LIVESTOCK LINE, SEPTEMBER 2018 1tezasvipublications.com/LLPDF/september2018.pdf · LIVESTOCK LINE, SEPTEMBER 2018 5 Schistosomes also known as “blood flukes” are the trematodes

LIVESTOCK LINE, SEPTEMBER 2018 1



VOL.12 ISSUE 5 SEPTEMBER 2018

CONTENTS

Editor : B. SHIV SHANKARAssociate Editor : B. KALYAN KUMAR

Printed, Published and Owned by B. Shiv Shankar, Printed at Karshak Art Printers, 40, A.P.H.B. Blocks, Vidyanagar, Hyderabad - 500 044. India.Published at 2-1-444/16, 1st Floor, O.U.Road, Nallakunta,Hyd-44. Editor: B. Shiv Shankar.

TECHNICAL EDITORIAL BOARDDr. P.K. Shukla, Jt.Commissioner Poultry, G.O.I., New Delhi.

Dr. V. RAMA SUBBA REDDY, Retd. Professor, Agrl. Uni. Hyd.

Dr. D. NAGALAKSHMI, Asst. Professor, S.V.V.U. Hyderabad.

Dr. S.T. VIROJI RAO, Sr. Scientist, AGB, S.V.V.U. Hyderabad.

Dr. M. KISHAN KUMAR, Sr. Scientist, S.V.V.U. Hyderabad.

Dr. M. KOTESWARA RAO, Vet. Asst. Surgeon, RAHTC, KMNR.

Dr. P.K. SINGH, Asst. Prof. (A.N.), Bihar Vet. College Patna.

Dr. S. NANDI, Sr. Scientist, CADRAD, IVRI, Izatnagar, U.P.

Dr. INDRANIL SAMANTA, Lecturer (Micro), WBUAFS, Kolkata.

Dr. M. KAWATRA, Sr. Manager-Bayer Animal Health, Thane (W), Mumbai.

Dr. DEVENDRA S VERMA, Tech. Mgr, Biomin Singapore B'lore.

Dr. R.K.S. BAIS, Sr. Scientist, CARI, Izatnagar, Bareilly.

Dr. VIJAY KUMAR M, Asst. Prof., Vet. College Bidar.

Dr. MD MOIN ANSARI, Asst. Prof., SKUAST, Srinagar, J&K.

Dr. AZMAT ALAM KHAN, Asst. Prof., SKUAST, Srinagar, J&K.

Dr. S K MUKHOPADHAYAY, Asst. Prof., (Vety Pathology) WBUAFS, Kolkata.

Dr. SUBHA GANGULY, Scientist, AICRP-PHT, Kolkata Centre.

Dr. AIJAZ AHMED DAR, Ph.D. Scholar, IVRI, Izatnagar, Bareilly.

Dr. SARADA PRASANNA SAHOO, Ph.D. Scholar, IVRI, Izatnagar.

Shrikant Katole MVSc, Ph.D.(Ani Nut) Asst. Prof Anand Agricultural University

DR RAKESH ROY, Ph.D, Uttar Banga Krishi Viswavidyalaya, Kalimpong,W.B.

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INDEX OF ADVERTISEMENTS

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9. Vetoquinol Title Cover III

1. Schistosomiasis an ...Diagnosis and treatment- Sukhdeep Vohra .................................................. 5-7

2. Abdominal Ultrasound ........ in Farm Animals- Dr.G.Senthil Kumar ............................................ 8-11

3. Antibiotics and chemical ......health concern- Jitendrakumar M Bhutediya ............................ 12-15

4. Babesiosis in livestock- Deepak Sumbria ............................................. 16-17

5. Evaluation of energy .....requirements for Horses- Neeti Lakhani .................................................. 18-19

6. Isolation and Propagation of Viruses in Cell Culture- Karam Chand ................................................. 25-27

7. Nipah Virus Infection – A Zoonotic Emergency- M.Sivakumar ................................................... 28-30

8. Recreational exposure ....public health impacts- Dr. Rizwan Khan ............................................. 31-35

9. Nutritional Management of Transition Buffaloes- Khwairakpam Ratika ....................................... 36-39

10. Press Release ............................................ 20, 40-42



Schistosomes also known as “blood flukes” are thetrematodes present in the mesenteric and nasal veinsof domestic animals. Unlike other trematodes, inschistosomes, separate male and female are present.They have fully developed miracidium inside the eggswhen laid. Further, radial and metacercarial stage areabsent during the life cycle and the cercariaepenetration the skin of the final host as a route ofinfection. India harbours maximum number ofmammalian schistosomes namely Schistosomaspindale, S. indicum, S. nasale, S. incognitum,Orientobilharzia dattai, O. turkesticum, O. harnasutaiand Bivitellobilharzia nairi. The first five schistosomesspecies occurs predominantly in domestic animals.These develop in Lymnaea luteola and Indoplanorbisexustus (Fig. 1) snails which inhabit the rivers, waterponds, lakes, ditches, paddy fields, road side water,marshy lands and other temporary water bodies. Thedisease is highly prevalent throughout the country,though not much detected by routine diagnosticmethods employed in parasitology laboratories.

Schistosomiasis an Emerging Disease in Domestic Animals inIndia - Diagnosis and treatment

Sukhdeep Vohra and Satyavir Singh, Department of Veterinary Parasitology, College of Veterinary Sciences, Lala

Lajpat Rai University of Veterinary and Animal Sciences (LUVAS), Hisar-125 004, IndiaU

incognitum and Orientobilharzia dattai. The diseaseshow no specific symptoms however, experimentallyinfected animals show clinical symptom of apparentdiarrhea or dysentery, anaemia, anorexia,dehydration, bottle jaw, reduced growth andproduction. However the presence of snails in thearea and eggs in the secretions/ faeces of the animalswill help in diagnosis of the disease. The nasalschistosomiasis is caused by Schistosoma nasale incattle and buffaloes. The disease was consideredmore prevalent than hepatic form because of easydiagnosis by snoring sound while in hepatic form noclear diagnostic symptoms are observed. The nasalschistosomiasis affected animals show snoring soundwhich are more audible during early morning and lateevening. In addition, the affected animal show highamount of nasal discharge which may be variable inconsistence. These two form of disease are mostcommon and widely prevalent, however, one caseon urinary schistosomiasis from Ratnagiri district ofMaharashtra has been reported.

The disease has peculiarity of passing very lessnumber of eggs in faecal sample which contain a fullydeveloped larvae (miracidium) inside it. As soon asthe sample come in contact with water the egghatches and the larvae is released. This results inlower reporting of the disease even though widelyprevalent. For the diagnosis of the disease specialmethods are used than the routine diagnosticmethods employed for trematodes.

DIAGNOSIS: The diagnosis of the hepato-intestinalschitosomosis can be divided into three subgroupsi.e. clinical, parasitological and immunologicaldiagnosis

I. CLINICAL DIAGNOSIS : The experimentallyinfected laboratory animals do not reveal any specificclinical symptom which may help in its diagnosis.Even these animals do not show apparent diarrheaor dysentery. In domestic animals, diarrhoea,anaemia, anorexia, dehydration may be observed butthese are non specific symptoms hence do not helpin diagnosis.

Fig.1: Lymnaea and Indoplanorbis snails asintermediate host for Schistosoma

The disease occurs in two forms i.e. hepato-intestinalschistosomiasis and nasal schistosomi-asis. Thehepato-intestinal schistosomiasis in domestic animalsis caused by Schistosoma spindale, S. indicum, S.


II. PARASITOLOGICAL DIAGNOSIS : During ante-mortem, faecal examination is the only way ofconfirming the infection parasitologically. Direct smearand sedimentation methods are commonly followedin the field for trematode infections but both fail todiagnose schistosomiasis. Specific methods are usedfor the diagnosis which are as follows:

Ante-mortem methods:

i. Formol–Ether or Acid–Ether : Take 2 gram offaeces and dissolve in 10 ml of 10% formalin (inherbivorus animals) or 10% acid (in carnivorusanimals). Mix in a mortor and sieve through filter in acentrifuge tube. Let the filtrate stand for 10 minutesand then add 2-3 ml of petroleum ether solution byvigorous shaking. Let the solution stand for 10-15min. discard the supernatant and check the bottom 2ml fluid for the spined eggs of schistosomes.

ii. Alkaline Digestion : Add 10 gm of faecal samplein 100 ml of N/10 NaOH or KOH in a conical flask.Place some glass beads along with the solution foruniform mixing of the faecal sample. Let the solutionstand for 12 hrs. Take 10 ml of uniformly mixedsolution and pass it through sieve. Collect the filtratein a centrifuge tube, centrifuge and examine the base1 ml for schistosome eggs.

iii. Hatching technique : It is a genus specific testwhere the properties of miracidium is utilized for itsdetection. Take 10-30 gm of faecal sample and mixin ice cold water in a conical flask of 500 ml capacity.Let the solution stand for 10 min and discard the upper2/3 fluid. Repeat the process twice to wash the debrisfrom sample. Then add chlorine free water of roomtemperature to the solution. Expose it to 40 W electricbulb or direct sunlight for 3 hrs. Afterward cover thewall of flask with black carbon leaving the brimexposed to light for 30 min. Miracidium beingpositively phototropic and negatively geotropic willconcentrate in the upper water of flask. Collect theupper 10-15 water in a watch glass and examineunder stereoscope for the presence of miracidium.The miracidium is recognized by its size, straightforward movement in the upper portion of water andpresence of cilia around its surface.

Postmortem methods:

The parasite is present in mesenteric veins, eggs inintestinal mucous membrane and adult pairing inportal veins of liver. So these three things i.e. liver,mesentery and intestinal scrapings should beexamined.

A. Liver examination

i. Liver chopping method : Cut the liver of deadanimal into pieces of 1-2 cm and place it into normalsaline solution (NSS) for 10-12 hrs. Afterward removethe pieces and filter the saline through muslin cloth.Revert the cloth in a petri dish, add some saline andremove cloth. The adult schistosomes are collectedand visible with naked eyes (0.7 – 2.0 cms). Thespecies identification can be made at highermagnification.

ii. Tissue press method : Take small piece of liveron a glass slide and with help of scissor chop it finely.Press the second slide on it and tie their ends withcotton thread. Let the slide containing tissue dry for12 to 24 hrs. Examination of material between twoslides under stereoscope will reveal the schistosomeeggs.

B. Intestinal scrapings examination : Scrap themucosa of caecum and colon with the edge of a slide.The scraped material should be place under two slidefor 8-12 hrs and then examined for Schistosomaeggs. The purpose of keeping for 8-12 hrs is that thesoft tissue is putrefied and the eggs become morevisible.

C. Mesentery examination : For this, separatemesentery from intestine, cut the mesentery into 1-2cm pieces and place in normal saline solution for 10-12 hrs. Afterward remove the pieces and filter thesaline through muslin cloth. Revert the cloth in a petridish, add some saline and remove cloth. The adult

Fig.2: Adult Schistosomes collected frommesentery of animals


schistosomes are collected and visible with nakedeyes (Fig. 2). The species identification can be madeat higher magnification.

III. IMMUNOLOGICAL DIAGNOSIS: Manyimmunological methods using live schistosomes, itsdevelopmental stages or preserved antigen are used.Most common methods used in laboratory and fieldare as follows

A. Cercarial hullen reaction (CHR) : The serum ofsuspected animal is placed around the live cercariaein a moist chamber. The positive serum will yield ahyaline membrane or precipitate around cercariae in12-24 hrs. Negative serum will not yield any hyalinemembrane or precipitate during the mentioned time.

B. Miracidial immobilization test (MIT) : Themiracidium is placed in test serum along with confirmpositive and confirm negative serum samples. Inpositive serum, miracidium immobilized after 12 hrstime. The immobilization in diagnostic serum incomparison with positive and negative serum willdetect its positivity.

C. Ring precipitation test (RPT) : The whole wormhomogenate when allowed to react with serum ofpositive sample it will form a white ring at their unionin 8-12 hrs indicating positive reaction. The principleis used for screening the schistosome positive andnegative samples.

D. Circum-oval precipitation test (CoPT) : Theserum of positive animal when allowed to react withschistosomes eggs, it will produce precipitationaround the egg in 8-12 hrs. The property is utilizedfor screening the positive and negative samples forschistosomosis.

E. Dot-ELISA : Nitrocellulose paper strips whencoated with cercarial antigen will yield positive blackdot when allowed to react with serum and conjugateusing Horse reddish per oxidase (HRPO) substrate.The method can be utilized for screening large herdfor the disease and can be used at different dilutionof serum and conjugate for different animal species.

F. Plate-ELISA : ELISA plates coated withschistosome antigens can be utilized for large scalescreening of disease at different dilution of serum andconjugate. The test detects positivity of schistosomeantibodies in the body. Now a days the antigendetecting ELISA which indicate presence of activeinfection is also used in human being and commercialkits of the same are also available.

G. Indirect fluorescence antibody test (IFAT) : Thetest is very sensitive for detection of positive serumwhen compared with negative serum sample. Theschistosome stages like miracidium and cercariae arealso used for this purpose. The positive serum samplewill show higher florescence when compared withnegative sample.

In humans even the polymerase chain reaction (PCR)is utilized for the detection of positive samples withvery high accuracy of sensitivity and specificity.

Detection of nasal schistosomosis is simple as thenasal sounds, presence of nasal granuloma alongwith high amount of nasal secretion can help us insuspecting the disease. Further the confirmation canbe made by collecting the nasal secretion in 2% NSS,warming in 10% potassium hydroxide (KOH) anddetection of boom rang shaped eggs of Schistosomanasale in it.

TREATMENT: Many drugs are used for the treatmentof hepato-intestinal schistosomosis like paziquintel,triclabendazole, tartar emetic, antimosan, stibophenand niridazole. No satisfactory treatment for thediseases except praziquintal. The drug, praziquintalis costly but the drug of choice for schistosomosis,given at the dose rate of 25 mg per kilogram of bodyweight. Two treatments at an interval of 3 to 5 weeksapart is recommended, by oral route.

For nasal schistosomosis the drugs are tarter emetic,antimosan, anthiomaline, triclorophon, niridazole andpraziquantel are recommended. Here also,praziquintal is the drug of choice.

CONTROL : For the control of disease followingmeasure should be like taken:• Treatment of definitive host.• Control of snails by methods like.Chemical control: Molluscicide like Baylucide (@0.14 ppm) and Copper sulphate powder in water (@1ppm).Biological control: Through raising of ducks (whichfeed on adult snails) and fishes like Gourami andGuppies which feed on snail eggs.• Proper disposal of faeces.• Proper drainage of water and fencing of waterbodies.• Storage of water for 48 hrs before watering theanimals.Education of human beings through extension worker.

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Abdominal Ultrasound and its Applications in Farm AnimalsDr.G.Senthil Kumar, Dr.K.K.Ponnuswamy, Dr.R.Rishikesavan,

Dr.P.Vikramachakravarthy, Dr.P.Sankar and Dr.R.Ezakial NapoleanDepartment of Clinics, Veterinary College and Research Institute, Namakkal- 637 001.

U

Introduction :

The ultrasonographic examination is unique in farmanimal disease diagnosis. It is a dynamicexamination technique with no risk to patient orsonographer. It has been said that ultrasonographyis the continuation of the clinical examination withother tools.

In the past, most food animal ultrasonography hadbeen applied to the diagnosis and management ofreproductive conditions. However, knowledge ofand experience with the application ofultrasonography in non-reproductive diseases hasincreased drastically over the last 10 to 15 years.

• Probe selection :

Ultrasound transducers are commonly in the 2to10 MHz range, with the most common probesused in large animal general practice being 3.5,5, and 7.5 MHz. Simple and convex linear arraytransducers are used most commonly in largeanimal practice because of their durability. Theirmajor disadvantages are the relatively large footprint surface area for patient contact, whichbecomes difficult in small areas such as theintercostal space and reduced penetrationdeath compared with some other technologies.

• Pros and cons :

There are no known side effects associated withultrasonography. Gas-filled bowel and bone areeffective barriers to ultrasonic imaging becauseof their large acoustic impedance differencescompared to soft tissues. It cannot be used toassess structures inside the skull. In addition,a successful ultrasound examination is highlydependent on the operator. Only trained andskilled ultrasonographers are capable ofgenerating and interpreting high- qualityimages.

• Patient preparation for ultrasonography isperhaps the largest drawback to the applicationof this diagnostic modality. Ideally, the hair isremoved with clippers and the skin is cleansedto remove all dirt and debris. Alcohol isfrequently used to clean and “degrease”the skinfurther.

Common uses of Ultrasonography in largeanimals :

• Ultrasound examinations are performed invirtual every facet of bovine and equine practiceand can be used to image essentially everyorgan system within the body.

Liver :

The costal part of the abdominal wall is scannedstarting at thr 12th intercostal space and movingcranially to the 7th ICS using a 3.5 MHz lineartransducer.

Indications :

• Determination of position of position and sizeof the liver and its vessels

• Visualization of diffuse and focal liver changesincluding hepatic lipidosis, abscesses, tumours,calcified bile ducts and cholestasis.

• Diagnosis of thrombosis of the caudal venacava

• Percutaneous ultrasound-guided centesis andbiopsy of the liver for histological, cytogical andbacteriological examination

• Percutaneous ultrasound-guidedcholecystocentesis for microscopic examinationof bile for liver fluke eggs

• Percutaneous ultrasound-guided centesis of theportal vein for experimental purposes.

Ultrasonography of ruminant forestomach :

Reticulum :

The reticulum is examined by scanning the ventraland lateral thorax on the right and left sides of the


sternum to the level of the elbows using a 3.5 MHzlinear transducer.

Indications :

• Evaluation of the contour and motility of thereticulum and adjacent organs (spleen,diaphragm, abomasum, liver).

• Visualization of lesions caused by traumaticreticuloperitonitis such as abnormal reticularmotility.

• Fibrinous deposits on the reticular wall andbetween the reticulum and adjacent organs.Adhesion of the abscess to the body wall wouldbe suggested by its immobility during reticularcontraction.

• Effusions.

• Reticular abscesses. The luminal contents ofthe forestomach are admixed with air, thus,magnets and foreign bodies inside the reticulumcannot be visualized ultrasonographically.

Omasum :

• The omasum is readily imaged in the mid lowerright seventh to tenth intercostal spaces andimmediately ventral to the costal arch. Theomasal wall is similar in appearance to thereticulum. Omasum is found to be largest atthe 10th intercostals space. The wall of theomasum appeared as thick echogenic line,similar to the wall of the rumen. The contentsof the omasum could not be visualized becauseof their gaseous nature, similar to that of thereticulum and rumen. The attachments of theomasal laminae were only occasionally visible.Useful to diagnose omasal transport failure.Lobed internal border can be identified, whichis unique to this organ by ultrasonography.

Abomasum, Small Intestine, Caecum andPeritoneum :

• Ultrasonography is of more limited value in theexamination of the intestinal tract of ruminantsbecause of the inherent limitations of thetechnique. The scanning depth is less thanapporoximately 20 EM with a 3.5 MHztranducer, or up to 30 EM with 2.5 MHz. Thus,

the size of the abdomen precludes completeexamination in larger animals. Also, the largeintestine and caecum generally containsufficient gas to prevent imaging beyond theirsurface.

• The flank and lateral and ventral abdominal wallare scanned on both sides using a 3.5 MHzlinear transducer.

Indications :

• Identification of free fluid in the abdomen,percutaneous ultrasound-guided centesis of thefluid for diagnostic purposes (ascites, peritonitis,uroperitoneum, haemoperitoneum).

• Evaluation and percutaneous ultrasound-guided centesis of the abomasum.

• Evaluation of the small and large intestine.Diagnosis of ileus of the small intestine.

• Differentiation between caecal dilatation andright-sided abomasal displacement when resultof transrectal palpation are unclear.

• Diagnosis of left sided abomasal displacementwhen clinical findings are not straight forward.

• Differentiation of peritonitis, omental bursitis,tumours and intra-abdominal abscesses

• Evaluation of the peritoneum and abdominalwall in cases with delayed healing afterlaparotomy, caesarian section, rumenotomy ortrocharization of the rumen.

Pancreas :

• The right side of the abdomen of standinganimals was examined by use of a 3.5 MHzlinear transducer from 12th intercostal spacecaudal to the costal arch. The region caudal tothe costal arch and intercostal spaces 10 to 12should be examined systematically from dorsalto ventral with the transducer placed parallel tothe ribs.

• Body and right limb of the pancreas couldconsistently be identified from the right flank.

• The right lobe of the pancreas could bevisualized from the right flank to the eleventhintercostal space and the body of the pancreasefrom the 12th to 10th intercostal space.


• Left lobe could not be visualizedultrasonographically because of its dorsomediallocalization which is beyond the penetrationcapacity of the ultrasonographic transducer.Unlike dogs, the bovine small intestine containslittle gas, because digestion of carbohydratesoccurs dominanantly in the forestomachs.

• Ultrasonographically the visible portions of thepancreas appeared as a triangle shapedstructure closely associated with the liver, portalvein, right kidney and duodenum. In comparisonto liver, it had an isoechoic or slightly moreechogenic parenchymal pattern.

Urinary Tract :

• The left kidney and ureter, bladder and urethraare scanned transrectally using a 5.0 or 7.5MHz linear transducer, whereas the right kidneyand ureter are scanned from the right flankusing a 3.5MHz linear transducer.

• In small ruminants, the left kidney cansometimes be imaged percutaneously in thecaudal right paralumbar fossa, however, it isfrequently covered by portions of the gaseouslarge intestine, in which case it cannot belocated.

Indications :

• Evaluation of the dimensions and appearanceof the renal medulla, cortex and pelvis and theproximal ureter.

• Identification of changes in the ureter andkidney associated with urolithiasis and ruptureof the ureter.

• Characterization of findings in cases withbacterial pyelonephritis, hydronephrosis andrenal amyloidosis. Evaluation of both kidneysbefore unilateral nephrectomy.

• Percutaneous ultrasound- guided biopsy of thekidney.

• Evaluation of the urinary bladder and itscontent.

Abdomen - Horses :

• Ultrasound is commonly used to evaluate theposition, contents and motility of intestinalstructures in colic cases.

• When the equine abdomen is scanned, it isimportant to use a systematic approach,scanning the left and right sides dorsally toventrally and then rostrally to caudally. Carefulattention should be pain to the spatialrelationship of the viscera because this may bethe key to distinguishing normal from abnormalfindings. The walls of some sections of the GItract appear strikingly similar and may not bedistinguishable if the clinician does not knowwhere the transducer is placed on theabdomen. Transabdominal ultrasonographyprovides not only structural information but alsofunctional information.

• Ultrasound windows to view different abdominalviscera in horse.

• Ultrasonographic anatomy of the left side of theabdomen.

• Left rostral side of the abdomen.

Stomach :

• Stomach-located deep to the spleen betweenthe ninth and 13th intercostal spaces atapproximately the level of the shoulder.

• Only part of the stomach that can be seen isthe wall of the greater curvature identified as acured hyperechoic line adjacent to the spleenand the gastrosplenic vein.

• If the stomach extends beyond the 14th

intercostal space in a horse that has not recentlyeaten, gastric distention may be present.

• Gastric fluid- a distinct gas- fluid interface maybe apparent in the lumen caudal from thestomach.

Spleen :

• Spleen- immediately adjacent to the body wall,from the left ventral eighth ICS to theparalumbar fossa. The size and location of thespleen vary greatly : the spleen may be left ofthe midline or extend slightly right of the ventralmidline.

• It appears as homogenous structure, withvessels that are rarely visible. The echogenicity


of the spleen is greater than that of the liver orkidneys.

Left Kidney :

• Left kidney found between the 16th and 17th

intercostal spaces and the first to third lumbarvertebrae, medial or deep to the spleen,between the level of the tuber coxae and thetuber ischii.

• Gas in the small colon or left colon or lung maypreclude transbdominal viewing of the leftkidney.

• The renal cortex is more echogenic than theadjacent medulla, except in areas of themedulla where interlobar vessels coursecentrally to form the renal pyramids.

Left Ventral Colon :

• Left ventral colon is identified by its sacculatedwall and “slugglsh”motility.

• Gas in the colon typically generates ahyperechoic wall with an indistinct luminalborder and intraluminal acoustic shadowing thatprecludes identification of the contents.

Ultrasonographic Anatomy of the Right Side ofthe Abdomen :

• Right rostral abdomen : liver, descendingduodenum, and right dorsal colon have acharacteristic proximity and can be identifiedin the right rostral abdomen at the level of theshoulder.

Liver :

• Located from the sixth to the intercostal spacesbetween the diaphragm and the right dorsalcolon.

• Only a small portion of the right side of the livercan be imaged.

• It is unusual for the liver to be seen beyoundthe 15th intercostal space or in the sametransverse plane as the right kidney.

• The vental edges of normal liver are distinctlysharp.

• Architecture of the liver is relativelyhomogenous, but more vessels are visible inthe liver and the general echogenicity of theliver is less than that of the spleen.

Duodenum :

• Duodenum - found descending the right middleabdomen at approximately the level of theshoulder and is located between the liver andthe right dorsal colon.

• The duodenum contracts one to four times perminute in horse.

Right dorsal and ventral colon :

• Has no sacculations, is immediately caudal tothe liver and duodenum.

• The wall of the right dorsal colon consistentlyappears as a hyperechoic curved line adjacentto the liver.

• The right ventral colon has sacculattons.

Cecum :

• Extends from the right paralumbar fossa to theventral midline.

• The cecum is sacculated and its motility isusually more apparent than that of the colonand gas in the lumen precludes imaging thecontents and far wall.

Right Kidney :

• Normally be found in the rostral rightparalumbar fossa to the 16th intercostal space.Gas in the cecum right dorsal colon or lungssometimes obscures visualization of the rightkidney.

Other Strucutures :

• The urinary bladder, non-gravid uterus, andovaries are best imaged transrectally in adulthorses.

• Because of the presence of mucus and calcium,urine in adult horses often appears veryechogenic.

• The transverse colon, adrenal glands, andpancreas are not usually identifiable viatransabdominal ultrasonography.

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Antibiotics and chemical residues in milk andtheir public health concern

Jitendrakumar M Bhutediya 1, Shumaila Malik 2, Kishor Pordhiya 3,Renu Chauhan 4, Laddika Lahri 5, Gulam Mohammad 6

1,2,3,4,5,6PhD scholar, ICAR- IVRI, Izatnagar-243122, Uttar PradeshU

Milk production is indistinguishably linked to theenvironment. Animals may become exposed toantibiotics and chemical substances during theirproductioncycle. These antibiotic and chemicalshave been identified to date could come from drugsaimed at treating diseases or application ofchemicals for the control of weeds, insects, fungiand rodents in order to enabled agriculturalproductivity. These antibiotics and chemicals areenvironmental contaminants linked to atmosphericpollution, feed, soil and water. Uncontrolled andindiscriminating use interfering with the natural fooddelivering ecological system lead to residues in milkand result risk to human and environmental health.Residues which have been found in milk areantibiotics, antihelminthicdrugs, pesticides,fungicides, disinfectants, mycotoxins and heavymetals. Any of these compounds may persist at acollection, preparation processes of dairy productsand they considered as residues.

The key use of antibioticsis the treatment ofinfectious disease and to treat and prevent udderinfections and as a growth promoter in the livestockindustry.Unauthorized antibiotic use may result inresidues of these substances in milk andmeat.Antibiotic residues are small amounts ofdrugs or their active metabolites, which remain inmilk after treating the animals. Because of thepublic health significance, milk and milk productscontaminated with antibiotics beyond a givenresidue levelsis considered unfit for humanconsumption.

In order to safeguard human health the WorldHealth Organization (WHO) and the FoodAgriculture Organization (FAO) have set standardsfor acceptable daily intake and maximum residuelimits in food.A regulatory limit for antibiotic residuesand other chemical residues imposed on the dairy

industry in many countries. However, there is noregulation in India, especially for use of antibioticsin animals for treatment and as a growth promoter.

Sources of Chemical Contaminants of Milk

Most of the chemical contaminants in milk and dairyproducts are antibiotics, antihelminthic drugs,pesticides, disinfectants, mycotoxins and heavymetals.

1) Veterinary drugs

Much of the veterinary treatment of dairy cattleinvolve the use of antibioticsin the infectiousdisease and to treat and prevent udder infectionsand as a growth promoter.Some drugs apply tocontrol endoparasites, ectoparasites and toincrease milk production. The most commonly usedantimicrobials in dairy cattle can group into fivemajor classes. These include the beta-lactams (e.g.penicillin’s and cephalosporin’s), tetracycline’s (e.g.Oxytetracycline and chlortetracycline),aminoglycosides (e.g. streptomycin andgentamycin), macrolides (e.g. erythromycin) andsulphonamides (e.g. sulfamethazine).

Antihelminthic drugs, Oxyclozanide, Closantel,RafoxanideAlbendazoleand Ivermectin which areused to remove parasites such as flukes,tapeworms (cestodes), nematodes (round worms)and external parasites are important in animalproduction systems.

2) Pesticides and insecticides

Chlorinated pesticides (DDT, BHC, lindane,dieldrin), Organophosphate pesticides (Parathion,Malathion) and carbamatecan enter milk and dairyproducts when the cow consumes contaminatedfeed.

3) Mycotoxins: Inappropriate temperature andmoisture conditions such as when feeds are


harvested damp, have not adequately dried, or areimproperly stored some of the molds producevarious toxic metabolites termed as mycotoxins.These metabolites may be hazardous to humanand animal health.Animal fed with feed containingAflatoxin B1 (AFB1) converted it into the AflatoxinM1 (AFM1) and it secrets into milk.Heat treatmentslike pasteurization were not effective in thereduction of the formation of AFM1.AFM1 withdifferent levels could be available in dairy productsmade from contaminated milk.

4) Nitrates and nitrites and Heavy metals

Nitrates and nitrites are chemicals used infertilizers, rodenticides (to kill rodents), and as foodpreservatives and Heavy metals mainly Lead (Pb)and cadmium (Cd)can enter to milk and dairyproducts and affect the health of people who haveconsumed contaminate milk and dairy products.

Toxic Agents in Animals

Toxic Agents in the animal can enter through themultiple way like oral (e.g. mycotoxins, pesticides),dermal (e.g. external antiparasitic agents),parenteral (e.g. antibiotic treatment), inhalation(anaesthesia before surgical procedures) and byintra mammary and intrauterine infusions.All ofthese routes may lead to residues appearing in milkand dairy products. In lactating cow, measurablelevels of the antibiotic are usually detectable in themilk for a few days after the last treatment.Risks tohuman health due to the consumption ofcontaminated milk and milk product by potentiallytoxic substances.

Chemicals in the animal body go through a seriesof stages including absorption, distribution,metabolism and excretion, forming part of thepharmacokinetics or toxicokinetics.

Absorption andDistribution: Absorption of toxicagent is depend on the route of the administration.After absorption, a toxic agent distributed through-out the whole body by the blood flows and storedin the fatty tissue because of their fat solubility.

Metabolism and Excretion

Metabolism of the toxic compound is occurred inthe liver and make them less toxic and watersoluble they are then excreted by the body butsometimes they are converted in more toxic formare termed as the bio activation (e.g. Aflatoxins).

Toxicants eliminated from the body by variousroutes, the kidneys being the most important organfor excreting chemicals since it is the mainelimination route. The other important eliminationroute is faeces and milk. Milk is an importantelimination route due to its chemical composition,a lipid emulsion in an aqueous protein solution.

Therefore there are Maximum Residues Limits(MRLs) for some drugs in milk that have beenstandardized. The withdrawal time is defined asbeing the time required after a drug administeredto an animal to ensure that drug residues inmarketable products (Milk, Meat, Eggs etc.) arebelow a determined maximum residue limit (MRL).

Methods for detection of antibiotics andchemical residues in milk

There isa variety of methods for reliably detecting,confirming and quantify a drug’s residues, whichcould be present in milk. These methods groupedinto bioassays, microbiological assays,immunochemical assays and physical-chemicalassays.

Public Health Concerns

Most of the antibacterial currently used in thecontrol and treatment of farm animal diseases arerelatively nontoxic even at higher concentration,but there are few antibiotics which pose a significantthreat to public health when present in sufficientlyhigh concentrations in milk.

The presence of chemical contaminants in milk isvery important for consumers and it can be a matterof public health concern as well as many ofunknown diseases in human because of milk anddairy products are widely consumed by humansthroughout the world.


Considering the issue of public health hazards, milkand milk products contaminated with antibiotics andother chemical contaminants beyond a givenresidue levels are considered unfit for humanconsumption. The residues of antibacterials maypresent pharmacological, toxicological,microbiological and immunepathological healthrisks for humans.

This concerns primarily antibiotics in use astreatment and feed additives. Overuse ofantimicrobial in livestock production cause totoxicity in human and animals. They can causesome disruptions like aplasia of the bone marrow(e.g. chloramphenicol), carcinogenic (e.g.furazolidone) and Penicillins have low toxicity buttheir most common adverse effects arehypersensitivity reaction, especially skin rashes,gastrointestinal disturbances diarrhoea, nauseaand vomiting. Nitrofuranscan react with nitrite toyield (carcinogenic) nitrosamines, benzimidazolesor their metabolites causes embryotoxicity andteratogenicity. Tetracycline can generate bacterialresistance. The emergence of resistant bacteriawithin animals and the transfer of antibioticresistance genes(R-factor)from non-pathogenicbacteria to other bacteria or human pathogens thatwill lead to widespread resistance.

Apart from the health hazards, antimicrobialresidues in milk are responsible for interferencewith starter culture activity and hence disrupt themanufacturing process of milk products.

The acute and malicious consumption of pesticidesinvolving higher dose results in death whereas,chronic insidious intake lead to elevated cancer riskand disruption of body’s reproductive, immune,endocrine and nervous system.

Mycotoxins can also present in milk and dairyproducts and can create public health problems inhumans. Aflatoxin M1 in milk is a carcinogenicmetabolite of Aflatoxin B1. Aflatoxin M1 in milk anddairy products led to increasing the risk of livercancer (hepatocellular carcinoma).

Exposure to higher levels of nitrates or nitrites hasbeen associated with increased incidence of cancerin adults, and increased incidence of brain tumors,leukemiaand “blue baby syndrome”(methemoglobinemia) in children.The healthimplications from heavy metals lead to kidneydamage, brain damage cardiovascular diseases,growth inhibition, interference in haemoglobinsynthesis, and also some of these residues areknown to be carcinogenic in nature.

Regulation and Risk assessment

The regulation of illegal residues in foods is acooperative effort of FSIS (Food Safety andInspection Services), FDA (Feed and DrugAdministration) and EPA (Environmental ProtectionAgency).

In India, Food Safety and Standards Authority ofIndia (FSSAI) under the Ministry of Health andFamily Welfare is the main authority for establishingthe scientific standards for articles of food includingmilk and milk products and to regulate theirmanufacture, storage, distribution, sale and import,to ensure availability of safe and wholesome foodfor human consumption under the rules specifiedby Food Safety and Standard Act, 2006.

To avoid risks related to Veterinary drug residuesin milk, in many countries maximum residue limits(MRLs) have been established for each antibioticand chemical substances. Milk withheld from salefor a specific period after veterinary therapy (usually72-96 h) to ensure that no residues persist.

MRLs for some commonly used antibioticdrugs and chemical residues in milk accordingto Indian regulations.


HACCP is a quality managementprogram to

identify hazards and to determine the acceptable

limits in the production process.

Possible strategies for prevention of

antibioticsand chemical residuesin Indian

scenario

Chemical contaminants in milk and dairy products

are results of environmental contamination, poor

veterinary service and misuse ofantibiotics,

uncontrolled use of pesticides and

insecticideingested by animals.Chemical

contamination not completely prevented, or

eliminated from milk and dairy products.However,

the implementation of food safety andregulatory

laws can reduce chemical residues in milk and

dairy products.

Possible strategies to prevent residues in milk:-

1) Good hygiene and management practices

at farm prevent the spread of disease among

livestock which could reduce the need for

antibacterial use.

2) Alternative use of antibiotic growth promoter

e.g. probiotic microorganisms, immune

modulators, organic acids and other feed

supplements.

3) Avoid using antibiotics in the veterinary field

without a veterinarian’s prescription.

4) Educate dairy owners on drug withdrawal

period of treated animals.

5) Development and validation of rapid

screening tests for detection of antimicrobial

residues in milk

6) Establishing the policy for use of antibacterial

in animals will help monitoring and

surveillance of the usage of these drugs.

7) Pharmacovigilance programme would be

developed for veterinary pharmaceuticals for

the risk assessment of antibacterial drug

residues for human and environment.

8) Strict national legislation passed on livestock

sector to avoid unnecessary use of

chemicals.

9) National chemical residues control and

monitoring program should be designed to

set standards on the use of chemicals

(antimicrobials, insecticides, pesticides,

etc.).

10) Training to farmers and personnel about

good manufacturing practices and

monitoring are useful to reduce chemical

contaminants in milk and dairy products.

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Babesiosis in livestockDeepak Sumbria a1, L.D Singla b

aPost-Doctoral Research Associate, Address: University of Tennessee, Knoxville, USAbDepartment of Veterinary Parasitology, College of Veterinary Sciences, Guru Angad Dev Veterinary and

Animal Sciences University, Ludhiana-141004, Punjab, India

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Intraerythrocytic protozoan parasites of the

genus Babesia causes Babesiosis in animal.

It is mainly transmitted by ticks and affects an

ample range of domestic and wild animals and

sporadically people. Even though the major

financial impact of babesiosis is on the cattle

industry, infections in other domestic animals,

including sheep, goats, pigs, and dogs can also

occur. Two important species in cattle-Babesia

(B) bigemina and B. bovis-are widespread in

tropical and subtropical areas. A loss of about

57.2 million US dollars annually occurs due to

babesiosis in India.

Transmission and Epidemiology:

The main vector of B. bigemina and B. bovis is

Rhipicephalus (Boophilus) spp ticks, in which

transmission occur transovarially. Moreover it

can also transmit experimentally by blood

inoculation, mechanical transmission by insects

or during surgical procedures. Intrauterine

infection has also been reported.

In Rhipicephalus spp ticks, the blood stages of

the parasite are ingested during engorgement

and undergo sexual and asexual multiplication.

Transmission to the host occurs when larvae

(in the case of B. bovis) or nymphs and adults

(in the case of B. bigemina) feed. In field

conditions, the rate of tick transmission is

generally higher for B. bigemina than for B.

bovis.

In prevalent region, three features are vital in

determining the risk of clinical disease: 1)

calves have a degree of immunity [related both

to colostral-derived antibodies and to age-

related issue] 2) animals that recover

from Babesia infections are usually immune for

their life and 3) the vulnerability of cattle breeds

to ticks and Babesia infections varies; e.g., Bos

indicus cattle be likely to be more resistant to

ticks and the effects of B. bovis and B

bigemina infection than Bos taurus-derived

breeds. At high levels of tick transmission,

nearly all calves become infected

with Babesia by 6 month of age. This condition

can be distress by either a natural (eg, climatic)

or artificial (e.g. acaricide action or changing

breed of flock) decline in tick numbers.

Babesiosis status in India

Walker and Edward first time reported

babesiosis in India in 1927. The occurrence of

B. bigemina has been reported from various

parts of India like Andhra Pradesh, Bengaluru,

Himachal Pradesh, Jammu and Kashmir,

Meghalaya, Punjab and Uttaranchal. Little

information of B. bovis is also there in buffaloes

and cattle. Prevalence of B. bigemina based

on blood smear examination in crossbred cattle

from north Bangalore, Andhra Pradesh and

Haryana state were reported to be 12.12, 8.02

and 3.22%, respectively. Due to B. bigemina

the prevalence of bovine babesiosis in Punjab

state was 5.94 % based on Giemsa stained

thin blood smear examination. Very few reports

are available in India on the prevalence of B.


bigemina based on PCR assay. Prevalence of

B. bigemina in north Kerala based on PCR

assay was 0.6%. Some cases of transmission

of babesia by Hyalomma anatolicum

anatolicum were also reported.

Clinical Findings and Pathogenesis:

Regarding virulence B. bovis is a much more

virulent organism than B bigemina. The

pathogenic effect of parasite is more relate

directly to erythrocyte destruction. Moreover in

case of B. bovis, a hypotensive shock

syndrome, combined with generalized

nonspecific inflammation, coagulation

disturbances, and erythrocytic stasis in

capillaries, contribute to the pathogenesis. In

acute case the infection runs for a course of 1

week. Main sign are fever (41°C), followed by

inappetence, amplified respiratory rate, muscle

tremors, anaemia, jaundice, and weight loss.

In the final stages hemoglobinemia and

hemoglobinuria occur. In B. bovis infections

Central Nervous System involvement occur

mainly due to adhesion of parasitized

erythrocytes in brain capillaries. Sometime

constipation/diarrhoea may also be present.

Abortion may occur in late-term pregnant cows,

and temporary infertility may be seen in bulls.

Animals that recover from the acute disease

remain infected for a number of years with B.

bovis and for a few months in the case of B.

bigemina. In carrier state no clinical signs are

visible.

Lesions:

Lesions (mainly with B. bovis) include an

inflamed spleen; a distended liver with an

engorged gallbladder including thick bile;

congested, dark colour kidneys; and

generalized anaemia and jaundice.Hemoglobinuria is seen in most clinical casesof B. bigemina, but this is not always the casewith B. bovis. Congestion or petechiae canbeen seen in other organs like brain and heart.

Diagnosis: Sometime other conditions havesimilar sign like fever, anemia, hemolysis,jaundice, or red urine so they can be confusedwith babesiosis. Therefore, substantiation ofdiagnosis by microscopic examination ofGiemsa-stained blood or organ smears isnecessary. Microscopically, the B. bovis issmall, with the parasites in paired form at anobtuse angle to each other and measuring 1-1.5 x 0.5-1 µm. B. bigemina is larger (3-3.5 x1-1.5 µm), with paired parasites at an acuteangle to each other. Sometime single forms ofboth parasites are also commonly seen.Reconfirmation should be done by a numberof serologic tests like indirect fluorescentantibody test, ELISA etc. Molecular test likePCR and real-time PCR are also availablewhich are competent of detecting extremely lowparasitemia.

Treatment and Control:

In the past mixtures of drugs have been usedto treat babesiosis, but only diminazeneaceturate and imidocarb dipropionate arefrequently use. These drugs are not availablein all endemic countries, or their use may berestricted. Diminazene should be used @ 3.5mg/kg IM for treating cattle. Imidocarb shouldbe used SC @ 1.2 mg/kg. Supportive treatmentis desirable which include the use of anti-inflammatory drugs, corticosteroids, and fluidtherapy. Blood transfusions may be life-savingin very anaemic animals.

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INTRODUCTION: Horses can use hay and otherroughages as nutrient sources much more efficientlythan other nonruminants such as poultry or pigs, butless than ruminants. A source of roughage shouldcomprise at least 50% of the total equine ration byweight. Current recommendations are that horsesreceive at least 1.5%–2% of their body weight inforage or forage substitutes such as hay cubes orother high-fiber source daily. The average maximumdaily dry matter intake is 2.5%–3% body wt therefore,forage or forage substitutes should be the majorcomponents of an equine ration. The main sites offermentation in horses are in the cecum and largecolons, where products of microbial fermentation,such as volatile fatty acids, amino acids, and vitamins,are also absorbed. Microbial fermentation also occursin the stomach and small intestine to lesser degrees,depending on the type of feed. Enzymatic digestionof carbohydrates, protein, and fats occurs only in theduodenum and jejunum. Any of these nutrient sourcesthat escape small-intestinal digestion are passed onfor microbial degradation in the large intestine, wheretheir fermentation will alter pH and microbial activity.

Eighty percent of the horse’s fat-free, moisture-freebody composition is protein. Protein is a predominantcomponent of blood, muscles, organs and enzymesand it is a critical part of the horse’s diet throughoutits life. The age and use of the horse are the mostimportant considerations in determining proteinrequirements. In addition, other important factorsconcerning protein which should be evaluated whenselecting a ration for a particular phase of a horse’slife are the digestibility of the protein, the amino acidcontent of the protein, and the protein to energy ratio(PER) of the ration.

ENERGY: Energy requirements may be classified intothose needed for maintenance, growth, pregnancy,lactation, and work. However, the need for energydiffers considerably among individuals; some horsesrequire much greater amounts of feed than others(“hard keepers”), and others are much more efficientat feed digestion/utilization (“easy keepers”).Digestibility of feedstuffs also often differs significantlyfrom published values. Therefore, the caloricrecommendations provided should be considered

only a starting point to determine the actual energyneeds of a given horse.

Maintenance: For maintenance of body weight andto support normal activity, the daily digestible energy(DE) requirement (in Mcal) of the nonworking adulthorse in good body condition is estimated to be onaverage 33.3 kcal/kg body wt, with a minimumrequirement of 30.3 kcal/kg for easy keepers or drafttypes and 36.3 kcal/kg for hard keeper adult horses.For obese or emaciated horses, the estimated idealbody weight in kg should be used in the equationrather than current body weight. For weight gain, it isestimated that 1 unit of change in body conditionscore takes 16–20 kg body wt gain and that each kgof gain requires 20 Mcal DE above maintenancerequirements. Caloric intake in obese horses shouldnot be restricted severely for prolonged periods oftime because of the risk of hyperlipidemia.

Cold weather increases the energy requirement by0.00082 Mcal DE/kg body wt for each degree Celsiusdrop below the lower critical temperature (LCT) ofthe animal.

Growth: For growth, the daily DE requirement of lighthorse breeds is estimated to be maintenance DEMcal/day = (56.5X–0.145)/1,000 times body wt in kg plusthe caloric requirements for growth = (1.99 + 1.21X –(0.021X2) × ADG, using the above equation(s) for themaintenance DE, and X as the age in months andADG as the desired average daily gain in kg.Warmblood, draft, and draft-cross breeds may require10%–20% less than calculated by the equationsabove to sustain rapid growth and avoid obesity.

Pregnancy and Lactation:

During pregnancy, if the mare is not exercised orexposed to extreme weather conditions, maintenanceDE intakes are usually adequate until the last 90 daysof gestation. Energy requirements during months 9,10, and 11 of gestation are estimated by multiplyingestimated maintenance requirements by 1.11, 1.13,and 1.20, respectively. Voluntary intake of roughagedecreases as the fetus gets larger, and it may benecessary to increase the energy density of the rationby using supplemental concentrates in latepregnancy.

Evaluation of energy and protein requirements for HorsesNeeti Lakhani 1, Preeti Lakhani 2 and Kambam Sudha Rani 1

1.Division of Animal Nutrition, NDRI, 2.Division of Animal Physiology, NDRI

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To support lactation, the NRC has estimated that 792kcal of DE/kg of milk produced per day should beadded to the increased (36.3 kcal/kg body wt)maintenance needs. Lactating light horses (eg,Thoroughbred, Quarter horses) maintained bodyweight when fed 28–31 Mcal DE/day. Draft maresmay require as much as 43 Mcal/day. However, thisrecommended level of energy intake has increasedbody weight gain in lactating pony mares, indicatingthat it may exceed the needs of some breeds orindividuals. The mare’s body condition should beevaluated on a regular basis and maintained in therange of 5 to 7 throughout pregnancy and lactation.

PROTEIN: Weanling horses require 50 g CP/McalDE (NRC, 1989). The lysine content of weanling dietsshould be at least 2.1 g/Mcal DE/day. Yearling andlong yearling horses require 45 g CP/Mcal DE and1.9 g lysine/Mcal DE/day. Two year olds require 42.5g CP/Mcal DE/day and 1.7 g lysine/Mcal DE/day. Theprotein to energy ratio and lysine to energy ratio areonly indirectly related to growth rate.

Although some amino acid synthesis and absorptionoccurs in the cecum and large intestine, it is notsufficient to meet the amino acid needs of growing,working, or lactating horses; therefore, the proteinquality of the feed provided to these classes of horsesis important. The amino acid balance in alfalfa andother legumes such as soybeans appears to be better

than that found in cereal grains or some grass hays.This should be considered when formulating rations,especially for rapidly growing young horses.

Growing horses have a higher need for protein (14%–16% of total ration) than mature horses (8%–10% oftotal ration). Aged horses (>20 yr old) may requireprotein intakes equivalent to those for young, growinghorses to maintain body condition; however, hepaticand renal function should be assessed beforeincreasing the protein intake of old horses. Fetalgrowth during the last third of pregnancy increasesprotein requirements somewhat (10%–11% of totalration), and lactation increases requirements stillfurther (12%–14% of total ration). Work apparentlydoes not significantly increase the proteinrequirement, provided that the ratio of crude proteinto DE in the diet remains constant and the increasedenergy requirements are met.

REFERENCES:

NRC. 1989. Nutrient Requirements of Horses. No. 6.(5th ed.). National Academy of Sciences. NationalResearch Council, Wash. D.C.

Ott, E.A., R.L. Asquith, and J.P. Feaster. 1981. Lysinesupplementation of diets for yearling horses. J. Anim.Sci. 53:1496

Ott, E.A. 1988. Protein and amino acid requirementsof the young horse. Horse Research Reports, Univ.of Florida, Gainesville. pp. 20-26.

Pagan, J.D. 1982. The digestible energyrequirements of lactating pony mares. M.S. Thesis,Cornell University, Ithaca, New York.

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An improved manufacturing method for handling,precision and uniformity in feed additives

By Angela Knezevich, Trouw Nutrition Global

PRESS RELEASE

Optisize™ technology creates uniform, low-dust trace mineral particles that are non-reactive, non-hygroscopic and which blend andmix more evenly into feed, meaning morenutrients make their way into the animal.

Some feed additive particles can create just asmany problems as they try to solve. Binding withother nutrients, blending unevenly or makingexcessive dust are all major detractors to otherwisehigh quality feed additives. Poorly made particlesturn into poor investments due to instability, caking,clumping and unnecessary messes, all resultingin fewer valuable nutrients being available for useby the animal.

Addressing the feed producers’ needs

These issues affect the bottom line for almost everyproducer and nutritionist, as feed and feed additivesare major investments. They need to haveconfidence that these issues will not get in the wayof the quality and quantity of each animal’s yield.

OptiSize™ Large Particle Technology was createdas a response to these needs. This technology ismeant toaddress these issues and it indeedboastsbenefits that traditionally manufactured traceminerals cannot provide, such as improved

handling, precision and uniformity in feed.Typicaltrace minerals, both organic and inorganic, lack theunique OH group covalently bonded to the metal,meaning OptiSize particles fall into a new categorycalled hydroxy trace minerals.

Making the process easier and increasing profit

The hydroxy trace minerals produced with thistechnology are uniform, non-hygroscopic, non-reactive and low-dust.Particles have an averagemean particle size of 175 microns, and all featurea uniform, spherical shape. These particles do notbind with other nutrients, promote oxidation orcreate excessive residue. This means they alsohave a reduced carryover riskwith less mess andless waste. Less wasted feed additives leads togreater yield from the animal, benefitting the needsof producers and nutritionists.

The OptiSize process also inhibits particles fromabsorbing moistureto prevent caking or clumpingin the mixers and bags. With this technology, lessproduct is rendered unusable before the customereven opens the bag.

OptiSize Large Particle Technology is a corefeature of theIntelliBond® line of hydroxy traceminerals.






1. INTRODUCTION

In the early 1900s the discovery of human cellsthat could be propagated in vitro providedvirologists with an alternative to embryonated eggsand laboratory animals for in vitro isolation ofviruses. Cell culture is the process by which cellsare removed from an animal or plant and grownunder favorable artificial conditions. Cell cultures,which are derived from dispersed cells taken fromoriginal tissue and disaggregated by enzymatic,mechanical, or chemical means, provided largenumbers of cells suitable for virus isolation,facilitated control of contamination with antibioticsand clean-air equipment, and helped decrease theuse of experimental animals. The cells may beremoved from the tissue directly and disaggregatedby enzymatic or mechanical means before cultiva-tion, or they may be derived from a cell line or cellstrain that has already been already established.

Primary cell culture: Cells that are directly isolatedfrom the tissue or organ and proliferated under theappropriate conditions are known as primary cellculture. Primary cells are prepared directly fromanimal or human tissues by enzymatic ormechanical means and placed under suitableculture conditions until they reach confluence. Theywill attach divide, grow and occupy the availablesubstrate i.e. reach to confluence. At this stage thecells have to be subcultured (i.e.passaged).

Cell lines: After the first subculture of primary cells,it is known as cell line. Cell lines derived fromprimary cell cultures have limited life span. Howeversome cell lines are immortal through a processcalled transformation, which can occurspontaneously, chemically or virus induced. Whena finite cell line undergoes transformation theyacquire the property to divide indefinitely. Thesecell lines are called continuous cell line

Isolation and Propagation of Viruses in Cell CultureKaram Chand, Sanchay Biswas and Bimlendu Mondal

Division of Virology, ICAR-Indian Veterinary Research Institute, Mukteswar, Uttarakhand

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Cell Strain: If a subpopulation of a cell line is

positively selected from the culture by cloning or

some other method, this cell line becomes a cell

strain. A cell strain often acquires additional genetic

changes subsequent to the initiation of the parent

line.

Cell culture is major tool in the cellular and

molecular biology which provides excellent model

for studying basic cell biology, normal physiology,

effects of drugs and toxic compound on cells,

mutagenesis and carcinogenesis. In virology cell

culture is used for isolation and propagation of virus

for diagnostic purpose, cultivation of virus for

vaccine production and also to study virus

infectious cycle. The major advantage of cell culture

for any of these applications is the consistency and

reproducibility of the result. Although

embroyonated eggs and laboratory animals are

very useful for the isolation of certain viruses, but

cell cultures are the sole system for virus isolation

in most laboratories. The cell lines amplify the

amount of virus present, express the viral antigens

and in many cases die as a consequence of the

viral infection producing characteristic cytopathic

effects (CPE) in the cell monolayer. Although in

virology, virus isolation in cell cultures was

employed by research laboratories by the early

1960s but diagnostic services were very limited,

varying from laboratory to laboratory and often not

available at all, except in major medical centers.

However, in the early 1970s, diagnostic virology

expanded dramatically, largely because of the

availability of highly purified reagents and

commercially prepared cell lines. Virus isolation in

cell cultures has long served as the “gold standard”

for virus detection, and it is the method to which all

others have been compared.


2. VIRUS ISOLATION AND PROPAGATION

The main advantage of the traditional cell cultureapproach is the capacity to isolate a wide varietyof viruses. By inoculating clinical samples intoseveral types of cell cultures, a suitableenvironment is provided for most of these viruses.The appropriate selection, collection, transports,and processing of clinical samples is important forsuccessful virus isolation. Collection of samplesthat contain the highest titer of virus is mostdesirable.

For infecting cultures, it is essential to understandthe concept of multiplicity of infection (MOI). MOI isthe average number of virus particles infecting eachcell.

MOI is related to pfu by the following formula:

Multiplicity of infection (MOI) = Plaque forming units(pfu) of virus used for infection / number of cells.

For example, if 2x106 cells is infected by 50 ml ofvirus with a titer of 108 pfu/ml. The MOI will be0.05*108/2*106= 2.5.

Different methods of infection practiced in viruspropagation are:

2.1. Infection by adsorption

Adsorption inoculation is thought to allow moreefficient adsorption of viral particles to the cells andto enhance rates of recovery of some viruses. At80-90% confluency, virus inoculum with known titeris inoculated into the flask at a multiplicity ofinfection (m.o.i.) of 0.01 to 0.1 TCID50/cell (approx).Cell monolayer is monitored under inverted

microscope daily for detection for virus growth byappearance of changes in cell. The spectrum ofchange is broad, ranging from swelling, shrinking,and rounding of cells to clustering, syncytiumformation, and, in some cases, completedestruction of the monolayer. These changes arecollectively called the cytopathogenic or cytopathiceffect (CPE) of the virus. Some viruses (e.g. FMDV)may produce easily visible CPE within the first 24h of incubation; other viruses demonstrate CPEonly after 3 to 10 days of incubation, with some,such as cytomegalovirus (CMV), averaging 10 to30 days for CPE production.

2.2 Infection by simultaneous inoculation

In this method, after sub culturing and plating theflask with cells, the virus with known titer isinoculated into the flask at a multiplicity of infection(m.o.i.) of 0.01 to 0.1 TCID50/cell (approx) andmonitored for CPE.

2.3. Estimation of virus titre

The end point is the dose or dilution that infects orkills 50% of the subject in the test system. Infectivitytitre which is the reciprocal of highest dilutionshowing 50% infectivity can be calculated byusing Reed and Muench methods.

Example:Calculation of 50% endpoints by Reedand Muench formula

Virus samples are usually titrated by inoculating into cell monolyers. Presence or absences of CPEis the indication for calculation of titre. The numberwells showing CPE in each dilution is calculatedas follows:

TABLE


Accumulated values for the total number ofwells showing CPE are obtained by adding inthe direction of lowest to the highest values.The accumulated infected ratios and thepercentage infected for each dilution iscalculated.

In the example depicted in the table it can beseen that infectivity in the 10-2, is higher than50%(67) and in the next higher dilution, 10-3 it isonly 14%. So, we need to find the 50% endpointdilution, which obviously lies between these twodilutions (10-2 to 10-3) First, we have to calculatethe proportionate distance (PD) between the 2dilutions where the 50% lies using a simpleformula.

The exponential of dilution of exactly 50% infectivity= PD X (ED next below 50% - ED next above 50%)+ ED next above 50%

= 0.3 X [(-3)-(-2)] + (-2) = -2.3;

So, the titer of virus = 102.3 TCID50/0.1ml, or 103.3

TCID50/ml

Further readings:

Freshney, R. I. 2000. Culture of animal cells, amanual of basic technique, 4th ed. Wiley-Liss, NewYork, NY.

Hsiung, G. D. 1984. Diagnostic virology: fromanimals to automation. Yale J. Biol. Med. 57:727-733.

Landry, M. L., and G. D. Hsiung. 2000. Primaryisolation of viruses, p. 27-42. In S.Specter, R. L. Hodinka, and S. A.Young (ed.). Clinical virologymanual, 3rd ed. ASM Press,Washington, DC

Mavromoustakis, C. T., D. T.Witiak, and J. H. Hughes. 1988. Effect of high-speed rolling on herpes simplex virus detection andreplication. J. Clin. Microbiol. 26:2328-2331

The proportionate distance obtained thus hasto be corrected to find out exactly 50% infectivityby the dilution factor, so called exponential ofdilution (ED).

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Nipah virus infection (NiV) is a viral zoonosis

caused by Nipah virus in both animals and humans.

It was first identified in fruit bats. The disease

causes respiratory and occasionally nervous signs

in pigs. It has devastating zoonotic potential

characterized by encephalitis and respiratory

disease, eventually become fatal in humans.

Synonyms

• Porcine respiratory and neurologic syndrome

• Barking pig syndrome

• Porcine respiratory and encephalitic syndrome

(PRES)

• One-mile cough

Etiology

• Nipah virus (genus Henipavirus, family

Paramyxoviridae), is an enveloped, negative-

sense, single-stranded RNA virus.

• Closely related to Hendra virus, the only other

member of the genus.

Susceptible species

• Fruit bats of the Pteropodidae family, which are

the natural hosts of the Nipah virus.

• Evidence of infection among several other

species of domestic animals, including dogs,

cats and horses.

• Clinical manifestation in pigs and humans. Pigs

act as intermediate host to cause infection in

humans.

Predisposing factors

Nipah viral infection is being an occupational

hazard to people involved in climbing palm trees,

working near mines, deep wells where bats are

inhabited; people handling pigs in intensive

farming; hospital workers, doctors and patient care

Nipah Virus Infection – A Zoonotic EmergencyM.Sivakumar 1 and C.Lavanya 2

1 M.V.Sc., Veterinary Public Health, Indian Veterinary Research Institute, Bareilly,2 Graduate Assistant, Veterinary College and Research Institute, Namakkal (TANUVAS).

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takers. They are at more risk of being infected by

the virus.

Transmission

Bats to human

• Consumption of fruits or fruit products (raw date

palm juice, sap or toddy) contaminated with

urine or saliva from infected fruit bats.

• Climbing trees coated in bat excrement.

Bats to pigs

• The virus is present in bat urine and potentially,

bat feces, saliva and birthing fluids, exposing

domestic pigs to infection.

Pigs to human

• Direct contact with sick pigs or their

contaminated tissues.

• Respiratory droplets, contact with throat or

nasal secretions from the pigs, or contact with

the tissue of a sick animal.

• Consumption of partially-cooked meat of

infected animals.

• Through contaminated fomites from pig farms

or carrying the virus on clothing, equipment,

boots and vehicles to other farms.

Human to human

• Close contact with infected people’s secretions

and excretions.

• Nosocomial infection.

• People working at hospitals who are taking

care of infected patients.

Outbreaks

• Nipah virus outbreaks have been reported

in Malaysia, Singapore, Bangladesh and India.

• First detected in Kampung Sungai Nipah,

Malaysia, in 1998.


• The highest mortality due to Nipah virus

infection has occurred in Bangladesh.

• For the first time in India, an outbreak has been

reported in the Kozhikode district of Kerala.

Morbidity and mortality

• Morbidity is high in all age groups of pigs.

• Mortality is low except in piglets, Overall

mortality is not more than 5 per cent among all

age groups.

• Many pigs remain asymptomatic or developed

clinical signs, recovered to a large extent.

• Mortality in humans is around 54 per cent out

of the affected cases.

Clinical signs in pigs

• Severe contagious disease in pigs, severity

depends on the age affected.

• A febrile respiratory disease with a severe

cough and difficulty breathing.

• A characteristic loud barking cough.

• Encephalitis.

• Nervous signs including twitching, trembling,

muscle fasciculation, paralysis, spasms,

muscle weakness, convulsions, incoordination

and death.

Clinical signs in human

• The symptoms appear within 3–14 days after

exposure.

• Fever, headache, altered consciousness,

drowsiness followed by disorientation and

mental confusion.

• Respiratory illness, influenza-like symptoms in

some cases.

• Sore throat, headaches, vomiting and muscle

pain (myalgia).

• Encephalitis and seizures.

• Can progress into coma as fast as in 24–48

hours.

• Atypical pneumonia and acute respiratory

distress, which further lead to death of theindividual.

Diagnosis

• Samples - throat swabs, cerebrospinal fluid,urine and blood.

• Isolation of virus from saliva of infectedpersons.

• Reverse transcriptase (RT) PCR.

• Immunohistochemical staining with specificantibodies.

• Indirect ELISA.

• Virus neutralization test.

Treatment

• Currently there is no effective treatment forNipah virus infection.

• The treatment is limited to supportive care.

• Ribavirin, a very broad-spectrum virustaticagent, which showed varying degrees ofefficacy against viruses such as respiratorysyncytial virus, influenza and measles, wastried on an empirical basis in NiV-infectedpatients, shown effective only in in vitro tests.

• Passive immunization using a humanmonoclonal antibody that targets the Nipah Gglycoprotein has been evaluated in the ferretmodel as post-exposure prophylaxis.

• The anti-malarial drug chloroquine was shownto block the critical functions needed formaturation of Nipah virus, although no clinicalbenefit has yet been observed.

• m102.4, a human monoclonal antibody, hasbeen used in people on a compassionate usebasis in Australia and is presently in pre-clinicaldevelopment.

• Human patients required intensive care withventilation support to manage the encephalitis;no specific treatment is available as all thetreatment trials are yet to be proven efficient

in humans.


Prevention

• It is important to practice standardinfection control practices andproper barrier nursing techniques toavoid the transmission of theinfection from person to person.

• Avoid close (unprotected) physicalcontact with infected people.

• Wear NH95-grade and highermasks.

• Avoid consuming partly eaten fruitsor unpasteurised fruit juices.

• Boil freshly collected date palm juice beforeconsumption.

• Thoroughly wash and peel fruits beforeconsumption.

• Maintain strict personal hygiene, wash handsregularly with soap.

• Follow protective precautions while handlingpigs.

• Immediate eradication by mass culling ofinfected and in-contact pigs and on antibodysurveillance of high risk farms to prevent futureoutbreaks.

• After culling, the burial sites are disinfected withchlorinated lime.

• Use sodium hypochlorite (bleach) to disinfectthe contaminated areas and equipment.

• Ban on transporting pigs within and out of theaffected areas, a temporary ban on pigproduction in the regions affected, as well asimprovement of biosecurity and quarantinepractices.

• Education and use of personal protectiveequipment (PPE) by persons exposed topotentially infected pigs is highlyrecommended.

• Decrease the likelihood of the bat reservoircoming into contact with pig production

facilities.

Prognosis and complications

• Poor prognostic factors for acute NiV

encephalitis included brain stem involvement,

presence of virus in the CSF and diabetes

mellitus.

• Although the mortality of acute NiV encephalitis

was high, the patients who completely

recovered did not suffer any serious sequelae.

• Clinical, radiologic and pathologic findings

suggested that, essentially, relapsed and late-

onset NiV encephalitis can cause fatality in

some recovered patients was the same

disease process that was distinct from acute

NiV encephalitis.

Conclusion

Nipah virus infection has been now identified in

Kerala, India, with number of human fatalities

reported. Hence there is no characteristic

symptoms, no definitive treatment or vaccine and

lack of awareness, it is not too late to adapt the

strict preventive and bio security measures in order

prevent further transmission of disease.

Veterinarians play a major role in disseminating

technical knowledge about the disease and

creating awareness among the public.

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IntroductionAlgae and cyanobacteria are present in all aquaticenvironments, and these organisms produce someof the most potent natural toxins known. We donot have a good sense of the extent of human andanimal exposures to these organisms or theirtoxins, nor do we understand the public healthimpacts from acute exposures associated withrecreational activities or chronic exposuresassociated with drinking water. To support publichealth decision-making about health risks fromexposure to cyanobacteria and algae blooms andassociated toxins, various efforts have beenundertaken to collect and assess data describingthe blooms, exposures, and associated human andanimal health outcomes.The term algae refers to microscopically small,unicellular organisms, some of which form coloniesand thus reach sizes visible to the naked eye asminute green particles. These organisms areusually finely dispersed throughout the water andmay cause considerable turbidity if they attain highdensities.Human activities (e.g., agricultural runoff,inadequate sewage treatment, runoff from roads)have led to excessive fertilization (eutrophication)of many water bodies. This has led to the excessiveproliferation of algae and cyanobacteria in freshwater and thus has had a considerable impact uponrecreational water quality.Harmful Algal BloomsAlgal blooms are a common occurrence in aquaticenvironments. A subset of these blooms posesenvironmental or public-health threats, and it istherefore referred to as “harmful algal blooms,” orHABs. Some HABs are harmful by virtue of theirsheer biomass, whereas others are associated withalgal blooms capable of producing toxins. Duringa HAB event, algal toxins can accumulate inpredators and organisms higher up the food web.Toxins may also be present in ambient waters,where wave action or human activities can create

Recreational exposure to Algal Toxins and its public health impactsDr. Rizwan Khan 1 Dr. S. Shakya 2

1 MVSc Scholar 2 Professor and Head, Department of Veterinary public Health and Epidemiology, Anjora, Durg, (C.G.)

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aerosols containing toxins and cellular debris.Animals, including humans, can thus be exposedto HAB-related toxins when they eat contaminatedseafood, have contact with contaminated water, orinhale contaminated aerosols.(Backer, L.C. 2012. Cyanobacterial harmful algalblooms (CyanoHABs): Developing a public healthresponse. Lake and Reservoir Management18(1):20–31.)Causes• Poisoning usually occur - heavy water bloom

that forms dense surface scum.• Factors- contribute to heavy water blooms are

nutrient-rich eutrophication, hypereutrophicwater and warm, sunny weather.

• Evidence -global climate change causes moreintense, and long-lasting warm weather- leadsto more extensive water blooms ofcyanobacteria.

• Agriculture practices (e.g. runoff of fertilizersand animal wastes) promote nutrientenrichment, also contribute to water bloomformation.

Formation of cyanobacteria bloomsIn contrast to true algae, many species of planktonic cyanobacteria possess specialize intracellulargas vesicles. Stacks of these minute (<300 nm)proteinaceous hollow cylinders maintain a gas-filledspace in the cell, which enables the organism toregulate its buoyancy and thus to actively seekwater depths with optimal growth conditions.However, regulation of buoyancy by changing theamount of gas in the vesicles is slow. Cells adaptedto turbulent mixing by enlarged gas vesicles willtake a few days to reduce their buoyancy in orderto adapt to more quiescent conditions. Thus,especially when the weather changes from stormyto fine (i.e., mixing conditions in the water changefrom turbulent to strongly stratified), manyexcessively buoyant cells or colonies mayaccumulate at the surface. Light winds drive themto leeward shores and bays, where they form


spp., Anabaena spp., Lyngbya spp. Nostoc spp.,some Oscillatoria spp. Schizothrix spp.The most widespread cyanobacterial toxins aremicrocystins and neurotoxins. Some speciescontain neurotoxin and microcystin simultaneously.Field populations of the most common bloom-forming genus, Microcystis, are almost always toxic(Carmichael, 1995), but non-toxic strains do occur.Generally, toxicity is not a trait specific for certainspecies; rather, most species comprise toxic andnon toxic strains. For microcystins, it has beenshown that toxicity of a strain depends on whetheror not it contains the gene for microcystinproduction (Rouhiainen et al.,1995; Dittmann et al.,1996) and that field populations are a mixture ofboth genotypes with and without this gene(Kurmayer et al., 2002).MicrocystinsMicrocystins are the most frequently occurring andwidespread of the cyanotoxins. They are cyclichepatic peptides containing a specific amino acid(ADDA) side chain which, to date, has been foundonly in microcystins and nodular in (a cyclicpentapeptide toxin of cyanobacteria from brackishwaters). About 70 structural analogues ofmicrocystin have been identified (Rinehart et al.,1994; Sivonen & Jones, 1999).Microcystins block protein phosphatases 1 and 2a(which are important molecular switches in alleukaryotic cells) with an irreversible covalent bond(Mackintosh et al., 1990). The chief pathway formicrocystins entry into cells is the bile acid carrier,which is found in liver cells and, to a lesser extent,in intestinal epithelia (Falconer, 1993).For vertebra-tes, a lethal dose of microcystin causes death byliver necrosis within hours up to a few days.Microcystins are found in most populations ofMicrocystis spp. (which frequently form surfacescums) and in strains of some species of Anabaena(which may also form scums). High microcystincontent has also been observed in Planktothrix(syn.Oscillatoria)agardhiiand P. rubescens(Fastner etal., 1999). P. agardhii, however, never formsscum’s, and where it occurs P. rubescens does notusually form scums duringthe recreational wateruse season, thus reducing the hazard to swimmers.

scum’s. In extreme cases, such agglomerationsmay become very dense and even acquire agelatinous consistency.When they are at 4m depth à 20 ì g/lit. of toxinsWhen they are at surface à 2000 ì g/lit of toxinsEffects• Harmful Algal Blooms(HABs)affect the quality

of fresh and marine waters and adversely affectboth animals and humans. Public health risksinclude exposure to toxins throughconsumption of contaminated drinking waterand fish and shellfish, and by recreating on orin contaminated waters.

• HABs have an adverse impact in recreationalwaters by fouling beaches andshoreline,affecting the quality of the water, andlimiting recreational activities such asfishing,swimming, and boating.

Algae’s Requirements• The Sun• Nitrogen & Phosphorous are the food.

PHOSPHOROUS CYCLE

CYANOBACTERIACyanobacteria are organisms with some character-istics of bacteria and some of algae. They aresimilar to algae in size and, unlike other bacteria,they contain blue-green and green pigments andcan perform photosynthesis. Therefore, they arealso termed blue-green algae (although theyusually appear more green than blue). Occurrence of toxic cyanobacteriaToxic cyanobacteria are found worldwide in inlandand coastal water environments.The most commontoxic cyanobacteria in fresh water are Microcystisspp., Cylindrospermopsin ,Raciborskii, Gloeotrichia


NeurotoxinsIrrespective of somewhat different modes of action,all three neurotoxins have the potential to be lethalby causing suffocation—anatoxin-a and a(s)through cramps, saxitoxins through paralysis.However, no human deaths from exposuretoneurotoxins associated with recreational use ofwater are known.Anatoxin-a(s) is the only known naturally occurringorganophosphate cholinesterase inhibitor andcauses strong salivation (the ‘s’ in its name standsfor salivation),cramps, tremor, diarrhoea, vomitingand an extremely rapid death (within minutes).Saxitoxins and anatoxin-a(s) are among the mostneurotoxic substances known. However, evidenceis accumulating that in lakes and rivers they do notoccur as frequently as microcystins. This appliesespecially to anatoxin-a(s): to date, it has beenfound only in a small number of Anabaena bloomsin North America.Further more, concentrations even of these highlytoxic substances in scums will scarcely reach levelsacutely neurotoxic to a human ingesting a mouthful.In contrast, neurotoxicity may be experienced bylivestock that drink many litres of contaminatedwater and pets—especially dogs—that gatherscum material in their fur and ingestit throughgrooming with the tongue.CylindrospermopsinCylindrospermopsin is an alkaloid isolated fromCylindrospermopsin raciborskii. It is a generalcytotoxin that blocks protein synthesis, the firstclinical symptoms being kidney and liver failure. Incontrast to the pure toxin, crude extracts of theorganism also cause injury to the lungs, adrenalsand intestine, indicating further, unknown toxins inthe organism. Clinical symptoms may becomemanifest only several days after exposure, so itwill often be difficult to determine a cause-effectrelationship. Patients intoxicated withcylindrospermopsin via drinking water in an incidentin Australia escaped death only through skilled andintensive hospital care (Falconer, 1996).Cylindrospermopsis raciborskii is considered to bea tropical and subtropical species, but has beenreported to form blooms as far north as Vienna(Roschitz, 1996).

Substantial populations have been reported fromnorth eastern Germany (C. Wiedner, personalcommunication), and generally C. raciborskiiappears to be invading temperate regions (Padisák,1997). Thus, cylindrospermopsin may becomerelevant in temperate zones in future.Evidence for toxicity of cyanobacteriaObservations of lethal poisoning of animals drinkingfrom water with mass developments ofcyanobacteria are numerous. The first documentedcase of a lethal intoxication of livestock afterdrinking water from a lake heavily populated withcyanobacteria was published in the 1800s (Francis,1878), and cases recorded since have includedsheep, cattle, horses, pigs, dogs, fish, rodents,amphibians, waterfowl, bats, zebras andrhinoceroses (Codd et al., 1989). Dogs have diedafter grooming accumulations of cyanobacteria outof their fur or after ingesting beached mats ofbenthic cyanobacteria.Human health risk from exposure to cyanobacteriaand their toxins during recreational water use arisesthrough three routes of exposure:Direct contact of exposed parts of the body,including sensitive areas such as the ears, eyes,mouth and throat, and the areas covered by abathing suit (which may collect cell material);Accidental uptake of water containing cells byswallowing; and uptake of water containing cellsby Aspiration (Inhalation).Different cyanobacterial metabolites are likely tobe involved in evoking symptom sassociated withthese exposure routes.Exposure through dermal contact: Allergic orirritative dermal reactions of varying severity havebeen reported from a number of freshwatercyanobacterial genera (Anabaena, Aphanizome-non, Nodularia, Oscillatoria, Gloeotrichia) afterrecreational exposure. Bathing suits andparticularly wet suits tend to aggravate such effectsby accumulating cyanobacterial material andenhancing disruption of cells and liberation of cellcontent. Reports from the USA have recordedallergic reactions from recreational exposure, andthe cyanobacterial pigment phycocyanin has beenshown to be responsible in one case (Cohen &


Reif,1953). In addition, cutaneous sensitization tocyanobacteria has been documented.Exposure through ingestion or aspirationSwallowing or aspiration was the exposure routein most of the documented cases of human illnessthat have been associated with cyanobacteria Incontrast to dermal contact, uptake of cyanobacteriainvolves a risk of intoxication by the cyanotoxins.This risk may be estimated from cell density, cellulartoxin content and known mechanisms of toxicity.Acute mechanisms of toxicity are well known forthe neurotoxins and microcystins, and someinformation is available to estimate risks due torepeated or chronic exposure.Case history of anatoxin exposure:In July 2002, five teenagers went swimming in apond at a golf course in Dane County, Wisconsin.The boys splashed around and two had their headsubmerged underwater. Of the two who wentunderwater, one boy died of acute heart failure 48hours later and the other became ill with acutediarrhea and abdominal pain. Blood tests on theboys confirmed the presence of Anabeana flosaquae and anatoxin-a. (Milwaukee JournalSentinel, Sept. 5, 2003).Case Reports :• In 1981, an incident of paralytic shellfish poisoningresulted in the hospitalization of 85 people anddeath of 3 persons due to consumption of the bloomin Tamil Nadu.• In Kerala, 5 children died and more than 300people were hospitalized in October 1998, due toshellfish poisoning from Gonyaulax polygramma(Karunasagar et al., 1997).• On 17 th September 2004, a massive fish kill wasnoticed along the Trivandrum coast. Many people,especially children, residing in the coastal districts,were hospitalized due to vomiting and nausea . Itwas later identified to be caused by a bloom of thetoxic dinoflagellates Gonyaulax diegensis andCochlodinium spp. (CMFRI Newsletter, 2004).• In India, livestock poisoning as well as skin lesionsin children were reported from the shores of lakesand reservoirs (Agrawal et al., 2006).• In March 2008, (U.S. EPA, 2008) listed theKlamath River from the California as impaired byexcessive concentrations of microcystin toxin.

• Australia has listed since 1989 ,many harmfulalgal spp. that they had been introduced toAustralia, i.e. further spreading via domestic ballastwater needs to be prevented. (PARK et al. AppliedEnvironmental Microbiology 2007.)Risk Levels & Standards of microcystin:Drinking water (provisional ): 1 ug/L microcystinTolerable Daily Intake (provisional): 0.04 ug/kg/dayRecreational Bathing WatersLow-risk of adverse effects: 20,000 cells/ml(4 ug/L microcystin)Moderate risk of adverse effects: 100,000 cells/ml (20 ug/L microcystin)High risk of adverse effects: scums.(WHO)Precautionary measures:• MonitoringWithin areas subject to the occurrence of marinetoxic algae or cyanobacteria, it is important to carryout adequate monitoring activities and giveinformation to the human population potentiallyaffected. Monitoring programmes should beplanned with the aim of preventing human exposurein areas affected by blooms of toxic algae orcyanobacteria. In some cases, satellite imagery canbe used as a part of a proactive monitoringprogramme. For example, movements of the GulfStream and subsequent elevated watertemperatures play a key role in Gymnodinium breveblooms; Gulf Stream temperatures monitored byremote sensing of infrared radiation can provideinformation on the likelihood of a bloom and itssubsequent movement (Hungerford & Wekell,1993)• InformationIn affected areas, it is appropriate to providegeneral practitioners and medical clinics withinformation regarding the health problemspotentially associated with algal blooms and toxicalgae, the diagnosis and treatment of poisonings,the surveillance of groups of people who could beat risk and procedures for reporting to public healthauthorities. Health information should also be madeavailable to the general public and to recreationalwater users in particular. As a precaution, thefollowing guidance is recommended for potentially


affected areas and should be included in publicinformation:• Avoid areas with visible algal concentrations and/or algal scums in the sea as well as on the shore.Direct contact and swallowing appreciable amountsare associated with the highest health risk.• If sailing, windsurfing or undertaking any otheractivity likely to involve water immersion in thepresence of algal blooms, wear clothing that isclose fitting in the openings. The use of wet suitsfor water sports may result in a greater risk ofrashes, because algal material in the water trappedinside the wet suit will be in contact with the skinfor long periods of time.• After coming ashore, shower or wash yourselfdown to remove any algal material.• Wash and dry all clothing and equipment afterany contact with algal blooms and scum.• If any health effects are subsequently experiencedand whatever the nature of the exposure, seekmedical advice.Prevention of marine algal blooms:There have been several attempts to developpractical methods for controlling algal blooms.Theuse of clays, herbicides, metals, chelators, artificialturbulence, dinoflagellate parasites andzooplankton all have been the subject of research.Algal blooms result from a complex interactionbetween hydrographic, meteorological, biologicaland chemical conditions, of which only a few canbe controlled. Without essential nutrients,principally nitrates and phosphates, algae willusually not reach bloom proportions.Excessive nutrient input from land-based sourcesis one of the most influential promoting factors, andminimization of nutrient availability will oftencontribute to controlling algal growth.Conclusion• Many algal blooms are caused by a major influxof nutrient rich run off into a water body, Programm-ing is necessary to treat waste water. Overuse offertilizers in agriculture should be reduced.• Reduce bulk flow of runoff as it can be effectivefor reducing severe algal blooms.• India is in much better position to establishnetwork as its long coast line is dotted with

institutions that deals with ocean research, fisheducation and technology.• We also have a dedicated ocean satellite IRS –P4 for ocean studies including bloom monitoring.We will now have to put them in use throughcooperative venture.References:CDC. Drinking water advisory communicationtoolbox. Available online: http://www.cdc.gov/healthy water/emergency/dwa-comm-toolbox/index.html (accessed on 25 March 2015).Backer LC, Carmichael W, Kirkpatrick B, WilliamsC, Irvin M, Zhou Y , Johnson TB ,Nierenberg K,Hill VR, Kieszak SM, Cheng Y-S. Recreationalexposure to microcystins during a Microcystisaeruginosa bloom in a small lake. Marine DrugsSpecial Issue.2008;6:389–406. [PMC free article][PubMed]Fleming, L.E.; Kirkpatrick, B.; Backer, L.C.; Bean,J.A.; Wanner, A.; Reich, A.; Zaias, J.; Cheng, Y.S.;Pierce, R.; Naar, J.; et al. Aerosolized red tide toxins(Brevetoxins) and asthma. Chest 2006, 131, 187–194.Gould, L.H.; Walsh, K.A.; Vieira, A.R.; Herman, K.;Williams, I.T.; Hall, A.J.; Cole, D. Surveillance forfoodborne disease outbreaks—United States,1998–2008. MMWR 2013,62, 1–34. 650–657.Geneva: World Health Organization; 2003. WHO:Guidelines for safe recreational water environments– Volume 1: coastal and fresh waters.[http://www.who.int/watersanitationhealth/bathing/srwgl.pdf].Graham JL, Loftin KA, Kamman N. MonitoringRecreational Freshwaters. Lake Line.2009;29(2):18–24.Anderson, D.M.( 2009) Approaches to monitoring,control and management of harmful algal blooms(HABs). Ocean & coastal management,342-347.Tian, D., Xie, G., Tian, J., Tseng, K.H., Shum, C.K.,Lee, J. and Liang, S.( 2017) Spatiotemporalvariability and environmental factors of harmfulalgal blooms (HABs) over western Lake Erie. PloSone,179-185.

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Nutritional Management of Transition BuffaloesKhwairakpam Ratika 1, 2, Avijit Dey 1*, S.S. Dahiya 1, I.N. Pathirana 3 and A.K.M. Anisur Rahaman 4

1ICAR- Central Institute for Research on Buffaloes, Hisar- 125 001, India2ICAR- National Dairy Research Institute, Karnal- 132 001, India

3University of Ruhuna, Mapalana, Kamburupitiya- 811 00, Sri Lanka4Bangladesh Agricultural University, Mymensingh- 2202, Bangladesh

*Corresponding author; email: [email protected]

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Transition period literally means the period duringwhich there is change from one state to another.In buffaloes, the transition period is oftenconsidered to occur from 3 weeks pre-partum to 3weeks post-partum where buffaloes transit fromnon-lactating state to lactating state. During thisperiod many essential processes undergo withinthe body of dairy animals preparing for the nextlactation. The dry period, and in particular the latedry period, should be considered a critical periodin which the quality of all inputs will directly impactthe productive performance in the next lactationas well as the incidence of disease associated withcalving and buffalo health.

Changes in the Transition period

Various physiological, metabolic and hormonalchanges occur during the transition period. Themost important physiological changes are thereduction in dry matter intake (about 1.7- 2% ofBW) around parturition and increase in nutrientrequirements for the rapidly growing foetus and milkproduction. These changes occurring in thetransition buffaloes further modify her metabolismdrastically. During the last trimester of pregnancy,the growing foetus occupies larger part ofabdominal cavity which reduces the volume ofrumen leading to decrease in dry matter intake.

The concentration of plasma insulin continuallydeclines in the transition period until calving, whilesomatotropin increases rapidly between the endof gestation and the initiation of lactation.Concentration of plasma progesterone, which ishigh in gestation, rapidly falls at calving. In addition,there is a transitory elevation in estrogens andglucocorticoids in the periparturient period. These

hormonal changes further contribute to decreasein dry matter intake.

Most of dairy animals at the onset of lactationexperience negative energy balance due to thereduction in dry matter intake and milk production.So, excessive mobilization of body lipid stores takeplace to support synthesis of milk and milk fat andincreased amounts of non- esterified fatty acid(NEFA) are released into the circulation which levelincreases gradually in the transition prepartumperiod.

Health Problems Coupled to Transition Period

The changes during transition period favour theoccurrence of health problems. The main disordersoccurring during the transition period are fatty liver,ketosis, sub-acute and acute ruminal acidosis(disorders related to energy metabolism); milkfever, sub-clinical hypocalcaemia, udder oedema(disorders related to mineral metabolism).

Moreover, the diet of most dairy animals’changes sharply at calving from being mainlyforage-based to concentrate-rich diets with highlevel of fermentable carbohydrates, the amount ofVFA produced exceeds the capacity of the rumento absorb them, leading to decreased pH in therumen environment. This situation leads to thephenomenon known as rumen acidosis andcontributes to reduced DMI and feed digestibilityin the early postpartum period.

The increased level of NEFA in the circulation dueto negative energy balance during the transitionperiod can be oxidized in the liver either completelyor incompletely, the latter resulting in the formationof ketone bodies causing a metabolic disorder,ketosis. The liver also re-esterifies NEFA into


triacylglycerol (TAG). To release TAG from the liver,it is packaged into very low density lipoproteins(VLDL). Fatty liver develops when the liver uptakeof lipids exceeds the oxidation and secretion oflipids by the liver. Excess lipids are stored as TAGin the liver and are associated with decreasedmetabolic functions of the liver.

The sudden start of milk synthesis in the udderresults in a tremendous demand for calcium. As aresult, blood calcium concentrations can dropprecipitously at calving, leading to milk fever.Smaller decreases in blood calcium, calledsubclinical hypocalcaemia, are believed to becontributing factors in disorders, such as displacedabomasum and ketosis, by decreasing smoothmuscle function, which is critical for normal functionof the digestive tract. Hypocalcaemia also leads toincreased secretion of cortisol, which is believedto be a factor in increased incidence of retainedplacenta.

Nutritional Management

Energy and protein are required for themaintenance, growth, development, reproductionand production performance of animals. Energy isgenerally acquired from carbohydrate such asstarch and cellulose. Energy requirement forpregnant buffaloes is 55.4 % TDN (2.00 Mcal/kgME) in DM between 240 and 270 days of gestationwhereas it is 60.6 % TDN (2.19 Mcal/kg ME)between 270 and 308 days. Paul and Patil (2006)reported that pregnant buffaloes require 12% CPduring 240-270 days and 14% CP during 270-308days of pregnancy. There is scanty informationregarding the nutrient requirement of pregnantbuffaloes. Lactating buffaloes require 36.34 g/W0.75

kg and 406.32 g/kg of TDN per kg 6% FCM formaintenance and lactation, respectively. Therefore,high demand of energy at lactation period shouldbe fulfilled by quality roughage and grains thatcontain copious amount of energy and should beintroduced in the ration gradually. Proteinrequirement in lactating buffaloes is high. For

maintenance DCP requirement is 3.14 g/W0.75 kg

and for lactation, about 55.24 g/kg 6% FCM isrequired. The protein requirement can be fulfilled

by supplementing high quality protein feeds like

cotton seed cake, groundnut cake, sesame cake,

soybean meal or mustard cake.

Bypass fat

Usually the extra energy required by the high

yielding dairy buffaloes cannot be fulfilled by

conventional ration. So, to increase the energy

density of the ration, fats can be added. As fats get

degraded in the rumen, which may adversely affect

the rumen microbes and feed intake it should be

given in rumen protected form. Supplementationof fat is recommended when the buffaloes are

yielding more than 18 kg of milk per day. The level

of total dietary fat in ration should not exceed 6%

of diet. Mixture of cereal grain and forages usually

contain about 3 % fat so up to 3 or 4 % of dietary

DM can come from supplemented fat.

Bypass protein

Bypass proteins are rumen undegradable proteins

that escape rumen fermentation and directly

degraded and get absorbed in the small intestine.

Lactating buffaloes yielding more than 15 kg of milk

per day should be given bypass protein as highamount of protein is required for milk protein

synthesis which cannot be met by conventional

ration. But when the diet is energy deficient, bypass

protein feeding is useful even in animals yielding

7- 8 kg milk per day. Bypass protein can be made

by treating conventional cakes either with

formaldehyde or heat. However, protein sources

like fish meal, blood meal, coconut cake and

cottonseed cake are good source of natural bypass

protein. Fish meal is used 1.5-2% of DM of ration

and blood meal at 0.3 -0.5% of ration DM of high

yielding buffaloes. Tanniferous leaves containingcondensed tannins (1.5% of supplement) can be

fed along with oil cakes as natural protectant of

dietary proteins.


Calcium and Phosphorus

Buffaloes require more calcium and phosphorus

as compared to other minerals. Calcium and

phosphorus required for maintenance of adult

buffaloes were found to be approximately 23-25g/

d and 12- 17 g/d, respectively. Buffalo milk contains

1.8-2.0 g Ca and 1.1-1.2 g P per kg milk. For per

kg milk production daily requirement of Ca is ataround 5.2-5.8 g and of P is 2.1-2.3 g. Good quality

mineral mixture should be supplemented (50- 60 g

/ d) to buffaloes for proper foetal growth and milk

production.

Buffers

Buffers combat acid production in the rumen and

help to reduce digestive upsets or to maintain milk

fat percentage when high grain diets are given to

the lactating dairy animals to meet out energy

deficiency. A mixture of sodium bicarbonate and

magnesium oxide (3:1) gives a better response

than either fed alone. Buffers should be fed at therate of 0.6 to 0.8 % of DMI or 1.2 to 1.6 % of

concentrate mixture. Sodium or potassium buffers

should not be fed during dry periods, because it

elevates dietary cation-anion balance (DCAD)

which predisposes the dairy buffaloes to milk fever.

Methionine and lysine

Methionine (Met) and Lysine (Lys) are considered

to be the two limiting amino acids for milk

production. Dietary supplementation of Met and Lys

can therefore be an effective approach to improve

amino acid balance for milk production. Methionine

also has an important role in the formation of verylow density lipoproteins which are necessary for

the export of stored fat in the liver and helps in

preventing fatty liver. Met and Lys easily gets

degraded in rumen. A source of ruminally-protected

methionine and lysine are available commercially.

Incorporation of 10g methionine and 30g lysine in

the ration has positive effects on milk production

and milk composition of lactating buffaloes (Ahmedet al., 2016).

Choline

Choline, a component of phospholipid and methyldonor, plays an essential role in very low densitylipoprotein synthesis and thereby contributes to fatexport from the liver. Choline is also required forbiosynthesis and secretion of milk. Fat metabolismcan be improved with the help of choline for betterenergy production. This also helps in improving milkproduction. As dietary choline gets degradedrapidly in the rumen, it must be supplemented inrumen protected form. Supplementation of 54g ofrumen protected choline 40 days before and 120days after calving increased milk yield and milkcomposition in dairy cows (Amrutkar et al., 2015).

Niacin

Niacin is a common feed additive in transition dietsfor its role in the prevention of ketosis throughreduced body fat mobilization. Dietary 14g/d niacinsupplementation also increases milk production inearly lactation of dairy cows (Karkoodi andTamizrad, 2009).

Rumen modifiers

Rumen modifiers act directly on rumen microbes,altering the balance between the different microbialpopulations and the proportions of the volatile fattyacids (VFAs) they produce. As such, they play apart in adapting the rumen. Ionophore rumenmodifiers include sodium monensin and lasalocid.Antibiotic rumen modifiers include virginiamycinand tylosin. The effects of sodium monensin areprimarily increased ruminal propionate balance,reflecting an increase in propionate producingbacteria compared to those producing formate,acetate, lactate and butyrate. There is aconcomitant decrease in methane production. Nowa day different plant secondary metabolites areused to modify rumen environment to increasepropionate production and reducingmethanogenesis in the rumen.

Selenium and Vitamin E

Selenium is one of the important minerals todecrease retained placenta, metritis and cystic


ovaries cases in buffaloes. Se requirement is0.3mg/ kg diet. This mineral along with vitamin Estrengthens the immune system. Vitamin E of dose500- 1000 IU per day may be fed to lactating anddry buffaloes daily. Panda et al. (2006) reportedthat supplementation of Vitamin E (1000-2000 IU/d) in late pregnancy reduces the incidence ofretained placenta in buffaloes.

Yeast Products

Yeast products are often targeted to transitionanimals to stabilize their rumen environment asthey shift from low- to high-energy diets. Severalresearch trials have shown increased DMI andreduced loss of body weight and condition scorein transition cows that were supplemented withyeast products. Feeding of 10g yeast was foundbeneficial to buffaloes with10-20 per cent increasein milk production.

Dietary Cation-Anion Difference (DCAD)

DCAD refers to the numerical difference betweenthe sum of certain dietary cations (positivelycharged minerals) and certain dietary anions.Primarily, the cations to consider are sodium (Na)and potassium (K) while the anions are chloride(Cl) and sulphur (S). Reducing DCAD in theprepartum transition period dramatically reducesthe risk for milk fever and subclinicalhypocalcaemia by improving calcium dynamics forthe buffaloes. A diet having 330 mEq/kg DM DCADhas promoted feed consumption, water intake andresulted in greater milk yield and milk fat in earlylactating buffaloes and occurrence ofhypocalcaemia was reduced by feeding dietcontaining -110 DCAD level, for last four to sixweeks before parturition.

Provision of adequate quantity and quality nutrientsas required by buffaloes during the transition periodgenerates positive effects on health, milkproduction and reproductive performance.

References

Agarwal, O. N., Nath, K. and Mahadevan, V. 1971.Phosphorus requirement of buffalo. J. Agric. Sci.(Camb.). 76: 83.

Ahmed, S., Gohar, M., Khalique, A., Ahmad, N.,Shahzad, F., Azam, B., Rahman, A. and Khan, M.I. 2016. Effect of Supplementation of RumenProtected Lysine and Methionine on ProductionPerformance, Milk and Blood Parameters of EarlyLactating Nili-Ravi Buffaloes. Pakistan J. Zool.48(2): 359-363.

Amrutkar, S. A., Pawar, S. P., Thakur, S. S.,Kewalramani, N. and Kaur, J. 2016. Effect of pre-partum supplementation of rumen protectedmethionine plus lysine and choline on theperformance of crossbred cows. Indian J. Anim.Sci. 86(1): 396- 404.

Bulbul, T. Energy and Nutrient Requirements ofBuffaloes. 2010. Kocatepe Vet. J. 3 (2): 55-64

Drackley, J. K. , Dann, H. M., Douglas, G. N.,Guretzky, N. A. J., Litherland, N. B., Underwood,J. P., Loor, J. J. 2005. Physiological andpathological adaptations in dairy cows that mayincrease susceptibility to periparturient diseasesand disorders. Ital. J. Anim. Sci. 4: 323-344.

Kara, C. 2013.Physiological and MetabolicChanges during the Transition Period and the Useof Calcium Propionate for Prevention or Treatmentof Hypocalcemia and Ketosis in PeriparturientCows. J. Biol. Environ. 7(19): 9-17

Karkoodi, K. and Tamizrad, K. 2009. Effect of niacinsupplementation on performance and bloodparameters of Holstein cows. South Afric. J. Anim.Sci. 39 (4): 349-354.

Melendez, P. Nutritional Management of theTransition Period to Optimize Fertility in DairyCattle. 2006. Proceedings 3rd Florida & GeorgiaDairy Road Show.

Panda, N., Kaur, H. and Mohanty, T.K. 2006.Reproductive performance of dairy buffaloessupplemented with varying levels of Vit. E. Asian-Aust. J. Anim. Sci. 19(1): 19-25.

Paul, S. S., Mandal, A.B., Pathak, N. N. 2002.Feeding standarts for lactating riverine buffaloesin tropical conditions. J. Dairy Res. 69: 173-180.

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PRESS RELEASE

CLFMA of India is the apex organization and thevoice of the country’s dynamic livestock sector. The51-year old industry association is recognized asone among the highly reputed in India. CLFMA OFINDIA is well recognized by livestock farmers,Central and State Governments, governmentdepartments, Agricultural Universities,Veterinary Colleges and also National ResearchInstitutes in India as well as outside the country.

On 7th September, 2018, CLFMA’s 51st AnnualGeneral Meeting was held and the new leadershipteam took charge for the period 2018-20. Speakingon the occasion the outgoing Chairman Mr. B.Soundararajan expressed his appreciations andconveyed best wishes to the new team led by Mr.S. V. Bhave, Managing Director, Berg and Schmidt

Change of Guard: New leadershipteam at the helmat CLFMA of India

India Pvt. Ltd, who got elected as the newChairman.

Mr. B. Soundararajan mentioned that CLFMA is wellrespected and well recognised in the LivestockIndustry. CLFMA is the pioneer organization andvoice of the sector, which actively works to protectthe industry’s interest through policy and regulatoryadvocacy.

“It wasmy great pleasure and honour to serve asthe Chairman of CLFMA of India for the last twoyears during which the organization madesignificant progress in terms of 3 I’s - “Image,Impact & Income”. I am sure under the ablestewardship of a visionary leader like Mr. S VBhave, CLFMA will continue to grow to newerheights. I wish the new Office Bearers and the


Managing Committee Members all the success.”Commented Soundararajan.

CLFMA OF INDIA has over 230 membersrepresenting diverse subsectors of animal proteinvalue chain including feed manufacturing, poultry,

dairy and aquaculture business, animal nutritionand health, veterinary services, machinery andequipment, processing, distribution and retailing ofmeat and ancillary services such as banking.

Following Office Bearers were elected for the period 2018 – 20.

Chairman : Mr. S. V. Bhave, Berg and Schmidt India Pvt. Ltd.

Dy. Chairman : Mr. Rajeev S. Murthy,Godrej Agrovet Limited

Dy. Chairman :Mr. Neeraj Kumar Srivastava, Novus Animal Nutrition (India) Pvt. Ltd.

Secretary : Mr. Divya Kumar Gulati, Nurture Aqua Technology Pvt. Ltd.

Treasurer : Mr. Naveen Pasuparthy, Nanda Feeds Pvt. Ltd.

Immediate Past Chairman : Mr. B. Soundararajan, Suguna Holdings Private Limited

Theother members of the Managing Committee 2018 - 20comprises of:

1. Mr. Sujit Komarla : Komarla Feeds

2. Mr. Vijay Bhandare : Bhavani Agrovet Pvt. Ltd.

3. Mr. Sumit Sureka : Shivshakti Agro (India) Ltd.

4. Mr. Anil M : KSE Limited

5. Mr. RamakanthVakula : The Waterbase Ltd.

6. Mr. Lakshmanan : Shanthi Poultry Farm Pvt. Ltd.

7. Mr. Suresh Deora : S. A. Pharmachem Pvt. Ltd.

8. Dr. Saikat Saha : Evonik India Pvt. Ltd.

9. Dr. Devender Hooda : Huvepharma SEA (Pune) Pvt. Ltd.

10. Dr. Sujit Kulkarni : Biomin India

11. Mr. S. Kannan :Suguna Foods Private Limited

12. Mr. Nakul Vakil : Cremach Private Ltd.

13. Mr. Abhay Shah :Spectoms Engineering Pvt. Ltd.

14. Mr. Nissar Mohammed : Coastal Exports Corporation

15. Dr. Vijay Makhija : DSM Nutritional Products India Pvt. Ltd.

16. Mr. Balaram Bhattacharya : Indian Herbs Specialities Pvt. Ltd.

17. Mr. Ramkutty : Niswin Enterprises

Mr. S. V Bhave, the new Chairman of CLFMA ofINDIA, gratefully acknowledged the critical role andvaluable contributions of the immediate pastchairman, Mr. B. Soundararajan and hispredecessors who played the vital role in buildingthe organization all along the past 5 decades.

“The new team of CLFMA has an apt mix of yourand experienced professionals.We will strive touphold the reputation and the legacy of CLFMAand work committedly towards its growth in theyears to come” concluded Mr. S V. Bhave.

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“Every industry needs fresh ideas from outside thesystem to survive and needs next-gen, young and brightminds with the clear vision and traits such as grit andperseverance to make a positive contribution to thesociety” said B Soundararajan, Chairman of CLFMA ofIndia, the apex association representing the livestockindustry in India on the occasion of International YouthDay (12th August).CLFMA of India is the apex body representing thedynamic livestock sector in India. The 50-year oldindustry association is recognized as one among theeldest and highly reputed in India. It currently has over240 members representing diverse subsectors of animalprotein value chain including feed manufacturing;poultry, dairy and aquaculture business; animal nutritionand health, veterinary services, machinery andequipment; processing, distribution and retailing of meat;and ancillary services such as banking.“It is impossible to achieve the 17 UN SustainableDevelopment Goals (SDGs) without significantparticipation and contribution from youth in every aspect.We strongly believe the country’s fast-growing livestocksector offers an ocean of opportunities for those whoare willing to explore” Soundararajan opined.Agriculture in India faces a number of importantchallenges: it needs to become more sustainable andproductive, while it must at the same time remainprofitable for farmers. This is particularly true forlivestock farming. Modern and innovative livestockequipment and technologies are important parts of thesolution to address and overcome these challenges.Furthermore, a number of innovations are occurring inplant agriculture to maximize all of the land we cansustainably cultivate. From advanced plant breedingtechniques to integrated pest management, to improvedvarieties, scientists, industry and farmers are workingtogether to ensure food and nutritional security of thecountry. Livestock is one of the fastest growingagricultural sectors driven mainly by rapid urbanizationand higher incomes.“In the last decade, the world is witnessing how Internetof Things (IoT) and cloud-based technologies aretransforming animal-agribusiness sector inunimaginable ways. For example, wearable devices onanimals provide real-time data to monitor feed intake,stress levels or disease symptoms so that these canbe addressed promptly not only to enhance productivitybut animal welfare as well. Similarly, soil sensors helpfarmers analyze moisture or nutrient levels to cut downunnecessary irrigation or fertilizer application and

CLFMA Symposium 2018 to focus on “GenNXT”aspects for Indian Livestock Sector

contribute greatly to cost savings as well asenvironmental sustainability. These innovations provideus wealth of information to analyze every processdeeper for continuous improvement. It is only a matterof time before we see all these are widely used in India”he added.This year’s theme for CLFMA’s annual symposium is‘GenNXT wave: People, Technologies and Innovation’and how this is going to impact the Indian livestocksector• People –perspectives from next-gen managing thebusiness and entrepreneurs• Technologies – perspectives including application ofIoT, Blockchain, digital applications• Innovation – in terms of products, marketing, andsupply chain on how these innovations can help improveanimal welfare, the environmental sustainability andboost farmers’ incomes.Now a days everything in the world has come down to‘one touch’, h How the Indian government’s full supportis needed to unleash the full potential of innovativelivestock technologies. Furthermore, innovations like e-commerce through mobile phones, coupled withanalytics positively disrupted retailing in India in therecent years. Nowadays, through mobile apps and withjust a few clicks, consumers can get their preferred type,preparation, and variety of meat and seafood deliveredat their doorsteps at affordable prices year-round withoutcompromising on their two most important needs -convenience and quality“It is high time we think about who is going to feed us infuture and how to ensure food and nutritional securityof the billion-plus population while remaining focusedon sustainability of our unique and precious biologicalecosystem. It is important to ensure India’s animal-agribusiness sector attracts the best talent, sparklingbrains and skilled hands from different fields and retainsthem. Traditional business paradigms; entrenchedperceptions and outdated practices must pave way tonewer and fresher ideas and concepts that only today’syouth can bring in. Only then innovations can sproutand flourish. This industry must be seen as one of thepreferred career paths by youngsters, who currently lackawareness about the ocean of opportunities available.Every one of us working in the industry must activelystep up to create awareness among students who areaspire to become tomorrow’s professionals,entrepreneurs, and leaders and CLFMA’s forthcomingsymposium would be a great platform for such in-depthdeliberations” Soundararajan concluded.

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PRESS RELEASE



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