Noble Desk

Etiology
This disease is caused by Pasteurella multocida type 1. It causes a form of acute pasteurellosis in bufallos and cattle.
Occurrence
Classical haemorrhagic septicaemia has been reported from all continents except Australia. The first regular occurrence is in the south east Asia where it appears every year with the monsoon rams and it is considered to be the most important infectious disease of cattle and domestic animals which are affected. Of the domestic animals, buffalos are the most susceptible followed by cattle.
Transmission
There is no satisfactory evidence that insect vectors are implicated or that infection persists in the soil. Healthy carriers of pasteurella organism have long been known in most susceptible species. About 5% of healthy cattle and buffalos are said to harbor the organism in the nasopharynx. Carriers or animals infected from them may under stress, breakdown into clear clinical cases. In the early clinical stage, there is salivation and nasal discharge containing numerous pasteurella organisms. The surrounding including drinking water becomes contaminated as bacteria can survive for some hours and the opportunity is there for other animals to become infected.
Clinical signs
Most cases in cattle and domestic buffalos are acute and sometimes peracute with death occurring 6-24 hours after the appearance of clinical signs. The first signs are dullness, reluctance to move about and fever. Salivation and nasal discharge appear. Commonly, swelling becomes visible around the laryngeal region and spreads around the head. The swelling is hot and doughy. The tongue may swell and protrude and mucous membranes are congested and breathing difficulty/respiratory distress appears. The animal usually goes down and dies within a few hours or lingers for 3-4 days. Recovery from the disease is rare.
Diagnosis
An outbreak of haemorrhagic septicaemia is readily identified but individual cases may be more difficult. The rapid cause of disease and higher occurrence of throat inflammation indicate haemorrhagic septicaemia. The lesions eliminate rinderpest, anthrax and black quarter. A snake bite near the head will simulate  haemorrhagic septicaemia but such cases are rare. Confirmations of diagnosis can be made by examining blood films from muribond or recently dead animals and by sending materials to the laboratory for culture. Films are stained by Leishmann or Giemsa stain.
Treatment
To be effective, treatment must start before bacteraemia becomes well established. In later stages, although the organism can be killed by chemotherapy, the animal will nevertheless die. The organism is sensitive to sulfonamide and broad spectrum antibiotic but when clinical signs are obvious, the prognosis is usually grave.
Control
In endemic areas, vaccination is indicated and should be carried out yearly with vaccine known to confer long immunity like the oil adjuvant vaccine which can produce solid immunity lasting for about at least one year. Prior to the establishment of protective immunity, healthy animals should be segregated from the sick and in contact animals.

Gas gangrene is due to infection by Clostridium septicum although other clostridia may be involved which includes Clostridium novyi and Clostridium sordelli. The organism is a common habitat of the intestinal tract of herbivores and occurs widely in faeces and soil. In most cases, it enters the body through contaminated wound and consequently produces a severe local reaction resulting in necrosis, edema and gangrene and profound systemic effects due to toxaemia with rapid deterioration and death.
Clinical signs
Incubation period is short. It is just within 1-2 days. There is depression, anorexia, high fever within a short time. Affected animals are completely recumbent. The infection site is swollen, hot and painful in the earlier stages. This rapidly progresses to a stage where swelling persist sometimes with a foul smelling sanguinous or bloody discharge but pain is no longer evident. The swollen area eventually becomes cold, discolored and sometimes emphysematous. Occasionally, a syndrome is encountered where the condition is initially limited to the head especially the intermandibular space. Death occurs within a few days. Commonly, animals are presented at sudden death.
Immunity
It is believed that infected animals are suddenly immuned to infection.
Diagnosis
Swabs may be taken from infected sites immediately after death to establish the identity of the causal organism. As with blackleg, examination of animal which has been dead for more than few hours especially in warm climates is likely to afford little or no information due to invasion of the tissue by clostridia organism.
Prevention and control
Proper management of surgical and accidental wound including administration of antibiotics is often adequate enough to prevent malignant edema. Where the disease is considered to be serious, vaccination is very important. In view of the possibility of mixed infection, it is wise to use polyvalent clostridia vaccine. When faced with outbreak for example after castration of a large number of animals, it is probably wise to carry out a herd vaccination and to administer large doses of long acting penicillin to each animal. Again, animals at risk must be moved to another grazing areas free of the disease.
Treatment
Treatment of individual cases is usually unsuccessful. Wounds should be carefully cleaned and drained adequately. This should be followed by massive doses of procain penicillin both intramuscularly and around infection site together with large frequently repeated doses of soluble penicillin given intravenously.

This is a chronic exudative dermatitis characterized by scab formation. The disease is caused by Dermatophylus congolensis. Horses, cattle, sheep and goats are commonly affected. It has been reported in pig, donkey, cat and dog. Bovine streptotricosis is of great economic importance in Nigeria because it destroys hide and skin. West African muturu and Ndama cattle are resistant to the disease.
Transmission
The organism is found on skin epidermis. It appears to be necessary for the skin to be broken before infection can occur. The skin may be damaged by ticks, biting flies or mechanically by barb wires.
Clinical features
In some animals, the lesions are found on the back, extremities like necks and face and others generalized all over the body. The commonest site of infection in goat seems to be the face, ears and inguinal region. In affected site, exudation and scab formation caused the hair to stand erect and become matted together to form paint brush lesions. These are so called because they resemble the hairs of the wet paint brush. The lesions increased in size and thick variable scabs are formed. Affected animals are emaciated and limp if the feet are affected. Death may occur eventually.
Diagnosis
This is based on the appearance of cutaneous scabs on endemic areas. Confirmation of diagnosis is by making a smear from scab which has been emulsified in water for some hours. The smear is stained by Gram’s procedure, Leishmann or Giemsa and examined for the presence of branching filaments and coccoid cells.
Fluorescent antibody technique is the most effective diagnostic method.
Establishment of experimental lesions in rabbits by skin scarification in the presence of suspension of lesion or culture the organism and rub it on scarified area.
Treatment
It is treated by removal of scabs and application of antibacterial substances like antibiotic cream/powder.
Give high doses of penicillin and streptomycin parenterally. This treatment is repeated after 2 weeks. This treatment is effective if it is given early in the disease.
Give long acting antibiotics.
Immunization
There is no available effective vaccine at the moment.
Control
It is necessary to eliminate those factors that predispose to the diseases like ticks (spray the animal), biting insects (insecticide).
Animals should be dipped regularly to rid them of ticks.
Sheep should not be sheared in wet hot weather.
All affected animals should be culled for meat or isolated and treated.
Increased herd resistance by selective breeding from resistant animals.

This is an infectious contagious disease primarily affecting cattle, swine and goats. It is caused by brucella organisms characterized by abortion in females, orchitis and infection of accessory sex gland in males and infertility in both sexes. The disease affects sheep causing abortion and infertility. It affects horses causing abortion, poll evil and fistulous withers. It cause undulant or Malta fever in humans. It is worldwide in distribution. It has been eradicated in some Scandinavian countries such as USA, France and UK. The disease is important because it is of economic and public health significance.
It is caused by Brucella melitensis but occasionally, Brucella abortus is involved. Infection arises through ingestion of the organism, conjunctival, vaginal and by inoculation. Also by contact through intact skin. It causes abortion about 4th month of pregnancy.
Clinical signs
They are as follows:
Abortion
Keratitis
Chronic bronchitis
Mastitis
Lameness
Unthriftiness
Hygroma
Orchitis
Osteoarthritis
Synovitis
It may cause nervous signs in sheep.
Diagnosis
This is based by bacterial examination of milk (milk ring test) or of the aborted fetus.
It is also diagnosed by serum agglutination test.
Control
Vaccination
Slaughtering reacting animaland compensation paid to the farmer.
Two types of vaccines available are:
Attenuated Brucella melitensis vaccine (strain Rev. 1vaccine).
Killed Brucella melitensis H38 adjuvant oil vaccine.
Treatment 
Not advisable.
It is caused by Brucella ovis. This has been reported in Australia and Brucella melitensis also affect sheep.
Clinical signs
They are as follows:
Acute edema and orchitis
Fever
Depression
Increased respiratory rate
Epididymis is enlarged and hard and testicles atrophy.
Abortion in ewes is characteristic of the infection.
Births of weak lambs and stillbirth
Treatment is not undertaken except in valuable rams.
In this case, streptomycin and chlortetracycline are given in high doses.
Control
Test and slaughter, pay compensation to the farmer.
Vaccination using Brucella abortus strain 19 vaccine because it gives high antibody titres of the serum or Brucella abortus killed adjuvant vaccine.
It is preferable to give Brucella melitensis strain Rev.1 vaccine.
Do not vaccinate within two months of mating.

This is widespread and of economic and public health importance in most world countries especially in dairy cattle. It is characterized by abortion in late pregnancy and high rate of infertility. The causative organism is Brucella abortus. Brucella melitensis occasionally affects cattle. The organism can be recovered from pregnant uterus, fetus, fetal membranes, milk and hygroma fluid. Cattle of all ages are affected. Infection is by ingestion, through intact and broken skin, through intact or broken conjunctiva and contamination of the udder in the course of milking.
Clinical signs
Abortion after 5th month of pregnancy in cows
Retained placenta
Metritis which may be acute with septicaemia and death following or chronic leading to sterility.
In the bull, orchitis and epididymitis. Occasionally, one or both scrotal sacs may be affected with acute painful swelling leading to sterility. There may be necrosis of scrotum leading to sterility in bulls. Infected semen can spread the disease by artificial insemination. There is hygroma of knee joints. Isolation is by guinea pig inoculation or by culture.
There are several serological tests used in diagnosis of bovine brucellosis and they are as follows:
Rose Bengal plate test
Slide agglutination test
Tube agglutination test/serum agglutination test
ELISA
Coombs agglutination test
Brucellin skin test is also done. Brucellin is an antigen obtained from brucella
Control and eradication
The disease has been eradicated from Scandinavian countries like Sweden, Norway and Denmark.
Bovine brucellosis can be controlled with effective vaccination programme or eradicated using test and slaughter programme. The vaccine used are Brucella abortus strain 19 vaccine (attenuated live vaccine) and is given to cows at 4 months of age. It is known to protect animals for 7 years.
Brucella abortus killed 45/20 adjuvant vaccine protect animals from 2 years and used for diagnosis of carrier animals.

Mastitis is the inflammation (puffiness) of the mammary gland regardless of the cause. It is a big problem in the dairy industry. In most cases, it is a bacterial infection which enters through teat duct. There is no evidence of viral mastitis. It may be secondary mastitis. Occasionally, there may be mycotic mastitis with mycoplasma being involved.
Etiology
It can be caused by staphylococci, streptococci, Corynebacterium pyogenes and Escherichia coli.
Three different types of mastitis are mild, subacute and peracute mastitis.
Mild mastitis
The milk is normal and udder may be warmed. It may be slightly enlarged and may be localized to the duct. The milk may be peculiar or watery containing small clot and granules. There is no fever. The cow may be eating well.
Diagnosis
This is based on taking milk sample and checking on sensitivity.
Treatment
Give intra-mammary antibiotics (through teat canal).
Give systemic antibiotics intramuscularly. The disease may be self limiting.
Prognosis
Generally good for the cow and calf.
Severe/acute mastitis
The cow is not normal. It is slightly febrile about 104oF. The udder is painful. The animal has abnormal gait. The udder is swollen. It is painful to touch and warm to touch. The milk is peculiar. It is difficult to collect milk from the udder. The milk secreted is small. The milk may contain serum, blood and clot. The milk may smell, for example in case of Corynebacterium pyogenes.
Treatment
Strip the udder.
Give parenteral/systemic antibiotic for 5 days.
Give intra-mammary antibiotics after stripping.
Prognosis
The cow will live but affected quarters will not recover. Prognosis is guarded to poor.
Peracute/ very severe and fatal
The cow is ill and may be recumbent. The temperature is high about 107oF and the cow may be lame and not eating at all. The udder is enlarged and milk may contain blood, serum, clot and there may be gangrene development. The cow gets sicker and sicker. The udder becomes blue and cold. The temperature goes down and the animal is still recumbent.
Prognosis
Very poor. This is caused by Corynebacterium pyogenes or staphylococcus.
Treatment
Save the cow, not the quarter.
Give high doses of parenteral or systemic antibiotics.
Do not give intra-mammary antibiotics (because it is a waste of time).
N/B: Severe mastitis can be confused with severe hypocalcemia.
Control of mastitis
Subclinical mastitis can result into acute mastitis. In this case, there is no clinical cure. Make attempt to eliminate current infection.
Prevent new infections. Current infections are eliminated by treating clinical cases properly after doing sensitivity test.
Cull any cow with chronic mastitis.
Dry cow therapy: In this case, infuse cloxacilin into the udder the last time it is milked.
Preventing new infections: Hygiene is very important. Do all teat dipping in iodophore after milking. Dry off the teats properly. Any animal that gets infection should be challenged with antibiotics.
Use milking machine in good working order and service it regularly (once in a month).
Treat clinical cases as they occur.
Back flush the teats cups after each milking.

Rabies is an infectious viral disease which is transmitted by the saliva of a rabid animal. It is characterized by nervous signs, paralysis and fatal termination.
Geographical distribution
It does not occur in Britain and Australia although it is widespread. All species of animals are prone to rabies. There is high occurrence in continental Europe as foxes are increasing in number. Cattle seem to be less susceptible than dogs and cats. It is not a serious disease in farm animals.
Etiology
It is caused by rhabdovirus. It appears to be only one strain of the virus. Isolates from different parts of the world are identical serologically but their pathogenicity differs. Bats seem to be the only symptomless carriers. Recently, a number of other viruses have been isolated. Not much is known about these viruses.
Clinical signs
Cattle are mostly affected. In Nigeria, dogs have most access to cattle. Incubation period is 2 weeks to 6 months but usually 3-4 weeks. In dogs, two distinct types are dumb rabies causing paralysis and strict rabies causing incordination may show straining/tenesmus, drooling saliva, bellows, recumbent and paralysis.
In bulls, there is increased sexual excitement. Affected animal may be hyperaestatic, charging people and objects. Bulls become sexually excited and can mount on anything. These signs occur for about 24-48 hours and the animal collapses and dies.
In sheep, the picture is similar in individual animal. In Europe, 2 or 3 animals may be affected.
Diagnosis
Diagnosis is not easy but important in human point of view. Demonstration of negri bodies in the brain is positive for this disease. Occasionally, these are not seen.
Inoculation of mouse is done and waited for 21 days.
Recently, fluorescent antibody technique has been used with fluorescent microscope. It is the best method because it is quick to perform. Take the head of the suspect to the laboratory in ice quickly. If the head is divided into two halves, the first half is put in 10% formalin and the second half is put in 20% glycine saline.
Treatment
There is no treatment for this disease.
Control
The animals should be vaccinated annually.
Stop them being exposed to the virus.
Destroy all wild fauna.
Vaccine used is passed in duck embryo. Vaccine protects for about 6 months and young dogs at about 4 months of age; after that, vaccinate annually.
Other rhabdoviruses are isolated from trade cattle in Nigeria.
208 viruses were isolated from 2179 samples.

This is an acute rickettsial disease of ruminants south of the sahara. It is caused by Cowdria ruminantium and transmitted by at least 5 species of Amblyoma. The name is derived from the frequent occurrence of the hydropericardium. The clinical disease is characterized by fever and nervous signs.
Etiology
Heart water is caused by rickettsia, Cowdria ruminantium. It occurs in closed packed colonies in endothelial cells of blood vessels in various organs. Multiplication of the organism appears to be by binary fission. It has been suggested that cowdria may arise at first in the reticulo-endothelial cells of lymphnodes before invading endothelial cells of the blood vessels and the organism has been reported to occur in various other cell types including macrophages, monocytes and cells of renal tubules. Although animal invasion shows that the organism occurs in blood smears.
Distribution
Heart water has been reported from several countries in Africa, south of the Sahara but in most areas, little is known about the incidence of the infection. The potential and possibly natural distribution of heart water covers at least that of the tick vectors, Amblyoma such as Amblyoma herbraeum, Amblyoma variegatum, Amblyoma pomposum, Amblyoma gemma and Amblyoma lepidum. These ticks occupy most of Africa south of Sahara and Madagascar and other offline Irelands.
Susceptibility
Apart from cattle, other domestic ruminants like sheep, goat and avian, buffalo are susceptible to infection and the disease is in fact as important for sheep and goat as it is for cattle. Some species of African antelopes and European deer have been shown to be susceptible to experimental infection. Other susceptible animals are Eland and spring buck.
Epidemiology
There is no doubt that heart water occurs only in Africa. It is apparent that natural reservoirs of the disease are undoubtedly wild African ruminants. Domestic ruminants suffice to maintain the disease at high level as is the case in Madagascar where wild ruminants are not existed. Five species of Amblyoma have been shown experimentally to be able to transmit Cowdria rumunantium. Recently, it has been demonstrated in Zimbabwe that elephant tick called Amblyoma tholloni is an experimental vector. Laboratory transmission of heart water by American tick, Amblyoma maculatum has been reported. It is believed that dissemination is only transtadial so that infected larva is free of infection. Transovarian transmission has been shown in one conclusive experiment in South Africa. The later transmission is probably infrequent. A larva feeding on infective ruminant is able to transmit the disease, not only in the next instar, the nymph but it is still infective in the adult stage. On the other hand, as the larva commonly feeds on non-susceptible animal, it is often the nymph which first gets infection and in that case, only the adult transmit the disease. As is in the case with other tick borne diseases, infected ticks do not start to transmit the disease immediately upon attachment. They usually feed for some time before transmission occurs. In heart water, this is said to be about 24 hours while in theleriosis and babesiosis, it is a matter of days. Artificial transmission is possible by means of blood and tissues of infected animals.
It is unanimously agreed that intravenous infection is necessary for successful transmission. Subcutaneous route of infection was achieved in brain tissue material obtained from infected animal. Calves even of highly susceptible stocks are relatively resistant to the disease for 2-3 weeks after birth. This resistance is independent of the immune status of the dam. Some calves infected throughout this period recover but as majority are not infected until later after the age, resistance (immunity) is lost. A state of endemic stability without apparent disease does not exist. In endemic regions, cattle usually suffer little mortality. A considerable degree of innate resistance presumably has been acquired through long natural selection. Where the vector population is low by acaricidal or unfavorable ecological factors, sporadic cases of heart water may occur with long intervals of seeming absence of disease. It has been reported that infection can be maintained in fasting adults for 15 months. The disease may be carried over long distances and reintroduced into pastures by nymphs or birds. If infection was acquired in larval stage, heart water occurs throughout the year but its incidence may reduce during dry season in countries with pronounced seasonal climatic changes which influence seasonal activity of different stages of the vector.
Clinical signs
Clinical reactions may be peracute, acute or subacute. Peracute cases exhibit sudden high fever, collapse and death in convulsion. Acute cases are manifested by fever and signs of nervous disturbance. Acute cases start with sudden high fever, nervous symptoms like staggering, drunken gait, cycling movement, abnormal postures, twitching of eyelid, frequent sticking out of the tongue, haggard facial expression, tremors of individual muscles which can often be provoked by touching the animal or by noise. Pregnant animals may abort. Finally, the animal may collapse in convulsion and with paddling movement of the limbs and frequently nystagmus, opisthtonus and chewing movement of the mouth. There may be profuse fetid diarrhea. Finally, death follows. Before dying, the animal may pass bloody faeces. In subclinical cases, there is transient or mild fever and sometimes diarrhea.
Diagnosis
This is done by microscopic detection of the organism in brain cortex, capillaries obtained by biopsy or inoculating blood from affected animal into susceptible ruminant.
The organism can be demonstrated after death in brain smears stained with methylene blue.
Differential diagnosis
Nervous symptoms or disorders may stimulate diseases such as rabies, cerebral babesiosis, hypomagnesemic tetany, tetanus, strychnine poisoning .
Haemorrhagic diarrhea is found in coccidiosis, hay fever and sudden death in peracute case of anthrax, high fever in foot and mouth disease, rinderpest, trypanosomosis, babesiosis and anaplasmosis.
Prevention and control
Disease transmission can be prevented by vector control. Amblyoma species are three host ticks and each stages remains on host for relatively short period. These ticks are less susceptible to most acaricides than Boophilus.
Frequent acaricidal treatment is necessary to prevent disease transmission as transmission may start within a day after tick attachment.
Dipping or spraying would have to be carried out at least every 3 days. If the acaricide used has a residual activity of 2 days, effective weekly acaricidal treatment will often bring disease incidence to low level. There is no effective vaccine for heart water disease prevention. The method adopted in some countries is to infect and treat. This involves infection intravenously of infective blood into animal to be vaccinated. The temperatures of the infected animals are taken regularly. Animals are then treated with tetracycline as soon as fever occurs. Antibiotics of tetracycline group are active in curing heart water in early stage. Oxytetracycline and clortetracycline have been found effective. Two therapies on consecutive days give a better result than only one treatment.
Suspension formulations administered intramuscularly areknown to give better results in small ruminants than soluble ones. This is possible because their actions are more durable. Sulfonamides possess chemotherapeutic activity against heart water disease but even less than that of tetracycline so that they are now being abandoned. Because of the presence of satisfactory strain of immunization and treatment, introduction of susceptible exotic animals into heart water disease areas must be strongly advised against. The importation can only be done where there is strict efficient acaricidal control.

Lumpy skin disease is divided into two types:
Neethling type is a true lumpy skin disease.
Allerton type is a false lumpy skin disease.
Etiology
This is not separate from sheep pox virus. It is identical to sheep pox virus. It is transmitted by flies. Although it is mild in indigenous cattle, it is severe in exotic cattle. Neethling type was first recognized in South Africa. It is now found to be a disease problem. It is also found in East Africa and Zaire. It has long incubation period of 2-4 weeks. Generally, it is a sporadic disease. Peracute form may kill the animal within 10 days without showing lesions. Lesions when they occur are generalized over the body.
Clinical signs include respiratory distress and pneumonia signs. In very severe case, fever occurs with depression, ocular and nasal discharges. Temperature may drop and shoot up again. Intra-dermal nodules vary in size from 1-5cm in diameter. They differ in size in different animals. There is lymphnode enlargement. The nodules are painful. Other signs are pain all over the body, necrosis of the nodules and sloughing off of the skin. Secondary bacterial infection may set in. in South Africa, attenuated vaccine is used to control the disease. In other parts of the world, no specific drugs are used for neethling type.
Allerton type is a simple disease caused by Herpes virus infection. There is a short incubation period. Skin nodules appear. More severely affected animals develop mild fever and it clears off in about 2 weeks.

This is a viral disease of cattle. If it is acute, very few animals die of it. It last for a few days. The disease has been recognized in Africa, Asia and slightly in Australia. It is transmitted by culicoides, midges and sandflies. There is a seasonal occurrence of the disease. It does not occur every year. Infected animals develop immunity lasting for several years. Insect activity plays very important role in epidemiology. The disease can be a big problem in an area in one year and does not show up again until after about five years. It is a cyclic type of disease and not specifically seasonal. Morbidity rate in exotic breeds is greater than that in indigenous breeds. In some cases, this may approach 100%. The disease may be seen in all ages of animal but more severe in adult cattle. Incubation period varies from 2-10 days and in experimental cases 2-50 days.
Clinical signs
There is oculonasal discharge. There is no erosions, ulcers or nostril blockage. There is high fever because temperature shoots up to 105oF-107oF.
Affected animals are slightly bright despite the high temperature. They are not totally depressed. At the end of the first day, animals are reluctant to work because of severe muscle and joint pains. This is transient. On the second day, the animal is recumbent and reluctant to stand up. There is enlargement of lymphnodes such as prescapular and femoral lymphnodes. On the third day, the animal rises again from recumbency. Milking cows stop milking on second day.
In severe cases, it appears to be inability to swallow. Death can occur if you try to give the animals water. They die of inhalation pneumonia. There is neutrophilia in this disease.
Diagnosis
This is based on clinical signs and recovery on third day.
Control
Vaccination control depends on the economics of the operation.
Treatment
There is no treatment.
For recumbent animals, try to make them stand. Advice farmers to tie the animals up to stand.

This is a viral disease of sheep characterized by fever and generalized pocks.
Etiology
Two types of viruses are incriminated. The viruses are not well defined. One of the viruses is believed to be specific for sheep while the other one affects sheep and goat.
Occurrence
It is endemic in southern Asia, Africa, north of equator and parts of Asia like India, Iran and neighboring countries.
Transmission
The virus specific for sheep occurs when there is direct contact between sick and healthy sheep. Infected dust helps in disease spread. Some virus strains affecting sheep and goats are spread by arthropods. Intrauterine infection occurs. Lambs have been born with pocks lesions.
Clinical signs
Clinical reactions may be peracute, acute or subacute. Peracute infections are seen in indigenous lambs and exotic sheep brought into endemic areas. It is characterized by generalized haemorrhages while spreading cutaneous ulceration and death before pocks develop.
In acute disease, there is fever, ocular and nasal discharge, salivation, papules emerge on mucous membrane and thin skin areas of the body.
Papules are crusted with exudates.
Crusts become scabs and darken. Irritation is intense and self mutilation is common. Death can occur at any stage after the appearance of pocks. Healing of lesion results in permanent scar formation.
Subacute reactions are characterized by low grade fever and lesions appear on restricted areas like head and under the tail.
Diagnosis
This is based on history, clinical signs and post-mortem lesions.
It is also diagnosed using agar gel diffusion test.
Differential diagnosis
Orf
Mange
Cutaneous streptotricosis
Blue tongue
Immunology
Each type of virus induces durable active immunity in surviving animals but there is no cross protection between the two major types.
Live and inactivated vaccines are available. The former is administered by scarification and produces immunity for a long time. The later vaccine produces immunity that last for about a year.
Control
For free areas, ensure their freedom from sheep pox by not importing sheep and goat from endemic areas.
Destruction of infected sheep and goat and vaccination of in-contact sheep and goat is necessary. In endemic areas,  it is recommendable to vaccinate regularly.
Treatment
Systemic antibiotic therapy should be administered.
Keep the animals warm in clean environment.

The malignant poxes of goats which include goat dermatitis or stone pox are characterized by fever and generalized nodular pocks.
Etiology
It is caused by virus. The organisms involved are ill-defined.
Occurrence
Goat pox is endemic in Africa, Asia and Europe where good number of goats are found. It has been reported from Australia and Paraguay South America. Goat dermatitis is found in India and South East Asia.
Species affected
Three viruses are involved in development of goat pox and two of the viruses appear to affect only goats. The third affect sheep and goats.
Transmission
One of the viruses affecting only goats is spread by direct and indirect contact. The others appear to be transmitted by arthropod. The virus affecting sheep and goat is spread by arthropod but the vectors are not known.
Clinical signs
General malaise
Fever
Lacrimation and rhinorrhea
There is papule formation in the skin and mucous membrane. They harden and thicken into circumscribed nodules. Some become unbilicated and exude. The exudates dry to form crust.
Others necrosed and shade leaving shallow ulcers which rapidly encrust.
Irritation can be enormous and self inflicted mutilation is common.
Crust persists for 3-4 weeks and drop off leaving permanent scars.
Diagnosis
This is based on history, clinical signs and lesions.
Biopsy of crusts is examined using electron microscope.
it is also based on isolation and recognition of the virus.
Immunology
Recovered goats are probably immuned forever. Vaccines both inactivated and attenuated are available.
Control
It can be controlled by prophylactic vaccination.

Orf is a benign pox of sheep and goat characterized by formation of centrifugally distributed exuding proliferative lesions. In lambs and kids, the lesions are commonly found on lips and muzzle and in ewes, the teats.
Etiology
It is caused by parapox virus. The disease is found all over the world.
Species affected
It affects domestic sheep and goats. Man is infected accidentally. It has been observed in dogs fed affected unskeamed carcasses.
Transmission
The disease is very contagious.
Clinical signs
The natural disease is proliferative and after a few days of incubation period, papules appear, enlarge and exude. This is followed by crust formation. The scabs are firmly adhered. The scabs fall of 3-5 weeks leaving white scar of new epithelium. There is no fever in this disease. The scabs are centrifugally distributed. In lambs and kids, the lesions cluster around the lips, muzzle and lower limbs. In sucking lambs, tooth eruption may favour development of oral lesions which spread to lips, muzzle. Lesions may also develop at castration and docking site. Outbreaks of induced balanoposthitis and vulvitis can also occur. Mastitis may occur when the teat are infected. The disease is rarely fatal but can cause significant loss in condition when the lesions make feeding very difficult.
Diagnosis
This is based on clinical signs, isolation and recognition of the virus.
It can be diagnosed using immunodiffusion test.
Differential diagnosis
Blue tongue
Labial streptotricosis
PPR
Rinderpest
Foot and mouth disease
Immunology
Animals that are recovered possess circulatory antiboby passed to the young in the colostrum. Majority of infected animals are able to resist the infection if re-exposed.
Prevention and control
Orf appears to be endemic in most flocks. Prevention is difficult. Live vaccines are commercially available. Antibody therapy, removal of scabs and application of antibiotic cream or iodine or antibiotic ointment is necessary.
Systemic antibiotic can be given to animals.

Laboratory amphibians include leopard frogs, African clawed toads and marine toads.
Not much is known about this class of animal. They are important especially in some schools where they are extensively employed in studying or teaching biology. Good husbandry and adequate feeding are recommended. It is our duty to observe their diseases and document them for future generation study.
This is a bacterial disease found in malnourished amphibians.
Etiology
It is caused by Aeromonas hydrophila. It is a facultative organism but under poor condition lead to clinical signs. Clinical signs are lethargy, weight loss, ulcers on skin, nose and toes, pinpoint haemorrhages on legs, abdominal tissues and nictitating membrane of the eyes. These clinical signs and lesions are characteristic.
Post-mortem lesions
There are haemorrhages of skeletal muscles, tongue and nictitating membrane.

This is an acute highly contagious viral disease of cattle and also sheep, goat, pigs, camels and buffalos. The disease is characterized by high necrotic stomatitis, gastroentreritis and fever.
Etiology
This is caused by paramyxovirus which is antigenically related to PPR, canine distemper and human measles virus.
Distribution
The disease is endemicin tropical Africa and Asia. It has been reported in Middle East.
Transmission
Transmission is by contact between infected/carrier animals and healthy ones. The virus is present in nasal and oral secretions, urine, faeces and expired air. Infected droplets are inhaled and the virus enters the body through the upper respiratory mucosa. Infection can be acquired by ingestion of contaminated feed and water.
Epidemiology
Cattle are susceptible to the disease but also pigs, bufallos, camels, sheep and goats. The later animals are relatively resistant but do not contract the disease in the field. Faeces, urine and discharges from the infected animals are infectious and transmission readily occurs. Close contact of infected and susceptible animals is necessary for transmission; aerosols and insects are most unlikely method of spread. Contaminated premises may be infectious for 6-8 hours after removal of affected animals. Contaminated urine without ventilation or sunlight may remain infective for 96 hours because rinderpest virus is very sensitive to environmental conditions and easily killed by heat and drying and by most disinfectants. After natural infection, animal develop protective immunity for a long time but the immunity is not lifelong. Other infected animals like camels, sheep, goats and bufallos may spread the infection to cattle if they are together.

This is a highly contagious acute febrile disease of cloven footed animals. It is characterized by vesicle formation on the tongue, mouth and in the rumen, teat and mammary gland and feet especially on the margin of the hoof in young animals. Degenerative changes occur in skeletal muscles; also extensive involvement of the cardiac muscle resulting in death. Human infection has been recorded but it is rare.
Etiology
It is caused by picorna virus (small RNA). There are 7 strains of the virus made of 3 standard or European strain and they are types O, A, C. others are African strains SAT1, SAT2 and SAT3 (sudan African territories type). The 7th strain is the Asian one found in far East. Each strain is made of many substrain which are antigenically different.
Distribution
Foot and mouth is widely distributed throughout the world and has been reported in almost all countries except Newzealand. The disease is endemic in Philipines, Africa, Europe, South America and Asia. The disease was last reported in USA and Australia about 75 years ago.
Epidemiology
Foot and mouth disease virus is found in body fluids, for example, milk, urine, faeces, saliva, blood and semen. The virus is most stable between PH 7.4 and 7.6 and rapidly destroyed by acid or alkali. It survives below 40C and may be stored for many years at temperature below freezing. It is resistant to heat. Most field strains are inactivated by heating at 560C for 30 minutes but a number of laboratory strains have shown ability to resist even 80oC for several hours. The disease spreads extremely readily when atypical type of virus appears in an area which it has not been affected before and so spread proceeds very rapidly. In the tropics, it is likely that spread takes place mainly by direct contact between animals. All formites are infective and contaminate the environment of an infected animal. Airborne spread can take place in temperate countries over considerable distances. In the tropics, airborne spread is likely to be limited to the night time when humidity is high. Since the virus can survive on material commonly found close to the animals like hair, straw, water and feed. Movement of material can lead to spread of the disease.

This is a viral infection of sheep and occasionally goats and cattle but mild infection. At least 16 strains of the virus are known. Disease is transmitted by culicoides. Disease is non-contagious and characterized by congestion of the hoof tissues, nasal and oral mucosae and and stiffness arising from muscle degeneration.
Distribution
Disease is endemic in many African countries like Tanzania, Morocco, South Africa, Sudan, Chad, Nigeria, Central African Republic, Zimbabwe and Kenya. Other affected countries are Cyprus, Middle East, USA and Spain.
Clinical signs
There is rise in body temperature which may be sudden or gradual. Temperature may fluctuate for a number of days. High temperature is ensued by hyperaemia of the nasal and buccal mucosae.
Later, it is accompanied by salivation and frothing at the mouth caused by peculiar and persistent licking movement of the tongue. The frothing around the lips is followed by appearance of watery discharge from the nostrils which become more prolific, mucocatarrhal and mixed with blood. Later on, the lips and tongue swell, the face only to a variable extent. The color deepens and small petechial haemorrhages appear on the mucous membrane of the mouth, muzzle and conjunctiva. This discoloration may deepen to an almost purplish blue from which the appearance of the tongue give rise to the description of the disease.
The lips or muzzle epithelium thicken and shade off. More severe changes may be observed in mouth where the gum, cheeks and tongue mucosae ulcerate leaving exposed irregular and haemorrhagic surface. As a result, saliva becomes mixed with blood and has the most offensive odour because of the presence of necrotic tissue. In a mean time, the nasal discharge has become purulent and dries leaving a crust around the nostrils.

This is a rinderpest-like viral disease of small ruminants like goats and sheep. Goats are more susceptible than sheep. The dwarf breeds of goats and red sokoto goats are known to be very susceptible to the infection. The disease is found in West Africa although it has been reported in the Middle East.
Etiology
The disease is caused by RNA virus belonging to the genus Morbillivirus. Morbilli means measles and the family paramyxoviridae. The virus is antigenically related to rinderpest, human measles and canine distemper virus.
Distribution
The disease is endemic in West Africa. It has been reported in the Middle East.
Transmission
The mode of transmission is by aerosols. Infection spreads readily when healthy and infected animals are in close contact. It is also possible by ingestion of contaminated food and water.
Clinical signs
The following are the clinical signs:
Fever
Anorexia
Shivering
Serous nasal discharge which later becomes mucopurulent
Erosions/ulcers in mouth; oral scabs
Coughing and fast breathing due to secondary pneumonia
Increased salivation
Emaciation and dehydration
Severe diarrhea

This is a viral disease of horses and also affecting cattle and pigs. Sheep are resistant. It is characterized by development of vesicles in mouth and at times on feet.
Etiology
It is caused by Arbovirus. Three strains of the virus are transmitted by mosquitoes mainly Aedes mosquitoes. Wild animals are reservoirs.
Epidemiology
Morbidity is low about 5% and mortality is zero. It is mainly seen in north and South America. One or two cases have been reported in South Africa. There is seasonal incidence of the disease. It disappears during winter. Outbreaks are not extensive.
Clinical signs
There are vesicles on the tongue dorsum, dental pads and lips. Vesicles may or may not develop. There is excessive salivation. Lesions appear on the teat only when they are being milked. Foot lesions are rare in cattle. There is quick recovery after 3-4 days. Animals become bright and milking cows milk normally. In pigs, lameness is common. Vesicles may be present on the snout. In horses, lesions are limited on tongue and lips dorsum. Immunity lasts for 6 months and then wanes. Immunity after infection is absolutely solid.
Treatment
Not necessary.
Control
Do not introduce animals from infected area.
A live vaccine is available for protection. The disease does not occur in Nigeria.

This is an almost invariably fatal disease in cattle characterized by fever (high body temperature), weakness, keratitis, dejection, profuse ocular and nasal discharges and encrustation, drooling of saliva, photophobia, erosion and diphtheresis of mucous membranes, generalized lymphoadenopathy, skin lesions and occasional cystitis and nervous involvement. The pathological lesions which affect all organs and tissues are cellular infiltration, necrotizing vasculitis and superficial necrosis of epithelial and mucous surfaces. The pathogenesis of the disease is unknown. In certain parts of East, Central and South Africa, the disease arises due to cattle acquiring infection from clinically normal wilder beast. The causal agent in these areas is the herpes virus. In other parts of Africa and elsewhere in the world, the etiology has not yet been established. The reservoir host in other areas is the sheep but the evidence is not conclusive. The diagnosis is based on its clinical signs and pathological features. Occasionally, transmission may help to confirm the disease.

This disease is limited to the teat skin of mammary gland. It is caused by poxvirus. It is a benign infection. Affected cows do not allow themselves to be milked because of pain. It predisposes cows to secondary mastitis; sometimes may cause hyperaemic lesion around it. It resembles bovine papular stomatitis.