1. The life cycle of Austrobilharzia terrigalensis Johnston, 1917 is described. The larval stages occur in Pyrazus australis, a common mollusc on sand flats of estuaries and coastal lagoons in New South Wales.

2. Austrobilharzia terrigalensis was originally described from the seagull, Larus novae-hollandiae. Experimental infections have been successful in young gulls of this species and in the budgerigar Melopsittacus undulatus and the pigeon Columba livia.

3. Under experimental conditions the cercariae will cause dermatitis, and cases of dermatitis resembling cercarial dermatitis have been reported after bathing in Narrabeen Lagoon, where about 4 % of Pyrazus australis carry forktail cercariae.

4. The cercaria was described previously (Bearup, 1955) as Cercaria variglandis subspecies pyrazi, new subspecies. Now that the adult form has been identified as a previously described species the subspecific name pyrazi lapses.

The present revision of the morphology, taxonomy and affinities of trypanosomes causing Surra in the Old World was undertaken in order to determine the status of the diverse geographical and hostal strains, the exact relation of which to Trypanosoma evansi and allied species was hitherto a subject of controversy. The material for this study was represented by thirty strains from diverse mammalian hosts and various countries, extending from Morocco to the Philippines.

One of the problems dealt with is the occurrence of polymorphism in T. evansi. When single samples of typical (monomorphic) strains from naturally infected animals were examined, only negligible numbers of stumpy forms (0·05–0·40 %) were found in a minority of cases. But in strains kept under continuous observation for several years the proportion of stumpy forms occasionally rose higher (2–25%), while one strain exhibited a remarkable and persistent degree of polymorphism in the course of 17 years, the proportion of stumpy forms—including numerous posteronuclear ( = posterior-nuclear) ones—fluctuating from 0 to 60%. It was shown that—as in the case of the Brucei group—the length distributions in polymorphic samples of T. evansi could be statistically resolved into distinct curves, corresponding to the three morphological components (stumpy, intermediate, slender).

1. Liver lesions were easily induced in hamsters with two strains of E. histolytica but not with six others.

2. Serial liver passage increased the invasiveness to the rat's caecum of one strain which had become attenuated by in vitro cultivation.

3. The invasiveness of one of the liver passage substrains was lost a second time after cultivation in vitro and a second series of liver passages restored some degree of virulence.

4. Serial liver passage did not increase the invasiveness of two avirulent strains.

5. The ease of production of amoebic liver lesions in hamsters is not correlated with invasiveness in the rat's caecum.

Epidemics in English crayfish, Astacus pallipes, were found to be due to micro-sporidia and yeasts similar to, if not identical with, those causing diseases in another Crustacean, namely, Gammarus pulex, in many parts of England.

1. The total bacterial floras from invasive strains of Entamoeba histolytica, when added to non-invasive strains, do not increase the invasiveness of the latter.

2. The bacterial flora of non-invasive strains do not inhibit the invasiveness of virulent strains.

3. Bacteria from a virulent substrain (revived by serial liver passage) do not increase the invasiveness of the attenuated parent strain.

4. It is concluded that the virulence of a strain of E. histolytica is primarily dependent upon the invasiveness of the amoeba itself.

1. The emergence of the gametocytes of Plasmodium gallinaceum from the erythrocytes and the exflagellation of the male gametocyte were inhibited completely when infected blood was exposed to an atmosphere of 5 % CO2 and 95 % O2, or 5 % CO2 and 95 % N2. When these gas mixtures were replaced by air, the gametocytes emerged from the erythrocytes and the male gametocytes exflagellated after approximately the same interval as they did in newly drawn blood exposed to air, or in blood ingested by mosquitoes. If pure CO2 were used instead of the gas mixtures containing 5% CO2, the development of the gametocytes, after the replacement of the gas by air, was uncertain.

2. The emergence of the gametocytes and exflagellation of the male gametocytes proceeded normally when parasitized blood was exposed to an atmosphere of N2.

3. The pH of freshly drawn normal chick blood was 7·38–7·46. The pH of blood exposed to air rose over a 20 min. period of observation, the highest pH recorded being 7·97. No significant difference in pH was observed between normal and heavily infected blood. It was not possible to correlate the stages of development of the gametocytes with precise values of pH of the blood.

4. The development of the gametocytes proceeded normally when parasitized blood was mixed with isotonic alkaline Tris buffer to give a pH of approximately 8·0; but it was inhibited, though not completely, when the pH was reduced below that of freshly drawn blood by the addition of isotonic acid buffer. The inhibitory effect of the acid buffer could be completely but not invariably reversed by alkaline buffer.

5. 5 % CO2 had no inhibitory action upon the gametocytes if the pH of the blood-buffer mixture was 7·62, but when it was 7·20 the inhibitory effect of the gas was complete.

6. The emergence of the gametocytes from the corpuscles and the exflagellation of the male gametocytes were completely inhibited when washed, parasitized corpuscles were suspended in isotonic buffer pH 7·78 or 8·20, but this inhibition was completely reversed when the corpuscles were resuspended in plasma. It is concluded that a factor present in plasma is necessary for the development of the gametocytes.

7. Further evidence that the pH of the blood, alone, is not the only factor affecting the emergence of the gametocytes and exflagellation of the male gametocytes was obtained from birds treated intravenously with Diamox. When blood from such birds was exposed to air the gametocytes emerged from the corpuscles and exflagellation took place, although the pH of the blood was as low as, or lower than, that of freshly drawn blood.

8. The emergence of the gametocytes from the erythrocytes and exflagellation of the male gametocytes were not stimulated by secretions from the stomachs or salivary glands of gorged or unfed mosquitoes.

9. The lowest measurement of pH of blood from mosquitoes' stomachs was 7·47 and the highest 7·90, the mean being 7·68, which is slightly higher than that of freshly drawn chick blood. No correlation could be found between the pH of the blood and the length of time since its ingestion by the mosquito.

The micro-glass electrode used in measuring the pH of blood from the stomachs of mosquitoes was a modification of that described by Caldwell (1954). The electrode was made of capillary tubing, drawn from Corning 015 glass, the outer diameter being 0·5–0·75 mm. and the length about 6 cm. As the electrode was used with a Pye Universal pH meter, and not with the electrometer impedance converter circuit used by Caldwell, it was important that the wall of the capillary tube should be very thin, in order that the resistance of the electrode should not exceed 500 MΩ, the maximum electrode resistance permissible with the Pye Universal pH meter.

The effect of combined doses of pyrimethamine and quinine has been studied in P. gallinaceum. No potentiation of the action of the drugs was observed.

Nine out of thirty-three specimens of the common shrew Sorex araneus, caught at Rosta in north Norway in August 1953, were found to be infected with Grahamella (Rickettsiales). Nine specimens of Clethrionomys rutilus, nine of Microtus oeconomus ratticeps and one of M. agrestis, caught at the same time and place, were found to be free of Grahamella. No other blood parasites were found in any of the animals examined.

Records by other authors of Grahamella in a variety of hosts are reviewed. The parasite is known to occur in mammalian hosts only: identifications of it in non-mammalian hosts can be discarded. Host specificity, tacitly assumed by most authors, is not proven, and therefore most of the specific names bestowed on Grahamella in different hosts are of doubtful validity. The morphology of the parasite varies little from host to host; and there is little evidence to show that its pathogenic effect on any host is serious. Grahamella has been cultured by a few authors: variations in characters of these cultures may be more reliable criteria for recognition of different species of Grahamella.

These small mammals were collected while I was a member of the University of Edinburgh Expedition to Arctic Norway, 1953. I wish to thank all who were concerned, in particular Dr D. M. Steven, with whom I did the trapping. The rest of the work was done during the tenure of a Research Studentship awarded by the Agricultural Research Council. I also wish to thank Dr P. Tate for his advice and his criticisms of the manuscript.

An account is given of some viruses affecting insects of economic importance. Twenty-six viruses are listed affecting twenty-two species of insects. Of these viruses eleven cause cytoplasmic, and eight cause nuclear, polyhedroses. Six are granulosis viruses and one virus has no intracellular inclusions. Most of these viruses are new or recently recorded. The granulosis viruses, affecting Pieris brassicae, P. rapae and Melanchra persicariae, and the diseases they cause, are described in some detail.

We are indebted to Dr L. L. J. Ossowski of the Wattle Research Institute, University of Natal, and to Mr T. H. Coaker of the Cotton Research Station, Namulonge, Uganda, who sent us, respectively, diseased specimens of the wattle bagworm and the American cotton bollworm, from which the viruses were isolated. Miss S. Vernon-Smith took the electron micrographs, and Mr Simon Frey the photographs on the optical microscope.