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This article was published in 1960
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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.
Avian Monocytosis
M. LINDTNER, D.V.M., Vetry. Research Station, Glenfield
Avian Monocytosis is a major problem of our poultry industry at the present time; accounting for 18-20% of losses from all poultry diseases. Its incidence appears to be closely associated with commercial poultry raising and hence its recent increase and spread results from rapid expansion of the industry itself.
Classically, Avian Monocytosis is a disease of adult flocks, affecting mainly the layers. However, in the last few years its incidence has shifted progressively towards the young birds; especially those in the 3-7 weeks age group, although one-week-old chickens are not excluded.
Etiologically, Avian Monocytosis is not yet defined in spite of various pathological conditions and theories claiming its identity.
American and Japanese workers have isolated an enteritis virus which closely simulates Avian Monocytosis, but in analysis the evidence fails to convince. The success of antibiotic treatment could support this theory.
Similarly, to ascribe the incidence of Avian Monocytosis entirely to high protein level diet cannot be confirmed experimentally. Starvation of sick birds, however, can bring about spontaneous recovery.
Fungal toxins in the ration or some fermentation products of newly germinated wheat are incriminated in some outbreaks, though in general they do not explain the disease itself. Simple change of ration or complete withdrawal of new wheat often have accounted for spectacular recoveries.
Again, stress factors like heat, chill, thirst, wet climate, muddy ground, excessive egg production and others could be seriously considered as trigger factors for this disease, but etiologically they do not withstand criticism.
Lately, nutritional imbalance and particularly that of potassium (the latter is supported by effectiveness of molasses treatment), were examined; but the result is still in doubt.
There are also hypotheses based on genetical factors, chemical poisons and allergic phenomena, each attempting to explain Avian Monocytosis, but none contributes decisively to the solution of the problem. Indeed, they add only further indications of the complexity of the disease.
Due to the uncertainty of the etiological classification, Avian Monocytosis is known under different names; each reflecting some features from clinical observations, suspected cause or some other characteristics. Blue Comb, Pullet Disease, New Wheat Disease, Avian Infectious Diarrhoea, Summer Disease, Mud Fever, Uraemia, X-disease,etc., are some examples. However, the term "Avian Monocytosis" is the only one scientifically accepted. At the present state of knowledge, Avian Monocytosis should be considered as a "disease complex" in which various factors contribute to the common clinical and pathological picture. Relative or absolute monocytosis associated with hepato-nephrosis at post-mortem is the basic diagnostic criterion.
Avian Monocytosis runs through three clinically and pathologically defined stages; acute, sub-acute and chronic.
The disease starts with enteritis and in some cases combined with proventriculitis. Enteritis can extend over the whole intestines or may be limited to the upper portion only.
In this condition the birds abandon food, and due to the increased excretion of fluid by intestines they try to maintain equilibrium by excessive drinking. In fact, the crop is filled with water and on lifting the bird by the legs the fluid often drips from the beak. Birds are droopy, have ruffled feathers, keep isolated and show signs of watery diarrhoea.
Mainly, the best birds are the first ones affected. Being more aggressive at the troughs they possibly have ingested higher doses of some unknown etiological agent. Accordingly, some birds may die at this stage showing at post-mortem only congested intestine and enteritis. In the blood picture monocytosis is present.
In the next step the liver and pancreas become involved. This is seen at post-mortem as enlarged congested liver, dark in colour and with rounded edges; whilst the pancreas is covered with whitish necrotic spots, giving the picture of "chalky pancreas".
From the liver the effect is spread primarily to the kidneys and heart. In the kidneys the damage is done to tubules and glomeruli, causing their dysfunction. Since in birds the final product of protein metabolism is uric acid, this in turn cannot be normally eliminated and its accumulation commences.
In the heart, capillaries are damaged; leading to various degrees of hydro-sero-pericardium, often accompanied with petechiae of the myocardium.
Breast muscles, too, start to show degeneration; seen as pale streaks or areas not unlike cooked meat or fish meat in colour.
The accumulation of uric acid in the kidneys causes distention of the organ and consequently displacement of blood; represented at post-mortem as swollen, pale kidneys with pronounced lobulation and canals crammed with a whitish mass of urates. Ureters are similarly distended and filled with uric acid crystals.
This altogether characterises the sub-acute stage of the disease and this is the condition most commonly seen in practice and easily diagnosed. Monocytosis of the blood picture supplements the diagnosis.
In this period, the birds remain the same; droopy, ruffled feathers, refuse to eat,etc. However, two additional symptoms appear. The first one is cyanosis of the comb, which becomes progressively darker in colour; finishing nearly blue in extreme cases. In taking the blood smear from the tip of the comb the drop hardly oozes out and is dark. Naturally the circulatory symptoms are of different degrees, relative to the internal damage. The second prominent symptom is whitish-watery diarrhoea. Large amounts of urates are present in the watery diarrhoea on the floor or are seen collected on the feathers around the cloaca.
If birds are not treated at this stage, high mortalities may result. Treatment is based on 5 oz. of molasses per gallon of water: with reduced protein mash prepared by mixing one half of the mash with another half of mixed pollard, bran and oats. Molasses acts as a slight laxative, sucrose nutrient and Potassium source; while the low protein ration preceded by 24 hours starvation relieves the damaged kidneys. Protein metabolism is thus reduced and the kidneys have a chance to handle smaller amounts of uric acid. Starvation itself can induce spontaneous recovery, but if this fails, the treatment should continue for 5-7 days.
Antibiotics such as Terramycin or Aureomycin in high levels, 30-40 lb. per ton of mash, given for 4-6 days are also very successful in treatment. A spectacular recovery may result in 24-48 hours if antibiotics are given in the form of a drench.
Recently Potassium citrate therapy (1 lb. to 4 gallons of water for one week) came into vogue, but the results obtained seem to parallel molasses; except that Potassium therapy is more expensive.
In the chronic stage of the disease the birds are mostly found dead. The carcases appear dehydrated, emaciated and cyanotic. The kidneys and ureters are immensely swollen and crammed with urates. Uric acid is spread over the liver in the form of whitish film or deposited in the pericardium; the heart being embedded in a whitish mass. Whitish dust-like areas in the peritoneum and air sacs are other deposits.
In adult birds it seems, however, that this stage is never reached — the birds die before or recover. The sub-acute stage seems to be of chronic duration in them, and symptoms and damage of that stage remain. At post-mortem, uric nephritis, haemorrhages on myocardium, chalky pancreas, ovarian and liver lesions are found. The spleen as a rule is not involved.
Ovarian lesions consist of under-developed ova; misshapen in form and abnormal in colour. The ova may be square-formed or flattened, greenish-blue or pale yellow, large or small. Occasionally misshaped ova and monocytosis in blood smears is the only indication that Avian Monocytosis is present. Such are mainly the cases in which the farmer comes to complain about persistent low egg production of his flock.
Liver lesions are significantly important; namely, from the initial inflammatory response of this organ (swollen congested liver) necrotic spots or areas progressively develop. These necrotic spots simulate liver lesions of Fowl Cholera, hence diagnosis easily can be mistaken, particularly if other signs such as haemorrhages on myocardium or misshapen ova are present.
If Fowl Cholera were wrongly diagnosed, Sulphaquinoxaline treatment most probably would be prescribed. This, however, is strongly contra-indicated in Avian Monocytosis and heavy mortality would result. Similarly in young chickens, when Coccidiosis and Avian Monocytosis are both present at the same time. Sulphaquinoxaline again is to be excluded from the treatment and should be replaced by some other drug.
In all Avian Monocytosis cases a differential diagnosis has to be made. In adult birds, between Avian Monocytosis, Fowl Cholera and Visceral Gout; while in chickens, between Avian Monocytosis and late Pullorum.
The duration of the disease in the flock without treatment may extend over the period of 1-3 weeks, with mortality arising to — 20-40%. However, if treatment has been commenced early enough the mortality is limited to approximately 5%; with birds returning to normal between 4-7 days.
Avian Monocytosis does not produce immunity in surviving birds. Therefore the repetition of an outbreak at any future period should not surprise.
Since the aetiology of Avian Monocytosis is not known, the preventive measures are hard to recommend. In practice it was found that if the birds are given at monthly intervals a one week's treatment of molasses, or if the animal protein of the mash is permanently replaced with vegetable proteins or the birds are fed on low protein diet the disease seems to vanish; or at least its incidence is considerably reduced.
The same applies to sanitation. There is not sufficient evidence that disinfection or other sanitary measures could check the spread of disease or prevent further outbreaks; although the virus theory claims that washing alone of the site, or spelling it for four days, is sufficient to prevent re-infection.
On the basis of the above review of Avian Monocytosis, difficulties in understanding this disease are seen. No hope for an early solution of the problem can be predicted, and at the moment an early correct diagnosis and prompt treatment are our only means of defence.