK-21 or IB-RS-2 cell lines). Serological tests: • The demonstration of specific antibodies to structural proteins in non vaccinated animals is indicative of prior infection with FMDV. This is particularly useful in mild cases or where epithelial tissue cannot be collected. • Tests for antibodies to some NSPs of FMDV are useful in providing evidence of previous or current viral replication in the host, irrespective of vaccination status. For laboratory diagnosis, the tissue of choice is epithelium or vesicular fluid. Ideally, at least 1 g of epithelial tissue should be collected from an un ruptured or recently ruptured vesicle, usually from the

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tongue, buccal mucosa or feet. The transport medium for epithelial samples composed of equal amounts of glycerol and 0.04 M phosphate buffer, pH 7.2–7.6, preferably with added antibiotics. If 0.04 M phosphate buffer is not available, tissue culture medium or phosphate-buffered saline (PBS) can be used instead. Samples should be kept refrigerated or on ice until received by the laboratory. Where epithelial tissue is not available samples of Oropharyngeal fluid can be collected by means of a probang (sputum). Treatment There is no specific treatment for FMD, other than supportive care. Treatment is likely to be allowed only in countries or regions where FMD is endemic. Prevention and Control In general, prevention and control strategies adopted can be categorized as those relating to a country where the disease is endemic and those in a country where the disease is usually absent. • In FMD-free countries the control policy includes slaughtering of infected and in-contact animals, restrictions on movement of animals and animal products. Vaccination under emergency circumstances where the outbreak is extensive and the slaughtering of large numbers of animals becomes unmanageable. • In countries or regions where FMD is endemic, the control measures usually employed include ο Prophylactic vaccination using vaccines containing strains of FMDV prevalent in the area. ο Strategic ring vaccination (during outbreaks) around the foci of infection ο Regulating and restricting movement of livestock and livestock products during an outbreak ο Disinfect the premises in order to reduce the amount of virus in the environment so as to prevent the spread of disease through indirect means. FMD Disinfectants: The following disinfectants can be used in the event of FMD outbreak Product Dilution Mixing Instructions Notes 5.25% Sodium Hy3% Add 3 gallons of chlorine bleach to pochlorite (NaClO) 2 gallons of water; mix thoroughly (household bleach) Acetic acid

Potassium Peroxymonosulfate and Sodium Chloride Sodium Carbonate (soda ash)*

Sodium Hydroxide (NaOH) (lye)*

4-5%

1%

4%

2%

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Add 6.5 ounces of glacial acetic Vinegar is a 4% solutions of acid to 1 gallon of water; mix thor- acetic acid oughly Follow label instructions Virkon-S

Add 5.33 ounces of sodium carbon- The solution is mildly caustic ate to 1 gallon of hot water (or 1 but can dull paint and varpound to 3 gallons of hot water); nished surfaces mix thoroughly Add 1/3 cup of NaOH pellets (2.7 This solution is highly caustic. Use protective rubber ounces of the lye) to 1 gallon of clothing, gloves and safety cold water; mix thoroughly glasses. WARNING: Always add the lye to the water. Never pour the water over the lye.

Volume No : 3 Issue : 08 01


qÁ . J£ï.©.²æÃzsÀgÀ. ¸ÀºÀ ¥ÁæzsÁå¥ÀPÀgÀÄ ¥À±ÀĪÉÊzÀåQÃAiÀÄ OµÀzsÀ±Á¸ÀÛç ªÀÄvÀÄÛ «µÀ±Á¸ÀÛç «¨sÁUÀ, ¥À±ÀĪÉÊzÀåQÃAiÀÄ ªÀĺÁ«zÁå®AiÀÄ, ºÉ¨Áâ¼À,¨ÉAUÀ¼ÀÆgÀÄ-560024. ªÉƨÉʯï: 94480 59777 E-mail:sridhar_vet@rediffmail.com ºÁ®Ä dégÀ JA§ÄzÀÄ «Ä±Àæ vÀ½ eÁ£ÀĪÁgÀÄUÀ¼À£ÀÄß PÀgÀÄ ºÁQzÀ £ÀAvÀgÀ PÁqÀĪÀ ¸ÁªÀÄ£åªÁzÀ MAzÀÄ PÁ¬Ä¯É. PÀgÀÄ ºÁQzÀ 12-24 WÀAmÉAiÀÄ M¼ÀUÉ EzÀÄ PÁt¹PÉƼÀÀÄzÀÄ. EzÀ£ÀÄß ºÁ®Ä dégÀ JAzÀÄ PÀgÉAiÀÄĪÀÅzÀÄ vÀ¥ÀàzÀgÀÆ ¸ÀºÀ ªÁrPÉAiÀÄ°è F ±À§ÝªÉà §¼ÀPÉAiÀÄ°èzÉ. F PÁ¬Ä¯ÉAiÀÄ°è DPÀ½£À°è dégÀ«gÀĪÀ¢®è §zÀ¯ÁV ±ÀjÃgÀzÀ vÁ¥ÀªÀiÁ£À PÀrªÉÄAiÀiÁUÀÄvÀÛzÉ. ±Éà 6 gÀµÀÄÖ ºÁ®Ä »AqÀĪÀ F PÁ¬Ä¯É aQvÉìUÉ ¸ÀÆPÀÛªÁV ¸ÀàA¢¸ÀÄvÀÛzÉAiÀiÁzÀgÀÆ ¸ÀºÀ PÉ®ªÉǪÉÄä ¸ÀÆPÀÛ ¸ÀªÀÄAiÀÄzÀ°è aQvÉì zÉÆgÉAiÀÄ¢zÀÝgÉ eÁ£ÀĪÁgÀÄ ªÀÄgÀtªÀ£ÀÄߥÀÅöàªÀ ¸ÁzsÀåvÉ EzÉ. gÉÆÃUÀPÉÌ PÁgÀtUÀ¼ÀÄ: ºÁ®Ä dégÀªÀÅ DPÀ¼ÀÄ PÀgÀÄ ºÁQzÀ DPÀ½¤AzÀ ºÁ®£ÀÄß »ArzÁUÀ §gÀĪÀ MAzÀÄ ¸ÁªÀiÁ£ÀåªÁzÀ MAzÀÄ PÁ¬Ä¯É. gÀPÀÛzÀ°è PÁå° ìAiÀĪÀiï ¥ÀæªÀiÁt UÀt¤ÃAiÀĪÁV PÀrªÉÄAiÀiÁzÁUÀ F gÉÆÃUÀ PÀAqÀħgÀÄvÀÛzÉ. EzÉà ¸ÀªÀÄAiÀÄzÀ°è J®Ä§Ä, ªÀiÁA¸À ªÀÄvÀÄÛ ¦vÀÛ d£ÀPÁAUÀzÀ°è ±ÉÃRgÀªÁzÀ PÁå°ìAiÀÄA gÀPÀÛPÉÌ ¸ÀÆPÀÛ ¸ÀªÀÄAiÀÄPÉÌ ©qÀÄUÀqÉAiÀiÁUÀzÉà ºÉÆÃzÁUÀ gÀPÀÛzÀ°è PÁå°ìAiÀÄA ¥ÀæªÀiÁt wêÀȪÁV E½ªÀÄÄRªÁUÀÄvÀÛzÉ. EzÀÄ PÉ®ªÀÅ ¸À® ¥ÁågÀxÁªÉÆðãï JA§ ZÉÆÃzÀPÀ zÀæªÀ ¸ÀÆPÀÛ ¥ÀæªÀiÁtzÀ°è ¸ÀÆPÀÛ ¸ÀªÀÄAiÀÄzÀ°è PÀgÀĺÁQzÀ vÀPÀët ¥ÀågÁxÉÊgÁAiÀiïØ ¤£Áð¼À UÀæAyUÀ¼À ªÀÄÄSÁAvÀgÀ ©qÀÄUÀqÉAiÀiÁUÀzÉà ºÉÆÃzÀ°è ªÀÄÄRåªÁV J®Ä§ÄUÀ½AzÀ PÁå°ìAiÀÄA ©qÀÄUÀqÉAiÀiÁUÀĪÀÅ¢®è. EzÀjAzÀ PÀgÀÄ ºÁQzÀ vÀPÀët eÁ£ÀĪÁgÀÄ ¥ÉÇõÀPÀgÀÄ DPÀ½¤AzÀ ºÁ®£ÀÄß »ArzÁUÀ ºÉaÑ£À ¥ÀæªÀiÁtzÀ°è PÁå°ìAiÀÄA ºÁ°£À°è ºÉÆgÀlÄ ºÉÆÃUÀĪÀÅzÀjAzÀ wêÀȪÁzÀ PÁå° ìAiÀÄA PÉÆgÀvÉAiÀÄÄAmÁV ºÁ®ÄdégÀ §gÀÄvÀÛzÉ. KPÉAzÀgÉ ºÀ®ªÁgÀÄ ±ÁjÃjPÀ QæAiÉÄUÀ¼ÀÄ PÁå°ìAiÀÄA£ÀÄß CªÀ®A©¹ªÉ. ®PÀëtUÀ¼ÀÄ: F

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Pashubandha 2014

Volume No : 3 Issue : 08 01


gÉÊvÀgÀÄ vÉUÉzÀÄ PÉƼÀÀÄzÁzÀ ªÀÄÄAeÁUÀÈvÉ: PÀgÀÄ ºÁQzÀ eÁ£ÀĪÁgÀÄ ºÁ®ÄdégÀ §AzÁUÀ vÀPÀët vÀdÕ ¥À±ÀĪÉÊzÀågÀ£ÀÄß PÀgɹ aQvÉì PÉÆr¸À¨ÉÃPÀÄ. DPÀ½£À ±ÀjÃgÀzÀ vÁ¥ÀªÀiÁ£À PÀrªÉÄAiÀiÁUÀzÀAvÉ vÀqÉAiÀÄ®Ä DPÀ¼À£ÀÄß ¨ÉZÀÑV£À ¸ÀܼÀzÀ°è ªÀÄ®V¸À¨ÉÃPÀÄ. PÉ®ªÀÅ ¸À® ¨Á¢üvÀ DPÀ½UÉ UÉÆÃt aî CxÀªÁ PÀA§½AiÀÄ£ÀÄß ºÉÆzɸÀ§ºÀÄzÀÄ. AiÀiÁªÀÅzÉà PÁgÀtPÀÆÌ AiÀiÁªÀÅzÉà OµÀ¢üAiÀÄ£ÀÄß PÀÄr¸À®Ä ¥ÀæAiÀÄw߸À¨ÁgÀzÀÄ. EAvÀºÀ ¸ÀAzÀ¨sÀðzÀ°è OµÀ¢üAiÀÄÄ ±Áé¸À£Á¼ÀPÉÌ ºÉÆÃV DPÀ¼ÀÄ ¸ÁAiÀÄĪÀ ¸ÁzsÀåvÉ EzÉ. DPÀ¼ÀÄ MzÁÝqÀĪÁUÀ UÁAiÀĪÁUÀĪÀ ¸ÁzsÀåvÉ EgÀÄvÀÛzÉ. C®èzÉà §ºÀ¼À ºÉÆvÀÄÛ ªÀÄ®UÀĪÀÅzÀjAzÀ ªÉÄʪÉÄÃ¯É MvÀÄÛ ºÀÄtÄÚUÀ¼ÁUÀĪÀ ¸ÁzsÀåvÉ EzÉ. PÁgÀt

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¤ÃqÀ¨ÉÃPÀÄ. gÉÆÃUÀ §gÀzÀAvÉ vÀqÉUÀlÄÖ«PÉ: GvÀÛªÀĪÁzÀ UÀÄtªÀÄlÖzÀ MtªÉÄêÀ£ÀÄß DPÀ¼ÀÄ UÀ¨sÀðzsÀj¹zÁUÀ ¤ÃqÀĪÀÅzÀÄ MAzÀÄ GvÀÛªÀÄ «zsÁ£À. PɯªÀÅ gÉÊvÀgÀÄ vÀªÀÄä DPÀ¼ÀÄUÀ½UÉ UÀ¨sÀðzsÀj¹zÁUÀ CzÀÆ 7 wAUÀ¼À £ÀAvÀgÀ PÁå°ìAiÀÄA ZÀÄZÀÄѪÀÄzÀÝ£ÀÄß PÉÆr¸ÀĪÀ ¥Àj¥ÁoÀ ºÉÆA¢gÀÄvÁÛgÉ. EzÀjAzÀ PÀgÀÄ ºÁQzÀ £ÀAvÀgÀ ¥ÁågÁxÁªÉÆðãï ZÉÆÃzÀPÀ zÀæªÀ PÀgÀĺÁQzÀ PÀÆqÀ¯Éà ©qÀÄUÀqÉAiÀiÁUÀzÉ DPÀ½£À°è PÁå°ìAiÀÄA ±ÉÃRgÀuÉ ¸ÁPÀµÀÄÖ EzÀÝgÀÆ ¸ÀºÀ CzÀÄ gÀPÀÛzÀ°è ©qÀÄUÀqÉAiÀiÁUÀzÉà ºÁ®ÄdégÀ §gÀĪÀ ¸ÁzsÀåvÉ EzÉ. ªÀÄvÉÆÛAzÀÄ «zsÁ£ÀªÉAzÀgÉ ¸ÀĪÀiÁgÀÄ MAzÀÄ PÉf ¸ÀÄtÚªÀ£ÀÄß 10 °Ãlgï ¤Ãj£À°è PÀgÀV¹ ¥Àæw¢£ÀªÀÇ ªÉÄÃ¯É ¸ÀAUÀæºÀªÁUÀĪÀ ¸ÀÄtÚzÀ w½ ¤ÃgÀ£ÀÄß ¸ÀĪÀiÁgÀÄ 100 «Ä°AiÀÄ£ÀÄß ¢£ÀPÉÆ̪ÉÄä ¤ÃrzÀgÉ ºÁ®Ä dégÀ §gÀ¯ÁgÀzÀÄ JA§ ¥ÀæwÃw EzÉ. DzÀgÉ ¸ÀÄtÚzÀ w½ ¤Ãj£À ¥ÀæªÀiÁt AiÀiÁªÀÅzÉà PÁgÀtPÀÆÌ ºÉZÀÄÑ ¤ÃqÀ¨ÁgÀzÀÄ. EzÀjAzÀ ºÉÆmÉÖAiÀÄ°è CªÀÄèzÀ ¥ÀæªÀiÁt eÁ¹ÛAiÀiÁUÀĪÀ ¸ÁzsÀåvÉ EzÉ. ¸ÀÆPÀÛªÁzÀ R¤d «Ä±ÀætªÀ£ÀÄß AiÀiÁªÁUÀ®Æ ¤UÀ¢vÀ ¥ÀæªÀiÁtzÀ°è ¤ÃrzÀ°è F PÁ¬Ä¯ÉAiÀÄ£ÀÄß vÀ¦à¸À§ºÀÄzÀÄ.

Dr. Madhukar* and Prof. H. A. Upendra# * Assistant Professor, # Director, Institute of Wildlife Veterinary Research, KVAFSU, Doddaluvara, Kodagu – 571232. (E-mail: madhukar262@gmail.com) Important facts •

Ebola is named after the river in the Democratic Republic of Congo (DRC) where it was first identified.

Bush meat from primates which are highly genetically similar to humans like chimpanzees (98% DNA similarity) and gorillas (97% DNA similarity) was the most important source of cross-species human infection.

First three outbreaks occurred in DRC and Sudan between 1976 and 1979. Five human outbreaks occurred between 2000 and 2004 in western central Africa. All these infections were traced back epidemiologically to multiple introductions from animal sources.

Initially hunters were affected and disease spread among humans to wipe out entire villages.

Zaire type and Sudan type of Ebola virus produce 90% and 50% case-fatality.

Ebola has been linked to declines in African great ape and other animals like duiker.

Fruit bats have been confirmed to be natural reservoir of Ebola.

Movement of non-human primates for research purpose is a proved source of Ebola spread.

Pashubandha 2014

Volume No : 3 Issue : 08 01


List of all Ebola outbreaks 2014: West Africa (Guinea, Liberia, Sierra Leone, and Nigeria) 2012: Uganda 2012: Democratic Republic of Congo 2012: Uganda 2011: Case in Uganda 2008: Ebola-Reston virus detected in pigs in Philippines

2007: Uganda 2007: The Democratic Republic of Congo (DRC) 2004: South Sudan 2003: The Republic of the Congo 2002: Gabon and The Republic of the Congo 2000-2001: Uganda

Symptoms • • • •

Diarrhea Vomiting Abdominal (stomach) pain Lack of appetite

• • • •

Fever (greater than 38.6°C or 101.5°F) Severe headache Muscle pain Weakness

Symptoms may appear anywhere from 2 to 21 days of post exposure, with an average of 8-10 days. Some infected individuals completely recover, reasons for which are not clear. However, dying patients usually do not develop a good immune reaction to Ebola. Transmission Because the natural reservoir of Ebola viruses has not yet been proven, the manner in which the virus first appears in a human at the start of an outbreak is unknown. However, researchers have hypothesized that the first patient becomes infected through contact with an infected animal. When an infection does occur in humans, the virus can be spread in several ways to others. The virus is spread through direct contact (through broken skin or mucous membranes) with • a sick person's blood or body fluids (urine, saliva, feces, vomit, and semen) • objects (such as needles) that have been contaminated with infected body fluids • infected animals Healthcare workers and the family and friends in close contact with Ebola patients are at the highest risk. During outbreaks of Ebola HF, the disease can spread quickly within healthcare settings (such as a clinic or hospital). Exposure to Ebola viruses can occur in healthcare settings where hospital staffs are not wearing appropriate protective equipment, such as masks, gowns, and gloves. Proper cleaning and disposal of instruments, such as needles and syringes, is also important. If instruments are not disposable, they must be sterilized before being used again. Without adequate sterilization of the instruments, virus transmission can continue and amplify an outbreak. Diagnosis Diagnosing Ebola HF in an individual who has been infected for only a few days is difficult, because the early symptoms, such as red eyes and a skin rash, are nonspecific to Ebola virus infection and

Pashubandha 2014

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are seen often in patients with more commonly occurring diseases. However, if a person has the early symptoms of Ebola HF and there is reason to believe that Ebola HF should be considered, the patient should be isolated and public health professionals notified. Samples from the patient can then be collected and tested to confirm infection. Laboratory tests used in diagnosis include: Timeline of Infection Within a few days after symptoms begin

Later in disease course or after recovery Retrospectively in deceased patients

Diagnostic tests available • Antigen-capture enzyme-linked immunosorbent assay (ELISA) testing •

IgM ELISA

Polymerase chain reaction (PCR)

• • •

Virus isolation IgM and IgG antibodies Immunohistochemistry testing

PCR

Virus isolation

Treatment Ebola does not have a known, proven treatment. Standard treatment for Ebola HF is still limited to treating the symptoms as they appear and supportive care. This consists of • balancing the patient’s fluids and electrolytes •

maintaining their oxygen status and blood pressure

treating them for any complicating infections Timely treatment of Ebola HF is important but challenging because the disease is difficult to diagnose clinically in the early stages of infection. Because early symptoms, such as headache and fever, are nonspecific to Ebola viruses, cases of Ebola HF may be initially misdiagnosed. However, if a person has the early symptoms of Ebola HF and there is reason to believe that Ebola HF should be considered, the patient should be isolated and public health professionals notified. Supportive therapy can continue with proper protective clothing until samples from the patient are tested to confirm infection. Experimental treatments have been tested and proven effective in animal models but have not yet been used in humans. Prevention Because mode of infection is still not clear, few primary prevention measures have been established and no vaccine exists. When cases of the disease do appear, risk of transmission is increased within healthcare settings. Therefore, healthcare workers must be able to recognize a case of Ebola and be ready to use practical viral hemorrhagic fever isolation precautions or barrier nursing techniques. They should also have the capability to request diagnostic tests or prepare samples for shipping and testing elsewhere

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Barrier nursing techniques include: • Wearing of protective clothing (such as masks, gloves, gowns, and goggles) • Using infection-control measures (such as complete equipment sterilization and routine use of disinfectant) • Isolating patients with Ebola from contact with unprotected persons. The aim of all of these techniques is to avoid contact with the blood or secretions of an infected patient. If a patient with Ebola dies, direct contact with the body of the deceased patient should be avoided. CDC, in conjunction with the World Health Organization, has developed a set of guidelines to help prevent and control the spread of Ebola. Entitled Infection Control for Viral Haemorrhagic Fevers in the African Health Care Setting, the manual describes how to • Recognize cases of viral hemorrhagic fever (such as Ebola) • Prevent further transmission in healthcare setting by using locally available materials and minimal financial resources. If you must travel to an area with known Ebola cases, make sure to do the following: • Practice careful hygiene. Avoid contact with blood and body fluids. • Do not handle items that may have come in contact with an infected person’s blood or body fluids. • Avoid funeral or burial rituals that require handling the body of someone who has died from Ebola. • Avoid contact with animals and raw meat. • Avoid hospitals where Ebola patients are being treated. • After you return, monitor your health for 21 days and seek medical care immediately if you develop symptoms of Ebola.

Kshama.M. A and Muralidhara. A Dept of TVCC , Veterinary College, Bangalore (kshamabopanna@rediffmail.com) Lhasa Apsos are cheerful, loyal, intelligent and trusty companion dogs who take their watchdog role quite seriously. The Lhasa Apso originated in the area of Tibet over 4,000 years ago as a small breed of mountain wolf . They were domesticated and actively bred perhaps as long ago as 800 BC by the monks who started using them to guard the monastery grounds. .Thus they are one of the oldest recognized breeds in the world. The monks also used the Lhasa Aspos in some religious ceremonies and generally held the dogs in highest regard.The name “Lhasa Apso” came from ‘Lhasa’ the capital city of Tibet and ‘apso’ meaning "bearded",in Tibetian language. In Tibet they are referred to as ‘Apso Seng Kyi’ which can be translated as "Bearded Lion Dog". The Lhasa's primary function was that of a household sentinel, guarding the homes of Tibetan nobility and Buddhist monasteries, particularly in or near the sacred city of Lhasa. It was believed that the bodies of the Lhasa Apsos could be entered by souls of deceased

Pashubandha 2014

Volume No : 3 Issue : 08 01


lamas while they awaited rebirth into a new body. Lhasas in Tibet were never sold. The only way a person could get one was as a gift. In the early 1900s, a few of the breed were brought by military men returning from the Indian subcontinent to England, where the breed was referred to as "Lhasa Terrier�.The original American pair of Lhasas was a gift from Thubten Gyatso, 13th Dalai Lama to C. Suydam Cutting, arriving in the United States in 1933. Certain characteristics which are part of the breed type such as head features, the coat, eye-fall, the musculature and body structure and the general hardiness evolved as a result of geographical and climatic conditions like high altitudes, the dry windy climate, the dusty terrain, the short hot summer and the long bitterly cold winter of the Himalaya region. DNA analysis has identified the Lhasa Apso as one of the 14 most ancient dog breeds, confirming that lap dogs and companion dogs were among the first dogs bred by humans. There is also some concern for Tibetan Lhasa Apso lines because many dogs were killed during & after the Chinese invasion of Tibet because of the breed's strong cultural symbolism to Tibetans. Breed characteristics Male Lhasa Apsos should ideally be 10.75 inches (27.3 cm) at the withers and weigh about 14 to 18 pounds (6.4 to 8.2 kg). The females are slightly smaller, and weigh between 12 to 14 pounds (5.4 to 6.4 kg). The breed standard requires dark brown eyes and a black nose, although liver-colored lhasas have a brown nose. The texture of the coat is heavy, straight, hard, neither woolly nor silky, and very dense. They come in a wide variety of colors including black, white, red, brown, yellow and gold with various shades. Lhasas can be with or without dark tips at the ends of ears and beard. The tail should be carried well over the dog's back.. Coming from the extremely cold weather of the Himalayas, the Apso has a double coat. Only the undercoat, which is soft, will shed out once a year; the outer coat, consisting of coarse outer guard hairs, does not shed. The average life span of a Lhasa Apso is about 13-15 years which is more than that of most other breeds. Temperament Lhasa Apsos’ can be willful, and if they decide they don't want to do something, they simply won't do it. Harsh treatment will often result in the dog retaliating. Lhasas respond best to food rewards, short training sessions and varied routines. Absolute consistency is important when working with a Lhasa Apso as they will see your bending the rules as an invitation to walk all over you. The time it takes to train a Lhasa is well worth the effort. Once leadership is established and the Lhasa learns that there is food in it for him, he will step up to the plate and perform the tasks at hand. Early and frequent socialization is important with this breed. They are naturally suspicious of strangers and this can get out of hand in the form of excessive barking and even nipping or snapping. It is imperative to teach a Lhasa to accept new people as welcome visitors. Lhasa Apsos don't require an excessive amount of physical activity to maintain health or happiness. Lhasa Apsos have no clue how small they are. They are fearless and often times bossy dogs who demand the attention of people whenever they are in the room. Some can be quite clownish, making mischief or performing for a laugh. They believe they are the center of the universe, and like any self-respecting diva, Lhasas can be quite moody.

Pashubandha 2014

Volume No : 3 Issue : 08 01


Despite their egos, Lhasas generally have a heart of gold and bring great joy to the homes they reside in. Training requires a lot of patience and a gentle hand. Lhasas are genetically hard-wired to be watch dogs, so even if you properly socialize your dog to accept visitors as welcome, it can be nearly impossible to train the barking alert out of them, and they will alert you (and the neighbourhood !) to every incoming person, vehicle or animal that comes his way. Issues regarding health Lhaso Apsos are known to suffer from sebaceous adenitis, a hereditary skin disease. They are also prone to patellar luxation, intervertebral disc disease and atlanto axial subluxation. They are also known to suffer from the genetic disease progressive retinal atrophy (PRA) which can render them blind. They are also prone to eye diseases, such as cherry eye (prolapse of membrana nictitans) and keratoconjunctivitis sicca (dry eye), glaucoma and cataract .They are also susceptible to perianal gland tumors.

Dr.Aparna Hebbar H and Dr.Veena M. P. Department of Veterinary Physiology and Biochemistry,Veterinary College,Hassan Email (appehebbar@gmail.com) Introduction Pig farming is very important in the livestock sector. Nowadays it is taken as entrepreneurship since the demand for the pork became very much high. Around 11.12 million pig population is seen in india. Much population is distributed in Assam, Kerala, Uttar Pradesh and also in Karnataka. However Piglet anemia is a big threat to the piggery industry since it causes severe economical loss to the farmers. Iron is a vital component in forming hemoglobin, a protein comprising about one-third of the weight of the red blood cell. It has got the function of carrying oxygen from the lungs to the tissues of the body and transporting carbon dioxide resulting from cellular metabolism back to the lungs. When there is a deficiency of iron, the piglet cannot synthesize an adequate amount of hemoglobin. They show microcytic, hypochromic type of anemia. Thus, piglet anemia is a condition of the blood in which the oxygen-carrying capacity is greatly reduced, and this condition is generally due to iron deficiency. Causes of Iron Deficiency Iron deficiency develops rapidly in piglets because • Pigs are born with low iron reserves about 50 mg. •

A sow's milk is low in iron. It contributes only 1 mg per day, but a piglet needs approximately 7 - 16 mg per day (depending on the rate of weight gain) for proper growth and health. • Modern pig breeding practices keep sows and piglets indoors in concrete pens that offer no chance for the animals to acquire iron from soil. • Piglets have an extremely high growth rate compared to other mammals. In fact, a piglet born at 1.5 kg will increase its weight tenfold in its first 60 days of life. And this growth requires a great deal of iron. • Sometimes pigs from sows consuming moldy feed or deficient in vitamin K may lose an excessive amount of blood from the umbilical cord at birth and quickly become anemic.

Pashubandha 2014

Volume No : 3 Issue : 08 01


Signs of Iron Deficiency Anemia Acute signs: In the most acute state, fast growing pigs may die suddenly from a shortage of oxygen. A characteristic sign of a more acute anemia is labored breathing or a spasmodic movement of the diaphragm muscles following exercise, and this is referred to as “thumps.” Chronic signs Poor growth, listlessness, rough hair coat, wrinkled skin and a paleness of the mucous membranes are seen. Anemia also lowers the resistance of the pig to disease and respiratory problems, and enteritis may appear more frequently in chronically anemic pigs.

A piglet having anemia Necropsy findings Carcasses are pale with thin watery blood and oedema of muscles are seen. Fluid exudates are common in the body cavity. Liver is enlarged in all cases and mottled greyish yellow colour due to fatty infilteration. Heart is flabby, enlarged. Enteritis is also there. Treatment If the hemoglobin value is below 9g/100ml, the pig is borderline anemic and needs supplemental iron. Injecting piglets with 100 to 200mg of iron in the first three days in the form of iron dextran, dextrin or gleptoferrin which serve to release iron from injection site or piglets are fed with oral iron supplements. Control and prevention • Add small amount of iron and copper in pigs diet at the rate of 25mg of iron and 5 mg of copper per day per piglet. • Paint the udder of the sow daily with the below mentioned mixure. • Ferrous sulphate-500g,Sugar-500g,Copper sulphate-70g and water-10liter.If an iron solution is swabbed on the sow’s udder daily throughout lactation, this will effectively prevent anemia. However, the labor required is too much for most of the modern swine producers. Conclusion Since the pig has got high fecundity and growth rate, pig production can yield a relatively rapid rate of return on the capital invested and provide income round the year. In this point piglet anemia may bring down their income rapidly. If the necessary care, Veterinarians suggestion and preventive measures are taken then chance of developing piglet anemia can be minimized.

Pashubandha 2014

PELVIC

Volume No : 3 Issue : 08 01


Dr. Tipshetti M.S, Dr. K. Satyanarayan, Dr. V. Jagadeeswary Dept. of Veterinary and Animal Husbandry Extension Education Email (ms.tipshetti@gmail.com) 1. Whether farmer / entrepreneur has aptitude for taking up Dairy Farming ? 2. Who has sponsored the application? DRDA or Voluntary Organisation ? 3. What is the subsidy available? If not, whether the applicant will bring sufficient margin money ? 4. Whether the land is suitable for construction of Cattle Shed ? 5. What is the design of shed? Whether adequate ventilation is available for animals ? 6. Whether the floor area available is adequate for animals ? 7. Ensure the floor is non slippery and provision for drainage of dung and urine is available. 8. What is the system of rearing animals (head to head or Tail to Tail) ? 9. What is the expected average milk yield / other parameters observed while selecting the animals ? 10.Whether concentrate feed is available at reasonable rate / arrangements for mixing the feed at farm ? 11.Whether adequate quantity of green fodder and dry fodder is available (Normally @ 25 kg green fodder and 5kg dry fodder /animal/day) ? 12. Whether the farmer has enough land to supply green fodder / arrangements for cultivation of green fodder ? 13. Have the applicants been informed of •

Installments due (monthly/ quarterly)

Rate of interest

Total repayment period (Normally 5 years)

14. Whether animals have been properly identified by tagging and insured. Whether the farmers are aware of their obligations to Insurance Company/Bank at the time of death of animal ?

Pashubandha 2014

PELVIC

Volume No : 3 Issue : 08 01


15. In case of Commercial Dairy (High value Dairy advances), whether you have ensured the following ? •

One acre land for fodder cultivation for every 5 animals.

Both leguminous fodders and non-leguminous fodders are cultivated.

A milking machine is included under the scheme.

A chaff cutter (Fodder Cutting Machine) is included.

Breeding facilities / Liquid Nitrogen Container for artificial insemination.

Land development and Fencing of the farm.

Silage pit - for 20 animals unit: 5, 610 cu.ft. @ Rs. 15/Cu. ft. Manure pit @ 2.2 cu.m/animal

Open paddock area - Simple 60' x 60' with fencing. •

Equipments such as Castrater, dehorner, Sickle, Wheel barrow, Milk pails, Buckets, Tie Chains, Milking machine, Bulk cooler, pasteurizer , transport vehicle, refrigerator etc. Any clarification / additional information contact ms.tipshetti@gmail.com

monthly e-Bulletin Published and circulated by Veterinary College, Hebbal Bengaluru Editor:

Associate Editior:

Dean, Veterinary College, Hebbal, Bengaluru

Head, Dept of Vety & Animal Husbandry Extension Education

Dr.S.Yathiraj (Ex-Officio)

Dr.K.Satyanarayana (Ex-Officio)

Contact : Dept of Veterinary and Animal Husbandry Extension Education Veterinary College, Hebbal Bangalore email: pashubandhavch@gmail.com Blog: pashubandhavch.blogspot.in

Pashubandha 2014

PELVIC

Volume No : 3 Issue : 08 01


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