This article throws light upon the ten main diseases caused due to bacteria in animals. The diseases are: 1. Fowl Cholera 2. Haemorrhagic Septicaemia 3. Pasteurollis of Sheep, Goat and Swine 4. Glanders and Farcy 5. Caseous Lymphadenitis of Sheep 6. Johne’s Disease 7. Joint-Ill Spirochaetosis (Dog) 9. Spirochaetosis (Fowls) 10. Strangles.
Contents
- Disease # 1. Fowl Cholera:
- Disease # 2. Haemorrhagic Septicaemia:
- Disease # 3. Pasteurollis of Sheep, Goat and Swine:
- Disease # 4. Glanders and Farcy:
- Disease # 5. Caseous Lymphadenitis of Sheep:
- Disease # 6. Johne’s Disease:
- Disease # 7. Joint – Ill:
- Disease # 8. Spirochaetosis (Dog):
- Disease # 9. Spirochaetosis (Fowls):
- Disease # 10. Strangles:
Disease # 1. Fowl Cholera:
Synonym:
Avian Pasteurollosis, Avian H. S.
Definition:
Fowl cholera is a highly infectious and contagious disease of fowls—usually of a septicaemic nature—and frequently occurring in epizootic form caused by Pasteurella aviseptica, which resembles other bacilli of the Pasteurella group. The other name of Pasteurella aviseptica is Pasteurella multocida.
Species Susceptible:
Fowl, geese, ducks, turkeys, guinea fowl, pigeons and many other birds including wild birds. All birds can be infected artificially, death occurring in 24 hours.
Modes of infection:
In the natural infection, the organisms probably enter the tissues through the mucosa of the upper air passages but the infection may occur through the conjunctiva and occasionally through the intestinal mucosa after ingestion of contaminated food and water.
Infection by direct contact with diseased birds is also possible.
Pathogenesis:
The bacilli first multiply through the tissue around the site of infection and they enter the blood where they multiply and increase in number. They exert a pathological action by means of a present toxic substance which causes a rise of body temperature and lethargy and by injuring the vascular walls gives rise to haemorrhage and effusion of blood in the serous cavities. This development is purely of septicaemic nature.
In other cases, the septicaemia is not fatal but subsides and the bacilli settle in different organs, specially liver, giving rise to inflammatory necrotic processes. In other cases, the bacilli after entering the blood—are carried directly to organs, where they set up similar inflammatory processes without multiplying in the blood.
In this way are produced chronic cases of fowl cholera with extensive necrosis of liver and joints. Such cases frequently appear at the end of an outbreak and also among birds which only attain medium degree of immunity after protective inoculation.
Postmortem lesions:
In acute cases, serous or sero-fibrinous pericarditis, petechial haemorrhage on the pericardium along the coronary groove. White necrotic foci over the surface of the liver and usually an acute haemorrhagic enteritis, specially in the duodenum, the contents of which are blood-stained. The lungs are usually congested and oedematous and there may be pneumonia with fibrinous deposits on the surface of the lungs. The spleen is usually normal.
In chronic forms, the lesions are localised to the head, the wattles, in particular, being swollen or oedematous, or shrivelled and sunken and containing cheesy substances.
In some chronic and sub-acute cases, changes are sometimes observed in the ovary, the ova are soft, flabby and frequently rupture. Dried, cheesy yolk – like material is found distributed over the abdominal organs.
Course:
Acute, chronic and mild forms occur. In acute form, the course is of a few hours only and in other forms, it is from 6 days and over and may last for several weeks or months.
Incubation period:
In a natural infection, the period varies from 12 hours to 3 days. The disease is usually acute in the beginning of an outbreak and becomes milder and more chronic as the progress of the disease goes.
Symptoms:
In per-acute cases, symptoms are almost entirely absent. If there is a chance to see a sick bird falling to the ground while running or while sitting on a perch, and—after beating their wings a few times—breathes its last.
However, in great majority of cases (acute form), the birds become apathetic and sit hunched up and trembling with their heads tucked under wings or bent backwards; or they stagger about with drooping wings and sunken heads. The temperature rises to 108° F (42.2°C) to 110° F (43.3°C) or more, which remains so till shortly before death. The appetite is completely lost and thirst increased.
Frothy mucus exudes from the nose and beak and the birds sometimes vomits grayish yellow shiny masses. The beak, comb and wattles become purplish in colour. There is usually severe diarrhoea. The faeces is greyish yellow and pulpy and later fluid and of a dark green or red colour mixed with flakes resembling coagulated albumin and has an offensive odour. The hinder parts of the body are soiled with faecal discharges. The feathers are ruffled and draggled.
The birds breathe with their beak open, both inspiration and expiration are accompanied by rattling sounds, specially in cases complicated by pneumonia. Later, the birds sit in a state of stupor with closed eyes and are seen to stand apart from the rest awaiting death which occur either after convulsion or in coma.
In chronic and mild form, the symptoms are slowly increasing anaemia, emaciation followed by obstinate diarrhoea. In other cases, the disease is localised to the head and some other organs.
Mortality:
In acute cases, about 95 per cent. Chronic cases often recover and remain as a carrier.
Diagnosis:
Postmortem lesions, specially the pericarditis are diagnostic. But to confirm the diagnosis, microscopical examination of the blood smear must be done. Injection of blood or tissue suspension of dead birds into pigeons is also diagnostic. If it is a fowl cholera, the pigeon dies within 24 hours and bipolar organisms can be detected in the blood of dead pigeon and also in tissue fluids.
If the material is suspected to be contaminated, then it should be applied to the conjunctivas sac of a healthy fowl. Death will result in about 18 to 24 hours if it is fowl cholera.
N. B.:
It must be remembered that pigeon is not susceptible to fowl plague and is only slightly to fowl typhoid.
Treatment:
If desired, the infected birds and those suspected to have been infected should be treated with immuned serum. In birds affected with the disease, the serum should be given intravenously. Methylene blue 0.8 gr XV in 12 to 20 litres of drinking water or 10mg gr 1/6 to 3mg gr ½ per bird in the form of pills are also known to give excellent results.
Sulphamezathine 0.5% in mash or 0.1% in drinking water reduces mortality in an outbreak by 50% to 75%. This treatment also permits development of a resistance to the disease in the treated flocks.
Prophylaxis:
Fowl cholera serum and vaccine in 5 and 1 ml dosage respectively is to be given simultaneously to each adult bird. The dose should be reduced proportionately in younger birds.
Healthy birds should be isolated and all sick birds destroyed and burnt with all dead birds. The runs and houses should be thoroughly disinfected. New arrivals should be isolated.
Disease # 2. Haemorrhagic Septicaemia:
Synonym:
Barbone.
Definition:
H. S. is an acute, occasionally subacute, infectious disease of a septicaemic nature in acute form affecting cattle and buffaloes, characterised by acute gastro-enteritis and extensive subcutaneous oedema and by acute Serofibrinous pleuropneumonia with oedema of the interalveolar tissue caused by Pasteurella multocida—boviseptica in cattle and bubaliseptica in buffalo.
Incidence:
H. S. in cattle occurs in nearly all countries, specially in tropical region. It is mostly prevalent in low lands subjected to periodic inundation and usually during and after the monsoon.
As has already been stated under Pasteurellosis, the organisms remain in the bodies of healthy animals as harmless saprophytes, specially in the upper air passages from where they invade the tissue and blood of their host when the resistance power of the host is lowered. The disease then spreads to other animals with low and reduced resistance. Eventually, the virulence of the organisms may be so increased as to affect comparatively resistant animals too.
Animals susceptible:
The disease occurs mainly in cattle and buffaloes, sheep, swine and other wild ruminants. It mainly affects young animals.
Modes of Infection:
Infection of non-carriers usually takes place by ingestion of contaminated food and water. It has occasionally be observed to infect through cutaneous lesions or through lesions in the naso-pharynx and also through the agency of ticks, fleas, lice and flies, as well as, mosquitos.
Experimental feeding of cultures infects only a small proportion of bovines, but minute doses of culture given subcutaneously or intravenously infect cattle with dead certainty.
Postmortem lesions:
The unopened carcass is negative exceptions the oedematous form where subcutaneous oedema of the head, neck, throat can be seen.
In very acute form with death in a few hours, petechial haemorrhages in the tissues and on the membranes and enlarged lymphatic glands.
On the average acute case, there is a clear yellowish or blood stained serous or serofibrinous exudate in the subcutaneous tissue of the head, throat, dewlap and thorax. Oedema of the buccal and pharyngeal mucosa and swelling of the tongue may be present. There is also present a severe gastroenteritis of a haemorrhagic nature with blood—stained intestine. Petechial haemorrhage on the tissue and membranes and enlargement of the lymphatic glands are very characteristic of both the forms. There is also a characteristic haemorrhagic endocarditis and sometimes a sero-fibrinous pericarditis. The spleen is usually normal excepting for the petechae of the capsule.
In the pectoral or thoracic form, the thoracie-cavity contains a serous infiltration or sero-fibrinous exudate with visceral pleura studded with haemorrhage. The lungs are oedematous with areas of red or dark brown consolidation, sometimes with small dry necrotic areas, which are prominent in some acute form.
The interlobular septa are yellowish white and are very prominent due to distension with serous fluid which escapes when the organ is incised. Due to thickening of the interlobular septa; this gives lung a typical and striking marbled appearance.
Incubation period:
6 hours to 2 days or even up to 5 days.
Symptoms:
Rapid rise of temperature (104° F or 40°C to 106° F or 41.6°C) with severe systemic disturbances and constipation. Later on, symptoms of colic appear, followed by evacuation after much straining of pulpy faeces which finally becomes thin fluid often containing flakes
of fibrin or mucus and sometimes blood. In the oedematous form, the head and neck, specially in the region of the throat and dewlap, as well as, thorax becomes swollen, which is tense, hot and painful.
The buccal membrane is oedematous and the tongue swollen rendering deglutition difficult and often impossible. The tongue may be swollen to such an extent as to fill the mouth and even protrude between the teeth and is of dark purple or reddish brown in colour. The respiration is laboured and often stertorous, all the visible mucosa are cyanotic and often studded with haemorrhage. Eventually, death takes place either from asphyxia or from exhaustion due to severe gastroenteritis.
In the pneumonic form, the characteristic symptoms are prostration, drooping ears, congested or haemorrhagic mucosa and there is complete loss of appetite and milk yield ceases. There is severe dyspnoea and is marked by extended head, open mouth and protruded tongue. Bloody diarrhoea is common and then may be haematuria.
Course:
In septicemic form—12 to 36 hours and in oedematous and pectoral form, about 3 to 6 days or still longer in some cases.
Mortality:
Recovery rare, — about 85% to 95% death rate.
It may be noted that the feature of this disease is that outbreaks frequently subside spontaneously.
Diagnosis:
Postmortem lesions supported by microscopical finding of the organisms. Rabbit injected with a tissue suspension or recently isolated tissue culture from a diseased animal dies within 48 hours and usually shows a very characteristic Haemorrhagic Tracheitis. Bipolar organisms are readily demonstrated in the rabbit’s blood.
The diagnosis of H. S. is really confusing. Because the normal habitat of the bacillus is on the mucosa of upper respiratory passages, so that its presence in the tissues of dead animal is not conclusive evidence. Secondly, a bacteriological examination of the animals died of this disease may be negative.
Treatment:
Affected cattle recover quickly if treated early with almost any common antibiotic or Sulphonamide. One treatment is sufficient but severely affected animals should be treated for 3 to 5 days. The choice of antibiotic or Sulphonamide will depend on economics and success rate in a particular area.
The following schedule may be followed:
Mass Medication:
Sulphamethazine:
100mg/kg B. w. in drinking water daily for 7 days.
Oxytetracycline:
3.5 mg/kg B.w. in Cattle feed for 7 days.
Prophylaxis:
Isolation, disinfection and disposal of carcasses should be carried out on the same line as that of Anthrax.
In the actual outbreak, the unaffected animals should be protected by H. S. serum—
Dose table — Cattle — 5 ml to 20 ml
Buffalo — 20 ml and upwards
Immunity is of short duration, approximately 2 weeks, so inoculation should be repeated if the outbreak continues for a prolonged period.
Immunity lasting about for 2 months may be produced by subcutaneous injection of H. S. Vaccine.
Dose table:
Cattle + Buffaloes — 5 ml below300 kg body weight and 10 ml from 300 kg and over.
N. B:
The vaccine should not be used during an outbreak. It is advisable to use the vaccine on animals in areas where there is a seasonal incidence of the disease, sometimes before the appropriate time of an outbreak.
Disease # 3. Pasteurollis of Sheep, Goat and Swine:
P. multiada (Types A and B) acting and secondary invader following enzootic pneumonia in pigs. P. haemolytica is the common cause of pleuro – pneumonia in sheep. Very young lambs and kids are more susceptible to P. haemolytica than adults.
Haemorrhagic Septicemia of Sheep:
Symptoms:
Animal dying of this disease shows the symptoms of general infection with extensive subserous and submucous haemorrhages on postmortem examination. The animals which survive longer the pneumonic form develops. Dullness and a discharge from the nose and eyes may be observed. There is no gastroenteritis and the temperature may remain normal.
Prophylaxis and Treatment:
Same as that has been advised for cattle.
Haemorrhagic Septicemia of Swine (Swine Plague):
Definition:
A sporadic enzootic pneumonia of swine caused by P. Suiseptica. It may be acute or chronic.
Symptoms:
The incubation period is from 4 days to 7 days. The onset is sudden and is marked by high rise of temperature and complete loss of appetite. Cough and dyspnoea are observed. It is characterised by catarrhal pneumonia and the prognosis varies according to surroundings, virulence of the infection and the age and resistance of animals.
Postmortem lesions:
Various stages of pneumonia are present. Hepatisation of cardiac and apical lobes, necrotic foci on-lungs and serous infiltration of the interlobular connective tissue may be seen.
Diagnosis:
Aqueous suspension of diseased tissue carrying P. Suiseptica injected subcutaneously to rabbit kills it in a few hours. Smears from heart blood of dead rabbit and stained with carbol-fuchsin may reveal bipolar organisms.
Treatment:
The treatment advised for pneumonic pasteurollis of cattle are equally effective in swine, sheep and goats. Penicillin has been described as a successful treatment in goats.
Disease # 4. Glanders and Farcy:
Synonym:
Malleus, Farcin, Gitty (Vernacular).
Definition:
Glanders is a contagious and usually chronic infective disease of the solipeds characterised by the formation of nodules and ulcers on the mucosa, skin and internal organs, specially the lungs, which exhibit a tendency to break – down and form ulcers and caused by Pfeifferella mallei.
Bacteriology:
Pfeifferella mallei is a straight or slightly curved, non-motile, non-sporulating rod – shaped organism with either rounded or somewhat pointed ends measuring 3 to x 0.5M. It is best stained by Loeffler’s alkaline Methylene blue.
The bacillus possesses only a slight resistance to external influences living outside for 3 to 4 months. Sunlight kills it in 24 hours, heating to 55° C in 10 minutes and the usual common disinfectants in half an hour.
It lives for about 20 days in clean water and probably not more than 6 weeks in contaminated stables. It does not multiply or live long outside the body.
Glanders is essentially a lymphatic infection, hence the organism cannot be found in blood (excepting when these are being carried by the blood to the seats predilction). They are abundantly found in all the lesions.
Animals Susceptible:
The disease is common in equines. Asses are more susceptible and the disease in these animals is nearly always acute. The horse is somewhat less susceptible and runs a chronic course in these animals, sometimes extending to several years, ultimately resulting in death. The mules occupy an intermediate place in susceptibility.
Man and even wild or domesticated carnivores also get the disease by ingestion of infected flesh and milk and also by inoculation. Cattle are immuned. Glanders in man is a distressing and nearly always fatal disease. Stable men, laboratory workers handling infected material or pure cultures of the bacilli are specially liable to infection, so that, every precaution must be taken. In fact, Glanders bacillus is the most dangerous of all disease-producing bacteria cultivated.
Modes of Infection:
In the majority of cases, by ingestion of food and water contaminated with discharges or excretions of diseased animals. In a few cases, it may occur through the pharyngeal mucosa. Infection through skin abrasions is also possible, but is comparatively rare. Droplet infection appears to be unusual.
Incubation period:
In the horse, there is probably a minimum period of 2 weeks but it may take 2 or 3 months or longer.
Symptoms:
As has already been told, glanders is primarily a disease of the lungs but has a tendency to localise also in the nasal mucosa and in the skin (Farcy). Involvement is usually chronic and presents no characteristic symptoms until it is far advanced.
For descriptive purposes, the symptoms are divided into three different types according to organs involved:
(a) Pulmonary type:
This form, usually turned as latent or occult glanders, may exist for months before any clinical symptoms are manifested and, when they appear, the symptoms are not – characteristic. These consist of gradual emaciation, loss of strength, dry cough with or without periodical rise of temperature. In advanced cases, there is often a blood – stained mucous expelled during coughing (which is highly infectious when fresh) and the hide appears to adhere to the ribs (hide – bound). This is usually followed by the affection of the nose or skin, or both.
(b) Nasal glanders:
This type too, may exist for a long time with only indication of a slight serous discharge often intermittent from one or both nostrils. As the disease progresses, the discharge becomes mucoid, then muco-purulent and finally purulent with a glistening oily look often streaked with blood. The discharge adhere tenaciously to the allae and surrounding area and may be thrown out from the nasal cavity in large quantity by coughing or snorting.
The inflammatory process in the beginning is in – distinguishable from ordinary nasal catarrh. Later on, small nodules covered by glistening epithelium develop, which soon break down and form minute ragged-edged ulcers with red bases. These coalesce rapidly to form large deep ulcers with a yellowish lardaceous bases and sharp but irregular edges.
At this stage, there may be a persistent bleeding from the nose if the animal is walked. Some of the ulcers may heal which are noticed by the formation of reddish or whitish irregular radiating cicatrices.
The inflammation of the sub-maxillary lymphatic gland is highly significant in glanders. The gland involved always correspond to the side of nasal passage affected. In the early stage, it is enlarged, painful and movable but soon shrinks, becomes indurate and knotty and is attached securely to the surrounding tissues and bones, when it becomes painless and has no tendency to break – down and suppurate. Nasal lesions are usually unilateral.
(c) Cutaneous type (Farcy):
Farcy is usually a chronic lymphangitis and lymphadenitis which usually affects one or more limbs, specially the hind ones. Small round nodules (Farcy buds) up to the size of a walnut occur singly or in chains in the subcutaneous tissues along the course of lymphatics. These buds soften, form abscesses, rupture and discharge an oily pus, leaving ulcers with ragged borders.
The superficial lymphatics near the buds become swollen and thickened (Farcy cords) and further buds are formed along their course. The lymphangitis may give rise to elephantiasis. Similar lesions may occur on the face, neck, sides of thorax and under surface of abdomen.
The nodules of the skin are surrounded by an area of oedema and eventually results in a doughy painless swelling involving the lower abdomen, the lower thorax and the limbs.
Diagnosis-(Microscopical):
Animal inoculation and allergic test.
Animal Inoculation:
Artificial inoculation produces a local lesion in 3 to 5 days. Guinea pigs are very susceptible, the male species is used for diagnosis. The animal is injected intraperitoneally with infective material. Orchitis and pus formation in the tunica vaginalis are produced in 2 or 3
days. Contaminated materials are better given subcutaneously than intraperitoneal.
One must find the organisms in the lesions of the guinea pigs culturally and microscopically before giving any diagnosis, but there is no difficulty in demonstrating them. This test is known as “Straris test” for glanders.
Allergic test:
The fact that in glanderous infection—as in tuberculosis—the tissues are affected by an allergic condition which is manifested by increased sensitivity to the toxins of the bacilli is utilised for diagnostic purposes by use of the toxins of the bacilli termed as Mallein.
Mallein is prepared from culture of glanders bacilli and contain the toxic substance dissolved in a glycerine containing fluid medium which may be introduced into the subcutaneous connective tissue (Subcutaneous mallein test), or cutaneous or skin (I. D. P. or cutaneous test) or applied to the conjunctival ophthalmic or conjunctival test).
Subcutaneous test:
The animal which is to be tested must be rested for a day and then its temperature taken morning and evening for two days. If the animal does not exhibit an unusually high temperature and maintains a regular morning and evening variation, it may be put to test.
The most convenient site for injection is a point estimated to be at the junction of two imaginary diagonal lines drawn across the area following the side of the neck, preferably the near side, which should be clipped in the form of a patch, about 10 inches square and some weak antiseptic applied.
The most convenient time for injection is 9 p.m. of the 2nd day. The dose for Mallein is 1ml injected subcutaneously at the centre of the clipped patch.
The temperature is to be taken just before the injection and then on the 9th, 12th, 15th and 24th hours afterwards. Then the morning and evening temperatures are to be taken on the day following and all recorded on a chart. A rise of 2° F or more above the normal daily fluctuations prior to the injection, points to a positive reaction, provided there is also a local reaction at the site of injection.
In a positive reaction case, the local reaction takes the form of a hot, tense and extremely painful swelling, which usually appears within 24 hours and tends to increase in size until the 48th hour, which persists for 2 to 3 days or even more and then gradually disappears. The swelling is a circumscribed one with raised edge and usually measures 8 cm to 10 cm but may measure up to 16 cm in diameter.
In normal animal, the swelling is not so conspicuous at any time and tends to disappear quickly after 24 hours, there may be no swelling at all.
N. B.:
This test must not be repeated before 3 weeks at least.
Intradermo-palpebral or cutaneous test:
This test is also termed as “Intra-dermal and Intracutaneous test”.
This test may be undertaken independently or in concurrence with the subcutaneous test to furnish corroborative evidence to the results obtained from that test.
This test consists in injecting 0.1 ml of a concentrated mallein with a fine sharp hypodermic needle into the cutaneous tissue closely attached to the epidermis near the rim of the lower eyelid about ¼ inch (0.6cm) from the inner can- thus. When the injection has been properly done, there will appear a minute circumscribed swelling (about 3/4 the size of a small pea) at the seat of injection after the needle is withdrawn.
The positive reaction is indicated by a marked swelling, usually of both the eyelids and which frequently extends down the face, marked conjunctivitis, photophobia (which may be present even 72 hours or longer after the injection) and a discharge from the eye, first artery and later mucopurulent, which tends to collect on the skin below the inner canthus.
There is constant blinking of eyelids, the eyelashes become matted together with discharge and the orbital opening much diminished in size. These changes are usually apparent within 24 hours after the injection but sometimes they are not distinct until between 24th to 48th hour and may persist for 3 or 4 days.
N. B.:
This test may be repeated in a few days in the opposite eye in case of a negative result.
Ophthalmic or Conjunctival Mallein Test:
This test consists in instilling about 0.2 ml of the concentrated mallein with an inoculation syringe without a needle or with a dropper into the inner angle of the lid sac of a normal eye. Animals under test should be rested, free from influenza colds and other conditions affecting the conjunctiva.
The positive reaction is manifested by the appearance of a purulent conjunctivitis in about 15% to 75% cases, also a rise of temperature over 101.5° F, sometimes associated with lassitude and loss of appetite. The reaction commences after 2 to 4 hours, reaches its maximum after 12 to 24 hours and subsides after 24 to 36 hours. Occasionally, the reaction does not appear till 24 or even 72 hours after instillation.
In case of a negative result in an otherwise suspicious case, it is advisable to repeat the test on the following day on the same eye which has been sensitized by the first test, when, if glanders, the reaction usually appears earlier and this time, more definitely. It is claimed that this test reveals 90 to 100 per cent of latent glanders.
Postmortem lesions:
For skin and nasal lesions, refer symptoms.
The respiratory organs are almost always affected. In the lungs are sometimes formed tubercle-like nodules arid sometimes broncho-pneumonic foci. The nodules are gray and transparent on the side and yellowish gray in the centre, vary in size from pinhead to a hemp seed surrounded by a red areola. Later these nodules may become gritty due to calcification. Pleurisy is not uncommon, the pleura being covered with fibrinous deposits.
The lymph glands in the region of the affected organs are usually involved but they rarely form abscesses and burst as in Strangles. On the other hand, they become hard and fibrous and, in case of the sub-maxillary gland, it is dense and irregular on the surface and firmly adherent to the bone and surrounding tissues. On section, it shows numerous cheesy foci, white in colour and surrounded by red zone.
Prevention:
Glanders and Farcy act.
All animals showing clinical evidence of glanders must be destroyed after Mallein test and, if necessary, the stables, utensils, harness etc. must be thoroughly disinfected. All in contact of animals must also be subjected to Mallein test and reactors destroyed.
Disease # 5. Caseous Lymphadenitis of Sheep:
It is a chronic disease of sheep characterized by the formation of abscesses in lymph nodes and exerting little effect on the general health of the sheep unless the disease becomes generalised.
Etiology:
Corynebacterium pseudotuberculosis is the specific cause of the disease. It is also the cause of Ulcerative Lymphangitis of cattle and horses and Suppurative Arthritis of lambs and Orchitis of rams.
Mode of infection:
Caseous lymphadenitis reaches its peak in adult sheep at each sharing. The source of infection is the discharges from ruptured lymph nodes. Contamination of soil on bedding grounds or in shelters may result in persistence of the organism in the environment for long periods.
It is assumed that infection occurs via wounds created by shearing, docking and castration. However, there is at least one other important source of infection, the sheep dip. The bacterium can survive in commercial sheep dips for at least 24 hours, and infection can occur through intact skin.
Pathogenesis:
Spread of infection from infected skin sites leads to involvement of local lymph nodes and the development of abscesses.
Clinical findings:
There is palpable enlargement of one or more of the superficial lymph nodes. Those most commonly affected are the sub-maxillary, prescapular, prefemoral, supra- mammary and the popliteal nodes. The abscesses commonly rupture and thick, green pus is discharged.
Diagnosis:
Palpable enlargements of peripheral lymph nodes in a flock of sheep are usually due to this disease. The caseous greenish pus is diagnostic. Examination of pus for the presence of corynebacterium pseudotuberculosis is the usual laboratory aid available.
Morbid Anatomy:
Caseous abscesses filled with greenish yellow pus occur chiefly in lymph nodes and to a lesser extent in interval organs. In the early stages, the pus is soft and pasty but in the later stages it is firm and dry and has a characteristic laminated appearance. Diffuse Broncho-pneumonia with more fluid pus may also be present.
Treatment:
Although the organism is susceptible to Penicillin but treatment is not usually attempted. The local formation of abscesses is unlikely to respond to other than surgical treatment and the usual non-progressive nature of this disease makes treatment unnecessary in most cases.
Disease # 6. Johne’s Disease:
Synonym:
Paratuberculosis enteritis of cattle, chronic bacterial enteritis of cattle, chronic pseudo-tuberculosis enteritis of cattle.
Definition:
It is a chronic infectious disease of cattle manifested clinically by periodical diarrhoea and progressive emaciation and caused by Mycobacterium paratuberculosis or Johne’s bacillus—an acid alcohol fast bacillus resembling T. B. bacillus—Mycobacterium tuberculosis.
Bacteriology:
The organism is a small non- mobile, non-motile, acid-alcohol fast bacillus, measuring 1µ to 2 µ x 0.3 µ to 0.5 µ. In tissues, they usually occur in clusters or clumps. They stain by Ziehl-Neelsen method like T. B. bacilli.
Animal susceptible:
It is commonest in cattle but also occurs naturally in buffaloes, sheep, goat and deer. It is not common in animals under 18 months old and the most susceptible is between 3 to 6 years. On account of the long period of incubation—from 6 month to a year—clinical symptoms are rarely met with until the animal approaches maturity.
Course:
Following an infection, the disease usually remains latent for months or years and symptoms usually do not appear until precipitated by parturition or some other circumstances which lower the animal’s resistance.
Modes of infection:
By ingestion of contaminated food and water.
Pathogenesis:
After the bacilli reach the intestinal canal, they penetrate the mucosa and submucosa and give rise to chronic enteritis. Here the organisms cause the infiltration with specific granulation tissue consisting chiefly of epitheloid cells but all containing giant cells, lymphocytes and polymorphs, as a result of which the mucosa and submucosa become greatly increased in thickness and the villi present a club – shaped appearance.
Postmortem lesions:
The carcass is extremely emaciated. The mucosa of the affected portion of the intestine, most commonly the Ileum, specially in the region of the Peyer’s patches, is 4 to 5 times its normal thickness and raised in irregular folds resembling the cerebral convolutions and coated with greyish white or greenish mucus and studded with small haemorrhagic patches and areas of erosions. The corresponding mesenteric glands are in most cases enlarged. Peyer’s patches are swollen and sometimes red and thickened.
Incubation period:
It varies up to 2 years.
Symptoms:
The initial symptom is gradual emaciation without exhaustion as seen in T. B. and reduced milk production. A few weeks or months later, the characteristic symptoms appear which are periodical and often painless evacuation of foetid, semifluid or watery faeces, mixed with gas bubbles and flakes of mucus, which soil the posterior region of animal and the floor, followed at a later stage with pallor of mucous membranes. There is little disturbance of appetite but there may be increased thirst.
Gradually, the diarrhoea becomes frequent and of longer duration. The emaciation and anaemia reach a high degree, the hide becomes bristly and the skin leathery. Oedematous swelling, develop in the sub-maxillary region and death occurs after long period of agony.
In rare cases, diarrhoea is absent, but fatal emaciation and anaemia develop in the same way and present similar postmortem lesions.
Diagnosis:
1. Microscopical examination of faeces or better pinched off portion or rectal mucosa offer staining by Ziehl – Neelsen method.
2. Allergic test by avian tuberculin or by the recent product Johnin.
(a) Subcutaneous injection of Avian tuberculin—
Preparation of animal on the same lines as subcutaneous injection in Glanders.
Temperature to be taken just before the injection and then on 9th, 12th, 15th, 24th and 48th after the injection.
Positive reaction:
A gradual rise of temperature recorded during the day of injection amounting to 2° F or over above the normal diurnal rise of temperature during the preinjection days.
Dose of Avian tuberculin:
8 -ml for a medium sized animal, therefore, the dose should be adjusted according to the size of the animal.
N.B.:
This test is not reliable in case of animal in the last state of disease or in animals injected with tuberculin within a period of two months prior to the test.
Double intradermal test, if required can be undertaken immediately after a subcutaneous injection.
Double intradermal test:
This test is performed by injection 0.1 ml of Johnin into the skin on the side of the neck in two successive doses.
Technique:
1. Clip on shave an area of skin of atleast 10 sq. cm. about the middle of the side of the neck and clean it.
2. Record by actual measurement the thickness of the fold of the skin at the seat of injection by means of a pair of callipers, the jaws of which grasp the fold of skin. The distance between the jaws is then read off on the callipers scale or else by means of a ruler.
3. Pinch up a fold of shaved area and hold it firmly between the thumb and forefinger of the left hand.
4. Insert obliquely into the fold of the skin, the needle of the fine syringe containing 0.1 ml of Johnin. The depth in which the needle is to be inserted is of great importance. It will vary with the thickness of the skin. On no account must the needle be allowed to pass too deeply into the subcutaneous tissue nor injection made superficially just under the epidermis. When the needle has been correctly inserted, inject the dose. A proper injection become evident immediately by the appearance of a pea – like nodule in the skin.
5. Inject the second or test dose into the skin in exactly the same place and in the same manner as the first injection, with the same dose after 48 hours.
6. Measure thickness of the fold immediately before the second injection and again 24 hours after the second injection.
7. Palpate the swelling at the seat of injection and record the consistence of the swelling, the presence or absence of heat, tenderness and oedema.
Estimation of the Results:
In animals that are not infected by the disease, a small swelling is produced after the first injection with increase in thickness of the skin which, however, does not exceed a few mms. Besides, palpation reveals absence of local heat and tenderness. A pea – like nodule is often fell which is not surrounded by any oedematous infiltration.
In animals that are infected, there’ is usually a considerable increase in thickness of the fold of skin at the 48th hour reading. Palpation reveals an appreciable degree of local heat and tenderness with a variable degree of oedematous infiltration of the surrounding area; these characteristics give the swelling a peculiar sensation to the touch, which is different from that felt on palpating the skin of an uninfected animal.
The most decisive information is given by examination of the skin, 24 hours after the second injection when the maximum swelling is usually reached. The most characteristic feature of a positive reaction as the presence of diffused oedema.
Treatment:
Mycobacterium paratuberculosis is very resistant to chemotherapeutic agents in vitro. Treatment with Streptomycin and Isoniazid give a transient improvement but has failed to cure clinical cases.
Control:
The lack of accurate tests and the long incubation period of the disease combine to make Johne’s disease difficult to control.
Disease # 7. Joint – Ill:
Definition:
It is an acute infective disease of a septicaemic nature affecting new born animals, specially foals—from the first day of their lives to several days caused by a number of bacteria of which E.coli, a bacterium of Coli- typhoid group is one. The other bacteria are Streptococci and Diplococci, Bacterium equirulis and Bacterium abortus equi.
In calves, the organisms include a species of Pasteurella, B.Coli, Corynebacterium pyogenes and Streptococcus.
In lambs — pyogenic cocci, specially Staphyococci and in older lambs—Erysipdothrix rhusiopathiae.
In pigs—B.Coli and pyogenic cocci.
Modes of infection:
Either intra-uterine or post natal, the latter being common and which in majority of cases results from umbilical infection.
Joint ill is not the only disease caused by these bacteria but is only one of the several forms of septicaemic diseases, new born animals are prone to e.g. Navel-ill, intramuscular pyaemic abscesses.
Symptoms:
The first noticeable symptoms which are usually noticed from the third day after birth are the usual signs of systemic disturbances including fever. These are followed by lameness in one or more legs with swelling of one or more joints of the affected leg. The joints usually involved are hock, knee and stifle.
The tendon sheaths and joints are either only filled with synovial fluid (acute cases) or may present a well-developed arthritis (chronic cases). Sometimes fistulae open to the exterior and discharge the offensive pus. The young animal become dull, takes no interest in dam, refuses to suckle. The breathing is rapid and the foal prefers to lie stretched out on its side and may have attacks of diarrhea or constipation.
Navel-ill:
In case of navel-ill, there is purulent discharge with inflammation of the umbilical vein and infiltration of the surrounding area. The navel is found to be wet and oozing with bloodstained serous material or it may be dry, hard, swollen and painful due to abscess formation.
Morbid Anatomy:
If the case has been a rapidly fatal one, as in septicaemic form, there may be no evident localisation but the whole carcass may give the appearance of a septicaemic condition with lymph glands enlarged and oedematous, serous membranes congested and petechiated and muscles and parenchyma of organs exhibit a boiled appearance. Abscesses may be found in the spleen, liver or lungs. The glomeruli of the kidneys are enlarged and many are converted into abscesses.
Treatment:
It is useless to try a treatment in well-developed cases showing severe arthritis, fistulae and intramuscular abscesses. However, Joint-ill in early stages and Navel-ill may be treated with fomentation with some astringent and antiseptic and application of some antiseptic dressing in case of Navel-ill. Joint-ill has been reported to respond with Sulphonamides and anti – serum. Antibiotics may be given parenterally or by intra-articular injection.
Injection directly into joints is presumed to overcome the inadequate levels in the joint following parenteral administration. The intra-articular administration of cortico-steroids and oral administration of phenylbutazone are used in an attempt to reduce pain and facilitate healing.
Immunity:
This is difficult owing to the pleurality of the organisms responsible for the disease. However, good results have been obtained in Streptococcal infection by the use of antistreptococcal serum followed by vaccine, which give an active immunity. If serum is used, it must be repeated every 10 days till the animal is over the susceptible age.
Prevention:
It must be impressed upon the owner of stock that eradication of Joint-ill from his flocks, herds and studs depends entirely on strict hygienic conditions. Strict and scrupulous attention must be paid to the cleanliness of the foaling box, calving-box and the lambing-pen calving and foaling should be done out of doors. While cutting the cord, it is necessary to maintain the strict cleanliness. An application of a sulphonamide dry dressing is indicated.
Disease # 8. Spirochaetosis (Dog):
Synonym:
Yellow jaundice, Enzootic jaundice, Canine typhus, Infectious icterus, Weil’s disease and Stuttgart disease.
Definition:
Spirochaetosis consists of two forms of diseases in dogs:
1. Infectious icterus (Synonym—Yellow or Enzootic jaundice and Weil’s disease) is caused by Leptospira icterohae morrhagiae and characterised by general icterus.
2. Canine typhus (Synonym—Stuttgart disease) is caused by Leptospira Canicola and characterised by haemorrhagic gastro-enteritis and no icterus.
Infectious icterus is a disease specially of young dogs and occurs sporadically—whereas canine typhus is a disease of older dogs which also appears sporadically but may sometimes occur enzootically.
N. B.:
Leptospira icterohae morrhagiae is also responsible for Weil’s disease in human beings.
Bacteriology:
Spirochaetes of the type Leptospira are very delicate organisms with shallow closed opposed spirals, demonstrable with difficulty. They measure 6µ to 9 µ x 0.25 µ and are actively motile. In the centre, they are almost straight but hooked at both ends. Leptospira icterohaemorrhagiae and Leptospira canicola are only distinguishable by serological test.
They are stained by Giemsa or by Fontana’s silver impregnation method; however, they are readily seen by dark ground illumination.
Modes of infection:
Probably, through rat -communicated food or bedding, through rat bites or through contact with water contaminated with rat’s urine. Recovered dogs are a source of danger for several weeks owing to the presence of Leptospira in the urine.
Postmortem lesions:
Apart from the lesions of the mouth, there is marked gastroenteritis, acute enlargement of the spleen and mesenteric lymph glands and congestion of the liver, pancreas, kidneys and lungs. These changes are seen in case of Canine typhus.
Yellow colouration of the organs with evidence of haemorrhage in some of them, specially lungs, enlargement of spleen and submucous and subserous haemorrhage are seen in Infectious icterus.
Symptoms:
In both the haemorrhagic and icteric types, the initial symptoms with a few exceptions, are practically identical. The onset of both is sudden and the temperature in the icteric type is usually around 103°F (39.5°C) to 105° F (40.5°C) while in haemorrhagic type, the temperature may be increased, normal or subnormal.
In both the types, a malaise is generally observed with a sort of lameness or unsteady gait, which is more marked in the haemorrhagic type. There is listlessness, constant vomiting, anorexia, dyspnoea, muscular tremors ‘and marked thirst. Epistaxis is also common.
At first, there may be a constipation followed by foetid diarrhoea, which at times are blood tinged. Marked ocular and nasal discharge of a greenish purulent character is frequently seen and the buccal mucosa at times show haemorrhagic to yellowish necrotic areas, specially in canine typhus with a strong offensive odour, which is said to be characteristic of this infection.
The urine is dark yellow coloured and albuminurea is almost constant. Convulsions and coma are seen in the later stage.
Course:
Rapid and causing death in 3 to 10 days.
Diagnosis:
If an animal dies of spirochaetosis, its liver and kidneys should be removed and a dark film examination undertaken of the tissue exudates.
At the same time, guinea-pigs should be inoculated either by scarification or by intraperito neal injection with macerated portions of these organs. Leptospira icterohae-morrhagiae is highly pathogenic for guinea pigs, killing them between the 8th and 15th day after inoculation.
In Leptospira canicola, about 40 to 50 per cent of the guinea pigs may be expected to die on the initial transmission; hence it becomes necessary to enhance the virulence of this strain by repeated passages. This is done by killing the inoculated animals surviving at the end of 10th to 14th day test period and removing the aforesaid organs, macerated portions of which are then inoculated again into other guineapigs. At times, it is necessary, to make 3 to 4 passages before success is attained in isolating Leptospira canicola.
N. B.:
Younger guinea pigs are superior to olders in yielding early successful isolation.
The examination of urine samples for the organism offers the most profitable opportunity of demonstrating the presence of infection. Examination of the centrifuged urine using dark- field illumination is considered to be a very useful diagnostic test.
Treatment:
Hyperimmuned serum taken from horses. Penicillin, Streptomycin and Tetracycline have been used with considerable success if the disease has been detected early. Once the kidneys have been damaged, treatment is for nephritis. At this stage, there is no specific line of treatment excepting symptomatic treatment.
During convalescence, the animal must be well cared for, and should be given nourishing food such as soup, milk, egg, essence of chicken etc. but no meat.
Prophylaxis:
A vaccine is now available and must not be given until the puppy is 5 months old before the first inoculation. Immune serum obtained from horses hyperimmunised with different strains of spirochaetes has given satisfactory results when injected to in-contacts.
Disease # 9. Spirochaetosis (Fowls):
Synonym:
Fowl tick fever.
Definition:
It is a septicaemic disease mostly affecting chicken (also geese and ducks) caused by Spirochaeta —Borellia gallinarum, (also known as Spirochaeta anserinum and Treponema anserinum) which is usually transmitted by the bites of the infected female ticks of the name Argas persicus. Ingestion of infected ticks or its faeces may also produce the disease.
N. B.:
The tick is infective in all its stages, infection passing through the eggs.
Red mites of chickens occasionally transmit the disease. Infection is also easily transmitted artificially by inoculation of infected blood.
Bacteriology:
The organism is a delicate, actively motile, spiral shaped, flexible organism measuring to 8µ 16µ long, which is found in the plasma of the blood of the diseased fowl.
Incubation period:
5 to 9 days.
Symptoms:
Rise of temperature—112° F (44.5°C) or near about, thirst, pronounced weakness and lethargy followed by somnolence. Emaciation, paleness of the comb and wattles, diarrhoea with greenish yellow foetid fluid evacuation, anaemia and paresis of the wings and limbs. A typical sign is drawing in or curving in of the claws.
These are followed in 1 to 2 days by purplish colouration of the comb and wattle, and a fall of temperature ending in death in severe convulsions.
Course:
In hyperacute cases, birds may be found dead without having shown any symptom. Acute cases last for 4 to 5 days and sub-acute or chronic cases may be deferred to 2 to 3 weeks.
Postmortem lesions:
Emaciated and anaemic condition, acute enlargement of the spleen and liver (in acute cases, the spleen may attain a size 4 to 5 times of the normal size). In chronic cases these organs may have necrotic foci. Enteritis usually present. Lungs are congested and fibrinous exudate usually present in serous cavities.
The blood is fluid and of a dark colour and abounced with spirochaetes until shortly before death. The blood is also incoagulable.
N. B.:
Smear should be made from the blood preferably before death or in acute stage during the height of the fever.
Treatment:
Specific therapy with various arsenical preparations give successful curative results, but the infection, though cured, often has a disadvantageous effect on growth. NAB—0.03 to 0.04 Gm/Kg intravenous.
Sulvarson, Arsenobillion—0.00 Gm/Kg. Atoxyl, Soamin etc.—0.05 Gm/Kg; intravenously or intramuscularly.
Prevention:
Prevention depends on eradication of the tick vector, Argas persicus or prevention of its access to poultry. The latter may be attained (the tick being active by night) by suspending the roosting perches from the roof, or if supported in the normal way, by baffling the supports with bands of grease.
Eradication of the ticks may be effected by keeping the poultry in movable poultry house and dipping these weekly in sheep dips. In case of built-on site houses, application of boiling water containing some disinfectant is the alternative method. Application of Painter’s Blow lamp is also effective but to a lesser degree.
Immunisation:
Recovered birds are permanently immuned. But birds can be artificially immunised by injecting subcutaneously 1 ml of virulent blood followed by a subsequent curative dose of any arsenical preparations suggested, after 48 hours.
Disease # 10. Strangles:
Synonym:
Adenitis equorum, Coryza contagiosa equorum.
Equine or cold distemper, Infectious adenitis.
Definition:
Strangles is an acute contagious infective disease, mainly of young horses, which in typical case runs a febrile course and is characterised chiefly by the inflammation of the upper respiratory tract and abscess formation in the sub-maxillary and pharyngeal lymph gland.
Etiology:
The disease is generally attributed to Streptococcus equi but some characteristics of the disease indicate, the primary cause may be a virus and that the streptococcus is merely the most important of the secondary invaders.
Animals susceptible:
It is exclusively a disease of the solipeds. The most susceptible age is between 6 months and 5 years. Animals over 5 year old are usually resistant.
An attack confers a fairly high degree of immunity that lasts for a number of years.
Modes of Infection:
Usually by ingestion of contaminated food and water. Infection by inhalation of coughed up materials or infection through wounds is also possible. The disease may also be transmitted by affected stallions while nosing the mare during coition.
Incubation period:
4 to 8 days.
Postmortem lesions:
Swellings are visible in superficial lymph glands due to formation of abscesses. The mesenteric and mediastinal lymph glands may be seat of abscesses several inches in diameter. Extensive suppuration may be seen in the liver, spleen, pleura, large vessels and the peritoneum and is due to extension from abscesses in the mesenteric lymph nodes.
Symptoms:
Rise of temperature (104° F or over) on the first day, which falls during the following days but rises again at the onset of suppuration and continues till the abscesses rupture, after which it falls rapidly and, in a few days, it becomes normal.
In most cases, there is a catarrh of the nasopharyngeal mucosa which runs rapidly through the stages of serous, mucous, muco-purulent and finally purulent, thick, yellow discharge from the nostrils. There is also an annoying unproductive cough. There is conjunctivitis, which is—more or less—severe.
Abscesses formed in the pharyngeal and sub-maxillary lymph glands. The former bursts either inwards or outwards and the latter bursting externally.
Sometimes, there may be seen cases with catarrhal bronchitis, pneumonia, pleurisy and pericarditis. In some cases, the guttural pouch may be involved by extension of infection through Eustachian tube. Pyaemia may arise from blood infection with formation of abscesses in the internal organs and from infection in the lymph stream, abscesses may form in almost any of the lymphatic glands. Pyaemia is caused by abscess in mesenteric lymph glands followed by rupture and peritonitis.
Nutrition is always impaired owing to the difficulty in mastication due to detention of the sub-maxillary tissues resulting from inflammation and partly from appetite.
Diagnosis:
Microscopical detection of the Streptococci, invariably present in the nasal discharges, as well as in the abscesses. Urine is passed in small quantity and Sp. Gr. is high. The albumin is increased in advanced cases.
Sequelae:
Apart from the chronic catarrh of the respiratory and digestive tracts, the most frequent sequela is paralysis of the Recurrent laryngeal nerve manifested by roaring. Other sequelae are staggers, permanent lameness and rarely paralysis of the facial nerve, pharynx or find quarter and chronic empyema of the accessory nasal sinus, guttural pouch, parotid glands etc.
Course:
In typical cases, the disease lasts from 2 to 4 weeks and results in complete recovery.
Treatment:
Medicated steam inhalation or nasal irrigation with some astringent lotion is useful to relieve the catarrh. The abscesses may be left alone or their suppuration expedited by hot fomentation and should be opened with long incisions and dressed with Sulphonamides. Internally, medicines should be prescribed according to symptoms such as for fever, heart weakness and loss of appetite.
Sulfanilamide and Sulphapyridine have proved to be beneficial. Sulphadiazene or Sulphamerazine are preferable to Sulphadiazene.
Penicillin 1, 00,000 i.e. intramuscularly every 4 to 6 hours, 5 to 9 injections give excellent result. Physiological salt solution is regarded as a better vehicle for penicillin than distilled water. Combined crystalline and procaine penicillin (2,000 to 5,000 i.u./kg/bw. is not excessive) and be followed by procaine penicillin alone for two further injections at 24-hour intervals. Tetracycline is also effective and at a later stage, intravenous injection of tetracycline will be more effective preceded by penicillin injection—should be continued for 4-5 days. But tetracycline may cause severe diarrhoea.
Sero-vaccine therapy:
Prophylaxis:
Segregate the animal for 3 weeks. Inject subcutaneously on arrival with a dose of Antiserum (15 ml), simultaneously with a dose of vaccine No. I (5 ml). After an interval of a week, inject a dose of vaccine No. II (5 ml), which is of an increased strength, and then after a further interval of a week, inject a third dose of vaccine No. Ill (5 ml) which is made of a still richer emulsion of organism, provided the animal has suffered no ill-effect following upon second injection.
At the end of segregation period, i.e. after a week of the last injection, allow the animal to mix freely with other horses, so that it may be given opportunities to contact strangles, which, when possible, run a mild course leaving the animal subsequently immuned to further attack and free from dangerous or lasting sequelae which often follow on acute attack.
If Strangles is not present when the vaccinated animal is liberated from segregation, it is advisable to repeat the injection of vaccine No. Ill every month or 6 weeks until all danger of natural attack is over, as the immunity conferred by the vaccine is not likely to be very durable.
Curative:
In animals showing commencing symptoms or in early stage of the disease, inject with frequently repeated doses of antiserum, 3 or 4 times of the preventive dose, every alternate day until the symptoms commence to subside.
In animals, showing the chronic or latent forms of Strangles with normal temperature or with only a slight degree of fever, inject repeated doses of vaccine at weekly intervals with gradually increasing doses until the animal responds by an appreciable thermal reaction or a slight exacerbation of other symptoms, when the dose should not be increased but given exactly at the same rate, until the animal has completely recovered.