Vet Facts Handout€¦ · VET FACTS ----- ANIMAL HEALTH COMMON DISEASES THAT AFFECT CATTLE, SHEEP,...
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Page 49 of 49 VET FACTS ------ ANIMAL HEALTH COMMON DISEASES THAT AFFECT CATTLE, SHEEP, GOATS AND POULTRY IN ZIMBABWE 1.0 GALL SICKNESS OF CATTLE A disease caused by a blood parasite causing high mortality in adults. Gall sickness or Anaplasmosis of cattle is a common disease in Zimbabwe caused by Anaplasma marginale which infects the red blood cells. OCCURANCE / PATHOGENESIS It occurs all year round but predominantly during the rainy season. This is due to the increase in the population of ticks and biting flies by which it is spread. It can also be spread on needles without sterilisation between animals. Susceptibility to infection increases with age and fatal cases often occur in animals over three years of age. Survivors need long convalescence due to anaemia and emaciation. Recovered animals develop some immunity but continued challenge is needed for it to persist. Young animals are relatively resistant to Gall Sickness and can have a symptomless infection. Infected animals remain carriers for life and breakdown to disease can occur in stress situations such as shortage of feed, transportation or pregnancy. CLINICAL SIGNS ➢ Gall sickness is acute in onset particularly in old animals. The clinical signs usually appear 2 to 5 weeks following tick bite and are as follows: ➢ Fever up to 41 degrees Celsius ➢ Loss of appetite, weakness and in-coordination. The animal sometimes chases people ➢ Laboured breathing ➢ Pale mucous membranes and jaundice ➢ Increased frequency of urination. The urine is of normal or strong yellow colour (not red as in Red water). ➢ Constipation is a characteristic sign. ➢ Dairy cows have a drop in milk production and abortion is frequently observed. POST MORTEM The most obvious sign is jaundice seen as yellow discolouration of mucous membranes and of the carcass after skinning. The blood is watery. The spleen and liver are enlarged. The liver is fragile, yellowish orange in colour and the gall bladder shows distension with thick bile; hence the common name of the disease. Haemorrhages may be present on the heart surface. Dehydration causes the contents of the rectum to be dry and the faeces is covered with mucus.
Transcript of Vet Facts Handout€¦ · VET FACTS ----- ANIMAL HEALTH COMMON DISEASES THAT AFFECT CATTLE, SHEEP,...
Page 49 of 49 VET FACTS ------ ANIMAL HEALTH COMMON DISEASES THAT AFFECT CATTLE,SHEEP, GOATS AND POULTRY IN ZIMBABWE 1.0 GALL SICKNESS OF CATTLE A disease caused by a blood parasite causing high mortality in adults. Gall sickness or Anaplasmosis of cattle is a common disease in Zimbabwe caused byAnaplasma marginale which infects the red blood cells.
OCCURANCE / PATHOGENESIS
It occurs all year round but predominantly during the rainy season. This is due to the increasein the population of ticks and biting flies by which it is spread. It can also be spread onneedles without sterilisation between animals. Susceptibility to infection increases with ageand fatal cases often occur in animals over three years of age. Survivors need longconvalescence due to anaemia and emaciation. Recovered animals develop some immunitybut continued challenge is needed for it to persist. Young animals are relatively resistant toGall Sickness and can have a symptomless infection. Infected animals remain carriers for lifeand breakdown to disease can occur in stress situations such as shortage of feed,transportation or pregnancy.
CLINICAL SIGNS
➢ Gall sickness is acute in onset particularly in old animals. The clinical signs usuallyappear 2 to 5 weeks following tick bite and are as follows:
➢ Fever up to 41 degrees Celsius
➢ Loss of appetite, weakness and in-coordination. The animal sometimes chases people
➢ Laboured breathing
➢ Pale mucous membranes and jaundice
➢ Increased frequency of urination. The urine is of normal or strong yellow colour (notred as in Red water).
➢ Constipation is a characteristic sign.
➢ Dairy cows have a drop in milk production and abortion is frequently observed.
POST MORTEMThe most obvious sign is jaundice seen as yellow discolouration of mucous membranes andof the carcass after skinning. The blood is watery. The spleen and liver are enlarged. The liveris fragile, yellowish orange in colour and the gall bladder shows distension with thick bile;hence the common name of the disease. Haemorrhages may be present on the heart surface.Dehydration causes the contents of the rectum to be dry and the faeces is covered withmucus.
DIAGNOSIS
The diagnosis is based on the history e.g. area, prevalence of the disease; presence of ticks;clinical signs and post mortem findings. Presence of Anaplasma organisms on examination ofspleen or blood smears is confirmatory of Gall sickness.
TREATMENTA number of drugs are effective. Treatment with regular Tetracycline Terramycin 100,Oxyvet or Hi-Tet 120 should be given for at least three days. Long acting Tetracycline suchas Terramycin LA, Coopermycin LA or Hi-Tet SA last in the animal for at least three daysand one treatment is usually enough. Injection of Imizol, given once only, can also be used.
CONTROLTo control Gall sickness an approached dipping schedule is effective. In addition, theVeterinary Research Laboratory can on request supply live vaccine for calves up to age of 9months. This age limit is imposed owing to the greater risk of fatal reactions developing inolder stock as direct result of inoculation. The vaccine must be ordered in advance and, aftercollection by the farmer, it remains viable for only a few hours. Therefore it must beinoculated into the calves as soon as possible after collection.
1.1. RED WATER FEVER OF CATTLE A disease caused by blood parasite causing high mortality in adults. Red Water Fever or Babesiosis is a common disease of cattle in Zimbabwe caused by Babesiabigemina which infects and destroys the red blood cells.
OCCURRENCEIt occurs all year round but predominant during the rainy season. This is due to the increaseof the blue tick (Boophilus decoloratus) by which it is spread. It can also be spread onneedles used without sterilisation between animals. The mortality is normally high in animalswhich show clinical symptoms. Survivors develop some immunity but can be carriers. RedWater Fever usually affects cattle above 12 months of age and calves rarely show symptomsof infection. Carrier animals can break down to disease in stress situations e.g. pregnancy,shortage of feed or transportation. Animals recovering from Red Water Fever need a longperiod of convalescence.
CLINICAL SIGNSRed Water Fever is sudden in onset and clinical signs usually appear 11-17 days followingtick bite infection. They are as follows:
➢ High fever up to 41 degrees Celsius
➢ Loss of appetite, dullness and staring coat
➢ Laboured breathing and pale, often jaundiced, mucous membranes
➢ Constipation which is later followed by watery diarrhoea
➢ Red to brown colour of the urine (cardinal signs) during the later stage
➢ Nervous signs may be seen in case of cerebral Red Water.
Dairy animals have an early drop in milk production and abortion may occur.
POST MORTEMThe most obvious sign is enlargement of the spleen up to double the size with a pulpyconsistency. The carcass is pale and the blood is watery. Jaundice is present and the bladdermay contain light to dark brown-red urine.
DIAGNOSISA presumption diagnosis is based on history e.g. area, prevalence of the disease, presence ofticks; symptoms-fever, dark brown-red urine, jaundice and post mortem findings. Presence ofBabesia organisms in blood, spleen or brain smears is confirmatory.
TREATMENTA number of drugs are effective. A packet of Berenil dissolved in 12,5 ml of water issufficient for treatment by treatment by injection of 300kg body mass. Larger animals needmore than one packet. Imizol should be given at a dosage rate of 1ml per 100kg body mass.For both Berenil and Imizol only one injection is needed.
CONTROL
To control Red Water Fever an approved dipping schedule is effective. In addition, theVeterinary Research Laboratory can on request supply live vaccine for calves up to the age of9 months. This age limit is imposed owing to the greater risk of fatal reactions developing inolder stock as a direct result of inoculation. The vaccine must be ordered in advance and,after collection by the farmer, it remains viable for only a few hours. Therefore it must beinoculated into the calves as soon as possible after collection. Exposure of young calves tonatural infection also induces immunity.
1.2. HEART WATER A serious disease in cattle, sheep and goats particularly occurring in thelowveld Heartwater is an acute, often fatal, disease in cattle, sheep and goats. It is caused by arickettsial organism, Cowdria ruminantium, which is transmitted by ticks.
OCCURRENCE
In Zimbabwe Heartwater occurs mainly in the southern lowveld area where the “bont- tick”,Amblyomma hebraeum, is found. Heartwater occurs all year round but predominantly duringthe rainy season due to the increase in populations of the bont tick. Young stocks arenaturally resistant, but animals over five months to six months of age are fully susceptible.Indigenous breeds are more resistant than exotic breeds in which the mortality usually ishigh. Often only a few animals in a flock are affected and those that survive develop animmunity which lasts for years. Recovered animals may act as carriers and so may certainnon-susceptible wild ruminants.
CLINICAL SIGNS
Signs of infection appear 10-14 days following tick bite and onset is acute. The clinical signsare as follows:
➢ Body temperature rises to 41-43 degrees Celsius
➢ Loss of appetite, depression and laboured breathing
➢ Nervous signs such as exaggerated blinking of eyelids, twitching of the eyes, walkingin circles and high stepping gait are all common
➢ Convulsions, lying on one side with limbs making running movements, followed bycoma and death
The disease lasts three to four days. In a typical case on the first day the animal shows loss ofappetite and altered movements. On the second day nervous signs become noticeable and theanimal lies down. On the third day the animal cannot raise, the nervous signs progress tocoma and death. Mortality is usually up to 60% or even higher. Cattle may drop dead withoutprior signs of illness. In the mild form of Heartwater clinical signs are seldom noticed underfield conditions although the animal is febrile.
POST MORTEM
The most common findings include fluid in the heart sac, chest and occasionally in theabdominal cavity. The lungs are oedematous and the trachea contains froth. The spleen isenlarged. Haemorrhage may be present on the surface of the heart and in trachea.
DIAGNOSIS
A tentative diagnosis is based on the history. Heartwater can be confirmed by microscopialexamination of brain crush preparations.
TREATMENT
Injection of Tetracycline is effective if given in the early stage of the disease. Once theanimal is lying down the drug must be given intravenously to have a reasonable chance ofsuccess. Treatment with Terramycin 100, Hi- Tet SA 120 or Oxyvet needs to be given dailyuntil the temperature returns to normal. With long acting Tetracycline such as Terramycinsuch as LA, Coopermycin LA or Hi-Tet SA treatment only needs to be repeated after 3 days.
PREVENTION AND CONTROLRegular dipping or the use of “pour on” preparations will control the tick infestation andprevent the occurrence of Heartwater in many cases. Excessive reduction in tick numbers,however, interfere with the maintenance of an adequate immunity through regular challengeand may result in heavy losses. Animals brought from the Highveld to Heartwater proneareas are susceptible. Such animals can be vaccinated by intravenous administration ofHeartwater infected blood. However this is a risky procedure which must be done underveterinary supervision. The temperature of the vaccinated animals must be monited. Whenthe temperature rises, usually after 10-12 days following inoculation, treatment withTetracycline must be given. This should reverse the febrile reaction and permit recovery withdevelopment of immunity.
1.3. THEILERIOSIS (JANUARY DISEASE / TOBACCO FARMERSDISEASE) A notifiable tick-borne disease of cattle Theileriosis is caused by the blood parasite Theileria parva bovis which is transmitted by thebrown ear tick Rhipicephalus appendiculatus. The parasite affects the white blood cellscausing swelling of the lymph nodes. The parasite is related to the organism causing EastCoast Fever which was eradicated in Zimbabwe in 1954.
OCCURRENCE
Theileriosis occurs between the months of December and March, with most cases seen inJanuary, hence the name “January disease”. The disease is mainly restricted to the Highveldwith high rainfall. In the low rainfall areas, outbreaks of Theileriosis are due to Theileriaparva lawrencei, which is transmitted from buffalo to cattle by the ticks R. appendiculatusand R. zambeziensis. Adult stocks are more susceptible to Theileriosis and higher mortalityoccurs in exotic than indigenous breeds. Recovered animals usually develop a solid immunitybut act as carriers despite drug treatment. Theileriosis rarely causes illness in sheep and goats.
CLINICAL SIGNS
➢ The disease, if untreated is rapidly fatal. Calves usually exhibit mild clinical signs
whilst adult susceptible animals show severe signs and death. Clinical signs occur 9-20 days following tick bites and include:
➢ Adult brown ear ticks are usually present
➢ Swelling of lymph nodes under the ears and opacity of eyes fever of up to 41.5degrees Celsius which is sustained until death
➢ Listlessness, loss of appetite and swelling of all superficial lymph nodes
➢ Terminally there is difficult breathing with froth exuding from the animal collapsesand dies.
POST MORTEMThe cardial post mortem findings are generalised swelling of lymph nodes, froth in thetrachea and fluid in the lungs. The abomasal wall is swollen and haemorrhagic ulcerationsmay be seen. Subcutaneous and intramuscular oedema are usually findings.
DIAGNOSISA presumptive diagnosis is based on history, clinical signs and post mortem findings. Lymphnode or spleen smears can be taken for microscopial examination and demonstration ofTheileria parasites is confirmatory. In live animals, smears from lymph nodes can beexamined microscopically. Theileriosis is a notifiable disease. If a farmer suspectsTheileriosis in his farm, he is compelled by law to report his suspicions to the VeterinaryDepartment. Once the disease is confirmed, the farm has to be placed in quarantine until 28days after the last confirmed case. During the quarantine period, a more intensive dippingschedule must be implemented. Tick attachment sites (ears, horn bases and tail brush) mustbe clipped of hair and hand dressed with tick grease.
TREATMENTIntramuscular injections of Butalex at a dose rate of 5ml per 100kg body mass effectivelycontrol Theileriosis. Usually one treatment is sufficient but in severe cases a further injectionwithin 48 to 72 hours may be required. Clexon at a dose rate of 7ml per 100kg body mass,given at a 48hours interval also effectively control the disease. Long Tetracycline given bydeep intramuscular injection at the recommended dose rate reduces the development of fever.The drugs must be administered early in the course of disease to be effective. One treatmentmay be enough as drug last in animal for at least 3 days. Recovered animals remain carriersof the disease.
CONTROLAt present, no vaccine against Theileriosis exists. The only effective is by controlling brownear ticks. This is achieved by dipping weekly or every second week in accordance with therecommendation for the acaracide used. The critical period is from December until March(the period when adults engorge and transmit the disease) and again at the end of July andduring August (the period when nymphs engorge on cattle and pick up infection).Irrespectively of the type of acaracide used, dipping is recommended for brief periods whenthe challenge is high and heavy rainfall may wash off the acaracide. This high risk periodnormally falls between mid-January to mid- February.
1.4. NECROTIC STOMATITIS NEPHROSIS SYNDROME A FATAL DISEASE OF CATTLE OCCURRING IN THE LATE RAINYSEASON Necrotic Stomatitis Nephrosis Syndrome occurs only from mid –December to April. All agegroups are susceptible but the disease is most common in beef cattle from 18 months to 2 ½years. It appears to be restricted to certain highveld areas of Zimbabwe with its rangecovering the area around Harare, east to Rusape and a belt south to the Gutu area. NSNS hasalso been recorded in the Chipinge area. Outbreaks are often sporadic and usually only one ortwo animals in a herd become affected. Sometimes the mortality rate may over 10%.Outbreaks of NSNS tend to be associated with particular paddocks, although there has beenno evidence to suggest that affected paddocks are more prone to the disease in subsequentyears. However, NSNS does seem to recur on particular farms over the years.
CLINICAL SIGNS
The majority of cases show a severe form of the disease and the clinical signs are as follows:
➢ Profuse salivation and dry crusted muzzle
➢ Poor appetite and occasional aggressiveness when handled
➢ Thick, pussy discharge from the eyes may be seen
➢ The gums, tongue and inner surface of the lips are covered by raw, bleeding ulcers oryellowish fibrinous membranes
➢ Foul rotting smell of the mouth
The condition is evidently extremely painful and the animal resents any attempts to forceopen its mouth, and is very reluctant to eat food. Affected cattle may persist for up to threeweeks before eventually succumbing to kidney failure. Occasional cases may show a milderform and recover after an illness of s few days.
POST MORTEMlesions similar to those in the mouth are found most of the length of the oesophagus. Thekidney are very pare in colour.
DIAGNOSISA presumptive diagnosis is based on history and clinical signs such as foul smelling changesof the mouth. High blood serum content of urea and creatinine indicating kidney failure arecharacteristic findings.
TREATMENTNo treatment for NSNS has yet been found to be effective. However, the small proportion ofmild cases which occur usually recover and can be sustained through good nursing and byadministration of a broad spectrum antibiotic to counter secondary bacterial infections.Streptomycin should be avoided as it may aggravate the kidney damage.
CONTROLOnce cases are diagnosed the herd should be moved to a different paddock, preferably not anadjacent one. The affected paddock should not be used for cattle until after April, when theNSNS season comes to an end.
2.0 WIREWORM DISEASE IN RUMINANTS One of the most serious round-worm infections of cattle, sheep and goats Wireworm Disease is caused by the internal parasite Hemonchus contortus which is found inthe fourth stomach (abomasums) and the small intestine of cattle, sheep and goats. Theparasites feed on blood and infected animals become anaemic and may die in poor condition.
OCCURRENCEWireworm disease in Zimbabwe occurs all over and is most common during the rainy season.All age group can become infected, but most serious effects are observed in lambs and kids.Animal get infected when they ingest infected larvae together with plants and water.
CLINICAL SIGNSAcute wireworm disease is seen primarily when young animals become heavily infected. Theanimals die showing signs of severe anaemia. In chronic cases the clinical signs are asfollows:
➢ Pale mucous membranes
➢ Swelling under the jaw (bottle jaw ) and occasionally along the ventral aspect of theabdomen
➢ Progressive weakness and unthriftiness
➢ Diarrhoea or constipation may occur.
➢ Shortly before death weakness may lead to prostration.
POST MORTEMThe carcass is markedly pale and the blood has a watery appearance. In chronic cases thecarcass is in poor condition and the chest, heart sac and abdominal cavity usually contain
fluid. The abdominal fat along the spine is jelly like. The fourth stomach contains reddishbrown fluid ingesta and numerous numbers of wireworms may be seen on the surface. Thewireworms are twisted, thin and 2-3 cm long. They are easily seen when stirring stomachcontents in a glass of water, but can be difficult to identify on direct examination.
DIAGNOSISThe clinical signs may lead to suspicion of Wireworm disease and identification of the wormsis confirmatory. Counts of parasite eggs in faeces above 200 per gram (cattle) and 2500 pergram (sheep and goats) are regarded as significant.
TREATMENTThere are various remedies available at present for treatment of wireworms. Panacur,Systamex, Valbazin, Valbantel, Ripercol, Tramisol and Ranide (also available for injection),are given orally. Ivomec, Seponver and Trodax are administered by injection. Be sure to usethe correct dose rate as different concentrations of some remedies are sold for cattle and smallruminants.
CONTROL
Provision of clean pastures, i.e. pastures that have not been grazed by ruminants for at least 8weeks. Dose animals a day before putting them onto clean pastures. Rotational grazing aidedby the strategic use of anthelmintics has proved to be an effective control measure forwireworms.During the rainy season sheep and goats should be treated every 3 weeks. If the raincontinues for 10 to 14 days reduce this to 2 weeks. During the dry months 6 weeks intervalshould be sufficient. Cattle require less frequent dosing. Treatment at the beginning of therains and at the beginning of winter is generally sufficient.It is important to avoid using one type of remedy all the time to prevent resistance of theparasite to specific drugs. In this respect Systamex, Panacur and Valbazin remedies are all thesame and the active component is benzimidazole. Ripercol, Tramisol and Tramizan have theactive component levamisole in common. Remedies should be alternated yearly.It should be kept in mind that drugs, alone are not able to keep the infection level low withoutrotational grazing.
2.1 STOMACH FLUKE IN RUMUNANTS Heavy infection with immature stomach flukes may cause serious lossesparticularly in young stock OCCURRENCEOutbreaks of infection by stomach flukes occur in the dry season with peak incidencebetween August and October. Animals become infected after ingesting of fluke larvae hostedin aquatic snails. The snails are the intermediate host and are found in flood-prone areas,low-lying marshes and along the borders of lakes and dams. All ages of cattle, sheep andgoats are susceptible but fatal infections are most commonly seen in young cattle. Themortality rate may be over 60%. Adult animals may develop some immunity to stomachflukes but become chronic carriers.
CLINICAL SIGNSThe disease follows a couple of up to 3 weeks. Death may occur any time from a few days inyoung sensitive animals to 3 weeks. The clinical signs are as follows:
➢ Persistent fetid diarrhoea
➢ Weakness, depression and poor appetite
➢ Pale mucous membranes and bottle jaw
➢ Weight loss and eventually death
POST MORTEMIn acute infection the immature flukes are seen in the first 2-3 metres of the small intestine.They might easy be overlooked but can be identified by scraping the intestinal inner surfaceand squashing the scraping between two glass slides. When held up to the light the flattenedflukes are clearly visible as small pinkish-white “seeds”. The mature flukes resemble smallcoffee beans and are found in the rumen mainly around the entrance of the oesophagus.
DIAGNOSISThe diagnosis is based on the history, prevalence of enzootic stomach fluke, clinical signsand post mortem findings. Dung from live animals can be examined for presence of stomachfluke eggs. However, it should be remembered that only mature stomach flukes produce eggsand no parasite eggs will be found in the case of acute infection by immature stomach flukes.
TREATMENTLintex-M is effective against immature stomach flukes and dosing should be done from Julyto November. Dosing with Terenol against mature stomach flukes should take place betweenNovember and May and it may reduce the magnitude of next generation infective flukelarvae on pastures. A count of stomach fluke eggs in stool samples might indicate thenecessity for treatment against mature stomach flukes in a herd.
CONTROLThe basic principle behind control is to keep snail and host apart. Piped water supplies aresafer than water-holes or dams. Snails can be controlled by drainage and fencing of water-holes and pools. Remedies that kill snails are available but expensive.
2.1 TAPEWORMS IN RUMINANTS Heavy infection in young animals may cause poor thrift Tapeworms are internal parasites of goats, sheep and cattle. Monieza expansa (sheep andgoats) and Monieza benedini (cattle) live in the small intestine, but Stilesia hepatica occurs inthe bile ducts of the liver, mainly in sheep.
OCCURRENCETapeworms occur commonly during the rainy season but the number of cases decreasestowards the dry season. The tapeworms are parasitic chiefly in young animals, especiallylambs, up to six months of age. Adult animals subjected to continuous low-grade reinfectiondevelop immunity. Stilesia hepatica, present in the liver, occurs throughout the year butinfection appears to cause little harm. The most serious loss is through condemnation oflivers at slaughter. Tapeworms are short lived, surviving for only a few months, during whichtime mature segments are continuously excreted in the dung. They resemble cooked ricegrains. The intermediate larval stage of the tapeworm develops in soil mites which remaininfective for up to 2 years. Animals become infected when the mites carrying tapewormlarvae are eaten along with forage.
CLINICAL SIGNSMost infestations do not cause clinical signs in adults or healthy carriers of low tapewormburdens. Heavy infestation in young animals may result in:
➢ Unthriftiness
➢ Starring coat and bot-bellied appearance
➢ Mild diarrhoea and sometimes anaemia
➢ Occasional convulsions and death
➢ Infected animals are more susceptible to other diseases or adverse environmentalconditions.
POST MORTEMThe lumen of the small intestine is packed with tapeworms which are 5 to 12mm broad andup to 5 metres long. Tapeworms of the liver can be drawn out of the bile ducts and appear asthin threads.
DIAGNOSISA diagnosis is based on history, clinical signs, observation of tapeworm segments expelledwith the dung and post mortem findings. Dung samples can be examined for the presence oftapeworm eggs.
TREATMENTAnimals should be treated against tapeworms at 5 to 6 weeks of age and thereafter three tofour times during their first year. Several drugs are available at present against tapewormssuch as Lintex-M, Panacur, Systamex, Valbazin, Valbantel, Rintal and Scolaban. Treatmentagainst S. hepatica is ineffective.
CONTROLRotation of pastures will avoid a build up of infective mites. If practical, young animalsshould not graze in the morning or evening or during damp, cloudy weather as the mites thenare very active and move on the grass leaves. Young and adult animals should be treated inthe rainy season. In some cases it may be necessary to deworm lambs born during the dryseason.
2.3 BILHARZIA FLUKE IN RUMINANTS A blood fluke causing loss of condition particularly in sheep Bilharzia or Schistosomiasis is a parasitic infection of the veins of the gut and liver caused bythe blood fluke Schistosoma mattheei.
OCCURRENCEBilharzia occurs near pools, backwaters, ponds and marshy pastures. The disease is seen allyear round although most cases occur during spring and summer. The parasite infects alldomestic ruminants and sheep are the most susceptible. The Bilharzia parasite can onlycomplete its life cycle using fresh water snail as its intermediate host. To become infestedruminants need direct contact with infested water. Infection occurs through skin penetrationby cercaria, a larval stage. Adult parasites are seen in the veins of the intestines of infectedanimals.
CLINICAL SIGNS
➢ The clinical course is insidious and the clinical signs include:
➢ Poor appetite
➢ Diarrhoea, occasionally blood stained
➢ Pale mucous membranes
➢ Loss of weight
POST MORTEM
The carcass is in poor condition, pale and it usually shows jelly like fluid in the subcutaneoustissue and along the dorsal part of the abdominal cavity. In fresh carcasses a closeexamination of the intestinal blood vessels may reveal thin, dark bilharzia parasites rangingfrom 10 to 20mm long. The consistency of the liver is hardened due to formation of fibroustissue. Fluid may also be present in the abdominal cavity.
DIAGNOSISA presumptive diagnosis is based on the history, clinical signs and post mortem findings.Presence of bilharzia eggs in dung samples is confirmatory of the disease. Microscopialexamination of tissue slides of gut wall and liver may show bilharzia eggs and chronicparasitic inflammation.
TREATMENTTreatment is not practised as the dung is expensive. Oral treatment with Droncit of individualvaluable animals might be considered.
CONTROLThe basic principle behind control of Bilharzia is to keep snail and host apart. Piped watersupplies are safer than water-holes or dams. Snails can be controlled by drainage and fencingof water-holes and pools. Remedies that kill snails are available but expensive.
2.4 LIVER FLUKES IN RUMINANTS An insidious disease predominantly occurring during the dry seasonThe disease is caused by flukes (Fasciola gigantica) which live in the liver bile ducts. Theflukes gradually result in destruction of the liver tissue and liver fluke infection causes majoreconomic losses due to infertility, poor growth, reduced milk yield and wool production.
OCCURRENCEInfection with liver flukes or Fascioliasis is common in ruminants and it occurs all overZimbabwe. The disease is most frequent in sheep and goats. Fascioliasis occurs all yearround, but most clinical cases are seen during the dry season. Animals become infected afteringestion fluke larvae hosted in aquatic snails. These snails are found in flood prone areas,low-lying marshes and along borders of lakes or dams. Animals of all ages are equallysusceptible and young animals may die during the acute stage. Surviving animals get chronicinfection and carry the mature flukes in the bile ducts. Chronically infected animals not onlyremain as carriers for the rest of their life but also progressively lose weight and mayeventually die.
CLINICAL SIGNSTwo stages of infection are seen. In the acute form of Fascioliasis, usually seen in sheep,animals may die without showing any symptoms and this occurs after heavy ingestion ofinfective larvae on a single occasion. The chronic form becomes apparent when larvae reachmaturity about 4 months after infection. The clinical signs are as follows:
➢ Pale mucous membranes
➢ Development of oedema of the throat (bottle-jaw)
➢ Loses of condition
➢ The animal may eventually die in poor condition.
POST MORTEMIn acute Fascioliasis, the liver is swollen with haemorrhagic tracts caused by migratinglarvae. In chronic Fascioliasis the carcass appears pale and may be in poor condition. Theliver is enlarged and on a cut surface the bile ducts are thickened and gritty due tocalcification. Leaf-shaped liver flukes measuring 20-30mm may ooze from the bile ductlumen.
DIAGNOSISThe diagnosis is based on the history, clinical signs and post-mortem findings. Faeces can betaken from live animals and examined for presence of liver fluke eggs. However, it should bekept in mind that liver fluke eggs only appear in faeces 3 to 4 months after primary infection.Unfortunately the number of eggs per gram of faeces provided no estimation of the severityof infection. In acute Fascioliasis eggs cannot be detected.
TREATMENTA number of drugs are available at present against mature liver flukes such as Trodax,Ranide, Seponver, Valbantel, Valbazen, I.C.I Liver fluke Remedy and Tramizan. Fasinex iseffective against all ages of liver flukes. Supportive vitamin and iron therapy should be given.
CONTROLThe basic principle behind control is to keep snail and host apart. Piped water supplies aresafer than water-holes or dams. Snails can be controlled by drainage and fencing of water-holes and pools. Remedies that kill snails are available but are expensive. Dosing of animalswith drug twice a year will keep the liver fluke infection rates low. First dosing should bedone at the end of the rainy season (March/ April) which will eliminate adult parasites. Avoidcontamination from dry season water-holes. Second dosing should be planned at the end ofthe dry season (September/October) when immature flukes migrate through the liver. Notethat only drugs which are active against immature flukes should be used for secondarytreatment.
2.5 COENURIASIS /GID A parasitic disease of the central nervous system particularly in sheep andgoats Coenuriasis or Gid is the presence of tapeworm cysts in the central nervous system. The cystsare the larval stage, Coenurus cerebralis, of the tapeworm, Taenia multiceps, of dogs.
OCCURRENCEThe adult tapeworm inhabits the small intestines of the dogs. Sheep, goats and cattle, and to alesser extent horses, become infected when they ingest feed or water contaminated withtapeworm eggs. The larvae are released in the gut and they migrate through the blood to thespinal cord and the brain where they develop to cysts within 2 to 7 months. The cysts causecompression and destruction of brain tissue resulting in nervous signs often referred to as Gidor Staggers.
CLINICAL SIGNSwhen animals start to show illness, the infection is already chronic and the clinical signs areas follows:
➢ The head is held to one side and the animal walk in circles
➢ Unsteady gait, impaired vision, falling, progressively the animal ceases to feed and
loss of condition develops.
POST MORTEMThe cysts are commonly located in the front part of the brain and occasionally along thespinal cord. The diameter of the cysts may be up to several centimetres. The bone over thecyst may be thin and even be perforated or bulging. Cysts observed in the abdominal cavityattached to the liver should not be mistaken for Coenuriasis; they are the intermediate stageof another dog tapeworm, Taenia Hydatigena.
DIAGNOSISNervous signs give suspicion of Coenuriasis but a confirmation is by post mortemexamination of the brain and spinal cord.
TREATMENTOnce cysts have developed in the brain there is no real treatment. In valuable animalsdrainage of cysts might be considered with the assistance of a veterinarian.
CONTROLThe only way to prevent Coenuriasis is by interrupting the lifecycle of the tapeworm usingthe following measures:Burning or deep burying of carcasses to prevent dogs becoming infected by swallowing theinfective cystsTreatment of dogs with drugs against tapewormsPreventing dogs especially stray ones, from frequenting the farm and thus contaminatingpastures and feeds with tapeworm eggs.
3.0 ANTRAX A notifiable disease which, if not controlled, may kill animal and man Anthrax is an acute, contagious disease characterised by septicaemia and sudden death. Thedisease is caused by the bacterium Bacillus anthracis. A unique feature of this organism is itsability to form dormant stages (spores) which may survive in the soil for many years.Animals become infected by ingestion of contaminated feed or water. In the body the sporesmultiply and produce a lethal toxin which kills the animal.
OCCURRENCEAnthrax occurs all year round although most cases are seen during the rainy season. Almostany animal species including man may become infected with Anthrax. Of the farm animals,cattle, sheep and goats are very susceptible to Anthrax whereas horses, pigs and dogs aremore resistant. If not controlled, Anthrax may reach epidemic proportions and kill livestockin large numbers. In addition, farmers and veterinarians attending to infected animals, orpeople eating meat from animals which have died of Anthrax may also become infected. Thiscan be illustrated by the fact that more than 4000 cases of human Anthrax were reported in
1980 when there was a breakdown in vaccination of animals. Anthrax is a notifiable diseaseand the Department of Veterinary Services must be notified of suspected cases. The carcassshould never be opened as air stimulates spore production causing the ground to be infectedfor many years. If possible a blood smear from the carcass should be taken and examined inorder to confirm the disease.
CLINICAL SIGNSThe clinical course of Anthrax is short and in ruminants often passes unnoticed. The historyusually is of a previously healthy animal being found dead. Such cases are often reported ascaused by snake bite or lightning strike. If observed the clinical signs are as follows:
➢ High fever, muscle tremor and laboured breathing
➢ Collapse followed by convulsions and death
➢ In horse, pigs and dogs (and man) the disease most often manifests itself as infectedwounds on the skin or in the mouth and throat, accompanied by swelling, fever anddiarrhoea.
POST MORTEMDead animals are found with tarry blood oozing from the nose, mouth and anus. Carcassesbloat and decompose very rapidly, and there is absence of death stiffness. Should the carcassbe opened inadvertently the most notable finding is an enormously enlarged spleen filled witha tarry pulp.
DIAGNOSISThe possibility of Anthrax should be suspected in all cases of sudden death. Without openingthe carcass a blood sample taken with a syringe or a blood smear on a glass slide should besent to the laboratory for the demonstration of Anthrax bacteria. If the carcass is opened apiece of the spleen securely packed in a strong container may be submitted for examinationalso.
TREATMENTAs the animals almost invariably die once symptoms are apparent, treatment usually comestoo late. However, Anthrax bacteria are very susceptible to penicillin, sulphonamides andother broad spectrum antibiotics. When the presence of Anthrax has been confirmed in a herdit is thus possible to give antibiotics to animals showing a rise in temperature during a one ortwo weeks period following the last case. It must be remembered, though, that vaccinationcarried out during this period is made ineffective by treatment with antibiotics, and must berepeated at a later stage.
CONTROLAnnual vaccination campaigns are carried out by staff from the Department of VeterinaryServices in prescribed Anthrax areas. It is compulsory for farmers to produce their cattle forthese campaigns as the success of the vaccination depends heavily on all animals beingvaccinated and thus protected. The vaccine is highly effective, and during the last decade thecampaigns have reduced Anthrax in Zimbabwe from epidemic proportions to a very raredisease. Should a case of Anthrax occur on your farm you may help to stop the spread ofinfection by burying or burning dead animals and disinfecting the place where the animalsdied . The most effective disinfectants are quicklime, formalin or caustic soda.
3.1 BOTULISM A fatal disease primarily in ruminants on phosphorus deficient diets Botulism is an acute often fatal poisoning of livestock which occurs after ingestion of the
toxin of Clostridium botulinum. The botulinum toxin interferes with nerve transmissionresulting in paralysis. Cattle, sheep and goats and horses are all susceptible to Botulism, butbirds, in particular waterfowls, have the highest sensitivity. Botulism may occur in pigs, butcats and dogs are highly resistant.
OCCURRENCEOutbreaks of Botulism are usually seen in winter, but individual cases may occur at any time.Cattle grazing on phosphorus deficient soils develop an appetite for bones and other unusualobjects such as dung, wood, carcasses, etc. The carcasses of an animal or bird that died ofBotulism may contain botulinum toxin. Thus phosphorus deficiency predisposes to Botulism.It must be remembered that most soils in Zimbabwe are deficient in phosphorus. The toxinmay also occur in decaying plant material or silage of high alkalinity. In sheep Botulism isusually associated with a dietary deficiency of protein or net energy. Horses most often getBotulism by eating rodent infested hay. Occasional outbreaks occur due to drinking watercontaminated by dead animals.
CLINICAL SIGNSIn cattle and horse signs usually appear 3 to 17 days after ingestion of toxic material and thesymptoms are as follows:
➢ Muscular weakness starting in the hind legs and moving forward
➢ Paralysis of the jaw and throat muscles
➢ The tongue hangs out of the mouth and saliva droolsThe animal become recumbent showing paralysis but usually retain consciousness until deathoccur 1 to 4 days laterSheep may exhibit similar symptoms but paralysis occurs at the final stage of the disease.Peracute cases die without prior signs of illness although a few fail to take water or food for aday beforehand.
POST MORTEMThere are no specific findings detectable at necropsy. Presence of bones or parts of carcassesin the stomach may be suggestive of Botulism. Cardiac haemorrhages and congestion of thegut wall be seen.
DIAGNOSISDiagnosis is based on the history and observation of dead waterfowls. A toxicity test in micefor botulinum toxin can be performed on liver or body fluids. However, this is not particularreliable test and a negative result does not rule out Botulism.
TREATMENTLittle can be done for animals that suffer from Botulism. Dehydration may be the main causeof death. Water may be given by stomach tube and this is repeated for several weeks. Supportin a sling may help to prevent pneumonia in horses.
CONTROLAnnual vaccination against Botulism in practised in endemic areas. Animals that have notpreviously been immunised should be given two injections of the vaccine at an interval offour to six weeks. Thereafter they are given only one injection annually. In range animalscorrection of dietary deficiencies by supplementation with phosphorus and protein should beimplemented. Disposing of carcasses and keeping stock out of animals “cemeteries” areimportant steps in controlling and preventing Botulism. Vaccination against Botulism willreduce the losses during an outbreak. Vaccination of horses is seldom practised as theincidence of Botulism in this species is low and usually due to accidental contamination offeed or water.
3.2 BLACKLEG (QUARTER EVIL) IN CATTLE An acute fatal disease often occurring in unvaccinated herds Blackleg or Quarter Evil is an acute infectious disease of cattle caused by the bacteriaClostridium chauvoei; but mixed infection with Clostridium septicum may occur. Blacklegdoes not spread from animal to animal, but infection is soil-born. It is presumed that entry isthrough the alimentary tract following ingestion of contaminated feed and soil. The bacterialspores lodge in the muscles where they lie dormant until stimulated to multiply possibly bycertain factors. The toxin formed by the clostridium bacteria produces a severe damage to themuscles locally and a generalised poisoning which is usually fatal.
OCCURRENCEBlackleg is seen in all parts of Zimbabwe and it can occur any time of the year although mostlosses are seen during the spring and summer. In some areas Blackleg may appear on severalproperties, while only isolated farms may be affected in other areas. Sometimes only parts ofa property are affected. Blackleg is largely confined to young stock between the ages of 6months to 2 years. In the field the disease appears to occur most frequently in rapid growingcattle on a high plane of nutrition. Usually a number of animals affected within a few days.The mortality rate in Blackleg approaches 100%.
CLINICAL SIGNSthe onset of Blackleg is rapid and the clinical symptoms are as follows:
➢ Lameness, depression and body temperature may rise up to 41 degrees Celsius
➢ Limb muscles are swollen and painful. Gas formation under the skin can be felt overthe affected muscle mass
➢ The animal goes down and usually dies within 12 to 36 hours after the onset.
➢ Affected animals may drop dead without signs of illnesshave been observed. After death blood-stained dischargeexudes from the nose and blood runs from the anus.Poisoning or snake bites are often suspected.
POST MORTEMBloating and putrefaction occur quickly in Blackleg. Dark blood-stained fluid with patches ofdark red haemorrhages is found under the skin. Incision of affected muscles reveals a darkred discoloured spongy surface with an excess of thin blood-stained fluid containing bubblesof gas. All the body cavities contain excess fluid. The spleen is swollen and firm. Patches ofhaemorrhages are present on the surfaces of internal organs including the heart.
DIAGNOSISIn typical cases of Blackleg in cattle a diagnosis can be made on the clinical signs and postmortem findings. Pieces of muscle and spleen combined with organ smears can be sent forlaboratory testing to confirm the diagnosis.
TREATMENTHigh doses of antibiotics in the initial stage of Blackleg may be tried. However, this is rarelysuccessful.
CONTROLThe only effective means of controlling blackleg is by annual vaccination of all cattlebetween 6 months to 2 years, usually during spring and summer. The vaccines usually usedagainst Blackleg in Zimbabwe are Blackleg vaccine (Cl. chauvoei), Blackleg/Braxy vaccine(Cl. chauvoei and Cl septicum) or Black quarter vaccine (Cl. chauvoei). Immunity takesabout 14 days to develop following vaccination and deaths may occur for some days ifvaccination is carried out during an outbreak. Vaccination does not always provide completeprotection against Blackleg and occasional deaths may occur in vaccinated herds. Theprotection provided by vaccination may last less than one year, so annual vaccination will notgive complete immunity. It is important that carcasses of animals dying of Blackleg are notopened but are destroyed by burning or deep burial to avoid soil contamination.
3.3 PULPY KIDNEY DISEASEA disease caused by a bacterial toxin causing high mortality particularly inlambsPulpy Kidney Disease is an acute enterotoxaemia caused by a toxin formed in the gut by thebacteria Clostridium perfringens type D. the growth and the ability of the bacteria to producetoxin in the gut stimulated in animals on a high nutritional plane particularly grain feeding.While enterotoxaemia is most common in lambs it also occurs in adult sheep, goats andcalves.
OCCURRENCEPulpy kidney Disease occurs all year round and is usually affects well nourished sucklinglambs between 4 and 10 weeks of age and weaned lambs in feedlots on a high-carbohydratediet. Animals grazing on lush, rapidly growing pastures are also susceptible. The mortality inaffected animals is high and up to 10% may contract the disease in a flock.
CLINICAL SIGNSPulpy kidney disease in lambs has a course of up to 12 hours but death often occurs in lessthan a few hours but death often occurs in less than a few hours. Often lambs are found deadwithout prior signs of illness. If observed the clinical signs are as follows:
➢ Depression and yawning
➢ The temperature is normal
➢ Convulsions with frothing at the mouth
➢ Cases surviving for more than a few hours may develop a green, pasty diarrhoea
➢ Adult sheep show weakness, in co-ordination and convulsions, and die within 24hours.
POST MORTEMPresence of Pulpy Kidney is a cardinal sign and may be found shortly after death. In additionan excess of clear, straw-coloured fluid may be seen in the heart sac of young animals.Haemorrhages on the surface of the kidneys, heart and intestinal wall may be observed. Therumen and abomasums are often overloaded in grain fed lambs. The carcass decomposesrapidly and the skin develops a purple discoloration. The wool is easily plucked. The animalis usually in a good condition.
DIAGNOSIS
A presumptive diagnosis is based on the history, clinical signs and post mortem findings.Growth of Clostridium perfringens from the small intestine may not necessarily be ofsignificance as the organism is a normal habitant of the alimentary tract. Presences ofcharacteristic haemorrhages of the kidney seen by tissue microscopy are indicative of PulpyKidney Disease.
CONTROLLambs should be vaccinated before they enter the feeding program with a oil-emulsionvaccine followed by a second injection of alum-precipitated vaccine 4 to 6 weeks later. Iflambs younger than 4 months of age are immunised a booster injection of the alum-precipitated vaccine should be given between 6 and 8 months of age. Hereafter an annualbooster injection of the alum-precipitate vaccine is recommended. The Pulpy Kidney vaccineis obtainable from the Department of Veterinary Services. Other vaccines used are Heptavac -P and Ovivac –P. lambs will get passively immunised via colostrums if ewes are vaccinatedbefore lambing. Vaccination does not always protect against Pulpy Kidney Disease and itmight sometimes be necessary to reduce amount of concentrate in the diet if best results areto be obtained.
3.5 PASTEURELLOSIS A bacterial infection associated with stress in cattle, sheep and goats Pasteurellosis, also known as “Shipping Fever” in cattle, is a bacterial infection affectingsheep, goats and cattle. The disease is caused by Pasteurella haemolytica or Pasteurellamultocida. The infection is characterized by acute bronchopneumonia, pleurisy or, lesscommonly, generalised infection.
OCCURRENCEAlthough Pasteurellosis occurs all year round, most cases are seen during winter and spring.The disease commonly affects young growing animals in feedlots; however all age groups aresusceptible. The pneumonic form of Pasteurellosis is usually caused by Pasteurellahaemolytica. Transmission of pneumonic Pasteurellosis occurs by inhalation of infecteddroplets coughed up by infected animals which may be clinical cases or recovered carriers inwhich the infection persists in the upper respiratory tract. The bacteria becomes pathogenicwhen associated with stress factors like draughty or poorly ventilated barns, exposure toinclement weather or transportation over long distances. Respiratory infections withmycoplasma or viruses are also predisposing factors. Sometimes, only a few animals in aflock or herd may become affected, whereas in other cases, outbreaks involving 30% or moreof the animals may occur. Death of affected animals varies from 5% to 10% in a herd.
CLINICAL SIGNSPasteurellosis develops within 10 to 14 days after the animals have been stressed. The clinicalcourse of the disease is usually short 2 to 4 days and the clinical signs are as follows:
➢ Poor appetite, depression and high body temperature up to 41 degrees Celsius
➢ Shallow, rapid breathing
➢ Pus like nasal discharge and crusty nose
➢ A mild diarrhoea may be present in some casesSudden deaths may occur without any premonitory signs of illness. If treated early, affectedanimals recover in a few days. Complications in affected animals which do not fully recoverinclude chronic infection of the lungs, thoracic cavity and heart sac. Outbreaks ofPasteurellosis in feedlots may last for 2 to 3 weeks.
POST MORTEMOne third or more of the frontal lobes of the lung may be consolidated. Pus may be present inthe bronchi, and affected lung tissue is haemorrhagic, edematous and firm. The surface of thelung is covered with yellow-green gelatinous exudates which may adhere to the chest wall.Varying amounts of straw-coloured fluid are found in the chest cavity and sometimes in theheart sac.
DIAGNOSISA presumptive diagnosis is based on the history, clinical signs and post mortem findings.Organ samples can be submitted for bacteriological and microscopial examination.
TREATMENTAny of the broad spectrum antibiotics, tetracycline or sulphonamide can be used fortreatment. Affected animals will recover within a few days if treated early. The treatmentregime will depend on the antibiotic used according to the manufacturer’s recommendation.If using long active tetracycline, then one treatment is usually adequate. If using regulartetracycline or a combination of penicillin and streptomycin or sulphonamides they have tobe given for at least 3 days.
CONTROLEnvironmental and managerial factors which may precipitate outbreaks of Pasteurellosisshould be controlled where possible. Pasteurella vaccine for sheep and goats can be obtainedfrom the Veterinary Department. Lambs and kids can have their first inoculation at 2 weeksof age followed by a second 4 weeks later. A booster injection must be given 6 months later.Thereafter a single vaccination annually is adequate. Ewes and goats vaccinated late inpregnancy will provide their offspring with antibodies against Pasteurellosis via colostrums.Vaccination does not necessarily produce complete immunity in all animals and breakdownmay occur under stress. Commercial vaccine such as Heptavac-P, Ovivac-P, Ovipast (sheepand goats) and Pastacidin (cattle and sheep) are also available.
3.6 SALMONELLOSIS (PARATYPOID) A serious disease affecting both domestic animals and humans Salmonellosis is an acute contagious disease of domestic animals and man, caused bySalmonella bacteria. The disease is characterised by diarrhoea and septicaemia. Recoveredanimals often become carriers of Salmonella bacteria, thus providing a source of infection forother animals. It should be remembered that humans can become infected via contaminatedmeat products, milk and drinking water. There is also a chance that contact between animalsand man in agriculture and in companion animals relationships, especially with horses andreptiles, can result in spread to man.
OCCURRENCE
In the newborn, infection with salmonellae is almost invariably fatal if not treated. In olderanimals, various predisposing factors such as transportation, intercurrent disease, severedeprivation of food, hospitalisation, dosing with antibiotics or anthelmintics, or parturition,are important for the development of Salmonellosis. Infection is transmitted mainly by theingestion of feed or water contaminated with faeces from sick or apparently healthy carrieranimals. Infected droppings from rats and birds are another source of contamination.Feedstuffs of animal origin, including blood and bone meal, have been incriminated in thespread of Salmonellosis.
CLINICAL SIGNSThree different syndromes occur:
➢ Septicaemia. This is the main form in the newborn animals. Affected animals showprofound depression, fever (40.5-42 C) and death within 24-48 hours
➢ Acute diarrhoea. This is the common form in adults, and in the newborn that survivedthe septicaemia state. The animal presents with fever (40-41 C), severe watery,
sometimes bloody diarrhoea, abdominal pain, and death in 2-5 days. Pregnant animalsmay abort, and the newborn may develop lameness or pneumonia
➢ Chronic diarrhoea. This is common form in pigs, and occasionally in cattle and adulthorses. The animal presents with an intermittent moderate fever and loss of weight.
POST MORTEMIn the septicaemic form extensive blood spots are seen in all organs. In the form of acutediarrhoea the intestinal content is watery, foul smelling, and contains mucus and blood. Theliver and intestinal lymph nodes are enlarged. The form with chronic diarrhoea shows areasof haemorrhage and ulceration of the intestinal wall. The spleen and intestinal lymph nodesare enlarged. Pneumonia may be present.
DIAGNOSISA presumptive diagnosis is based on history, clinical signs and post mortem findings.Isolation of Salmonella bacteria is confirmatory. For bacterial cultivation, faeces can besubmitted from the live animal and from dead animals: spleen, liver, lung, intestinal lymphnode and small intestine.
TREATMENTAmpicillin, neomycin, and nitrofurazone are recommended antibiotics, although the choice ofdrug preferably should depend on a test of drug sensitivity in each case or outbreak.Treatment must be accompanied by the administration of fluids. It should be noted thatantibiotics may prolong the shedding of bacteria, increasing the chances of a prolongedcarrier state, and presenting a potential source of infection to other animals.
CONTROLIn open herds or flocks, new animals should preferably be introduced directly from aSalmonella-free farm. Carrier animals should be identified and either culled or isolated andtreated rigorously. Rat infestation of feed stores and pasture should be controlled. The watersupply should be provided in troughs which should not be capable of faecal contamination.Static drinking water or pasture may remain infected for as long as 7 months. Rigorousdisinfection of animal houses is important. An all-in, all-out policy should be adopted.Disposal of infected material should be carried out with great care. Carcasses should beburnt. A live paratyphoid vaccine is available from the department of Veterinary Services forthe prophylactic immunisation of calves from 2 to 3 weeks of age. A commercial vaccine,Ecosan is also available at present. The vaccine can be administered to the dry cow, whichwould impart colostral immunity to the calf until 6 weeks old.
3.7 CONTAGIOUS ABORTION OF CATTLE A disease seriously affecting the reproductive performance of cattlePart One: Occurrence, Clinical Signs, Diagnosis and TreatmentContagious Abortion, or CA, is an infectious disease of cattle which specifically affects thereproductive organs. CA is caused by the bacterium Brucella abortus, and is characterised byinflammatory changes in the foetal membranes which lead to abortion of the foetus. Animalsbecome infected by ingestion of pasture, drinking water, fodder and bedding contaminatedfrom discharge from animals which have aborted. Bulls are not considered important in thespread of CA, but they can be affected.
OCCURRENCECA occurs all year round all over the country. It is, however, most prevalent in areas ofintensive cattle raising, particularly among dairy stock. Due to vaccination and other controlmeasures the prevalence in Zimbabwe is low, but if CA is not controlled “abortion storms”may occur with abortion losses as high as 30 to 40 %. Farmers and Veterinarians attending to
infected animals, or people drinking untreated milk, may also become infected. A similardisease caused by the bacterium Brucella melitensis occurs in sheep and goats.
CLINICAL SIGNSNon-pregnant cattle may show no signs of infection at all. In pregnant cattle the clinical signsare as follows:
➢ Abortions in late pregnancy, or even birth at full time of weak, stillborn or deadcalves
➢ Retained afterbirth
➢ Increased incidence of metritis and prolonged calving- to –conception intervals.In some animals the infection may occur only as a local swelling of the knee, hock or, in thebull, the testicles.
In man, infection is manifested as a general illness called “Undulant Fever” which is oftenconfused with influenza or malaria. The main symptoms are sweating, chills, headache andfever periods. The disease in man may last for several months or even years.
DIAGNOSISCA may be diagnosed either by laboratory isolation of Brucella bacteria from aborted calves,milk or vaginal discharge, or by demonstration of Brucella antibodies in blood samples. IfCA is suspected the following samples should be submitted to the laboratory:
➢ From the foetus a piece of foetal liver, lung, spleen, kidney and stomach contents. Abutton (cotyledon) of the afterbirth
➢ From the dam a blood sample drawn from the jugular vein and a milk sampleA second blood sample taken from the dam three weeks after the abortion will help inconfirming the diagnosis of CA, or to differentiate from other infectious causes of abortion.
TREATMENTAt present there is no effective treatment for CA.
3.8 CONTAGIOUS ABORTION OF CATTLEA disease seriously affecting the reproductive performance of cattlePart 2: Control Contagious Abortion CA or Bovine Brucellosis is an infectious disease of cattle whichspecifically affects the reproductive organs.
CONTROLThe control of CA is based on vaccination coupled with blood testing, identification andculling of infected animals. In addition, all dairy producers have their milk tested once amonth, and their CA status is incorporated into the Quality Premium Scheme.Vaccination of all female animals between 4 to 10 months old is compulsory in commercialfarming areas as well as for dairy producers in communal and resettlement areas. Animalsshould only be vaccinated once as the vaccine offers a life-long protection. The vaccine isobtainable from local veterinary offices and from the veterinary research laboratory, Harare.Blood testing of animals is carried out on request, or on a routine basis s part theAccreditation Scheme in the dairy herds. Positive animals are called REACTORS, andaccording to Animal Health Regulations they must be branded and are not allowed to leavethe premises except for slaughter. As infected animals remain infected for life they should beculled as soon as possible. Animals which show only positive reaction are calledINDEFINITE REACTORS. As these animals may have reacted due to previous vaccination a
second sample is required some weeks later for retesting, and a decision on the status of theanimals then made.A declared policy of eradication of CA from the dairy herds was formulated in 1987 withintroduction of the Brucellosis-free Accreditation Scheme”. The scheme is implementedthrough the Veterinary offices which arrange for blood samples to be tested and issueAccreditation Certificates. The components of the scheme are as follows:
➢ Initially, all female animals over 18 months old in the herd must be bled at intervalsof not less than 3 months. Positive animals are identified and must be culled. When 3consecutive negative tests have been achieved an Accreditation certificate is issued,and herds are then only required to be bled on an annual basis
➢ The herd must remain closed. Addition of stock must only include animals born onthe farm, or bought in from other accredited herds
➢ Vaccination of young calves is compulsory as CA may be introduced with stray cattle,wild animals etc.
4.4 EPHEMERAL FEVER (THREE- DAY SICKNESS)A viral disease causing drop in milk production in dairy cattle Ephemeral Fever, also known as Three-day sickness, is a disease of cattle caused by a virus.It is transmitted by biting insects. The condition is characterised by fever, stiffness andlameness. The word “Ephemeral”, which means “transient”, describes the most importantaspects of the disease: sudden onset, short course and abrupt recovery.
OCCURRENCEOutbreaks occur during the rainy season when mosquitoes and other biting insects areprevalent. Although all age groups are susceptible to Ephemeral Fever, it is most common inadults. Up to one third or more of animals in a herd may become affected; however, themortality is low. Recovered animals develop a solid immunity for up to 2 years.
CLINICAL SIGNSIn most cases, the animal is sick for 3 to 5 days. Recovery is usually spontaneous. Theclinical signs are as follows:
➢ Sudden onset of high fever, which lasts a few days
➢ Sudden drop in milk production
➢ Muscle shivering, weakness and laboured breathing
➢ Watery discharge runs from the eyes and nose
➢ Stiffness, lameness and recumbency, which may persist for 3 or more daysFat cows and bulls are worst affected. They can lose condition rapidly and are slow torecover body weight. Ephemeral fever is usually milder in calves under 12 months of age.Occasionally, animals die of secondary infection or prolonged recumbency.
POST MORTEMFew characteristic lesions are evident at necropsy. Yellow inflammatory material is seen inthe joint cavities and excess joint fluid may be present. The trachea contains froth and thelungs may be oedematous. The lymph nodes are enlarged.
DIAGNOSISThe seasonal occurrence of a transient illness with typical signs of stiffness would suggestEphemeral fever. Blood samples can be tested for presence of antibodies against EphemeralFever. A rise in antibody levels in 2 blood samples collected 14 days apart is supportive.
TREATMENTThere is no specific treatment. Drugs like Aspirin or Tomanol that reduce joint and musclepain and lower the body temperature are useful. Recumbent animals should be provided withadequate shelter, water and food. In prolonged recumbency, treatment with antibiotics may benecessary to avoid secondary bacterial infection.
4.5 BLUETONGUE OF SHEEP An acute infectious disease causing death and abortions in pregnant ewes Bluetongue is an acute viral disease of sheep transmitted by midges. Occasionally cattle andgoats can become mildly affected.
OCCURRENCEBluetongue is prevalent throughout Zimbabwe and it occurs only during the rainy seasonwhen the insect’s vectors are most numerous. Bluetongue is most common in low-lying areas,next to rivers, dams and pans. Because of midges’ nocturnal feeding habits, animals becomeinfected mainly at night. Sheep of all ages can become infected, young sheep about a year oldbeing the most susceptible. Indigenous sheep are more resistant than exotic breeds. The deathrate is high among non-immune animals.
CLINICAL SIGNSThe incubation period is less than a week and the clinical signs are as follows:
➢ Body temperature up to 41 degrees Celsius
➢ Discharge from eyes and nose which may become purulent
➢ Lips, gums and tongue show intensive reddening and ulcers appear
➢ Tongue, cheeks and ears are swollen and the smell from the mouth is offensive
➢ Reddening of unpigmented skin above the hooves and animals are disinclined tostand
➢ Recumbency and deaths may occur after a weekRecovered animals may be in poor condition and convalescence often takes several months,particularly in lambs. The hooves may separate or crack. Pregnant ewes may abort andinfection during early pregnancy can cause brain damage in the offspring.
In cattle and goats, the infection is mild and clinical signs are usually not noticed.
POST MORTEMUlcers are seen on the tongue, gums, lips and oesophagus. Haemorrhage in the wall of the
large vessel which leads from the right side of the heart to the lungs is a characteristicfinding. The skin above the hooves is swollen and inflamed.
DIAGNOSISA presumptive diagnosis is based on clinical signs and post mortem findings. Blood can betested for antibodies against Bluetongue virus. A rise in antibody level in blood samplescollected 2 to 3 weeks apart, is indicative of infection
TREATMENTAffected sheep should be housed and protected from adverse weather conditions and strongsunlight. Antibiotic treatment to control secondary bacterial infection may be desirable.
CONTROLVaccination can control Bluetongue infection in sheep. Immunisation should be done fromAugust to October, before the breeding season. Pregnant ewes must not be vaccinated duringthe first half of pregnancy. Re-vaccination annually is recommended. Lambs born to immuneewes receive a solid passive immunity lasting 3 to 6 months. In addition, Bluetongue can beprevented by ensuring the protection of sheep during the time of the year when the risk oftransmission by biting insects is greatest. Animals should be kept away from low lying areas,next to rivers, dams and pans. Night housing of sheep is also recommended.
4.6 BOVINE VIRUS DIARRHOEA/ MUCOSAL DISEASE A disease causing infertility and abortions in cows and unthriftiness anddeath in young stock Bovine Virus Diarrhoea/ Mucosal Disease is a viral infection in cattle. In adults the disease isknown as Bovine Virus Diarrhoea and it has mild clinical course. Infected pregnant cowsmay pass on the infection to their foetuses. Infected offspring may later on develop thedisease called Mucosal Disease which has a severe clinical course.
OCCURRENCEThe infection appears to be common in cattle. However, only now and then clinical outbreaksoccur dependent on the state of immunity within the herd. Bovine Virus Diarrhoea istransmitted between adult cattle through infected saliva, discharges, urine and faeces.Outbreaks tend to occur only on particular farms or on premises where cattle are frequentlybrought in.
CLINICAL SIGNS
A. Adult cattle. Usually adult cattle only become mildly affected. If noticed the clinicalsigns are as follows:
➢ Transient fever
➢ Mild depression and drop in milk production
➢ Discharge from eyes and nose
➢ Erosion in the mouth are seen occasionally diarrhoeaHowever, infection of cows early in pregnancy may result in abortion or infertility withincreased return to service. Calves may be born dead or with malformations. Some calvescarry the virus infection and later on develop mucosal disease.
B. Young cattle. Mucosal disease often precipitates in young cattle between 6 monthsand 2 years of age and the course of the disease is usually fatal. Chronic cases mayoccur and present with:
➢ Intermittent diarrhoea and unthriftiness
➢ Rough dry coat and hoof deformities
➢ Persistent epithelial erosions in the mouth and of the skin
➢ Secondary bacterial infection is often seen
POST MORTEMIn mucosal disease the most characteristic finding is the presence of erosions in the mouth,oesophagus, stomach and intestines. The intestinal contents are dark, watery and foul-smelling.
DIAGNOSISIn cows the clinical signs and a history of animals recently brought in are suggestive ofBovine Virus Diarrhoea. The diagnosis can be supported by laboratory examination of pairedblood samples collected 3 to 4 weeks apart. A rise in antibody level is indicative of infection.
In young cattle unthriftiness and the presence of typical post mortem lesions in the mouth. Onthe hoofs and skin may suggest Mucosal disease. Calves born carrying the infection and thosethat later develop mucosal disease, usually do not have antibodies to Bovine Virus diarrhoeavirus. Therefore confirmation of mucosal disease in young animals requires the detection ofthe virus in tissue or blood.
TREATMENTThere is no specific treatment. However, supportive treatment with alimentary tractastringents and the provision of oral electrolyte solutions may be attempted.
CONTROLVaccines are available but are not in common use in Zimbabwe.
4.7 INFECTIOUS BOVINE RHINOTRACHEITIS A contagious disease of cattle causing abortions and drop in milkproduction Infectious Bovine Rhinotracheitis is a viral infection of the upper respiratory tract of cattle. InZimbabwe, a high percentage of cattle have antibodies against Infectious BovineRhinotracheitis virus. However, the significance of the disease is relatively unknown.
OCCURRENCEInfectious Bovine Rhinotracheitis occurs all year round and is mainly seen in animals over 6months of age. The disease occurs most commonly in large groups of cattle and feedlotsappear to experience a higher number of infected animals than do dairy or range cattle. IBRvirus is transmitted by direct contact among animals and is highly contagious. The number of
affected cattle in a herd may be high but the mortality rate is low. The main production lossesoccur as a result of abortions, stillbirths and a temporary drop in the milk yield. Outbreaksusually occur if infected cattle are brought into a non-immune herd or by contact withbuffaloes and wildebeest, which can also contract the disease.
CLINICAL SIGNSUsually the infection is mild and the only clinical sign noticed is a temporary drop in milkproduction. In more severe cases however, the clinical signs would be as follows:
➢ High fever and poor appetite
➢ Drastic drop in milk production
➢ Intense reddening of unpigmented areas of the muzzle and occasionally involving theeyes
➢ Profuse watery nasal discharge and shallow breathing
➢ Abortions may occurRecovered animals may become latent carriers of the virus indefinitely.
The IBR virus can occasionally affect the genital organs of cattle causing Infection PustularVulvovaginitis in females. It is manifested by the development of Pustules and a discharge.Infertility may occur temporarily. Infected bulls can transmit the disease during mating andcan contaminate semen collected for artificial insemination
POST MORTEMLesions are confined to the upper respiratory tract with reddening of the nasal cavity, throatand trachea. The trachea may contain cheesy material. Pneumonia may be present.
DIAGNOSISA presumptive diagnosis is made based on the history and clinical signs. Two blood samplescollected 2 to 3 weeks apart can be submitted for laboratory examination. A rise in theantibody level to the IBR virus is indicative of infection. Swabs from the nose and genitalorgans, if affected, can also be submitted for virus isolation and identification.
TREATMENTThere is no specific treatment. Antibiotics are indicated in cases complicated by secondarybacterial infection.
CONTROLVaccination against IBR virus can be done. The vaccine is included in Preg-Guard 9.
4.8 BOVINE MALIGNANT CATARRH/ SNOTSIEKTE A serious disease of cattle associated with contact with wildebeest Bovine Malignant Catarrh is an acute, often fatal disease of cattle caused by a virus.
OCCURRENCEBovine Malignant Catarrh occurs when cattle and wildebeest are grazed closely together.Outbreaks are usually associated with the wildebeest calving season and most cases areisolated within the herd. The disease is seen most often in adults and occurs most commonlyduring summer. The incubation period is up to 8 weeks or longer.
CLINICAL SIGNS
Bovine Malignant Catarrh sometimes occurs in an acute form, resulting in death within a fewdays. More often however, the animal is sick for a week or two. The clinical signs include:
➢ Persistent high fever and loss of milk production
➢ Severe depression and loss of appetite
➢ Eye discharge and opacity of the cornea
➢ Excess nasal discharge with crusting around the muzzle excessive salivation
➢ Diarrhoea may occurMuscle tremors and nervous signs such as loss of co-ordination, weakness and dementedappearance may be seen. Most infected cattle die.
POST MORTEMIntensive reddening and erosion of the trachea is seen. Secondary bacterial pneumonia maybe present.
DIAGNOSISA presumptive diagnosis is based on the history of contact with wildebeest, clinical signs andpost mortem findings. Characteristic microscopic findings in brain, liver and kidney areregarded as confirmatory evidence of Bovine Malignant Catarrh.
TREATMENTThere is no specific treatment. Antibiotics may control secondary bacterial infection.
CONTROLContact between cattle and wildebeest should be avoided, particularly during the wildebeestcalving season.
4.9 BOVINE LEUKOSIS A viral disease of adult cattle particularly affecting dairy herds Bovine Leukosis, also known as Enzootic Bovine Leukosis, is an infectious disease of cattlewhich specifically affects the white blood cells. Bovine Leukosis is caused by a virus and ischaracterised by increase in the number of white blood cells in the blood stream. At an earlystage of infection there are no clinical signs and most infected animals remain symptomlesscarriers for life. However, some infected animals may after several years develop masses(tumours) of malignant white blood cells which infiltrate various internal organs.
OCCURRENCEBovine Leukosis was diagnosed for the first time in Zimbabwe in 1989, but it is likely thatinfected animals were in the country for some years before then. The department ofVeterinary services has adopted an eradication scheme in collaboration with the commercialdairy sector and the necessary regulations are due to be gazetted. A survey has shown thatone in six or seven commercial dairy herds were infected. In general one animal in 200 wasfound to be positive by serological tests of blood samples. Bovine Leukosis has in othercountries been more common in dairy than beef herds. It is presumed that Bovine Leukosis inbeef cattle in Zimbabwe plays a minor role in the spread of the disease. Most animals becomeinfected when they are over 2 years old and clinical signs are usually first seen between theages of four and eight years. Close contact between animals is necessary for infection to takeplace and it seems that spread occurs when infected blood is transferred to susceptibleanimals via unsterilized needles or surgical instruments. Biting insects and ticks have alsobeen considered as vectors but the importance of these is uncertain. Infected dams can pass
the infection to foetuses during pregnancy and the offspring can become infected by ingestionof colostrums from infected cows. There is no evidence that semen from infected bulls viaartificial insemination can transmit the infection to cows. However, transmission can takeplace by rectal palpation.
CLINICAL SIGNSAn animal infected with BL virus may never show signs during its life and tumours may notbe present at post mortem. In instances where tumours develop, the disease is characterisedby chronic ill health, loss of appetite, progressive loss of condition and general weakness.Lymph nodes may be visibly enlarged. Affected animals will eventually die.
POST MORTEMThe lymph nodes are enlarged. Diffuse enlargement or firm whitish tumour masses may befound in the liver, kidney, spleen, heart or in any other organ. Microscopial examination ofaffected organs reveals infiltration with numerous white blood cells.
DIAGNOSISEnzootic Bovine Leukosis can be confirmed only by serological tests of blood samples.
TREATMENTThere is no treatment
CONTROLThe control of Bovine Leukosis I based on blood testing, identification a culling of infectedanimals and quarantine measures. A declared policy of eradication of Bovine Leukosis fromthe dairy herd was formulated in 1989 with the introduction of an accreditation scheme forLeukosis-free dairy herds. The scheme is implemented through the local Veterinary Officeswhich arrange for blood testing and issue accreditation certificates. Blood testing is carriedout on request, or on a routine basis as part of the accreditation scheme in the dairy herd. Thecomponents of the scheme are as follows:
➢ Animals found serologically positive must be re-bled for confirmatory diagnosis
➢ A dairy herd is accepted as being Leukosis-free when it is:EITHER—retested at least three months after the last positive animal has been branded andisolated or slaughtered, and is shown to be serologically negative at three consecutive testscarried out at intervals of not less than three months;OR—tested at least one month after the last introduction of dairy cattle with negative resultsThe certificate remains valid for two years and to retain accreditation, all dairy cattle over 18months must be tested on expiry of the accreditation. cattle from a non Leukosis-freeaccreditation of the herd falls immediately away. As infected animals remain carriers for lifethey should be culled as soon as possible. However, there is no extreme urgency and farmershave time to take advice where necessary and think about the most economical way toslaughter infected cattle. During the quarantine period, infected farms have no value assuppliers of breeding stock, but the value of pasteurised milk and of the beef produced isretained.
5.0 VITAMIN E/ SELENIUM DEFICIENCY A disease, primarily of young sheep and cattle, caused by low dietarycontent of Vitamin E and selenium Vitamin E/ Selenium deficiency, also known as white Muscle disease, is caused byinadequate dietary levels of either selenium or vitamin E or a combination of both. In the
body, selenium and vitamin E form part of various enzymes which protect cells. Thedeficiency will result in the breakdown of skeletal system and heart muscle fibres.
OCCURRENCEAlthough most cases develop during spring and summer vitamin E / selenium deficiency mayoccur all year round. The disease is most common in rapidly growing animals of 2 to 4months of age born from mothers which have been grazing selenium deficient pastures and or/ fed diets low in selenium and vitamin E. lambs are most susceptible but the disease alsooccurs in calves and in beef cattle up to 18 months of age under feedlot conditions. Thedisease occurs clinically in an acute or sub acute form. Unaccustomed exercise, vaccinationor dehorning procedures are precipitating factors.
CLINICAL SIGNSThe acute form mainly affects the heart and affected animals may die without showing anypremonitory signs if illness especially after unaccustomed exercise. When observed, theclinical signs are as follows:
➢ Dullness and severe respiratory distress
➢ Frothy and blood-stained nasal discharge
➢ Lateral recumbency
➢ The temperature, eyesight and temperament remain normal
➢ Death usually occurs within 6 to 12 hoursThe sub acute form mainly affects the skeletal muscles and the clinical signs are as follows:
➢ Stiffness and trembling of the limbs
➢ Weakness and inability to stand for more than a few minutes
➢ Stiff, goose-stepping gait
➢ Temperature remains normal and laboured breathing may occurSubclinical cases occur in apparently normal animals during an outbreak. Primary seleniumdeficiency may also cause retained placenta and in young animals weakness, diarrhoea andunthriftiness.
POST MORTEMThe skeletal or heart muscles show defined white or grey areas of tissue degeneration withthe appearance of fish flesh. These lesions may be in streaks and involve all or part of amuscle. Lung oedema may be present.
DIAGNOSISA presumptive diagnosis is based on the history, clinical signs and post mortem findings.Blood and muscle samples can be taken and sent to the laboratory for examination. Increasedlevels of muscle enzymes in blood serum and presence of muscle damage observed bymicroscopial examination are confirmatory of vitamin E/ selenium deficiency. Levels ofselenium can be estimated in the blood.
TREATMENTIntramuscular injection of a mixture containing 2,5 mg selenium and 750 mg of vitaminE(tocopherol acetate) per 45 Kg body weight is recommended. Following treatment, affectedanimals usually show marked improvement within 3 to 5 days and are able to walkunassisted. Treatment of all animals at risk should be done.
CONTROL
The disease can be prevented by injection of vitamin E/ selenium mixture to ewes and damsduring pregnancy or directly to the young animals at 1 week of age followed by secondinjection 2 to 3 months later. Incorporation of vitamin E and selenium in mineral mixtureeffectively prevents the disease. Vitamin E oil can be added to the diet.
5.1 IODINE DEFICIENCY (GOITRE) A condition causing abortion, stillbirths or weak offspring Certain areas in Zimbabwe are iodine deficient in the soil and goitre occurs when animals arefed on a diet which contains insufficient amounts of iodine. Goitre is a swelling on the ventralaspect of the throat caused by enlargement of the thyroid gland.
OCCURRENCELow dietary iodine is not only cause of Goitre. Certain feeding systems can also be directlyresponsible for iodine deficiency in animals: for example diets rich in cabbage, rape, linseedmeal or soyabean products. Such diets and highly fertilized star grass contain glycosideswhich interfere with the uptake of iodine by the thyroid gland and cause enlargement of theorgan. Iodine deficiency may cause increased incidence of abortion, stillbirth, and lowsurvival rates in new born animals. Sheep and goats are more susceptible to iodine deficiencythan cattle, pigs and horses. Animals lambing or kidding for the first time are more likely tobear goitrous offspring than adult animals.
CLINICAL SIGNSThe most obvious symptoms is goitre, but abortions, stillbirths and birth of weak offspringare common manifestations of iodine deficiency. The offspring usually are unable to stand orsuckle and die within a few days of birth. Adult animals often look healthy but the herdexperiences an increased incidence of anoestrus, repeat breeding and low libido in bulls.
POST MORTEMThe thyroid gland is enlarged to 2 or 3 times its normal size. In young animals partial or totalabsence of the hair coat may be seen.
DIAGNOSISThe presence of goitre makes diagnosis easy. The history of the farming area, type of pastureand feed use are useful aids.
TREATMENT AND CONTROLIodine deficiency can be prevented by providing animals with salt lick containing 0.02 %potassium iodate. The amount of goitrogenic food in the diet should be reduced.
5.2 GRAIN OVERLOAD IN RUMINANTS Usually a fatal condition due to ingestion of feed with high contents ofcarbohydrates Grain overload or Ruminal Acidosis occurs in cattle and small ruminant which suddenlyingest large amounts of carbohydrate-rich feed such as maize, wheat or molasses. It causes anacute disease due to excessive production of lactic acid in rumen. The pH of the Ruminalcontent drops from the normal values of 6-7 to below 5. The lowered pH destroys theRuminal microflora and impairs the Ruminal motility.
OCCURRENCERuminal Acidosis occurs throughout the year but is especially common during the wintermonths, when animals are fed concentrates. Accidental access to concentrate feed is the mostcommon cause of Ruminal Acidosis but mixing of concentrate e.g. maize corn and roughagein the winter in the wrong proportions may also result in Ruminal Acidosis is not uncommonin feed-lot cattle or dairy cows on high concentrate feeding which at the same time getinadequate supply of roughage.
CLINICAL SIGNSUsually clinical signs occur within 1 to 2 days after engorgement and they are as follows:
➢ Loss of appetite, depression and weakness
➢ Body temperature usually remains normal
➢ Respiration and pulse accelerate
➢ Immobilized rumen and dehydration
➢ Diarrhoea and grain may appear in faeces
➢ Recumbency followed by coma and deathMildly affected animals show less pronounced symptoms and usually recover after 3 to 5days. Such animals may develop inflammation of hoofs resulting in irregular outgrowth ofthe claws weeks or, even months later.
POST MORTEMIn acute cases which die within 1 to 2 days, excess grain and fluid may be found in therumen. The content has a typical odour suggestive of acid fermentation. Estimation ofRuminal pH values below 5 strongly suggests Ruminal Acidosis. Shortly after death therumen pH begins to increase and its measurement may not be reliable. The lungs areoedematous and froth is present in the trachea. Fluid may be seen in the heart sac and thechest cavity.
TREATMENTIn serious grain overload emergency slaughter should be considered. In moderately affectedcases, 50 gram of magnesium hydroxide in 1 litre of water per 100kg body weight isdrenched into the rumen followed by kneading the rumen to promote mixing. Water intakeshould be restricted for the first few days and good quality palatable hay provided equal tohalf of the daily allowance per head. Exercise every hour encourages movement of theingesta through the digestive tract. Treatment with antibiotics and adding of electrolytes inthe drinking water may reduce problems with Ruminal inflammation.
5.3 UREA POISONING IN RUMINANTS Usually a fatal condition if urea is fed in high concentrations or notintroduced gradually to the animals Urea poisoning is an acute often fatal intoxication of cattle, sheep and goats due to excessivebreakdown of dietary urea and formation of ammonia in the rumen. Presence of soyabeanmeal in the feed increases the ammonia formation. Urea is used as a feed additive inruminants to provide a cheap protein substitute. Urea also serves as a fertilizer on crop andpasture fields. Urea poisoning occurs if urea is not gradually introduced into the animals dietso that the animals can get accustomed to it. Urea poisoning also occurs when ruminantsaccidentally gain access to large quantities of urea, or when feeds are improperly mixed. Itshould be kept in mind that tolerance to urea is lost rapidly and animals which do not receiveurea for a few days are fully susceptible. The diet must contain adequate amounts of
carbohydrate when urea is fed.
CLINICAL SIGNSSigns of illness show within 20 to 30 minutes after ingesting a toxic amount of urea and thesymptoms are as follows:
➢ Severe abdominal pain
➢ Weakness and laboured breathing
➢ Excessive salivation and bloat
➢ Muscle tremor, in-coordination and staggering backwards
➢ Violent struggling and bellowingThe course is short and death usually occurs a few hours after ingestion.
POST MORTEMSigns of circulatory distress are usually seen in the form of generalised congestion, froth inthe trachea, lung oedema and increased fluid of the heart sac. Haemorrhages may be presenton the heart surface. Ammonia dissipates rapidly but ammonia odour may be emitted fromthe opened rumen. The pH rumen content may be over 7.
DIAGNOSISA diagnosis is based upon the history of urea ingestion and post mortem findings. Oftenseveral animals are affected at the same time. Toxic levels of urea in feed can be verified bychemical analysis.
TREATMENTIf not administered early, treatment is unlikely to be effective, however, oral administration of½ to 1 bottle (sheep), 3 to 4 bottles (cattle) of vinegar or 5 % acetic acid mixed with equalamount of water and drenched to the animal might be tried. Repetition of the antidote isrecommended as clinical signs tend to recur about half an hour after treatment.
PREVENTIONIn general urea should not constitute more than 3 % of dietary concentrate, or 1 % of the totaldry ration. As a rule of thumb, an adult cow should not be given more than 60 gram urea perday. Urea must be introduced slowly to animals and evenly mixed in the feed. Urea fertilizershould be kept away from animals.
5.4 TWIN LAMB DISEASE A disease of malnutrition in pregnant ewes carrying twins Twin Lamb Disease, also known as Pregnancy Toxaemia, is a metabolic disease of pregnantewes especially those carrying twins. The disease is caused by a decline in the plane ofnutrition during the last two months of pregnancy.
OCCURRENCETwin Lamb Disease is primarily a disease of intensive farming systems and is relatively rarein intensive grazing units. The disease occurs only in ewes in late pregnancy, usually duringthe last month in those carrying more than one lamb. Twin lamb disease occurs most often inoverweight sheep in which dietary deficiency of net energy is exacerbated by the increaseddemand for energy in the latter part of pregnancy. Precipitating factors include reduced feed
intake following sudden feed change, exposure to inclement weather, an absence of shelter ora heavy worm infestation. Twin lamb disease also occurs in goats. In cattle it is known as FatCow syndrome.
CLINICAL SIGNSThe clinical course usually lasts up to a week and is characterized by nervous signs. Theclinical signs are as follows:
➢ Poor appetite, separation from the flock and aimless walking
➢ Apparent blindness and pressing of the head against obstacles
➢ Constipation and dry scanty faeces
➢ Grinding of the teeth, usually posture, tremor of the head and neck muscles whichlater may involve the whole body
➢ Odour of acetone may be present on the breath
➢ Convulsions followed by coma and deathTwin Lamb Disease is usually fatal.
POST MORTEMThe main pathology is confined to the liver which is enlarged, friable and yellowish. There isevidence of constipation. Twin lambs are usually present and the foetuses may show varyingdegrees of decomposition.
DIAGNOSISA presumptive diagnosis is based on the history, clinical signs and post mortem findings.Analysis of blood samples reveals low sugar content and presence of ketone bodies (fatmetabolites). Ketone bodies can also be detected in the urine.
TREATMENTAffected animals must be given adequate food and water and protected from extremes ofweather. Oral treatment with 120ml of either glycerine or propylene glycol may be given inthe early stage of the disease. The treatment needs to be repeated regularly. Removal of thelambs by caesarean section or hormonal induced abortion early in the course of the diseaseusually leads to recovery, and, if near term, the offspring may be saved. In the later stages ofpregnancy the ewe’s condition is irreversible and the foetuses are often dead anddecomposed. All animals at risk should be given supplementary feed which is high incarbohydrates.
CONTROLObesity should be avoided in early pregnancy and sufficient exercise ensured through thewhole period. During the last 2 months the provision of a concentrate containing 10% proteinat a rate of 0.25 kg/day, increasing to 1 kg/day in the last 2 weeks, provides good protection.
5.5 LANTANA CAMARA POISONING OF CATTLE A poisoning weed causing liver and kidney damage and subsequent skinphotosensitization Lantana camara is a poisonous weed which contains a toxic factor causing liver and kidneydamage in cattle. The skin photosensitization is due to inability of the damaged liver toexcrete break-down products of chlorophyll on the food. These accumulate in the blood andsensitize the skin to the ultra-violet rays of the sun which result in sunburn especially of thewhite areas of the skin. Lantana is a scrambling shrub up to 3 metres tall. The leaves are
cordite with a short stalk. The flowers are small trumpet-shaped and born in dense terminalclusters. The outer petals are red with either yellow or white centres. The fruits are small andblack and are much relished by birds that spread the seeds.
OCCURRENCELantana poisoning can occur all year round but is more common in the dry season wherethere is lack of grazing. All age groups are susceptible, however serious cases are usuallyseen in young stock. Pregnant cows may abort. The clinical course depends on the amount ofweed ingested.
CLINICAL SIGNSThe cardinal signs of poisoning are as follows:
➢ Unpigmented skin, particularly muzzle, lips and teats become reddened and cracked.Portions of tissue peel away leaving ulcerated areas
➢ The mouth is similarly affected causing drooling of saliva and refusal to eat
➢ As the condition progresses affected skin become thickened, raw, hairless andcracked
➢ The membranes of the mouth, nose, eyes and vagina may be yellow from jaundice.The urine is noticeably yellow. Recovery may take few weeks. The most severe forms areacute often being fatal following three to four days of illness. Clinically there are signs ofmarked weakness, jaundice and bloody faeces.
POST MORTEMThe carcass is jaundiced. The liver shows yellow to orange-brown discoloration and swelling.The gall bladder may be extended and impaction of the large intestine is usually seen.
DIAGNOSISA presumptive diagnosis is based on presence of Lantana camara plants which show signs ofhaving been grazed, clinical signs and post mortem findings. Evidence of characteristicmicroscopic degenerative changes of the liver and the kidney are confirmatory.
TREATMENTAffected animals should be kept in shade and a purgative administered. Treatment withTerramycin has been reported to reduce the clinical course. In addition injection ofmultivitamins is recommended. Skin lesions should be kept clean and treated with antisepticointment. Unaffected animals should be removed to Lantana-free grazing areas.
CONTROLLantana camara has been declared a noxious weed. Farmers are urged to collectivelyparticipate in the eradication of Lantana. It can be controlled in the following ways:
➢ Seedlings less than 40cm can be pulled by hand
➢ Larger plants have to be cut close to ground level and the stump dressed with oldengine oil, roundup or tordon.
➢ Re-growth may be cut and sprayed.
5.6 EAR INFECTION OF CATTLE A bacterial infection of the external or inner ear which may cause loss ofcondition and death
Ear infection also known as Bovine Purulent Otitis affects cattle of all age groups but ismainly seen in young stock. Initially the external ear canal is affected and the infection mayprogress to the middle and inner ear. The cause of the disease and how it spread is not fullyclarified. Worms and different bacteria have been isolated from ear discharges. It is supposedthat small midge-like flies, which hover around the cattle in summer, might be involved inthe transmission of the disease.
OCCURRENCEThe ear infection starts late in the rainy season. Once the disease is first seen in a herd itspreads rapidly and up to one third of the animals may be affected. Subclinical cases appearto occur and they may serve as a reservoir of infection. Major outbreaks have occurred in thepast predominantly in the Mashonaland Province, but the disease has also been observed inthe Manicaland and Masvingo provinces.
CLINICAL SIGNS
Ear infection may affect the external and or middle and inner ears.The EXTERNAL FORM of the ear infection is characterised by oozing of large amounts offoul-smelling, thick white or yellow pus which runs down the cheek from one or both ears.The head is held to one and occasionally shaken. The animals show poor appetite anddepression. Several animals are usually affected at the same time in a herd. In some cases theexternal form may penetrate the ear drum and infect the middle and inner ear.In other cases the INTERNAL FORM develops without prior signs of external ear discharge.This form usually has an insidious course with drooping of the ear on one side being acardinal symptom. As the condition progresses paralysis of the face and tongue may occur,affecting food intake. It gives the animals an odd facial expression and the mouth droolsaliva. Some animals circle and gradually lose condition eventually dying of starvation.
POST MORTEMIn the external form of the disease sloughing of the ear epithelium is seen and the denudedareas are covered with large amount of pus. In the internal form bacterial infection isobserved of the middle or inner ear. Formation of abscesses may result in compression offacial nerves, destruction of cranial bones and consequential meningeal and braininvolvement.
DIAGNOSISIt is based on history, clinical signs and post mortem findings. Bacterial isolation from pus ofexternal ear infection usually reveals growth of a variety of bacteria includingCorynebacterium pyogenes, Pseudomonas and Proteus spp.
TREATMENTTreatment at an early stage of the external form prevents the infection spreading to middleand inner ears. A thorough cleansing of the ears and irrigation with disinfectant followed byinstillation of penicillin and streptomycin into the ear canal two to three times a week, controlthe infection. Animals showing signs of either the external form or the internal form wheredroopy ears are seen, should be given intramuscular injections of penicillin and streptomycin,at the maximum recommended dosage rate, for 4 to 5 days. However, animals with infectionof the middle and inner ear do not always respond successfully to treatment as the infection atthat stage of the disease is often too advanced.
CONTROLAffected animals should be isolated immediately from the rest of the herd and treatment outthoroughly to avoid spread in the inner ear. Measures to ensure effective tick and fly controlon the cattle should, be taken. Slaughter of animals that develop droopy ears might be
considered if they have not responded to treatment.
6.0 FOWL CHOLERA A killer disease of poultry Fowl cholera is an infectious bacterial disease caused by Pasteurella multocida that affectsdomestic fowls and wild birds. Outbreaks of Fowl cholera in Zimbabwe have been restrictedto Mvurwi, Mazowe and Concession areas of Mashonaland Central.
OCCURRENCEPasteurella multocida is capable of causing mortality of up to 90% in a flock. Waterfowl(ducks and geese) and turkeys are more susceptible to the disease than chickens. It isunknown whether Fowl cholera can affect Ostriches.Pasteurella multocida may be introduced into a flock by adding newly acquired, infectedstock to the old flock or by contact between infected wild birds and domestic birds. Survivorsof an outbreak or birds dying from fowl cholera may act as reservoirs of infection tosusceptible birds. Similarly contaminated crates, feed bags or any other equipment used in aninfection flock may serve as source of infection to the next flock. It is known that rodents canact as carriers of the infection. Pasteurella bacteria from mammals do not affect fowls exceptstrains from swine and possibly cats.
CLINICAL SIGNSFowl Cholera may present different clinical forms depending on the pathogenicity of thebacteria and the flock resistance.
➢ The per-acute form is characterised by sudden death in apparently healthy birds: theowner may not see a sick bird.
➢ In the acute form non-specific symptoms such as listlessness, poor appetite, rufflingof feathers, and discharge from the mouth are common. In some cases there is alsodiarrhoea, and respiratory involvement can occur. The chronic form of the disease isusually seen in birds that survive the acute form. Infection localizes in the wattles,sinuses, legs and wings joints, footpads and sterna bursae, which may be swollen.Noisy and difficult breathing results from respiratory infection. Twisted neck is afrequent sign in turkeys. Chronically ill birds may die after a protracted illness orrecover to become chronic carriers of infection.
POST MORTEMThere are no gross lesions in the per-acute form. In the acute form pin-point haemorrhages onthe heart, proventriculus, gizzard and intestines may be seen. The liver surface may havegrayish sports of dead tissue, which is a cardinal sign. Peritonitis may be present. In thechronic form of fowl cholera the bird is in poor condition and the wattles and joints areswollen.
DIAGNOSISA presumptive diagnosis is based on the history of the flock and the post mortem findings.Isolation of Pasteurella multocida from affected birds is confirmatory of f owl cholera.
TREATMENTSulpha drugs such as Sulphaprim, sulphamentazine and mezenol in feed or water usuallycontrol mortality. Tetracycline can also be used with good results. It is always advisable tocarry out a sensitivity test on the isolated Pasteurella bacteria as this will help choose themost effective drugs.
CONTROLIt must be emphasized that drugs alone cannot control an outbreak without accompanyinghygiene measures to prevent further contact between the Pasteurella bacteria and the birds. Inan outbreak (suspected or confirmed) the following measures should be attended:
➢ All movement of birds to and from affected farms should be suspended
➢ Dead birds should be destroyed preferably by incineration
➢ Daily disinfection (quaternary ammonium, hypochlorite or iodine containingdetergents) of all utensils especially drinkers and feeders used in affected houses andlocation of foot baths on entrances of all houses
➢ Houses should be thoroughly cleaned and disinfected between batches
➢ An all-in all-out policy will avoid carryover of pathogens to new flocksVaccination against Fowl Cholera would be ideal but the vaccine is not at present available inZimbabwe. Emphasis should therefore be put on management and hygiene.
6.1 COLI INFECTION IN BROILER CHICKENS A disease secondary to stress Infection with E. coli bacteria is an important infectious disease of poultry. These bacteria arenormal inhabitants of the intestine of birds but only a few cause diseases. These organismssurvive for long periods outside their hosts and are very widespread in all poultry housesespecially in the litter and dust. In Zimbabwe we can assume that up to 30% of all losses dueto mortality and condemnation at slaughter are related to secondary E.coli infections.
OCCURRENCEE. coli rarely causes primary disease. Environmental stresses such as high levels of dust,humidity, concentrations of ammonia, overstocking, insufficient ventilation or the presenceof other infectious conditions are some of the predisposing factors to produce diease. Mostoutbreaks of coli infection in broilers occur between 4 to 6 weeks of age. High mortalities cancontinue until slaughter age. The disease may occur as early as the first week of life.
CLINICAL SIGNSThe first sign of disease is an increase in daily mortality. This is accompanied by respiratorysigns such as sneezing, coughing, gurgling sounds and listlessness. Loss of appetite,diarrhoea and ruffled furthers may also be seen. Gradually the flock may start to look unevenwith many stunted and retarded birds.
POST MORTEMThe findings are quite characteristic. The pericardium and liver surface are covered with awhitish elastic and thin membrane. The air sacs are cloudy and thickened and the trachea ishaemorrhagic. Patchy congestion of the large muscles is frequent.
DIAGNOSISA presumptive diagnosis of Coli infection is based on the history of the flock, course ofinfection and the post mortem findings. Isolation of the bacterium E.coli will confirm thediagnosis
TREATMENTA number of drugs such as neomycin, tetracycline, furazolidone and sulpha-drugs areeffective. However certain strains of E.coli may be resistant to some of these drugs.Preferably an antibiotic sensitivity test should be carried out at laboratory before treatment. Inaddition, determination of the environmental factors causing stress and predisposing the birdsto infection should be done.
CONTROLNo commercial vaccine is available at the moment. Good management practices are the bestcontrol measures. Vaccination against diseases, disinfection of the houses between crops,elimination of environmental stresses and an “all-in all-out” system may reduce susceptibilityto E.coli infection.
6.2 INFECTIOUS CORYZA IN CHICKENS A highly contagious disease of the upper respiratory tract particularlyoccurring in the winter season The winter season always means an increase in the incidence of respiratory diseases which isendemic in Zimbabwe and which recurs regularly during the cold season is InfectiousCoryza.
OCCURRENCEInfectious Coryza is an acute upper respiratory disease caused by a bacterium Haemophilusgallinarum. Chickens of all ages are susceptible after the seventh day of age but the diseaseseldom occurs in birds younger than five weeks of age. Chronically ill or healthy carrier birdsare the reservoir of infection. New outbreaks result from the mixing of susceptible birds withcarriers. Further spread of the disease takes place by direct contact, airborne droplets and bythe contamination of drinking water. The incubation period is from 1 to 3 days with durationin complicated cases of about 2 weeks.
CLINICAL SIGNSUnder field conditions the disease can last much longer than 2 weeks persisting for severalweeks (four or more) depending on the presence of other complicating diseases such asMycoplasmosis. In the uncomplicated form, there is nasal discharge and an occasionalswelling of the face. This is common in young birds. The severity of disease increases withage. In the more severe form there is marked swelling of one or both sinuses behind the eyes.With secondary infection, the swelling may persist for months. Sneezing and gurgling noisesare heard. Egg production is reduced. Mortality is generally low, but can reach 20% in mixedinfections.
POST MORTEM
There is excess mucus and a catarrhal inflammation of the trachea and the sinuses below theeyes. There may be an occasional pneumonia and cloudiness of the air sacs.
DIAGNOSISA presumptive diagnosis is based on the history and clinical signs. The condition may beconfused with other diseases such as Mycoplasmosis, newcaastle disease, Infectiousbronchitis and Vitamin A deficiency. The diagnosis can be confirmed at the laboratory byisolation of the causal bacterium.
TREATMENTVarious Sulpha-drugs and antibiotics can be used for treatment of Infectious Coryza.Sulphaprim, Furazolidone, Neomycin and Streptomycin have been used with success.
CONTROLAn “all-in all-out” system, combined with efficient disinfection of the premises is an effectiveway of minimising the spread of disease to the next flocks. Vaccination for broilers once atabout 3 weeks of age and layers twice at 6 and 10 weeks of age is effective. Goodmanagement can reduce disease incidence on the farm.
7.0 INFECTIOUS BRONCHITIS IN POULTRY A disease causing drop in egg production and infection of the respiratorysystem in young chickens Infectious bronchitis is a disease of domestic poultry and has a worldwide distribution.Although playing a minor role as a single disease entity in Zimbabwe, its contribution todisease problems when combined with other disease agents is undoubted. The disease iscaused by a virus which is transmitted by air or mechanically by contaminated farmimplements. Outstanding characteristics of the disease are respiratory disturbances and injuryto the reproductive organs resulting in reduced productivity. Some strains affect the kidneyscausing kidney failure.
OCCURRENCEInfectious bronchitis affects birds of all ages. In the young birds respiratory signs are mostevident. This is rare in adults which only show reproductive disturbance. Outbreaks of thisdisease are most common in winter.
CLINICAL SIGNSYOUNG BIRDS
➢ In the young birds, head shaking, gasping, sneezing, eye-watering, facial swelling,nasal discharges and increased mortality are common. In the absence of othercomplicating diseases such as Mycoplasmosis or E. coli infections, Infectiousbronchitis usually lasts 1 to 2 weeks. Mortality is very low although it may be higherin young birds. In immature female birds, besides the respiratory signs, developmentof the oviduct may be prevented partially or completely resulting in reduce or no eggproduction at laying age.
ADULT FEMALES
➢ In adult females Infectious Bronchitis is manifested by typical egg deformities anddecreased egg production which may be as high as 40%. Eggs may be smaller, eggshells are deformed, pigmented, have calcareous deposits, and may be thinner than
normal or absent. The egg white is often watery. Fertility and hatching are reduced inbreeder stock. Recovery in production may take up to 8 weeks
POST MORTEMIn the respiratory form, there is excess mucus in the trachea. The lungs are congested and theair sacs are cloudy. When the oviduct is affected, it may be underdeveloped, vestigial orabsent. Kidneys are swollen due to the accumulation of urate. Visceral gout may be present.
DIAGNOSISA presumptive diagnosis is based on history and clinical signs e.g the respiratory signs,reduced egg production and egg abnormalities. The presence of antibodies in blood samplestested for infectious bronchitis is indicative of Infectious bronchitis.
TREATMENTThere is no specific treatment against Infectious Bronchitis. Broad spectrum antibiotics e.gtetracycline are given during the course of the disease to control secondary infections thatmay prolong the disease and increase mortality.
CONTROLInfectious bronchitis can be controlled by vaccination. Live and inactivated vaccines areavailable. Live vaccines can be administered by spray, beak dipping, nasal or eye-drops inday old chicks. Drinking water and spray is used in older birds. If using chlorinated water,powdered milk at 1 tablespoon per 5 litres of water should be added to neutralise the chlorinewhich can kill the virus and so prevent the development of an immune response. Inactivatedvaccines are given by injection in laying stock at 18 weeks of age.
7.1 INFECTIOUS BURSAL DISEASE IN CHICKENS A fatal viral disease affecting the immune system of young chickens Infectious Bursal Disease, also known as Gumboro Disease, is highly infectious viral diseaseof young chickens causing destruction of the immune system. The disease is common inZimbabwe.
OCCURRENCEInfectious Bursal Disease occurs throughout the year with little seasonal variation. Chickensbetween three and seven weeks of age are most commonly affected. Older birds up to the ageof twelve weeks may also be affected. The disease is usually subclinical in turkeys and ducks.Poor flock isolation and mismanagement can increase the risk of infection. In an outbreak allchickens are affected and mortality varies from 5 to 30%. The disease may be spread by thewind, and the movement of people, animals and vehicles.
CLINICAL SIGNSThe incubation period of Infectious Bursal Disease is 2 to 10 days. An outbreak in a flocknormally lasts 5 to 7 days. The clinical signs observed are:
➢ Ruffling of feathers
➢ Diarrhoea and soiling of vent feathers
➢ Vent pecking due to bursal irritation
➢ Severe depression and droopy appearance
➢ Trembling, prostration and death
POST MORTEMThe cardinal sign of Infectious Bursal disease is enlargement of the bursa which containscreamy whitish contents. At a chronic stage of the infection the size of the bursa diminishes.The liver and kidney become swollen and haemorrhages of the breast and thigh muscles mayoccur.
DIAGNOSISA presumptive diagnosis of Infectious Bursal disease is based on the history and the clinicaland gross findings. Presence of characteristic microscopial changes in the bursa confirms thedisease
TREATMENTThere is no treatment for Infectious Bursal Disease. Broad spectrum antibiotics such asTetracycline and sulpha-drugs can be used during the course of the disease to controlsecondary bacterial infections that may prolong the disease and increase mortality.
CONTROLVaccination, if well implemented, can control Infectious Bursal Disease effectively.Inactivated vaccine is given to parent stock to protect the progeny. Commercial birds arevaccinated with a live vaccine at 10 and 21 days of age. The Infectious Bursal Disease virusis very persistent in the environment and may survive in contaminated feed for up to 3months. Disinfectants containing formaldehyde and organic iodine have been found effectiveagainst the virus. Other important measures for disease control include:
➢ Restricted movement between farms
➢ Prohibiting backyard flocks on poultry farms
➢ Fencing of farms to isolate them
➢ Use of effective disinfectants at entrances into farms or poultry houses
➢ Provision of special clothing for farm duties only
➢ Correct disposal of litter and disinfection between different flocks of chickens
7.2 SWOLLEN HEAD SYNDROME IN POULTRY A disease in broiler of 4 to 6 weeks of age Swollen Head Syndrome is an infectious disease of chickens characterized by a generalswelling of the head affecting particularly the wattles and the space between the lower jaw.This relatively new infectious disease of poultry was first noted in South Africa in the early70’s and subsequently reported in many other parts of the world including Zimbabwe. Atpresent the incidence of the disease in Zimbabwe is very low. Up until now all cases havebeen confirmed in broiler flocks. The specific cause of Swollen Head Syndrome is unknownbut various infectious agents including viruses and bacteria have been incriminated
OCCURRENCESwollen Head Syndrome most commonly affects broilers of four to six weeks of age. Usuallyless than 10% of the birds in a flock become affected but the incidence may be much higherwhere unfavourable environmental conditions are present. The mortality rate varies from 1 to20%.
CLINICAL SIGNSThere is sneezing, swollen eyelids and accumulation of fluid under the skin of the head
region. The swelling starts around the eyes and eventually cover the whole head, includingthe wattles and the throat. The eyes become closed. The birds cannot see or find the feed.This results in starvation and death.
POST MORTEMThe accumulation of a clear to blood-tinged fluid underneath the skin of the head region isthe most characteristic feature. Haemorrhages of the trachea may be present. There may be anoccasional lung infection
DIAGNOSISThe clinical picture of head swelling and swollen eyelids is quite characteristic.
TREATMENTThere is no specific treatment against Swollen head Syndrome. Broad spectrum antibioticssuch as tetracycline and neomycin may be used. Where a virus is involved, antibiotics willminimise secondary bacterial infection
CONTROLThere is no vaccine against Swollen Head Syndrome. Strict hygiene and sound managementpractises are the best control measures
