Trypanosomiasis

 Trypanosomiasis

Trypanosomiases is a group of protozoal infections of both man and animals caused by trypanosome parasites. The species of trypanosomes consist of T. brucei, T. vivax, T. congolense, T. simiae and T. evansi. Animal trypanosomiasis in Africa represents one of the most serious veterinary problems in the world, and while most other animal diseases have been successfully controlled during this century, trypanosomiasis continues to represent a major threat to animal production in sub-Saharan Africa. The parasites causing the disease are largely transmitted by tsetse flies. Approximately ten million km2 of Africa are infested with tsetse flies and approximately 30 percent of the 150 million cattle in these countries are exposed to the infection. Most infected cattle die if they are not treated. No vaccines are available, however, the disease can be prevented by the use of prophylactic drugs. Another effective control method is to prevent tsetse flies from biting animals.
 
Clinical signs:
Anaemia and general loss of condition are the first clinical signs, when trypanosomes invade and multiply in the bloodstream of the affected animals. About one or two weeks later, the sick animals usually have recurrent fevers for up to three months. There are about twelve days between the bouts of fever. Although after the first bout of fevers, the number of parasites in the circulation declines, the animals continue to be anaemic and lose condition. Some animals can survive many months before dying. A few animals can survive the disease. In the case of T. brucei and T. evansi infections, the parasites can invade brain, eyes and skin and clinical signs like nervous signs, discharges from the eyes, oedematous swellings under the skin can occur.
 
Treatment:
Trypanosomiases can be treated by trypanocidal drugs. In order for the drugs to be effective, early treatment is essential. The drugs can be classified as for therapeutic and prophylactic purposes. The therapeutic drugs for cattle include diminazene aceturate, homidium chloride and homidium bromide. The prophylactic drugs for cattle include homidium chloride, homidium bromide and isometamidium. Because most of these drugs have been in use for many years, many stains of trypanosomes have developed drug resistance towards these drugs. In order to try to overcome this difficulty, some countries have policies in restricting the use of drugs. Some drugs are reserved in the case of that drug resistance develops towards the drugs in use.
 
Control measures:
Trypanosomiasis can be prevented by the use of prophylactic drugs. The prophylactic drugs currently used for cattle are homidium and isometamidium. After properly injecting into the animals, these drugs can usually provide three months protection. Prophylactic drugs are very effective to be used to protect animals at times when they are exposed to constant disease challenge. Unfortunately, because these drugs have been in use for many years and in many places they were not properly used, resistance has been developed in some places. Another effective control method is to eradicate the vectors, tsetse flies, which transmit the disease. Various strategies have been used to control tsetse flies. These include spraying insecticide on tsetse habitat, destruction of tsetse habitat and alteration of vegetation so that it becomes not suitable for tsetse flies. It appears that trypanosomiasis can be eliminated, at least from much of Africa, by eradicating tsetse flies. However, this method is very costly and requires a high level of management, organisation and specialist expertise.

Anthrax

ANTHRAX

Anthrax is a bacterial disease of animals and man caused by Bacillus anthracis. It can occur almost anywhere around the world, but most commonly in tropical and sub-tropical countries.
The disease is spread through the sick animals' blood, faeces and other excretions to the environment where they sporulate (form spores) on exposure to air. Pasture, food and water supplies contaminated with spores are the usual source of infection to susceptible animals. Once infected, the animals develop the disease in a rapid course. Therefore, if anthrax is suspected, it is essential to confirm the diagnosis and then take prompt actions to prevent the widespread of the disease. Vaccinating animals annually a few weeks before the known expected season for outbreaks may be the most effective control method. In many countries, annual vaccination of ruminants is a legal requirement.
 
Clinical signs:
Anthrax may be peracute, acute and subacute. Peracute cases is the usual form in ruminants in which animals have a short illness of fever and difficulty in breathing, rapidly followed by collapse, convulsions and death. This form of the disease may last from a few minutes to a few hours and typically animals are found dead. After death, the most common features of the disease are discharges of thick and dark blood from mouth, nostrils, anus and vulva. In the acute forms, animals usually survive two to three days before death. The typical clinical signs of the acute cases are: high fever, depression, listless, congested and haemorrhagic visible mucous membranes (e.g. in the eyes and gums), difficulty in breathing, and oedematous swellings in ventral aspects of the body. Subacute cases last about a week and some may recover. In acute and subacute forms, female animals may abort and have a reduction in milk which may be bloodstained or yellow in colour.
 
Treatment:
Because of the rapid course of the disease, infected animals are often found dead or too sick to be treated. However, anthrax can be treated effectively if it is still in early stages when fever is the only clinical sign. The treatment for anthrax is to use antibiotics, such as oxytetracycline and penicillin, given at the maximum recommended dosages for at least five to six days.
 
Control measures:
When a anthrax case is diagnosed, all the animals in contact must be carefully examined for up to two weeks and their temperatures be taken regularly. If an animal is found to have fever, it should be given antibiotics immediately.
 
In the case that an animal died of anthrax, the carcass should not be opened and should be disposed by burial or burning  to prevent and minimise the spread of  the infection. Contaminated food, water, premises, etc. should be disinfected or even destroyed.
 
In areas where animals are at risk of anthrax, vaccination should be annually a few weeks before the known expected outbreak seasons. The live Sterne-strain spore vaccine is now used all over the world. It is relatively easy to prepare in the laboratory and safe to be used in all species. This vaccine has proven to be effective in field situations and can protect animals for about one year.

Acidosis in Dairy Cattle

Acidosis

 

Under extreme conditions, such as grain overload, large amounts of lactic acid are formed in the rumen. Acid may be produced faster than it can be absorbed or buffered. When lactic acid continues to build up, the rumen pH decreases (becomes more acidic) and microbial activity slows down. When the microbes stop working, fibre digestion is reduced and voluntary food intake is depressed.
In a normal, healthy rumen, lactic acid production equals lactic acid use.  Thus, lactic acid is rarely detectable in a healthy rumen.  However, a number of different factors can easily lead to an imbalance in lactic acid metabolism  resulting in acute or sub-acute acidosis. They include:
·        Diet too high in fermentable carbohydrates.
·        Too high concentrate:forage ratio.
·        Too fast a switch from high forage to high concentrate.
·         Too fast a switch from silage to high levels of green crop forage.
·         Low fiber content in diet.
·         Diet composed of very wet and highly fermented feeds.
·         Too finely chopped forage.
·         Over mixed TMR resulting in excess particle size reduction.
·         Mycotoxins.
One of the most common causes of acidosis occurs when switching from a high fiber to high concentrate diet that is rich in fermentable carbohydrates (starches and sugars).  Large amounts of starch and sugar stimulate bacteria that make lactic acid.  In this instance, bacteria that normally use lactic acid cannot keep up with production.  The amount of acidity in the rumen is measured by pH readings.  The optimal rumen pH should be between 6.0 and 6.2, but there is daily fluctuation below this level even in healthy cows.  Lactic acid is about ten times a stronger acid than the other rumen acids and causes the rumen pH to decrease.  As the rumen pH drops below 6.0, bacteria that digest fiber begin to die and thus, fiber digestion is depressed.  Because the end products of fiber digestion are used for milk fat synthesis, a drop in milk fat test is a sure sign of acidosis.  In, addition, the accumulation of acid causes an influx of water from the tissues into the gut and thus a common sign of acidosis is diarrhea.  If the rumen pH continues to decline and falls below 5.5, many other normal healthy rumen bacteria also begin to die.  As lactic acid accumulates, it is absorbed and lowers the pH of the blood.  High levels of acid in the gut can also cause ulcers in the rumen resulting in infiltration of bacteria into the blood that can cause liver abscesses.  Endo-toxins resulting from high acid production in the rumen also affects blood capillaries in the hoof, causing them to constrict resulting in laminitis.  Sub-acute acidosis is also characterized by cycling intake because animals eat less during times of distress, then if the rumen adapts, their appetite returns.  If blood pH drops too low, this can result in death of the animal in acute acidosis.
Another common cause of acidosis is having diets too low in effective fiber (see last newsletter) or too small particle size.  When animals don’t chew their cud normally, lack of saliva (that contains a natural buffer) contributes to low rumen pH.  Recently, researchers at the University of Wisconsin have found that some mycotoxins can alter the metabolism of lactic acid causing it to build up and cause acidosis.  This may explain why acidosis and laminitis are also commonly observed when mycotoxins are a problem.
The common symptoms of acidosis include: 
·        Low milk fat test; < 3.0 to 3.3%.
·        Sore hooves; laminitis.
·        Cycling feed intake.
·        Diarrhea.
·        Liver abscesses.
·        Low rumen pH (< 5.8) in 30 to 50% of animals tested.
·        Limited cud chewing. 
Veterinarians and nutritionists also use a procedure called rumenocentesis to measure rumen acidity.  A needle is pushed through the flank of the animal into the rumen and ruminal fluid is withdrawn into a syringe.  The rumen fluid is then measured with a pH meter.  In my opinion, a low milk fat test (less than 3.3 to 3.0%) is one of the best measures of acidosis.  Fat tests less than 2.7 to 2.8% will more than likely be accompanied by cows with laminitis.  In order to prevent acidosis good management practices are needed to prevent the situations in Table 1 from occurring.  Several pounds of long hay (or even straw) can go a long way in helping cows but the root of the problem must be found and corrected.  Buffers can also be useful in keeping rumen pH high, especially in corn silage-based diets.  Use common sense when changing diets and ensure that there is effective fiber in your diets for production of saliva.
Also to avoid acidosis, grain should be introduced gradually (ie. 0.5 kg grain or

pellets/cow/day) so that the population of rumen microbes can adjust according to the type of fermentation that is required (more starch fermenting microbes may be needed). Remember, though, that different cows respond differently to grain feeding. Some cows can handle 6 kg of grain per day while others will get sick on 3 kg per day and there is always a cow that will eat more than her share. The key to success is to make it a gradual daily increase and to WATCH your cows and check for symptoms of acidosis or grain poisoning.

Vitamin deficiencies

Introduction

The important vitamins for survival and growth of grazing animals are either manufactured in the rumen by the rumen microbes, in the body from sunlight, or are stored in sufficient quantity in the liver or contained in adequate amounts in available feed.

Even under drought conditions, grazing animals almost never require expensive vitamin supplements or injections. In ruminant diseases, only fat soluble vitamins A, D and E have a real importance.

Vitamin A

Vitamin A itself does not occur in plants, but its precursor carotene in green plant material is converted in an animal's body to vitamin A.

Green pasture, tree or shrub leaves, hay with good green colour and yellow maize all contain sufficient carotene to allow the animal to produce enough vitamin A to top up the reserves stored in the liver. These reserves are readily available for use by the animal, even during drought, and will compensate for any dietary inadequacy; supplementary vitamin A is not generally required.

For a vitamin A deficiency to occur, the diet would need to be completely devoid of green plant material for a considerable period of time. As little as 28 g of green material per day will provide the animal's vitamin A requirements almost indefinitely. This can be obtained from any green plant material, including browse leaves and shrubs.

Adult wethers or ewes and cattle can store sufficient vitamin A in the liver to provide for a period in excess of one year with no access to any green plant material (at all), including mulga and other fodder trees or browsed leaves.

There is no evidence available to indicate that sheep wholly or largely eating scrub require vitamin A supplementation. One possible exception is rams and perhaps bulls required for breeding after some months on dry pasture containing no green material. The fertility of rams is seriously reduced after they have been without any green feed for 2-6 months. Rams that are to be used for breeding and that have not had access to any green feed or leaves for 2-6 months should be given 1,000,000 I.U. (International Units) of vitamin A, a minimum of 6-8 weeks before joining, if there is no green feed available at the time.

A second possible exception is lambs and calves weaned from drought-affected mothers with depleted liver stores. Lambs and weaners that have been reared without any access to green feed or tree leaves for 3-4 months should be supplemented with 500,000 I.U. of vitamin A from the cheapest source available; 350,000 I.U. is sufficient for lambs. These amounts will give a high degree of protection for the subsequent 6 months, improving survival, growth and wool production.

Where administration of vitamin A is necessary, use the cheapest form available.

There is no evidence available to show the superiority of injecting vitamin A over drenching with vitamin A.

On the one hand injection gives quicker and slightly higher liver storage, while drenching results in similar levels fairly quickly.

Over the long term, neither method of administration has shown to have an advantage over the other in vitamin A storage or utilization. For drenching purposes, oil base, emulsion, and water-soluble forms of vitamin A are equally effective.

It may be advisable to give vitamin A to sheep and cattle given high-energy diets with little green feed in feedlots if they have been brought in after 3 or 4 months on dry feed; the recommended dose is about 1 million I.U. for cattle and 100,000 I.U. for sheep.

The supplement will generally not be necessary if the animals have been brought in from green pasture because their requirements not met by feed will probably be provided from reserves in the liver.

Clinical signs of Vitamin A deficiency:
Includes the following:

1.     Decreased appetite leading to reduced growth

2.     Impaired night vision

3.     Increased still births in pregnant animals due to affected reproductive function especially in cases where dry cows are offered poor diets

4.     Fainting fits in calves: the calf collapses as if in a deep sleep then gets up and walks away quite normally

5.     In latter stages of deficiency, bone growth is affected and this may cause pressure on the nerves to the eye which may lead to total blindness

Diagnosis of Vitamin A deficiency

This can be one by investigating the history of animals and their diets, analysis of blood and liver samples in a laboratory.

Vitamin D

There is little vitamin D in plants and animals obtain most of it by synthesizing the vitamin in the skin by action of ultra-violet rays from the sun. It is involved in the absorption of calcium and phosphorous from the intestines and the deposition of the minerals in bone together with maintenance of normal blood levels. Vitamin D deficiency in young calves is likely to occur when they are housed in houses with dim lights and offered poor quality diets. The body also stores sufficient vitamin D to overcome dietary deficiency for several months. Supplementation of drought or feedlot rations is unnecessary. Vitamin D deficiencies only occur occasionally in the southern areas of Australia.

Clinical signs of Vitamin D deficiency

Includes the following:

1.     Reduced growth rates

2.     The legs may be bent and swollen with abnormal swellings with stiffness and lameness in a number of animals

3.     The teeth may be pitted out of line and the jaw bone deformed

Treatment

Is done by injecting vitamin D and by correcting the ration, which may include oral supplementation with vitamin D.

Vitamin K

This is synthesized by the ruminal microorganisms and is available in leafy forages in plenty. Primary deficiency does not occur though can be induced by the action of dicoumarol poisoning such as warfarin rat poison and mouldy clover hay which inhibit the action of vitamin K. Vitamin K is involved in blood-clotting mechanisms.

Clinical signs of vitamin K deficiency

Include the following:

1.     Failure of blood clotting including excessive bleeding from cuts

2.     Appearance of large red hemorrhagic areas in the membranes of the mouth, eyes and nose

3.     Abdominal pain and lameness

Treatment and prevention

1.     To identify and remove the source of poison

2.     Give vitamin K by mouth or through injection.

Vitamin E

Vitamin E is contained in green plant material, hay and grain; the concentration in grain decreases during storage.

There are currently no confirmed reports of vitamin E deficiency in cattle and deficiencies in sheep are rare.

Vitamin B

This group of vitamins is synthesized by micro-organisms in the rumen and any excess is absorbed by the cow. They are also present in ample quantities in milk and therefore primary dietary deficiency is never seen.

Vitamin C

This is produced in tissues of all farm livestock and dietary supply is unnecessary.

Dentition in Sheep and Goat - Dental Formula of Animals

Introduction:

Type and number of teeth in a species. Different kinds of teeth have different functions; a grass-eating animal will have large molars for grinding its food, whereas a meat-eater will need powerful canines for catching and killing its prey. The teeth that are less useful to an animal's lifestyle may be reduced in size or missing altogether. An animal's dentition is represented diagrammatically by a dental formula.

Facts:
1- All domestic animals have two successive sets of teeth; Deciduous teeth, or milk teeth, are the first set of teeth in young animals.These are replaced by a permanent set of teeth as animals age.  In an anatomic tooth- identification system, permanent teeth are designated as incisor (I), canine (C), premolar (P) and molar (M) ; deciduous teeth are designated as Di, Dc, and Dp. The canine tooth of domestic ruminants has commonly been counted as a fourth incisor.

2- The number of each type of tooth varies from one species to another and the conventional way of describing them is a "dental formula". The type of teeth are indicated by the first letter, and the number of teeth on one side of the upper jaw is indicated over the number of the same type of teeth on the lower jaw. Because the formula is on one side of the mouth, the total number of teeth is the total in the formula x 2.

3- Goat Deciduous Teeth Dental Formula: 2(Di 0/4; Dc 0/0; Dp 3/3) = 2(10)=20 Goat Permanent Teeth Dental Formula: 2(I0/4; C0/0; P3/3; M3/3)= 2(16)=32 The dental formula for different species are as follows where I = incisors, C = canines, P = premolars and M = molars

4- Old animals with worn teeth and broken mouths will not eat as well as younger animals and will lose condition. How to check the teeth Baby teeth (milk teeth): under 1 year of age 2 tooth: 1 to 1½ years 4 tooth: 2 years 6 tooth: 2½ years Full mouth: 2½ to 3 years Worn to broken mouth: over 3 years of age Gummy: aged.

5- 2 tooth: 1 to 1½ years 4 tooth: 2 years 6 tooth: 2½ years Full mouth: 2½ to 3 years.

6- Worn to broken mouth: over 3 years of age Gummy: aged.

7- The teeth of a sheep are divided into two distinct sections namely, eight permanent incisors in the lower front jaw and twenty-four molars, the latter being divided into six on each side of the upper and lower jaw. Sheep have no teeth in the front part of the upper jaw which consists of a dense, hard, fibrous pad. Sheep dentition.

8- Dentition of a 2-year-old sheep. Four incisors are permanent (black arrows). Dentition of a 4-year-old sheep or "full mouth." All incisors are permanent. Dentition of a 68-year-old sheep. Notice the wide spacing between the teeth. Dentition of an extremely aged sheep (from 8- 12 years of age), frequently referred to as a "broken mouth."

9- Dentition of a yearling sheep. Two incisors are permanent (black arrows Dentition of a 2-year-old sheep. Four incisors are permanent (black arrows).

10- Dentition of a 4-year-old sheep or "full mouth." All incisors are permanent. Dentition of a 68-year-old sheep. Notice the wide spacing between the teeth.

11- Dentition of an extremely aged sheep (from 812 years of age), frequently referred to as a "broken mouth."     

 The morphology of mammalian teeth correlates closely with the animal’s alimentation. This explains the large variety in dental morphology between different species of animals. All domestic animals, however, have a diphyodont dentition. The dental formulas are listed in the following formulas:

 Horse:

Deciduous:

  Permanent:

Cow, Sheep, and Goat:

Deciduous:

 

Permanent:

In an anatomic tooth identification system, permanent teeth are designated as incisor (I), canine (C), premolar (P), and molar (M); deciduous teeth are designated as Di, Dc, and Dp.

Some Examples:

Sheep less than 1 year:

Sheep (1-1.5 years):

Sheep (1.5- 2 years):

Sheep (2.5 - 3 years):

Sheep (3.5 - 4years):

Extremely aged Sheep ( more than 6 years):

Note: there is a wide space between the teeth

Milk Fever in Cows

Milk Fever (Hypocalcaemia) in Cows

Introduction
Milk fever is a disorder mainly of dairy cows close to calving. It is a metabolic disease caused by a low blood calcium level (hypocalcaemia). Between 3% and 10% of cows in dairying are affected each year, with much higher percentages occurring on some properties. Jersey cows that are mature and fat and graze lush, clover dominant pasture before calving are most susceptible.
Milk fever, post-parturient hypocalcemia, or parturient paresis that most common in the first few days of lactation. It happens when demand for calcium for milk production exceeds the body's ability to mobilize calcium reserves.
Fever is a misnomer, as body temperature during the disease is usually below normal. Low blood calcium levels interfere with muscle function throughout the body, causing general weakness, loss of appetite, and eventually heart failure.
Losses are due to:
1. Deaths (about one in 20 affected cows dies).
2. A reduction in the productive lifespan of each affected cow of about three years.
3. Reduction in milk production following each milk fever episode.
4. Costs of prevention and treatment.

Signs
In typical cases cows show some initial excitement or agitation and a tremor in muscles of the head and limbs. Then they stagger and go down to a "sitting" position, often with a 'kink' in her neck, and finally lie flat on their side before circulatory collapse, coma and death. A dry muzzle, staring eyes, cold legs and ears, constipation and drowsiness are seen after going down. The heart beat becomes weaker and faster. The body temperature falls below normal, especially in cold, wet, windy weather. These signs are due mainly to lowered blood calcium levels. Sometimes there are additional signs due to complicating factors. Bloat is common in cows unable to "sit up" because the gas in the rumen is unable to escape. Pneumonia and exposure may affect cows left out in bad weather.

Causes
About 80% of cases occur within one day of calving because milk and colostrum production drain calcium (and other substances) from the blood, and some cows are unable to replace the calcium quickly enough. High producers are more susceptible because the fall in their blood calcium level is greater. Selecting cows for high production may, therefore increase the problem with milk fever. Some individual cow families or breeds (for example, Jerseys) are more susceptible than others. Age is important. Heifers are rarely affected. Old cows increase in susceptibility up to the fifth or six calving because they produce more milk and are less able to replace blood calcium quickly.
The feeding management of dry cows in the 2 weeks before calving is very important, because it affects both the amount of calcium available to replace blood calcium and the efficiency with which the available calcium can be used. When the amount of calcium in the diet is greater than is needed, the efficiency of absorbing calcium from the intestine and the efficiency of transferring calcium from the skeleton both become very sluggish and the chance of milk fever is greatly increased. Also, grazing pastures in Southern Australia winter and spring results in alkaline blood which creates conditions unfavourable for the availability of calcium in the body and predisposes the cow to milk fever. Feeding hay prior to calving and restricting access to green feed results in acidic blood which favours calcium mobilisation from bone and improves calcium absorption from the intestines, both of which are important factors in preventing the occurrence of milk fever.
Fat cows are at a greater risk than thin cows. This is partly because their feed and calcium intake has been higher and partly because fat cows produce more milk at calving time. Some cows get milk fever several days or even weeks before or after calving. This is usually due to the feed, especially the dietary calcium, being insufficient to meet the heavy demand due to the rapidly growing foetus or milk production in early lactation. In early lactation, cows should receive as much calcium as possible, and clover-dominant pasture are therefore desirable. They will help to prevent grass tetany as well as milk fever.


Treatment
Treatment should be given as soon as possible. Use 300 ml, or more, of a 40% solution of calcium borogluconate or, preferably, a combined mineral solution such as "three-in-one" or "four-in-one". Often 600 ml may be required. The combined solutions contain additional ingredients such as magnesium, phosphorus and dextrose (for energy), which may also be at low levels in the blood while cows have milk fever. Packets of solution together with an injection kit are best kept on hand for emergencies.
All equipment should be kept sterile to avoid abscess formation at the site of injection. Injection of the solution by farmers should be in several places under the skin on the neck or behind the shoulder, unless the cow is in a coma or there are other reasons for desiring a quick response. Injection into a vein should be left to a veterinarian as it can cause sudden death if not carried out properly. Veterinary assistance is also advisable if there is not a quick response to treatment, because other problems may also be present. Cows that are "flat out" should be propped up into a normal resting position to relieve bloat.
If weather conditions are bad, or the response to treatment is slow, transfer the cows to shelter to prevent exposure and other complications. Provide feed and water. Some cows that have been comatosed may have regurgitated and inhaled rumen content into the lungs. If there is ruminal material around the nose one should be suspicious that this may have happened and intensive antibiotic treatment should be commenced as soon as possible as inhalation pneumonia is often fatal. Recovered cows should not be milked for 24 hours; then the amount of milk taken should be gradually increased over the next 2-3 days.

Prevention
Management of the diet can be a valuable aid preventing milk fever. Cows should be kept on a low calcium diet while they are lactating (dry). This stimulates their calcium regulatory system to keep the blood levels normal by mobilising the body stores of calcium from the bone. When the demand for calcium increases as calving, calcium can be mobilised much more rapidly from bone than the feed, therefore preventing milk fever. With cows at greater risk - Jersey cows of mature age and in forward to fat condition - green feed should be restricted and plenty of hay fed for at least 1-2 weeks before calving, neither should contain a high percentage of clover or capeweed.
If it is necessary to improve the body condition of cows in order to improve milking performance, feeds high in energy but low in calcium may be used, for example cereal grain or oaten hay. Cereal grain is also high in phosphorus content, and this is of additional value. Cows close to calving should be kept in a handy paddock to enable frequent observation and early detection of milk fever. On the point of calving, and afterwards, the available feed and calcium should be unrestricted.
Calcium feed supplements may be helpful at this point, but should not be given earlier. Where dietary management is inadequate, other methods are sometimes used. Vitamin D3 given by injection 2-8 days before calving may be useful. As the calving date is often difficult to predict, repeated treatments are sometimes necessary. A common treatment used to prevent milk fever is the injection of calcium borogluconate just before or just after calving. Some cows are given more than one treatment. This is quite successful because the calcium provides a reservoir to increase blood calcium just at the time it is needed for milk and colostrum. The danger is that it may not last long enough and milk fever may still occur before the calcium-regulating mechanism of the cow is working efficiently.
Drenching cows with Unimix on the day before and then twice daily for 1 to 2 days after calving has considerably reduced the incidence of milk fever in some herds where other methods alone have been unsatisfactory. Unimix is a registered product containing a mixture of calcium and magnesium. Cows that have required injections to treat milk fever will benefit from a drench of Unimix to help prevent relapses.

CRD

ChChronic respiratory Disease
(CRD) (Airsacculitis)

Cause
Mycoplasma gallisepticum

Transmission

The main problem is that parent birds infected with
Mycoplasma gallisepticum can transmit the organism through
the egg to their offspring. In addition, infection can occur by
contact or by airborne dust or droplets.

Species affected
Chickens and turkeys.

Clinical signs
In chicks:
respiratory distress.
The birds frequently show a lack of appetite.
decreased weight gain and increased feed conversion ratios.
In adult birds :
sneezing,
coughing and general signs of respiratory congestion. In
laying birds a drop of egg production between 20-30 % can
occur.

Internal lesions
A reddish inflamed trachea and/or cheesy exudate in airsacs,
especially in complicated cases (e.g. with secondary E. coli
infections) are observed. In mild Mg infections the only lesion
might be slight mucus in trachea and a cloudy or light froth
in the airsacs.
Turkeys with Mg infection usually have swollen sinuses under
the eyes.
Diagnosis

Diagnosis of Mg infection can be made by blood testing of
chickens, post-mortem examination and ultimately by
isolating the causative Mg organism from tracheas or airsacs
of affected birds.

Differential diagnosis
Respiratory virus infection (Newcastle disease or infectious
bronchitis) with secondary infection (E. coli, etc.) can give
similar lesions.
Treatment
Treatment of Mg-infected chickens or turkeys with suitable
antibiotics or chemotherapeutics has been found to be of
economic value. However, control by medication or vaccination
and eradication of Mg infections has been by far the
most effective method of combating the disease. Fertile eggs
from infected birds can be treated with antibiotics such as
tylosin to eliminate the Mycoplasma gallisepticum organisms.
Methods used are the injection of fertile eggs or egg dipping.
Blood serum testing of breeder chickens for Mg antibodies
has become a routine to test flocks for a Mg infection.

Castration in camel

Castration 

Definition of Castration
Removal of the sex glands of an animal, i.e., testes in the male, or ovaries and often the uterus in the female. Castration of the female animal is commonly referred to as spaying. Castration results in sterility, decreased sexual desire, and inhibition of secondary sex characteristics. It is performed for the purpose of improving the quality of meat and decreasing the aggressiveness of farm animals.

Operative Steps:

1. The upper (right) testicle was pushed forward towards the midline in the prescrotal region and was immobilized there by firmly grasping it between the fingers and thumb of the left hand. A small incision was then made on the midline with the right hand which was just enough to squeeze out the testicle. In case of a small sized testicle, as seen in the young animals of 2-3 years of age; it was difficult to perfectly stabilize it with a single hand. In such a situation, the assistant immobilized the organ with his both hands while the operator made a small incision exactly on the midline to exteriorize the testicle (Fig. 1).

2. After exteriorizing the testicle, the tunica vaginalis was freed from its attachments as high up as possible and incised longitudinally with an operating scissors.

3. The vascular and non-vascular portions of the spermatic cord were separated from each other through the mesorchium.

4. The non-vascular portion was securely transfixed with USP-2 chromic catgut and severed distal to the transfixation.

5. The vascular portion was maximally exteriorized and was first simply ligated with USP-2 chromic catgut and then transfixed distal to the ligature using the same suture material and was severed below the transfixation ligature (Fig. 2). This technique provided a full security against slippage of the ligature.

6. The lower (left) testicle was then pushed towards the incision in the prescrotal region, slightly incised and squeezed out. The spermatic cord was ligated and severed the same way.

7. The skin incision was cleaned with a sterile gauze swab and closed with one interrupted, horizontal mattress suture using USP-2 chromic catgut, (Fig. 3). The reason for using catgut to suture the skin incision was that it did not need to be removed.

The end.

Animal Welfare In Japan

The number of dogs in Japan more than (exceeds) the number of children under the age of ten.

Trading in animal Kimono is the prosperous trading.

Hanary saloon: Shampoo washing and trim nails (100$) in Shirokane town

 

Coat to prevent cold condition

End of the topic