The present figures show that the virus may be present in the blood as early as 18 hours and as late as 90 hours after the onset. It was not found in the blood 130 hours and 190 hours after the onset.

The virus outside the body has been found alive, if kept reasonably cool, in several instances up to 48 hours, and in one instance after 99 hours.

It is not possible from this series to draw deductions from the negative cases on this question.

Several mosquito experiments in this series have not therefore added to our previous knowledge, but the one satisfactory experiment with Culex fatigans tends to support the view we hold that this species is probably not a vector of the disease. The results previously published by us support the opinion of Bancroft (5) and show clearly that, whether or not C. fatigans may also play a part in Australia, Stegomyia fasciata is capable of spreading the infection of dengu.

Two instances are described of sera showing abnormal anti-complementary power. The amount of complement fixed by the serum was in the one case about six times, in the other about four times, greater than is normal. Examination of subsequent specimens from the patients showed that this inhibitory character was transient only. No feature common to the two cases was found to which the abnormality could be attributed. Attention is drawn to the rarity of this condition, but it is of practical importance in that such sera would be regarded as giving a positive Wassermann reaction if their behaviour in the absence of antigen were not observed.

The question of standardising bacteriological methods is at present under discussion and, although it is most undesirable that any one method should be forced on all bacteriologists, it is certainly resonable that any method which has given excellent results in the hands of a number of independent workers should have a strong recommendation.

Experiments I–VIII.

I shows that under the conditions shown the plates were covered with innumerable colonies 7 feet above ground level to ground level. The beds and trestles were used to keep the hut always uniform.

II shows that 8 feet above ground, i.e. on top of the crossbeams, the same conditions obtain.

III, IV, V, and VI show that the same condition exists in the area between the beds or trestles. The beds make no difference, better or worse.

VII shows practically the same condition high up on the beam between the beds. The inverted plates naturally show less colonies, as the organisms mostly fall on to the plates.

VIII confirms the above.

There is only one conclusion to draw from these experiments, and that is that practically speaking there is no difference in the number of organisms on the ground floor and 8 feet above it, in the ordinary men’s sleeping huts, Barrack Design 230/14.

1. The disease is an acute encephalo-myelitis produced by a virus akin to, but not identical with, that of the Heine-Medin disease.

2. The disease was readily communicated, with fatal results, to monkeys (Macacus rhesus) by intracerebral inoculation of a suitably-prepared emulsion of nervous substance (brain, cerebellum, pons, medulla and spinal cord) from the human subject dead from “X disease.” Moreover, the virus was found to breed true in a succession of thirteen monkey (Macacus rhesus) generations.

3. The disease was not communicated to Macacus cynomolgus (several trials).

4. The disease was communicated by the above-mentioned method from monkey to sheep (10 times), from sheep back to monkey and on again from monkey to monkey.

5. A certain number of sheep, perhaps 50 per cent., were found wholly insusceptible to the disease; others suffered lightly and recovered.

6. The disease was communicated, with fatal results, by the same method, from monkey to horse (1 case) and to calf (1 case). Two calves suffered lightly after intracerebral inoculation of the usual virus-containing material taken from monkey and horse respectively.

7. The virus appears to be held back completely, or to a great degree, by the pores of a Berkefeld filter.

8. Storage of the virus-containing material in diluted glycerine, under cool conditions, for longer than a few days, reduced or annulled its nocive properties.

9. Drying of the virus-containing material in Petri dishes, in an incubator, probably destroys its activity.

10. In the case of the sheep, there was failure to induce the disease by swabbing the nostrils with virus-containing emulsion.

11. There is some evidence that in the case of the sheep and the calf a previous inoculation with the virus confers immunity.

12. One experiment suggested that artificial immunity might be induced in the monkey by inoculation of virus treated with serum from an “X disease” sheep.

13. Intracerebral inoculation of three dogs, one kitten, two rabbits and one hen failed to produce any signs of the disease; and similar inoculations of two guinea-pigs gave doubtful results.

14. Treatment of the virus-containing emulsion with (a) normal human serum, (b) serum from recovered human cases of “acute poliomyelitis” and (c) serum from “X disease” sheep prolonged the incubation period of the disease in the monkey but did not destroy the virus.

15. Normal sheep serum and serum from “X disease” sheep did not neutralise the virus in its operation on other sheep.

16. Two experiments suggested that the virus was no longer present in the monkey on the eighth or tenth day of illness.

17. Two experiments towards the end of the investigation suggested a waning in strength of the virus.

18. Intraperitoneal and intrasciatic inoculations of virus-containing material, also intracerebral inoculations of cerebro-spinal fluid, of a filtrate of faeces, of a “Noguchi culture,” of an emulsion of fowl ticks, of naso-pharyngeal swabs from human cases and contacts, and inoculations into veins, all failed.

In December 1917, Lieut.-Col. MacGilchrist of the Indian Medical Service published a paper on the necrosis produced by intra-muscular injections of strong solutions of quinine salts. It might be an advantage to quote the first few lines of this communication: “Advocates of intra-muscular injections of strong solutions of quinine salts for the treatment of malaria seldom omit to state that no local ill-effects are produced”. He records a case of tissue necrosis following on the intra-muscular injection of eleven grains of quinine bi-hydrochloride in thirty-four minims of water. Death supervened thirteen hours later. MacGilchrist especially noted, owing to rapid tissue necrosis, that the track of the needle remained patent. He regards as an established fact that most of the quinine injected is precipitated and probably chemically combined with serum proteins in the necrosed tissues and for this reason intramuscular injections of concentrated solutions of quinine salts are not to be recommended for cases of emergency. Very dilute solutions of quinine salts are, in his opinion, rapidly and completely absorbed whether employed subcutaneously or by the intra-muscular route. If the views which MacGilchrist puts forward in this and other communications are to be accepted without reserve then intra-muscular injections of strong solutions of quinine should no longer be employed. It was for this reason that Major-General Sir M. P. C. Holt, K.C.B., K.C.M.G., D.M.S., B.S.F., asked me to carry out an experimental enquiry on animals as to the effects produced by intra-muscular injections of strong solutions of quinine.

The action of univalent and bivalent salts on bacteria in affeting the conductivity of thick emulsions of the meningococcus and B. coli demonstrates the important fact, that they alter the conductivity of these germs in the living condition, in a very definite manner. In this alteration, the predominant part is played by the cat-ion.

All monovalent cat-ions, with the exception of the H-ion, such as those of Na, K, Li, Rb, produce a rapid increase in conductivity or a fall in resistance. In its early stages this increase in conductivity is readily reversible in these solutions. If allowed to follow its due course, however, it leads finally to death in about two hours, when the bacterial cells no longer offer any resistance to the passage of the ions. The conductivity of the emulsion then becomes that of the fluid in which the emulsion has been suspended.

Bivalent cat-ions and the H-ion, on the other hand, at first produce a slight fall in conductivity or an increase in resistance, followed, swecondly, by an irreversible increase in conductivity which is slow and gradual resulting finally in death after 48 or more hours. This is shown by the car-ions of Ca, Sr, Ba, and Cd.

In a balanced solution such as sea-water, blood plasma, Ringer's solution, van't Hoff's solution, where a certain quantity of CaCl2 antagonises a larger amount of NaCl and KCl, the conductivity of bacterial emulsions undergoes no change, but remains constant.

Dead in distinction to living bacteria offer little resistance to the passage of ions of a solution. It would seem the relativity high resistance of the bacterial cell is due to some condition present in the living and absent in the dead state.

It has been shown by experiments on animals that the condition of increased conductivity of the cell is coupled with a loss of virulence in the case of some pathogenic bacteria. It is not clear from these experiments if this is due to the actual death of the germs in a monovalent salt solution, or to a detoxicating action of these solutions on the germs. It would seem there is some evidence for believing that the latter takes place, as the lost lethal power returns in the presence of a small trace of Ca. In bivalent salt solutions no loss of toxicity takes place. It has been pointed out that the action of monovalent and bivalent salts on bacteria offers a new explanation of certain experiments with gas gangrene organisms, where it is at present considered that the action of the salts are on the tissues of the animal and not on the bacteria.