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This article was published in 1959
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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.
Sudan Grass Poisoning in Cattle
A. R. OMAR, B.V.Sc. (Sydney), Malaya.
SUMMARY
General considerations of cyanogenesis and factors affecting it, are reviewed. Some new experimental data as well as theoretical discussion on cyanide poisoning are described; these consisting mainly of the assumption that death in cyanide poisoning is due to the attainment of a critical level of HCN in the body, which in turn results from the interaction of the following factors:
(a) The rate of hydrolysis of glucoside
(b) The rate of absorption of the formed HCN
(c) The rate of detoxication of the HCN.
The fact that toxicity in Sudan Grass can develop at any stage of growth, and the fact that the problem of control and prevention is difficult, are emphasised.
Summary of the recent outbreak in the far North Coast of New South Wales is tabulated. Certain aspects of this outbreak are discussed under the appropriate headings; as affirmations of, or points of variance from, the generally accepted picture of cyanide poisoning.
INTRODUCTION
Despite extensive research which has been carried out by many workers, especially at Glenfield Veterinary Research Station, into the problems of poisoning through grazing on the Sorghum species, such poisoning still occurs. The recent outbreak of poisoning on Sudan Grass (Sorghum Sudanese) in the Far North Coast of New South Wales serves as an example. This outbreak occurred in the months of December, 1957, and January, 1958; involving three properties in the Pastures Protection District of Casino. A total number of 55 cows was affected; 30 dying as a result. A summary report of this outbreak is given in a Table which follows later.
This article attempts a survey of the available literature on general aspects of Sorghum species poisoning in general, and Sorghum Sudanese poisoning in particular; as well as evaluating the special aspects of the recent outbreak to fit into the general clinical picture of such poisoning.
GENERAL CONSIDERATIONS
Cyanogenetic glucoside
Free Hydrocyanic Acid (HCN) does not occur in plants. It is found always as a complex glucoside, the HCN fraction being bound up to glucose and an aldehyde or ketone fraction. Although more than 1,000 species of plants are known to be cyanogenetic at one stage or another of their growth, only about twelve different cyanogenetic glucosides have so far been isolated,e.g. amygdalin from Prunus species and Lotausralin from white clover. The glucoside from Sorghum species of grass is called dhurrin; the aglycone of which contains p-hydroxybenzaldehyde.
Bound up HCN in the form of glucosides or the intermediate cyanhydrins is harmless to animals. It is when these cor hydrolysed that free HCN is liberated; and when absorbed, exerts its toxic effects.
Liberation of HCN
The liberation of HCN from glucosides requires the action of a specific enzyme. Most plants that contain the glucoside, also contain the enzyme. Some plants,e.g. Native Fuchsia, contain the glucoside alone; others like gidgee contain the enzyme alone. When ingested together, hydrolysis of the glucoside occurs in the gastro-intestinal tract and HCN is set free. The process takes place after the following general equation;
Cynogenetic glucoside ⇒ Glucose plus Cyanhydrin ⇒ Aldehyde or ketone plus HCN
In cyanide poisoning from cyanogenetic plants the presence of the enzyme was first thought to be essential. Later, however, it was shown that hydrolysis of the glucoside can take place by the action of micro-flora of the gastro-intestinal tract (Boyd et al. 1938: Coop and Blakely, 1949). Ruminants with their relatively higher population of micro-flora are more susceptible to cyanogenetic glucosides than monogastric animals. Ruminal pH of 6-7 provides the optimum condition for bacterial hydrolysis of cyanogens, whereas the pH inside the stomach of monogastrics is more acidic and hence less suitable. Further, Boyd (loc. cit.) believes that monogastrics and horses readily detoxify liberated HCN in the stomach by converting it into formic acid.
HCN in Sudan Grass
The presence of HCN in the Sorghum was discovered in 1902 by Vinall. The amount present in Sudan grass is variable; depending on many factors. Francis (1915) gave an average figure of 0.0068 per cent. HCN of the fresh weight of the plants. Analysis of Manuel and Dowell (1920) showed a range of 0.0035 per cent. to 0.0105 per cent. of fresh weight.
Analysis of various parts showed that there is an unusual distribution of HCN in the plants. Swanson (1921) found that in the early stages of growth there is little variation in HCN content of stem and leaves. As growth and maturation proceed, the leaves' HCN level becomes higher; so that when the plants are mature only a trace of HCN can be found in the stem; the main bulk being concentrated in the leaves (about 60 per cent.). A small amount may be present in the roots; as is the case with Sorghum, where the ratio of the total cyanogen compounds in leaves, stems and roots of a plant is 9:3:2 (Acharya, 1933).
There is also diurnal variation in the HCN content of Sudan grass. Estimation of Manuel and Dowell (1920) showed that the morning content is some two per cent higher than the afternoon. Boyd et al. (1938) analysed the content of plants cut at 8 a.m., 1 p.m. and 7 p.m. and found that the 1 p.m. results were three per cent higher than the others. This difference, however, is of no significance with retard to toxicity when the overall amount is high: but in border-line cases it may well decide the point of safety and danger to grazing stock.
Factors affecting concentration of HCN in Sudan grass.
(1) Stage of growth
Young and second growths can develop more HCN than older plants. The general tendency is for the HCN content to diminish more or less regularly as the plants mature. The following table (modified from Hurst) gives an idea of the HCN content at various stages of growth:
TABLE ONE
| Height of Plants (in inches) | % HCN of Fresh Weight | Authority |
|---|---|---|
| 4 | 0.020 | Swanson 1921 |
| 10 | 0.0035 | Frances 1951 |
| 15 | 0.0042 | Frances 1951 |
| 17 | 0.0021 | Frances 1951 |
| 30 | 0.0042 | Frances 1951 |
It is believed generally that past eighteen inches tall equivalent to a month or more of growth the plants are quite safe for feeding to stock. Rose (1941), however, strongly emphasised the fact that the plants can be dangerous at any stage; even when they are in seed. This is especially true in cases where there is uneven growth, so that while some of the plants are in seed, others may still be very short. The writer encountered several cases of poisoning on such an uneven sward (see Table of Casino outbreak, 1957/58).
(2) Weather and Climatic Conditions
Records of Sudan grass poisoning in New South Wales over many years show that the majority of outbreaks occur in the months of December, January and February. This has a significant relation to climatic conditions. Normally, Sudan grass is grown in the spring (October) and usually is subjected to a long, hot, dry period in the early summer. Plants under this condition are poor and stunted, but when grazed by stock do not give toxic effects (Rose, 1941). This indicates that prolonged hot and dry weather alone does not increase the HCN content of the plants. Boyd (1936) states that stunted drought growth actually contains less HCN than plants growing under more favourable conditions. However, the HCN content tends to rise after a fall of rain.
In the summer-rainfall areas, the onset of rain in mid-summer causes prolific re-growth of Sudan grass; hitherto stunted. Grazing under such conditions can be expected to result in high mortality (Rose, loc. cit.) The recent outbreak in the Casino District of New followed the same general pattern: a long hot and dry period caused stunting of Sudan grass, and a sudden hall and heavy rain early in December brought about rapid and prolific re-growth. The first incidence of poisoning occurred later in the same month.
In short, it can be said that the effect of prolonged hot, dry weather on the HCN content of Sudan grass is indirect; i.e., such condition per se does not increase cyanogenesis, but a period of rapid re-growth caused by rain after a long period of drought weather favours it particularly.
Very high temperature, on the other hand, causes wilting of plants. It is believed that wilting releases HCN from the bound form and that ingestion of such material causes rapid absorption and onset of symptoms. If left standing for some time, part of the HCN volatilises and the material may become non-toxic. This is the basis for cutting and drying cyanogenetic herbage before feeding to stock as a method of prevention of cyanide poisoning. This point will be discussed later.
Frost, like hot weather, has an indirect effect. While it does not actually cause HCN content to rise (Boyd et al. 1938), the rapid re-growth following it may prove highly toxic. Swanson (1921) suggested that freezing tends to cause bursting of the plant cells and the release of HCN. Therefore, the rate of evaporation of HCN from the frozen material determines the margin of safety of such material for grazing.
(3) Soil Conditions
Boyd et al. (loc. cit.) state that the addition of nitrogen fertilisers to soil poor in nitrogen results in high HCN content of Sudan grass grown on it. But the HCN content of plants growing on soil containing of nitrogen is not affected by nitrogen fertilisers.
Boyd also found that the addition of phosphorus to soil deficient in the mineral results in only a small amount of HCN being formed. But plants at the same age grown on phosphorus deficient soil have a high HCN content.
He concluded that high nitrogen and low phosphorus content both favour high HCN production.
Low soil moisture is another factor which favours production (Gardner and Bennetts, 1956). This becomes an important factor in low rainfall areas where the long dry summer gives rise to low soil moisture. The Far North Coast of New South Wales is subjected to frequent drought or semi-drought conditions. The soil of the area is also generally low in phosphorus. These two factors may well contribute to the high incidence of Sudan grass poisoning in this part of New South Wales.
(4) Hybrids and strains of Sudan Grass
In the past it was thought that only certain strains of Sudan grass or Sudan-Sorghum hybrids caused HCN poisoning; while ordinary 'pure' strain can be fed to stock with impunity. The hybrids are said to acquire a toxic property from their Sorghum 'parentage'. While it is true that Sorghum generally contains more HCN than an equivalent growth of Sudan grass (some two-thirds or so more according to Manuel and Dowell 1920), analysis of pure Sudan grass and hybrids by Seddon (1932) showed very little difference in their HCN contents.
TABLE TWO
(from Hurst)-Seddon's analysis of plants from the same crop:
| HCN % of fresh weight | ||
|---|---|---|
| No. of Crop | Sudan Grass | Hybrids |
| 2a | 0.026 | 0.014 |
| 3 | 0.029 | 0.039 |
| 4 | 0.063 | 0.065 |
| 5a | 0.027 | 0.018 |
| 5a | 0.018 | 0.018 |
| 6 | 0.011 | 0.015 |
| 6 | - | 0.008 |
| 7 | 0.026 | 0.024 |
| 8 | 0.006 | 0.008 |
This analysis, as well as observations by many workers including Rose (loc. cit.), disprove the earlier concept. The Casino outbreak occurred on stands of pure Sudan; and in one case of Sweet Sudan (see Table). It is accepted now that any strains of Sudan grass, pure or hybrid, can cause poisoning.
(5) Insect Attack
Rose (loc cit.) considers that attack by insects, grass-hoppers in particular, is a major factor in producing high toxicity in Sudan grass. There is though, no proof that destruction by insects actually causes a rise in HCN content of the plants. It seems that re-growth after an attack by the insects is the factor responsible for toxicity.
However, since the conditions under which Sudan grass is grown also favour the breeding of grasshoppers, the question of insect attack becomes important in regard to seasonal occurrence and outbreak of cyanide poisoning.
TABLE THREE
SUDAN GRASS POISONING
SUMMARY OF CASINO DISTRICT OUTBREAK, 1957/1958
| Date | Locality | Pasture | Soil | Weather | Animals Affected | Treatment and Results |
|---|---|---|---|---|---|---|
| 25/12/58 | TABULUM | "Sweet Sudan" Fed off safely once - regrowth occurred. Present state 8-10" high. | Black alluvial flat | Very hot and humid. Max. Temp. 106 deg. F. | 150 Hereford cows were put on pasture. Animals began collapsing within 5 min. 35 down before removal from pasture. 25 died. Deaths in 15 min. to 2 hrs. after onset of symptoms. | Owner claimed he saved 10 cows by drenching with "Rinso". |
| 14/1/58 | PIORA | Sudan grass 12" high | Light sandy | Hot and humid | 34 Jersey milkers put in paddock. 2 seen staggering in 10 min. After removal 13 collapsed, 4 staggering. 5 died in 30 min. | Treatment with Sod. thiosulphate-2 oz. given i/v followed by same dose i/ruminal. No more mortality even in apparently moribund cases. 1 animal treated twice, showed tremor of head and neck muscles and champing of jaws during recovery. |
| 30/1/58 | THE BEND via. CASINO | Sudan grass uneven growth. Some 6" high. Some in head. | Dry and sandy | Hot and humid | 7 aged cows put on as "pilots". Grazed for ½ hr. then removed. 3 collapsed 15 min. after removal. | Owner drenched with Na2S2O3. Recovery slow. Animals still down after 2 hours. Then given i/v 2 oz. Na2S2O3. Animals were on feet 15-20 mins. later. |
CLINICAL CONSIDERATIONS
Aetiology
As has been stated previously, the mere ingestion of a cyanogenetic glucoside will not cause ill-effects unless it is broken down by enzymatic or bacterial hydrolysis in the rumen and absorbed. Granted that hydrolysis and absorption occur, a certain amount of HCN (the Critical Level) will have to be present in the body before its toxic property can exert itself. The attainment of this critical level depends upon:
1. The rate of hydrolysis of glucoside.
2. The rate of absorption of HCN.
3. The rate of detoxication of HCN.
The rate of hydrolysis and absorption can be considered as one single factor because absorption of free HCN is almost as rapid as it is formed. Therefore, in effect the attainment of the critical level is the result of two factors; namely, the rate of absorption tending to increase the concentration of HCN and the rate of detoxication tending to lower it. Death occurs when the former overwhelms the rate of detoxication and upsets the balance. An estimate of 0.5-1.0 mg./Kg. of HCN represents the critical level to which the HCN content of the body must rise in order to cause death.
(a) Detoxication and Factors Affecting It.
Detoxication mechanism consists of oxidation of HCN by sulphur-donors H2S in particular forming HCNS. This non-toxic oxidised product is excreted rapidly in the urine and saliva. In the sheep some 10 per cent of this is excreted via the lungs (Coop and Blakely, 1949).
The rate of detoxication, in accordance with all reversible reactions, varies with the concentration of the reagents. Liver tissue in vitro can detoxify HCN at the rate of 2.1 mgm. HCN/kg./hour. Intact and in vivo the liver would do this at a faster rate; probably of the order of 3.9 m.g. HCN/kg./hour (Coop and Blakely, 1950). If the liver is damaged,e.g. the result of fluke infestation and tape-worm cysts, then its capacity to detoxify is reduced; and hence the natural tolerance of the animal is also reduced.
Since the rate of detoxication is important in regard to the attainment of the critical value, the tolerance value is also the function of detoxication; the faster the detoxication the higher the tolerance. And since the S-donors play a major role in detoxification, a question arises as to whether or not these compounds will set a limit to tolerance.
The body contains reserves of cystine and methionine while the food also contributes large quantities. Relative to HCN, H2S, the most effective S-donor, occurs in the rumen in considerable quantities and can be absorbed rapidly (Coop and Blakely, 1950). Therefore, under normal circumstances S-donors do not limit the rate of detoxication except when the animal has been starved for long periods and its S-donor reserves are exhausted. The remaining factor which can upset the balance and reduce tolerance is then, the rate of hydrolysis and absorption.
(b) Hydrolysis and Absorption
Micro-flora of the rumen can hydrolyse glucoside rapidly. In sheep the peak production, concentration and absorption of HCN in most circumstances takes place within less than ten minutes of dosing free glucoside, and within 10-20 minutes of animal eating cyanogenetic plant materials (Coop and Blakely, 1949). In cattle, the rate is of the same order, or possibly even slightly higher; judging from the fact that animals grazing on toxic materials begin to show symptoms within 5-10 minutes. (Blood. 1946). The larger population of micro-flora of the bovine may contribute also to the more rapid hydrolysis of glucoside in this species.
(e) Factors affecting the Rate of Hydrolysis and Absorption
(i) In determining the rate of hydrolysis and absorption, two factors are of special importance; namely, the population of micro-flora and the pH of the rumen. These two are inter-related. The right pH will favour a high micro-flora population and therefore a higher rate of hydrolysis and absorption. The pH most favourable is somewhere in the vicinity of neutrality, so that the normal ruminal pH of 6-7 is optimal (Coop and Blakely. 1949). On a full stomach, the micro-flora density is high and the pH close to the optimum; so that rapid hydrolysis can take place. On the other hand, in a starved stomach bacterial population is low and pH more acidic than optimal; hydrolysis therefore being slower.
Under grazing conditions, even if the stomach is empty initially ingestion of herbage tends to increase the micro-floral density and induce the right pH; so that while hydrolysis may be slow to begin with, it will increase with time. For this reason, starved animals tend not to show symptoms until one or two hours after ingestion of the cyanogenetic plants. On pasture, this delay in the onset of symptoms would cause the animal to go on eating and by the time discomfort is felt, large quantities of toxic material would have been ingested. The seriousness of this can be appreciated easily. On the other hand, non-starving animals will commence to feel disturbed after 10 to 15 minutes of grazing, and then stop feeding. The chance of their not having ingested a lethal amount of toxic material is higher, and consequently while they do show symptoms, their chances of recovery are more favourable.
(ii) Readily metabolised carbohydrate tends to delay or reduce hydrolysis. Coop and Blakely, 1949 In Vitro experiments found that glucose reduces hydrolysis very markedly. A dose of 30 gm. glucose, equivalent to 10 mgm./ml. in a three litre rumen (sheep) reduces hydrolysis to 10 per cent. of normal rate; while a dose of 50 mgm./ml. reduces it to 5 per cent. The explanation for this is that glucose supplies a readily available substrate for bacterial metabolism at the expense of the glucoside. This also may be the explanation of the observation of Bunyea (1934) that cattle fed on a high starch diet develop a resistance to cyanide.
(iii) Coop and Blakely (loc cit.) also found that salts such as Sodium sulphate and Sodium nitrate reduce bacterial hydrolysis. But the extent is not as marked as inhibition of hydrolysis by glucose.
(d) Toxic Dose
Avery (cited by Udall) estimated that the minimum amount of HCN sufficient to cause toxic affects is about 0.4 grams. Udall (1954) suggested a lethal dose of 0.4 - 0.6 grams for adult cattle. Figures from other workers (Swanson, 1921; Hindmarsh, 1930; Finnemore and Cox, 1931) were slightly higher; 1 gram HCN being lethal for 1,000 lbs. beast, or an M.L.D. of 2.0 mgm./kg. bodyweight. As a general rule sheep are more tolerant; the M.L.D. being of the order of 2.2 - 2.3 mgm. HCN/kg. bodyweight (Coop and Blakely, 1950).
The actual bulk of Sudan grass which has to be ingested to cause death will then vary according to the HCN content of the grass. Udall (loc cit.) gives an estimated average value of 18.9 lbs. Seddon (1932) gives the following:
TABLE FOUR
| % HCN of fresh wt. | Lethal amount for Bovine | |
|---|---|---|
| of Sudan grass | grams | lbs. |
| 0.01 | 7500 | 16.5 |
| 0.02 | 3750 | 8.3 |
| 0.03 | 2500 | 5.5 |
| 0.04 | 1875 | 4.0 |
| 0.05 | 1500 | 3.3 |
| 0.06 | 1250 | 2.8 |
| 0.08 | 937 | 2.0 |
| 1.10(sic) | 750 | 1.7 |
| 0.15 | 500 | 1.1 |
| 0.20 | 375 | 0.83 |
Considering the capacity of the bovine rumen, it can be said as a general rule that plants containing a minimum of 0.02 per cent. fresh weight of HCN should be regarded as dangerous for grazing stock (Seddon and King. 1930).
(e) The possibility of Nitrite as an aetiological agent
Sorghum (S. vulgare) can contain as much as 7 per per cent. of Nitrite (Blood, 1946). Since the plant is closely related to Sudan grass, one would expect the latter to contain quite a high amount of nitrite. Hence, the possibility of nitrite being the aetiological agent in Sudan grass poisoning should not be overlooked.
Pathogenesis
The cyanide ions interfere with tissue oxidation, or more specifically with cytochrome oxidase, causing an anoxia of a histo-toxic type. Cellular respiration is suspended and oxygen is retained in the blood, giving it the characteristic bright red colour. If the course is prolonged the blood may become dark red in colour due to low oxygen intake resulting from inhibition of respiration. The final stages in cyanide poisoning are the arrest of respiration and death due to asphyxia. Cardiac activity continues for some brief period after the cessation of respiratory movements.
Udall (loc cit.) mentioned that the action of concentrated solutions of cyanide on the mucous membrane of the alimentary tract is corrosive. But since the absorption of HCN is rapid, one does not expect a high concentration of the acid to accumulate in the rumen. Consequently, corrosion of the ruminal mucosa may never occur at all in field cases of cyanide poisoning. However, Burnside (1954) states that formation of HCN by bacteria can go on after the death of the animal; the action of this on the ruminal mucosa post-mortem leading possibly to erroneous conclusions with regard to corrosion.
In experiments with monkeys, Hurst (1940) found that sub-lethal doses of cyanides cause massive necrosis and demyelination of white matter of the brain. Clinically this is seen as progressive paraplegia. However, the natural occurrence of the chronic form of cyanide poisoning is doubtful. Van der Walt (1944) failed to produce chronic poisoning in sheep, after administering 3.2 mgm. HCN/Kg. for over two years. Similar results in rabbits were reported by Worden (1940).
Clinical Signs
The onset of symptoms has been quoted always as occurring some 5-15 mins, after the animals are put on toxic pasture. But in the Casino outbreak, animals were seen to show symptoms 15 mins. after they had been removed from pasture on which they had grazed for about half an hour. There is thus a big variation which depends on factors already discussed under the heading of aetiology; namely, the HCN level of the grass, general body condition of the animals and whether or not the animals commenced grazing the Sudan grass sward on an empty stomach.
(i) The symptomatology is rather complex and often variable. Blood and Steel (1944) in their clinical studies on HCN poisoning of sheep via the agent of linseed cakes, described six stages in the development of the clinical signs. These are briefly as follows; lassitude and apathy initially, followed by muscle twitchings; then ataxia, inability to stand and convulsions; animals may show running movements; vomition may occur: the final stage being respiratory arrest and death due to asphyxial respiratory failure. The point is that all these signs may not be shown by all affected animals. In cattle the first signs are agitation and restlessness. There is a sudden onset of dyspnoea. Staggering is quite marked and the animals invariably down; lying in sternal recumbency with the legs tucked in under the body. Foaming at the mouth is a constant feature.
In the acute form death occurs as early as 2-3 mins after the onset of symptoms; usually preceded by convulsions.
In the less acute form, animals may remain prostrate for a long period and if not treated death may occur as late as two hours or longer after first signs are shown. Tympany, which may develop following a long period of recumbency, may be the actual cause of death.
Other signs which may be shown during prostration are pupil dilation, lachrymation and muscular twitchings.
(ii) Cardiovascular System
There is an initial tachycardia which may be followed by a slight fall and then a secondary rise. In the terminal stages a sudden fall occurs. This follows more or less the findings of Blood and Steel (loc cit.)
Jugular pulse is very prominent in all cases. Arterial pulse is rapid (140-160 per minute) but generally weak, with low maximum and minimum pressures. This persists until just prior to death, when irregularity and deficit occur. With treatment, the fall in pulse rate to within the normal range is rather slow. The animal may regain its feet while the pulse rate is still above normal.
(iii) Respiration
Increase in rate and depth of respiration is seen from the beginning. When in sternal recumbency the respiration becomes shallow and forced and the rate is 40-45 per minute. The animal may stretch its neck and breath through the mouth.
Autopsy Findings
Unfortunately, no autopsy was carried out on cases the writer has seen, but the usual text-book report is that post-mortem findings are often negative. The blood is bright red, especially if death is sudden. The characteristic bitter almond smell from the rumen was described by many early workers, but Udall (loc cit.) Smith and Jones (1957) and many others could not substantiate it.
Diagnosis
This is based mainly on symptoms and history of grazing of Sudan grass. A simple quantitative test for the presence of HCN in the Sudan grass can be done using Henrici Picric Acid technique. Ruminal contents also can be subjected to this test and the result is quite dependable, provided that the sample is taken immediately after death. Formation of HCN post-mortem by bacteria can confuse the issue if the sample is taken some time after death. It should be remembered that the HCN content of the rumen can be variable, even in positive cases; since death can occur before or after the HCN has been completely absorbed.
Quantitative laboratory tests may be made on ruminal contents liver, blood and muscle specimens. No preservative should be added when despatching these specimens to the laboratory; the specimens being placed in air-tight containers to prevent volatilisation of freed HCN.
For ruminal contents Coop and Blakely (1950) regarded 10 mg/gm. of HCN as positive. As far as the liver is concerned, a piece from the left lobe should be taken. A minimum of 1.4 mg/gm. of HCN from this organ can be considered positive (Van der Walt, 1944).
Treatment
Since asphyxia caused by HCN is the result of interference with respiratory enzymes, it follows that any form of antidote for cyanide poisoning must have one of two actions. Either the cyanide must be removed or detoxified, or the inactivated enzymes replaced (Best and Taylor, 1950). The first line of attack is the more practicable. The following methods of treatment have been used by various people from time to time:
1. Intravenous injection of sodium nitrite and sodium thiosulphate
This was described by Bunyea (1935), who claimed that given at a dose of 10 ml. of 20 per cent. NaNO2 and 30 ml. of 20 per cent. Na2S2O3, these chemicals would be effective in cattle against two lethal doses of cyanide. Rose (1941) claimed equal success with a dose of 3 gm. NaNO2 and 15 gms. Na2S2O3.
2. Intravenous injection of sodium thiosulphate alone
Was described by Stanton (1934) and the dose recommended was 40 ml to 80 ml of a 20 per cent. solution. Blood (1946) recommended an equal amount of a 10 per cent. solution. We found that a dose of 2 oz. of thiosulphate (dissolved in water is very effective.
3. Intravenous Injection of sod. nitrite alone at a dose of 1 ml. one per cent. soln. per 10 lbs. bodyweight (Blood 1946).
4. Sodium thiosulphate orally (Maunder 1944) or intra-ruminal injection: 2 oz. dissolved in water.
5. Methylene Blue also has been used with some success.
6. Sub-cutaneous ether was tried by Rose (1941) but was of no value.
Relative merits of the various methods of treatment:
Sodium nitrite and sodium thiosulphate given together are very effective and justify the claims of Bunyea and Rose. But our own finding is that Sod. thiosulphate alone given intravenously is just as effective and less cumbersome to use. At a dose of 2 ozs. per animal, we found that it is effective even in animals apparently moribund (some of these regained their feet in 10 minutes). In an animal which was treated twice within a space of two hours a slight untoward effect was noticed during the recovery stage. This consisted of tremor of muscles of the head and champing of the jaw. On the whole, however, the danger of overdosing is small. Animals that received intravenous injections followed by intra-ruminal injections, each of 2 oz. of sod. thiosulphate dissolved in water, recovered uneventfully. Further, sod. thiosulphate is easily prepared and administered by the farmers themselves in a case of emergency.
Given as a drench or into the rumen by trocar and cannula, sodium thiosulphate takes effect rather slowly, so that while it will save the less acute cases, it will not be rapid enough to offset the effect of the more severe intoxication. Farmers may give it as a drench; as a temporary measure while waiting for the arrival of the veterinarian.
Methylene Blue is not recommended because its potency as an antidote for cyanide poisoning is rather low (Blood 1946). With sodium nitrite there is always the danger of producing nitrite poisoning with over-dosing.
Theoretical aspects of treatment
1. The thiosulphate injection supplies the sulphur-donor for oxidation of HCN into thiocyanate which is non-toxic (cf. discussion under Aetiology).
2. Sodium nitrite and methylene blue react with blood haemoglobin, forming methaemoglobin; which will combine with HCN to form cyanmethaemoglobin. The cyanide later is released slowly from this combination and is detoxified by the normal mechanisms of the body. If thiosulphate is given simultaneously the released HCN is dealt with rapidly as in (1) above.
3. In the recent Casino outbreak, an owner claimed that he saved 10 cows by drenching with 'RINSO' (see Table Three) may not be justified in that the animals, while having eaten sufficient toxic material to show symptoms, may not have ingested a lethal quantity and possibly recovery would have taken place regardless. On the other hand, the treatment may have a sound scientific basis in that the soap created an alkaline condition in the rumen; thus reducing hydrolysis of the glucoside and delaying the absorption of HCN. In this way the detoxication mechanisms of the body are not overtaxed and the critical level is not attained.
Prevention and Control of Sudan grass poisoning is quite a problem because the grass is grown extensively in certain areas as a fodder crop which is relied upon to provide grazing for cattle at a time when the natural pastures are generally poor. A simple measure which is adopted for other toxic herbage, namely avoidance of the suspected plants by fencing off, is often not applicable since this would defeat the purpose for which the grass is grown. Unless it is known without doubt that the plants are toxic, the usual practice is to withhold grazing until the plants are taller than eighteen inches. But in view of the fact that the plants can be highly toxic at any stage of growth, such a practice is not reliable. Other methods of prevention have to be used, especially when weather conditions and other factors are such that high toxicity can be expected.
1. Pilot Grazing.
The N.S.W. Dept. of Agriculture recommends that farmers should allow one or two of their less valuable animals to graze on pasture before putting the rest of the herd on it should no toxic symptoms develop in the 'pilot' animals the pasture can be regarded as safe.
This system is far from being foolproof, especially if the number of pilot animals is small. The reaction of animals to toxic materials and the rapidity with which the symptoms are shown vary from individual to individual depending on grazing habits, body conditions and so forth. In one instance in the Casino outbreak, where a farmer put seven aged cows to graze as pilots (see Table Three) only three of these showed symptoms after half an hour of grazing. The fallacy of the pilot grazing system can be appreciated fully from this example; particularly should only one or two animals be used instead of the seven. There is no reliable guide by which 'suitable' pilots may be chosen.
2. Pre-feeding.
Starved animals tend to feed greedily and in no time literally engorge themselves with herbage; thus increasing the chances of becoming affected rapidly should the pasture be toxic. Therefore, animals should not be allowed on to a Sudan grass lot on empty stomachs.
Pre-feeding with foodstuffs high in starch or carbohydrate is another approach which may be adopted. We have mentioned that high carbohydrate and starch diet tends to delay hydrolysis of the cyanogenetic glucoside.
3. Air-drying and Ensilaging have been adopted as measures of reducing the toxicity of Sudan grass. This was done in the belief that such treatment caused the release and evaporation of HCN. This has been disproved. In air-drying, while it is estimated that some 75 per cent. of the HCN is released, not all of this volatilises (Dowell, 1919). Air-drying and sun curing do not appreciably reduce HCN content if the grass contains a high percentage when cut (Boyd et al. 1938). Oven-drying at 115 degrees C. is effective, but is not practicable.
Ensilage is also ineffective in reducing HCN content of Sudan grass (Hurst, 1942).
4. Time of feeding will have a small bearing on toxicity because of the presence of diurnal variation in HCN content of Sudan grass. It may be of assistance of animals are allowed to graze only in the afternoon.
5. Soil management. Correction of soil with regard to nitrogen and phosphorus content will help to reduce the tendency to high HCN of Sudan grass grown on it.
Discussion
Prom the foregoing, it can be said that the occurrence of Sudan grass poisoning is dependent on two major factors; namely, the plant factors and the animal factors. A comprehensive treatment of the plant factors is given under general consideration at the beginning of this paper of the animal factors, perhaps the general body condition of the animal is of greatest importance, mainly due to its relation to the tolerance capacity of the animal. An animal in good physiological state would have a high reserve of the Sulphur-donors, so essential in detoxication of HCN, and hence a high tolerance value. On the other hand an animal in poor condition generally would tend to suffer more severely from the toxic effect of HCN. So that under conditions which tend to cause debility (e.g. low nutritional status) in animals, poisoning is apt to occur even if the HCN level of the pasture is non-toxic under normal conditions. In other words there is a lowering of the tolerance value, due to inability to detoxify HCN. In the northern parts of this State, conditions tending to reduce the tolerance of the animals (drought and consequently low nutritional status) tend also to increase the toxicity of Sudan grass. The relatively high incidence of Sudan grass poisoning in that part of NSW. hence is the result of both animal and plant factors.
Despite the significance of the animal factors, poisoning is still largely dependent on the plant factors. And since Sudan grass can be highly toxic at any stage of growth, the danger from poisoning is ever-present.
On the whole stockowners are quite aware of this potential danger of Sudan grass to stock. The practice of cultivating the grass for feeding to cattle during the summer months, however, has not been abandoned; primarily due to the fact that it gives bulky feeds, is drought resistant and can be left standing in the paddocks right through winter. In these respects the Sorghum species as a whole is more suitable for the Far North Coast of NS.W. than other summer-growing species such as maize. But with regard to their food value, both maize and the Sorghums are on equal status in that they are essentially carbonaceous fodders; being high in carbohydrates and low in protein. As such, Sudan grass is not a suitable foodstuff per se, for dairy cattle for which it is grown. Its main value is merely roughage.
Further, the unreliable nature of the Sudan grass with regard to safety for grazing, especially in the northern dairying districts where the soil is generally low in phosphorus and weather conditions erratic (both being favourable to the development of high toxicity) offsets any advantage of the grass over other forms of summer-growing, fodder crops. Another point against the cultivation of Sudan grass is the lack of a highly reliable yet practicable method, under field conditions, for the detection of toxicity and hence prevention of poisoning. The only factor which prevents Sudan grass poisoning from claiming very high mortality is the effectiveness of the methods of treatment. Even so, the inconvenience caused to the farmers is quite extensive. In addition, once a pasture has proved toxic no further use can be made of that particular growth. There is no method by which toxic materials can be rendered safe. It has been seen that ensilaging and air-drying do not reduce appreciably the HCN content of the Sudan grass. The economic loss arising from deaths of stock as well as wastage of Sudan grass pasture during an unfavourable season must be quite high. Hence the writer is of the opinion that Sudan grass should not be grown at all for stock feeding. Other summer growing crops (e.g. 'Poona peas') which thrive very well in the north should be grown as an alternative. Even the less drought-resistant maize, in view of its freedom from cyanogenetic glucoside, may be preferable.
Conclusions
1. Sudan grass can be highly toxic at any stage of its growth. Toxicity is highest when the plants are young and growing rapidly. Any conditions tending to cause rapid growth will tend to cause high toxicity.
2. In the production of toxicity in animals, not only the plant factors are responsible, but also the animal factors, such as nutritional status, greediness of feeding,etc.
3. Prevention and control is difficult because Sudan grass is grown for stock.
4. Treatment is very effective and recovery is possible even in the apparently moribund cases.
5. In view of the fact that it is unreliable with regard to safety for grazing, and also in view of the fact that it is a poor foodstuff for dairy cattle, we suggest that Sudan grass should not be cultivated for fodder but replaced by other summer-growing crops.
Acknowledgment
The writer wishes to thank Mr. J. M. Wilson, B.V.Sc., Veterinary Inspector, Casino, for supplying details of the Casino outbreak in Sudan grass poisoning in 1957/58. The Table covering the outbreak is compiled from information supplied by him.
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NOTE: This article was submitted by Mr. Omar (an Asian student) as his Final Year (1958) Thesis, and although publication here is a new departure, such is thought to be warranted: considered to be a particularly thorough and useful review of the subject. Especially, perhaps, as one of our members apparently is entitled to bask in any reflected glory there may be—EDITOR.