veevernuf stocksense 2013 ISSUE 3 3 Understanding Conical Flukes in Ruminants Jacques van Rensburg 6 Zoonoses: Campylobacteriosis Dr Mats Abatzidis KALF- GESONDHEID Dr Adél de Haast 8 KNOPVELSIEKTE Dr Brand van Sittert Wat is die belangrikste siektetoestand in kalwers? Kalwerdiaree is die belangrikste siektetoestand in veral suiwelkalwers en het die grootste finansiële verliese tot gevolg as enige ander siektesindroom. Afhangende van die oorsaak, kan kalwerdiaree enige tyd voorkom van die eerste paar ure na geboorte tot n paar weke van ouderdom. Hoe ontstaan diaree? Bakterieë, virusse of parasiete heg aan die selle van die ingewande van die kalwers vas en beskadig die selle sodat geen absorpsie van vloestowwe en voedingstowwe kan plaasvind nie. Waterige diaree is gewoonlik die gevolg en die kalfie dehidreer. Indien die lading van infeksie baie hoog is kan die kalfie doodgaan, maar selfs as die kalfie oorleef sal die kalfie nie goed prestreer as volwassene nie. 10 LIVERFLUKE & Decreased Milk Production Dr Johan Cloete Wat is die hoof oorsake van kalwerdiaree en hoe kan ons die oorsake onderskei van mekaar? Rotavirus Coronavirus E.coli Salmonella spp. Coccidia spp. Cryptosporidium spp. Ouderdom 5 14 dae 5 28 dae 2-3 dae 3 12 weke 2 3 weke 1 4 weke Diaree voorkoms Waterig en groot volumes Waterig met slym, en groot volumes Waterig geel tot grys-geel Stink en puttylike, baie slym. Sag en bloederig Geel en waterig 12 Kalfgesondheid Dr Adél de Haast Ander simptome Baie skielike siekte, depressie Nie so depressief as met Rotavirus nie, drink nog melk. Dehidrasie, swak, koors en dood Koliek, swak. Geen eetlus, swakheid, geen koors Geen eetlus, depressief, gewigsverlies Intervet SA (Pty) Ltd. Reg. No. 1991/006580/07 20 Spartan Road Isando 1600 R.S.A Private Bag X2026 Isando 1600 Tel +27 (0) 11 923 9300 Fax +27 (0) 11 974 9320 www.msd-animal-health.co.za Hoe kan ons kalwerdiaree voorkom? Daar is n paar faktore wat nie onderhandelbaar is as dit by die voorkoming van kalwerdiaree kom, 1. Higiëne van kalfhokke Goeie higiëne verminder die risiko vir verspreiding van siekte tussen kalwers. Droë en skoon beddegoed is noodsaaklik in kalfhokkies. Moenie ou beddegoed net omdraai nie. Organismes vermeerder baie gou in ou beddegoed. Verwyder siek kalfies so gou as moontlik na n isolasie eenheid apart van die res en behandel. Ontsmet klere, hande en skoene na die siek kalfies hanteer is om verspreiding na ander diere te voorkom. 2. Biesmelk (Kolostrum) kwaliteit Korrekte voeding tydens die maand voor geboorte wanneer kolostrum gevorm word, bepaal die
kwaliteit daarvan. Goeie kwaliteit biesmelk is die sleutel tot goeie immuniteit in die kalf en bied beskerming teen die oorsake van kalfdiaree. 3. Verminder stres voor- en naspeen Kalfbehuising behoort droog en vry van trekke te wees. Die temperatuur daarbinne behoort so konstant as moontlik te wees. Wanneer kalwers op ongeveer 6 weke ouderdom gespeen word moet hulle minstens al vir n week 1 kg aanvangsrantsoen per dag ingeneem het en minstens 60 kg weeg. Kalwers wat nie hierdie teikens behaal het nie, sal dit moeiliker vind om na speen aan te pas en word makliker siek as gevolg van die mindere tot meerdere mate van immuunonderdrukking wat die speen proses tot gevolg het. Voldoende skadu en beskutting, drinkwater en gereelde lewering van n kwaliteit rantsoen sal verseker dat die kalf die teiken teelmassa betyds bereik (15-18 maande ouderdom). Hoe verseker ek dat my biesmelk n goeie kwaliteit is? n Kolostrometer behoort roetinegewys gebruik te word om kolostrum kwaliteit van elke vers of koei wat kalf te evalueer. Die kolostrometer meet die proteïene en dus teenliggaampies in die biesmelk. Die soortelike gewig (SG) moet meer as 1.045 wees. Hoe beter die kwaliteit van die biesmelk, hoe beter is die beskerming teen diaree. Beskerming teen spesifieke siektetoestande kan aangehelp word deur die dragtige droë koei 4 6 weke voor geboorte te ent met entstowwe soos, ROTAVAC CORONA, BOVILIS S, RESPIRAVAX. Hoeveel biesmelk vir hoe lank? Die kalf moet ten minste 2 4 liter biesmelk binne 4 6 ure na geboorte ontvang waartydens die dermwand se deurlaatbaarheid opname van teenliggaampies toelaat. Die beskerming (teen die besmetlike oorsake wat die eerste dosis biesmelk bied) werk net vir 3 4 dae, terwyl dermkanaal infeksies kan voorkom tydens die eerste paar weke van ouderdom. Daarom is herhaalde dosisse van biesmelk (ten minste 2.5 liter elke dag vir twee tot drie weke ) belangrik. Die teenliggampies word nie meer betekenisvol na 6 ure vir sistemiese beskerming geabsorbeer nie, maar bly op die oppervlak van die dermslymvlies om plaaslike beskerming te bied teen infeksies. Kan ek biesmelk vries en dit weer later gebruik? Ja, indien jy wel gevriesde biesmelk gebruik is dit baie belangrik om dit reg te ontdooi. Dit moet in warm water ontdooi word en nie in die mikrogolfoond nie, aangesien die teenliggaampies in die biesmelk vernietig word in die mikrogolf. Rotavac Corona (Reg no. G2955 (Act 36/1947)) contains inactivated bovine rotavirus, inactivated coronavirus and inactivated E.coli K99 antigens. Bovilis S (Reg no. G3763 (Act 36/1947)) contains organisms of inactivated Salmonella Dublin and organisms of inactivated Salmonella typhimurium Respiravax (Reg no. G3867 (Act 36/1947)) contains inactivated BHV1 (IBR), PI3 and BVD type1, as well as Mannheimia haemolytica 236A/1305 2
UNDERSTANDING CONICAL FLUKES in RUMINANTS Jacques van Rensburg Conical fluke belongs to the family Paramphistomatidae (recently changed to Calicophoron) and presents itself as small, red pear-shaped, parasites found in the rumen of cattle, sheep and goats. The adult conical flukes cause little or no physical damage, however the young stages found in the intestine may be very harmful and can even cause death if present in large enough numbers. Conical flukes (Calicophoron microbothrium) are found worldwide but are most prevalent in the warmer regions of Australasia, Africa and India 1. C. microbothrium seems to be the most important fluke in domestic ruminants in South Africa 1. Life cycle The life cycle of the conical fluke is similar to the gastrointestinal trematodes or liver flukes (Fasciola spp). They both require water sources and a water snail as an intermediate host. One of the main differences is that the immature stages of the conical fluke causes the majority of it s damage in the small intestine (duodenum), and not in the liver, as with liver flukes. The adult parasites attach to the lining of the rumen 2. In the host animal the adult conical fluke will pass it s un-embryonated eggs into the environment through the hosts faeces and will hatch within 12-26 days if the eggs are deposited into water. After being freed from the faeces the miracidia hatch from the eggs within 12-16 days and penetrate the intermediate host snail Bulinus tropicus (Fig.1) Only snails less then three weeks of age are infected, older snails do not become infected 3. These snails multiply very rapidly in warm, watery environments and can be found on pastures prone to flooding, on herbage in and around ponds, streams and other water sources. Due to the adaptability of these snails they occupy a far more diverse habitat than the lymnaeid snails which are the intermediate hosts for Fasciola spp (liver flukes). Endemic areas for conical flukes and liver flukes therefore do not necessarily coincide. Fig. 1 Bulinus tropicus Within the snail, sporocysts are formed and release free swimming cercariae which encyst to metacercariae, on water plants which will later be ingested by the ruminant host while grazing in these watery marshy areas. Cercariae, if kept moist and cool, may survive for two months but metacercariae die off if they become dessicated or completely submerged in water. Young conical flukes are released from the metacercariae when in contact with digestive fluids and bile in the duodenum and attach to the mucous membrane with their posterior sucker. It is in this part of the small intestine where they will feed from the hosts stomach contents for 5 8 weeks before crawling back into the rumen and reticulum to become adults. Adult flukes may start passing eggs from as early as day 56 in calves and day 70 in sheep following ingestion of metacercariae. The entire life cycle, from egg to egg, takes a minimum of 110 days in sheep and 132 days in cattle 1. Distribution The infestations of cattle, sheep and goats with flukes are very common. These parasites may survive for years providing a virtually constant source of infestation for successive generations of snails. The intermediate hosts are extremely adaptable and prolific breeders, which ensures a widespread availability of the snails within infested areas 1. Clinical signs ascribed to severe conical fluke infestations are usually confined to the drier months of the year (autumn and winter months in summer rainfall areas) due to concentration of snail populations around smaller concentrated water resources. The latter areas may also provide the last available green grazing. A more constant but lower challenge may be seen during periods of higher rainfall, due to the infested water snails being distributed over a larger area and a resultant lower concentration of parasites per potential host 3. The moisture on irrigated pastures is often adequate for the survival of water snails and metacercariae. Outbreaks of conical flukes may occur throughout the year on irrigated pastures 3. Recorded studies showed an extensive distribution in KwaZulu-Natal Province, the Limpopo Province, the coastal areas of the Eastern Cape Province and the south-eastern part of the North West Province. Several investigations have shown that mild temperatures and frequent rainfall throughout the year are suitable conditions for the infestation of cattle with trematode parasites like conical fluke 2. Clinical signs 1,2,3,4 Adult conical flukes are found in the rumen and are not responsible for the clinical signs seen in the infested host animal. Clinical signs of conical 3
fluke infestation are caused by the immature flukes that attach in the first 3 meters of the small intestine. These immature flukes attach themselves to the intestinal mucosa and may even penetrate as far as the intestinal muscular layer. A plug of mucosa becomes drawn into their posterior sucker, with potential strangulation and necrosis of the mucosa causing severe discomfort and loss of appetite leading to progressive weight loss. Severe enteritis is associated with high numbers of migrating flukes in the duodenum. A drop in food consumption may occur from around day 8 after initial infestation and could progress to complete anorexia by day 21. Water intake may also drop to about half the normal level. A characteristic and persistent foul smelling foetid diarrhoea is caused by the decomposition of intestinal mucosa and intestinal content. The diarrhoea is seen in adults and young animals. Leakage of blood protein into the intestinal lumen may also lead to the plasma protein levels dropping and may lead to signs of anaemia, pallor of mucosae and bottle jaw. These signs could be accompanied by weakness, intestinal discomfort, reduced appetite, loss of weight, rough dry coat, a drop in milk production, depression, dehydration and eventually anorexia. Bleeding from the rectum may be observed in heavy infestations. Mortality rate in heavily infested animals is high and may occur 5 20 days after the first clinical signs appear. Reinecke (1983) reports that cattle develop a strong immunity to C. microbothrium which may be dependent on the presence of adult parasites in the rumen. Sheep were reported to be less resistant after attempts to immunise them by artificial infestation 1. Diagnosis 1,3 The clinical diagnosis of conical fluke infestation remains challenging as immunological techniques and serum antibody detection is usually not conclusive. Therefore a diagnosis in live animals still depends on faecal detection of eggs, in conjunction with a typical clinical history and clinical signs. In some cases one may not find eggs, or only very few, due to massive infestation with young flukes and the relatively long pre-patent period before adult parasites start to produce eggs. Another drawback is that with many standard flotation methods of faecal egg identification, it may not be possible to detect conical fluke infestation. Currently, post mortem findings combined with the presence of flukes in the affected intestines serve as a confirmative diagnosis (Fig. 2). Treatment and control Effective treatment and control of conical fluke infestation is challenging. Immature flukes cause the physical damage in the host animal that should be addressed, while adults are mainly responsible for laying eggs and contaminating the environment again with potential future reinfestation of available hosts. The control of most trematode infestations, including conical fluke, should be two-fold: 1. The strategic use of an effective and registered chemical product for the treatment of immature as well as adult conical fluke. 2. Adressing the environmental impact and potential ways to manage and limit the contact between the intermediate and final hosts. A sound knowledge of the historical parasite prevelance, environmental conditions and effective farm management guidelines will assist the farmer to better understand the various management guidelines and methods available for managing fluke infestations successfully 1 : 1. Prophylactic treatment of animals towards the end of a period of reduced activity of the parasites and the intermediate hosts (eg. during a prolonged dry season, or extreme cold). The latter removes adult conical flukes and reduces the pasture contamination levels with eggs before favourable climatic conditions for larval development and snail activity resume during the summer months. 2. Curative treatment is applied one to two months after expected peak host infestation to remove the residual fluke burden acquired from metacercariae which have survived. Animals showing signs of clinical infestation and with a history of grazing on infested pasture, should immediately be treated with a reputable product registered for the treatment of both adult and immature conical flukes and moved to uninfested pastures. The treatment will prevent egg laying from adults, thus breaking the life cycle of the parasite and will also treat the clinical signs by killing the immature flukes. 3. Additional treatments should be considered in highly contaminated areas where seasonal variations do not significantly affect the life cycle of the flukes. These strategic, additional treatments may be required when the seasonal climatic conditions are favourable for parasite and snail development, or in areas where high metacercariae intake often occurs as a result of restricted grazing of wet areas during dry seasons. 4. Prevent snail habitats from developing by regular clearing of drainage channels of vegetation which provide suitable sites for snail development. Good drainage and the building of dams at appropriate sites in marshy and low lying areas may reduce the snail problem. Fig. 2: Adult conical flukes in the rumen. 5. Fence off infested areas where possible to minimise contact with infectious, swampy water areas. Younger animals like calves, lambs and heifers are more at risk for severe infestation and should be kept away from these infested areas if possible. 4
6. Establish proper watering facilities to prevent animals from drinking from lakes, ponds and streams. It is also important to repair any leaks in dams and water troughs. Leaking dams and troughs can create an ideal habitat for the survival of water snails. 7. Chemically controlling water snails in marshy areas is potentially toxic to livestock and the environment, but also often unsuccessful and impractical. MSD s anthelmintic answer to conical fluke infestation: The choice and implementation of the correct chemical product into the overall herd health program of each herd should be discussed together with your local veterinarian and your MSD agent. MSD has two active ingredients available for the control of conical fluke. Oxyclosanide and Closantel. These actives can be found in the following two well-known and regularly used anthelmintics, namely Nem-a-Fluke and Tri-Dose respectively. Nem-a-Fluke, with it s broad spectrum of efficacy against major economically important internal parasites, including liver fluke, seems to be the product of choice for the treatment of conical fluke. Nem-a-Fluke contains Levamisole hydrochloride 2,5 % m/v PLUS Oxyclozanide 3,4 % m/v which gives it its efficacy to control both adult and immature stages of conical fluke (Calicophoron spp.), wireworm, brown stomachworm, bankruptworm, cattle bankruptworm, longnecked bankruptworm, large-mouthed bowelworm, hookworm, nodular worm, lungworm as well as both adult liver flukes (Fasciola hepatica) and giant liver fluke (Fasciola gigantica) in cattle, sheep and goats. Nem-a-Fluke is widely used in dairy cattle as there is no milk withdrawal, which means you may treat cows before, during and after lactation without the loss of income due to the loss of milk. The convenient dose rate of 15 ml / 50 kg live mass for cattle and 3 ml / 10 kg for sheep and goats makes Nem-a-Fluke just as popular for use in a variety of species. Specific strategic treatment of conical fluke infestation can be done at a dose rate of 3 ml /10kg live mass for cattle, sheep and goats and to ensure optimal efficacy against both adult and immature flukes a second identical dose 72 hour later is recommended. Nem-a-Fluke comes conveniently packed in 1 l, 5 l and 10 l containers. Product information: Nem-a-Fluke (Reg. No. G3563 (Act 36/1947), Namibia Reg. No. V05/18.1.8/46) contains Levamisole hydrochloride 2,5 % m/v and Oxyclozanide 3,4 % m/v. Tri-Dose ORAL (Reg. No.G3103 (Act 36/1947, Namibia Reg. No V02/18.13/654) contains Closantel 5% m/v. References: 1. www.cpdsolutions.co.za, CONICAL FLUKES IN RUMINANTS. Dr. J.H. Vorster, BVSc, MMedVet (Path), Vetdiagnostix, Veterinary Pathology Services and Dr. P.H. Mapham, BVSc (Hons) Veterinary House Hospital. 2. www.fivetanimalhealth.com, Flukes in Cattle, Sheep and Goats Fivet Animal Health. 3. www.afrivet.co.za, Conical Fluke (Calicophoron microbothrium) 4. www.merckmanuals.com, The Merck Veterinary Manual, Paramphistomes in Ruminants: (Amphistomes, Rumen flukes, Conical flukes). 5. Reinecke R.K. (1983), Veterinary Helminthology 1983, Butterworths, Durban/Pretoria. 235/1305 2013 ISSUE 3 5
ZOONOSeS Dr Mats Abatzidis MSD Animal Health would like to take this opportunity to inform you, the reader, regarding the importance of gaining knowledge on zoonotic (diseases that can be transferred from animals to humans) diseases. These diseases will be dealt with in alphabetical order. CAMPYLOBACTERIOSIS Synonyms: Classification: Direct Distribution: Previously vibriosis in animals and man and previously referred to as micro-aerophilic vibrios. First recognised over 70 years ago by two veterinarians McFadyean and Stockman, Campylobacters remarkable association with disease is only now becoming appreciated. The breakthrough came when human microbiologists accepted from veterinary microbiologists that a difference can exist between surface mucosal and general luminal flora. Campylobacter organisms are amongst the most frequent causes of bacterial diarrhoea in man, enzootic sterility in cattle and sporadic abortion in various domestic animals. Widespread, but not yet positively identified in all countries. AGENT DETERMINANTS Gram NEGATIVE bacteria, characteristically curved, S-shaped or spiral morphology and highly motile. The catalase POSITIVE group c o n t ains those Campylobacters n o w recognised as pathogens in humans i.e. Campylobacter fetus subsp. fetus and Campylobacter jejuni. HOST DETERMINANTS Immune status and age are important determinants. C. fetus subsp.fetus attacks debilitated people with impaired defences against infection and rarely causes disease. C. jejuni attacks the healthiest people and is one of the most common causes of acute diarrhoeal illness - even more predominant than Salmonellae, Shigellae and enteropathogenic Escherichia coli. It is frequently isolated as the SOLE presumptive pathogen. C. jejuni is an important cause of diarrhoeal illness in all age groups in developed countries, but in developing countries the prevalence of infection amongst children (2-5 years old), regardless of climate, is greatest. There is, however, a BIMODAL tendency in developing countries, with a high incidence also occurring in the 20-30 year age group. ENVIRONMENTAL DETERMINANTS In the RSA there is a definite summer time peak of Campylobacter infection (season or temperature). So far, sero-epidemiological studies support the thought of a relationship between Campylobacter infection and occupation, and in particular carcass and meat handlers and abattoir workers. The major identified reservoirs of Campylobacter are animals and products obtained from animals. C. jejuni exists as a commensal in the intestinal tracts of a wide variety of wild and domestic animals. The species of animals and handling practices pertaining to them are important environmental determinants. These are as follows: Poultry Bovines Pigs Sheep Dogs Cats & birds Humans intestinal content contaminates carcasses during slaughter. carcass contamination from intestinal contents: INFREQUENT unpasteurised milk is a problem - origin faecal or mastitis. Campylobacter coli more common than C. jejuni. Carcass soiling during slaughter spreads the organisms. Sausage casings can also be contaminated. C. jejuni causes epizootic infectious abortion: common in the intestines. found in stools MORE in puppies and kennel populations. also harbour Campylobacter - unlikely to be a major reservoir or vehicle to humans. play a role in developing countries in the transmission due to a carrier state. 6
CAMPYLOBACTERIOSIS Inanimate reservoirs: C. jejuni is NOT adapted for free living in water. If it is found in water (usually with Escherichia coli) then this suggests FAECAL contamination. Campylobacteriosis is a principal cause of bacterial diarrhoea in humans and appears to be an emerging zoonosis of importance. Mode of spread: Usually from animal reservoirs to humans, but it can differ. 1. Direct animal contact: There is increased RISK from contact with diarrhoeic puppies (also kittens - less important), farm animal stools (especially in summer), pregnant sheep and laboratory animals - especially primates. Regular contact results in high seropositivity. 2. Ingestion of contaminated foods: Campylobacteriosis has been associated with uncooked or poorly cooked meat or poultry products, uncooked foods contaminated by meat and poultry products, unpasteurised dairy products (particularly RAW milk) and seafood contaminated by sewage. In such cases, isolations of campylobacter are often sporadic and the history of transmission is vague. The world picture of travellers diarrhoea suggests MULTIPLE vehicles with intermittent contamination. 3. Ingestion of contaminated water: This can occur indirectly, in the case of eating shellfish which are taken from contaminated water, or directly where drinking water was involved. RISK of disease is highest in rural areas where surface water is used for drinking. 4. Person to person transmission: faecal - oral and birth canal transmission is suspected. There is strong evidence of diarrhoeal disease in families where a neonatal gastroenteritis was found. Sexual transmission has not been proved. 5. Perinatal transmission: C. jejuni bacteraemia has caused in utero foetal death and neonatal meningitis has been reported. Generally, however, neonates acquire infection from faecal contamination at delivery. SYMPTOMS The incubation period is about 1-5 days. This is followed by a moderate to severe diarrhoea but less acute and more prolonged than Shigellae or Salmonella. It can become protracted in infants and children. Apart from diarrhoea and abdominal pain, symptoms are mainly afebrile with occasional vomiting and blood in the stool. The course of the illness is usually benign and the patient recovers spontaneously in a week to ten days. More severe symptoms may resemble ulcerative colitis or salmonellosis and may even lead to a suspicion of appendicitis. Septicaemia has developed in some cases, either simultaneously to the enteric disorder or afterwards. Complications are rare, but consist of meningitis and abortions. PREVENTION AND CONTROL Control is based on good hygiene principles (especially in the handling of animals and animal products) and is identical to the control of Salmonellosis. Introduction of some BASIC HYGIENE swings the picture from that of a developing country to that of a developed country. NB: Pasteurisation effectively eradicates Campylobacter from milk and chlorination of water helps eradicate campylobacter from water. Reference: Prof. B Gummow and Dr M More O Ferrall-Berndt, Veterinary Public Health and Applied Epidemiology Course Notes: Zoonoses and Food Associated Diseases, BVSc, University of Pretoria, Onderstepoort, 2000 edition, pp 15-17. Photograph: istockphoto.com 2013 ISSUE 3 7
KNOPVELSIEKTE Dr Brand van Sittert Perseel veearts MSD Malelane Navorsings Eenheid Knopvelsiekte is een van die belangrikste erosiesiektes van beeste in Afrika. Dit word veroorsaak deur n pox virus wat simptome soos permanente huid skade en skerp dalings in die vrugbaarheid en produktiwiteit van die kudde veroorsaak. Hoe kan jou beeste knopvelsiekte kry? Daar word vermoed dat die siekte hoofsaaklik deur bytende insekte soos stalvlieë oorgedra word 1, en kan dus oor n groot gebied versprei vanaf n enkele besmette dier. Die meeste gevalle kom gedurende laat somer en vroeë herfs voor, gewoonlik tydens jare van bo-gemiddelde reënval 2. Binne in kuddes versprei die siekte ook waar diere drink- en voerbakke deel deurdat besmette diere se speekselafskeiding in die voerbakke beland. Koeie skei die virus deur die melk af en kan hul kalwers ook só besmet. Die mens kan ook die siekte versprei deur naalde tussen beeste te deel indien geënt word tydens uitbrake, of deur beeste kunsmatig te insemineer met besmette semen 3. Watter diere is vatbaar vir die siekte? Alle ongeënte beesrasse is vatbaar, en tussen 3% en 85% van n kudde kan geaffekteer word 4. Kalwers van ongeënte koeie is ook vatbaar, maar kalwers van koeie wat geënt is word beskerm tot op ongeveer 6 maande. Sover as wat vasgestel kon word speel wilde diere nie n betekenisvolle rol in die verspreiding van hierdie siekte nie 1,4. Watter tekens wys beeste met knopvelsiekte? Beeste ontwikkel eers n koors en wys tekens soos verhoogde speeksel-, traan- en neusafskeidings. Soms kan daar ook bindvlies ontsteking (konjunktivitis) in die oog en vergrote limfknope op die lyf voorkom. Daarna begin die bees uit te slaan in vel knoppe van ongeveer 1 tot 5 cm in deursnit 4. Op korthaar beeste kan hierdie knoppe veral prominent vertoon en is gewoonlik oor die hele lyf teenwoordig. Letsels strek soms dieper as net die vel en kan tot in die pees/sening skedes op die bene strek waar dit dan ook mankheid en onderhuidse wateraansameling (edeem) veroorsaak. Verswering van die bek, lugpyp en pens kan ook voorkom. Sekondêre longontsteking kan n nagevolg wees in gevalle van waar lugweg verswering plaasvind. Letsels kom ook op die skrotum en peester voor, en kan lei tot ontsteking van die testes wat weer tydelike of selfs permanente onvrugbaarheid veroorsaak. Speenletsels lei dikwels tot mastitis en gevolglike verlies aan uier funksie 4. Skerp dalings (tot 50%) in melk produksie kan verwag word in koeie met knopvelsiekte 2,4. Is daar ander siektes wat soos knopvelsiekte lyk? Ja; die belangrikste hiervan is skynknopvelsiekte (Pseudo-lumpy skin disease). n Veearts kan in samewerking met n laboratorium jou help om te onderskei. Hoe voorkom mens hierdie siekte? Beheer is eerstens deur enting. Beheer van bytende insekte soos steekvlieë kan ook help om verspreiding te beperk. Vatbare diere moet jaarliks geënt word, verkieslik in die lente voor insek populasies drasties toeneem. Omdat die entstof n lewende (verswakte) entstof is, kan daar n tydelike afname in melkproduksie wees in melkbeeste. Diere jonger as 6 maande van geënte koeie moet nie geënt word nie, terwyl kalwers gebore van ongeënte koeie so vinnig moontlik geënt moet word. Dragtige koeie kan ook geënt word met LUMPYVAX 6. Omdat siekte uitbreke in siklusse van n paar jaar kan plaasvind, is sommige produsente geneig om op te hou ent gedurende die goeie jare. Die gevolg is dat groot dele van die nasionale kudde onbeskermd gelaat word wat tot massiewe uitbreke kan lei, dikwels met n tekort aan entstof gedurende sulke tye as gevolg van laer entstof produksie in die vorige jare 2,7. Beplan dus vooruit en moenie onverhoeds betrap word nie. Kan diere steeds knopvelsiekte kry na enting? Dit is moontlik dat daar steeds gevalle van knopvelsiekte in n geënte kudde kan voorkom, maar dit is meer dikwels as nie, die gevolg van sekondêre redes 4 : Behandeling Behandeling is slegs simptomaties, en dit is baie beter om eerder die siekte te voorkom (sien hieronder). Simptomatiese behandeling hang af van hoe erg n bees geaffekteer is en sluit rehidrasie, antiinflammatoriese middels en antibiotika in. Melksalf/agriflaviengliserien kan ook oor letsels gesmeer word indien dit versweer 5. 8
Indien diere alreeds die siekte inkubeer tydens enting (soos wat dikwels die geval is wanneer n produsent eers ent wanneer sommige diere simptome toon). Onbehoorlike entstof hantering (bv. verbreking van die koueketting vanaf die verskaffer tot by die dier, blootstelling aan sonlig, entstof wat vries in die yskas, vervaldatum wat verstrek en klaar opgemaakte entstof wat nie dadelik gebruik word nie). Verkeerde toediening van entstof (bv naald steek per ongeluk reg deur vel en nie onder die vel nie of verkeerde dosis word gebruik). Enting van kalwers gebore by beskermde koeie voor 6 maande ouderdom. In enige populasie diere is daar n baie klein persentasie individue wat nie n goeie immuniteit opbou ten spyte van enting nie 7. Verder kan baie groot virus ladings (baie hoë besmetting) sommige diere se immuunstelsel oorweldig 8 Verwysings: 1. Coetzer, J. A. W. Lumpy skin disease. In Infectious diseases of Livestock; Oxford University Press Southern Africa: South Africa; Vol. 2, pp. 1268 1276. 2. Hunter, P.; Wallace, D. Lumpy skin disease in southern Africa : a review of the disease and aspects of control. Journal of the South African Veterinary Association 2001, 72, 68 71. 3. Annandale, C. H.; Holm, D. E.; Ebersohn, K.; Venter, E. H. Seminal Transmission of Lumpy Skin Disease Virus in Heifers. Transboundary and Emerging Diseases 2013, n/a n/a. 4. Tuppurainen, E. S. M.; Oura, C. A. L. Review: lumpy skin disease: an emerging threat to Europe, the Middle East and Asia. Transbound Emerg Dis 2012, 59, 40 48. 5. Blignaut, D. Re: [ruralvet] Disease rapport - LSD. Ruralvet Yahoo Group 20110610. 6. Malan, F. S. FW: [ruralvet] Lumpy skin. Ruralvet Yahoo Group 20060421. 7. Du Preez, E. Re: [ruralvet] Disease raporting October 2012 - Drs Eben & Shaun. Ruralvet Yahoo Group 20121105. 8. Van Vuuren, M. Re: [ruralvet] Lumpy Skin Disease. Ruralvet Yahoo Group 20110312. Produkinligting: Lumpyvax, G3673 (Act 36/1947) Bevat 10 4 TCID 50 gevriesdroog, lewendige, verswakte virus (SIS type). VCN 214/1304 Jaarlikse enting word aanbeveel; indien nie is dit moontlik dat sommige diere hul immuniteit kan verloor. Wegneemboodskap Knopvelsiekte kan n ekonomiese verwoestende siekte wees, maar kan voorkom word indien entings jaarliks en korrek gedoen word. 2013 ISSUE 3 9
LIVERFLUKE & Decreased Milk production Dr Johan Cloete Similiarity between South Africa and Australia Regrettably in South Africa we do not have significant dairy production trials related to the loss of milk production in dairy cattle due to the effect of liver fluke infestation. When one takes the climatic conditions and the geographical zone in which Australia and South Africa occur into consideration there are many similarities. It could then also perhaps be extrapolated as a fair comparison that the challenges in Australia could easily be found present on many dairy farms in South Africa. Fasciola hepatica and Fasciola gigantica do occur in both regions. In interesting work conducted in Australia by the SADRI (South Australian Research and Development Institute) they have illustrated the importance of controlling liver fluke infestations in dairy cattle. Impact of Parasitism on Dairy Production in South Australia Trials (1) In recent years the Parasitology Group of SARDI Livestock Services has examined the transmission and economic implications of roundworms and liver fluke on dairy production in South Australia. In the 1994 1995 season 560 adult cattle on 7 properties were included in a drench productivity study. From 60 120 adult milkers on each property were alternately allocated to either a drenched or an undrenched control group in order of expected calving date. Treated animals were drenched once in the dry period for roundworms and for liver fluke and twice for roundworms in the first 80 days of lactation. Milk production data (including total milk, protein and fat) for each cow were obtained over a 200 day period from herd testing records. Increased production responses to treatment for fluke and roundworms in 6 of the 7 herds ranged from: [milk], 2.3-9.2% (mean 4.9%); [butter fat], 1.3-14% (mean 4.9%); and [protein], 3.1-9.6% (mean 5.8%), and were consistent at both 100 and 200 days of lactation. Another productivity study was conducted the following season using 630 cattle from 8 herds. The same drenches were used, but this time animals were only treated in the dry period for liver fluke and roundworms. Consistent, but lower, average production responses of 2% - 4% were again recorded in 7 herds. Using a modified ELISA test developed in NSW for the detection of antibodies to liver fluke a bulk milk survey of all 753 South Australian commercial dairy herds for antibodies to liver fluke was conducted, followed by field visits to every farm with unusual or unexpected results. The following positive tests were recorded by geographical region: Meningie (Murray) Lakes 39%; Murray Flats 34%; Fleurieu Peninsula 25%; South East 10%; Mid-North 8%; Adelaide Hills 6%. The bulk milk ELISA is not quantitative but can be used to identify herds which merit further attention because they may be heavily infected. It can also provide peace of mind where the geographical distribution of liver fluke is discontinuous and the infection status of herds is uncertain. For these reasons it has been immensely valuable in providing the appropriate directions in the SA studies. Do not forget to control roundworm infestations in your dairy cattle Do not forget the concomittant effect of roundworm infestations in dairy cattle. In recent local trials conducted by MSD Animal Health on the weight gain of beef cows and heifers in 2013, it was found that roundworms occurred more frequently than liver fluke in the sampling conducted. The conclusion was also that it was strategically important to remember to treat simultaneously for roundworms and liver fluke. (2) 10
The effect of roundworms in beef and dairy cross cattle in Brazil (3) Table 1. Egg counts in feces from cows during the prepartum, calving and postpartum periods, in the rainy and dry seasons, at Pesagro-Rio from 2008 to 2009. Season Prepartum Eggs per gram Calving Eggs per gram Postpartum Eggs per gram Rain 210 605 500 Dry 285 590 550 Table 2. Egg counts in feces from cows with annual milk production of less than 1500, between 1500 and 3000 and greater than 3000 kg/cow/ year, during the prepartum, calving and postpartum periods, at Pesagro-Rio from 2008 to 2009. Milk production Kg/cow/year Prepartum Eggs per gram Calving Eggs per gram Postpartum Eggs per gram <1500 190 420 380 >1500 a <3000 240 510 359 >3000 656 982 1090 MSD Animal Health roundworm and liver fluke treatment products Do not forget the concomittant effect of roundworm infestations. Combat the roundworm and liver fluke infestation in your dairy herd with one of a number of the MSD drenching remedies i.e. 1. Roundworm and liver fluke combination drench with NEM-A- FLUKE for lactating cows with zero milk withdrawal or any age of dairy cattle. 2. Roundworm and liver fluke (from earliest immature liver fluke stage) for non-lactating cows, heifers older than 4 months and pregnant heifers with FLUXACUR NF 3. Roundworms in lactating and non-lactating dairy animals with PANACUR BS or any age of dairy cattle. 4. ELISA tests can be conducted for the detection of antibodies to liver fluke in individual or herd group animals. Contact the local MSD agent for more details regarding this service structure. References: 1. Dr Ian Carmichael, Chief Veterinary Parasitologist, SARDI, Australiaend_of_the_skype_ highlighting) 2. MSD Animal Health, local trials 2012, South Africa, data on file. 3. Silva, J., Rangel, C., Baêta Bde, A. & Fonseca, A., 2012. Risk factors relating to helminth infections in cows during the peripartum.. Rev Bras Parasitol Vet, 21(2), pp. 92-96. Product information: NEM-A-FLUKE Reg. No. G3563 Act 36/1947, Namibia Reg. No. V05/18.1.8/46 Composition Contains Levamisole Hydrochloride 2,5 % m/v and Oxyclozanide 3,4 % m/v FLUXACUR NF Reg. No. G3202 Act 36/1947, Namibia Reg. No. V03/18.1.8/679 Composition Contains 0.2% m/v Abamectin and 10% m/v Triclabendazole PANACUR BS Reg. No. G1481 Act 36/1947, Namibia Reg. No. V03/18.1.1/655 Composition Contains Fenbendazole 5 % m/v. SOVEREIGN Reg. No. G3831 Act 36/1947, Namibia Reg. No. V09/18.3.9/195 Composition Contains Ivermectin 15 g and Triclabendazole 240 g/l. 234/1305 2013 ISSUE 3 11
KALF- GESONDHEID Dr Adél de Haast Ons het gepraat oor die bakteriese en virale oorsake van kalwerdiaree, maar watter wurms is belangrik in kalwerdiaree? Die melklintwurm (Monïeza spp) is n belangrike oorsaak van slegte kondisie in kalwers. Kalwers word geïnfekteer met die melklintwurm as hulle begin wei op die lande en dan neem hulle die klein geïnfekteerde grasmiet in. Hierdie miet bevat die lintwurm sist wat dan vrygestel word as dit die kalf se spysverteringskanaal bereik. Diaree is die gevolg. Watter produkte is beskikbaar vanaf MSD vir ontwurming in kalwers? 1. Panacur BS Effektief teen onvolwasse en volwasse haarwurm, bruinmaagwurm, bankrotwurm, knoppieswurm, haakwurm en longwurm. 2. Gardal 10% Effektief teen onvolwasse en volwasse haarwurm, bruinmaagwurm, bankrotwurm, knoppieswurm, haakwurm en longwurm. Ook effektief teen volwasse melklintwurm en volwasse lewerslak (Fasciola hepatica) Watter effek het wurminfestasies in kalwers? Kalwer wurminfestasies veroorsaak n verswakking van die immuunstelsel wat dan weer tot bakteriële en virussiektes kan aanleiding gee. Wat se rol speel Bees Respiratoriese Siektes in kalwers? Dit is n sindroom wat veroorsaak word deur infeksie en inflammasie van die boonste lugweë en longe. Kalwers is baie vatbaar vir Bees Respiratoriese Siektes en baie omgewingsfaktore, soos stof, onhigiëniese hokke en koue lug soos trekke maak hulle meer geneig om siek te raak. Hoe sal n kalf met Bees Respiratoriese Siektes simptomaties voorkom? Kliniese simptome sluit in slegte eetlus, lusteloos, afskeiding van neus en oë, moeilike asemhaling, hoes en koors. Die simptome kan verskil van bees tot bees. Dit maak egter nie saak hoe subtiel die simptome is nie, dit sal groei en produksie negatief beinvloed. Wat is die algemeenste agente wat Bees Respiratoriese Siektes veroorsaak? Virale infeksies 1. Herpes Virus wat Infektiewe bees rhinotracheitis veroorsaak (IBR) Draer diere is n belangrike bron van herhaalde infeksies Kan ook aborsies veroorsaak in dragtige diere 2. Bees Virus Diarree (BVD) Veroorsaak immuunonderdrukking en lei tot ander kalfsiektes Die ontstaan van permanente draers, is altyd n belangrike aspek en kan n konstante bron van infeksie wees in die kudde 3. Para influenza tipe 3 Maak die kalwers meer genieg tot sekondêre infeksies soos bv Pasteurellose, n aggressiewe vorm van longontsteking deur Mannheimia haemolytica bakterieë. Bakterieë gewoonlik sekondêr tot stres geïnduseerde virale infeksies Mannheimia Haemolytica (Pasteurella) Dit vorm deel van die normale flora van die boonste lugweë van gesonde diere. Virale infeksies en ander stressors bv. ontwatering, stowwerigheid, koue lug en vervoer van diere, veroorsaak dat die bakterieë oorgroei en dan siekte veroorsaak. Hoe kan ons help om hierdie siektes te voorkom in kalwers? Kalf se immuunsisteem is nog nie ten volle ontwikkel met geboorte nie, en dus is die enigste manier hoe n kalf siekte kan beveg deur die teenliggaampies wat die kalf ontvang van die ma d.m.v. kolostrum. Om te verseker dat die kalf die korrekte en genoeg teenliggaampies ontvang teen die belangrike siektes moet die dragtige bees met die korrekte kombinasie van entstowwe geënt word. Watter entstowwe, stel u voor, moet die bees mee ingespuit word en wanneer? Naïewe diere met onbekende inentings geskiedenis, asook nuwe kalwers wie se ma s nie ingeënt is nie, moet eers n eerste enting ontvang en dan gevolg word deur n skraagdosis 4 weke later. Daarna kan enkel jaarlikse dosisse geskied in die droë periode. Die volgende entstowwe moet ten minste 2 maande voor kalwing aan dragtige diere gegee word: 1. Rotavac Corona beskerm teen Rota- en Coronavirus sowel as E.coli 2. Bovilis S beskerm teen paratifus. 3. Respiravax Beskerm teen die hoofoorsake van Respiratoriese siektes, IBR, BVD, PI3 en Mannheimia haemolytica. 4. Multiklostridiale entsowwe soos Multiclos en Covexin. Produkinligting: Panacur BS Reg.nr G1481 (Act 36/1947) Fenbendazole 5% m/v (Benzimidazole). Gardal 10% Reg.nr. G3201 (Act 36/1947) Ricobendazole 10% m/v (Benzimidazole). Rotavac Corona Reg no. G2955 (Act 36/1947) Contains inactivated bovine rotavirus, inactivated coronavirus and inactivated E.coli K99 antigens. Bovilis S Reg nr. G3763 (Act 36/1947) Contains organisms of inactivated Salmonella Dublin and organisms of inactivated Salmonella typhimurium. Respiravax Reg nr. G3867 (Act 36/1947) contains inactivated BHV1 (IBR), PI3 and BVD type1, as well as Mannheimia haemolytica. Verwysings: 1. Bovine Health and Production BVSc IV notes, University of Pretoria. 2. Respiravax brochure, MSD Animal Health 3. Rotavac Corona brochure, MSD Animal Health 4. A practical guide to diagnosis, neonatal health, MSD Animal Health. 236B/1305 Intervet South Africa (Pty) Ltd, Reg. No. 1991/06580/07 20 Spartan Road, Spartan, 1619, RSA Private Bag X2026, Isando, 1600, RSA Tel: +2711 923 9300, Fax: +2711 392 3158, Sales Fax: 086 603 1777 www.msd-animal-health.co.za