Document MMpyJGoX1pm2mjoBp5Gb8beMa

PLAINTIFFS EXHIBIT SA-386 The Response of Peritoneal Tissue to Industrial Dusts 4 ... i' By JOHN W. MILLER and R. R. SAYERS / / REPRINT No. 2234 ROM THE PUBLIC HEALTH REPORTS Vol. 56. No. 7 Febbcaht 14,1941 - Paces 264-272 01 501 0010 FEDERAL SECURITY AGENCY UNITED STATES PUBLIC HEALTH SERVICE Thomas Pauah. Surgeon General DIVISION OF SANITARY REPORTS AND STATISTICS Cuno V. Aun. Auituiu Svpn Cmttrai, Chief / Duriuen + UNITED STATES GOVERNMENT PRINTING OFFICE, WASHINGTON : 1941 For ule by cbo Superintendent of Documents, Vuhin|ttB D. C. Pitee S cents 01 501 0011 hi Kl THE RESPONSE OF PERITONEAL TISSUE TO INDUSTRIAL DUSTS 1 By John W. Miller, Pathologist, and R. R. Savers,3 Senior Surgeon, United States Public Health Service The reaction of the peritoneal tissue to injected dusts has been described in previous reports3 and attention has been called to the possibility of using the results of such a biological response to predict the pneumoconiosis-producing potentialities of industrial dusts. From time to time, minor modifications in the method of introducing the dusts into the animals have been made to simplify the procedure without altering the results. As now practiced, the test is briefly as follows: Two cubic centi meters of a 5-percent suspension of air-elutriated (or 325-mesh screened), heat-sterilized dust in sterile, physiological saline solution is injected into the peritoneal cavities of a number of guinea pigs. Animals are killed and examined 14, 45, and 90 days after injection (in earlier experiments at intervals up to 1 year). The nodules produced by the dust on the anterior abdominal walls or in the omentum at the various intervals are compared. The gross appearance is usually sufficient for interpretation of results. Three general types of reaction are produced by the various dusts. These have been designated as absorptive, proliferative, and inert. Dusts of the absorptive group produce nodules which progressively decrease in size as the interval between injection and examination increases. Eventually the dust disappears from the peritoneal tissue. From the Division of Industrial Byyiene, National Institute ol Health. 1 Director of the Bureau of Mines. * Miller. J. W,, and Sayers. R. R.: The response of peritoneal tissue to dusts introduced as foreign bodies. Pub. Health Rep.. 40: 80-S (January IP, ISM) (Reprint No. 1808). J. Am. Med. Assoc.. 103 : 007-012 (Sep tember 22.1034). Am. J. Pub. Health, tt: 482-456 (April IBM). Pub. Health Rep., 51:1677-1680 (Decem ber 4.1038) (Reprint No. 1787). Miller. J. W,, and Sayers. R. R.: Microscopic appearance ol experimentally produced dust nodules in the peritoneum. Pub. Health Rep., SO: 1610-1628 (November IS, 103S) (Repnnt No. 1717). 308594--(1 1 o i 5 Oil 0012 2 REACTIONS TO INDUSTRIAL DUSTS Microscopically, & typical early nodule consists of a mass of the dust mixed with fine, granular, necrotic material. A zone of fibroblasts with an occasional macrophage surrounds this more or less centrally placed mass. With time the necrotic material becomes less and finally disappears. Brown pigment particles, apparently of endogenous origin, are usually found rather early, and in an experiment of a year's duration are the only evidence that the dust was introduced into the peritoneal cavity. Dusts causing a proliferative type of reaction produce nodules which progressively increase in size as the interval between injection and examination increases. The maximum growth, using & O.i-gm. dose for each guinea pig, is reached in about 90 days. Microscopically the nodules 7 days after injection are similar to those produced by the dusts of the absorptive group. As the process continues, the fibro blasts in the cellular zone about the central mass of dust and necrotic material are largely replaced by macrophages which are usually filled with dust particles. This is most marked in the 30-day series. Later, the engulfed dust particles appear to decrease in numbers and fibroblasts and adult connective tissue cells predominate. The area of necrotic material persists throughout the duration of the test. After 90 days fat cell formation in the cellular zone and calcification of the necrotic material is noted. All of the dusts classified in this group studied thus far are various forms of naturally occurring silica. The nodules produced by the inert group of dusts are, in the early stages, grossly similar to those of the other two groups. As the interval between injection and examination increases the nodules become flattened with irregular edges, and numerous dispersed partides are present in the adjacent peritoneum. These are often found a considerable distance from the original nodules. The amount of dust found in the peritoneal cavity 1 year after injection is essentially the same as noted in 7 days. Histologically, the fibroblast is the early predominating cell. An increase in macrophages is noted at the 30-day interval and eventually fibrous tissue and accompanying fat cells predominate. No necrosis is noted at any interval in the entire process. The response is characteristic of that caused by a nonirritat ing foreign body. It has been possible to correlate the response of peritoneal tissue to certain dusts with the results of X-ray examination or of post-mortem study of workers exposed by inhalation to high concentrations of the same dusts for protracted periods of time. These records are far from complete, because medical and roentgenographic surveys are available for only a limited number of the dusty trades. Neverthe less, the preliminary results of such comparisons can be summarized: (a) No cases of pneumoconiosis have been reported and confirmed among workers exposed solely to dusts of the absorptive group; (6) all REACTIONS TO INDUSTRIAL DUSTS 3 of the dusts so far examined that fall into the proliferative group are known to produce a nodular, pulmonary fibrosis (silicosis); (c) pneu moconioses caused by dusts of the inert group (asbestos,* anthracite mine dusts,* bisque ware,* mica,7 pyrophyllite,* and talc *) have been reported as a result of X-ray examination of industrial workers. Where autopsy material is available, certain of the dusts of this group are known to produce a diffuse, interstitial, pulmonary fibrosis, or a mixed nodular and diffuse fibrosis, such as is produced by anthracite coal containing free silica. Interpretation of the response produced by a dust in the peritoneal tissue in animals can be used as an index to determine the potential harmfulness of an industrial dust to which workers are exposed. Thus, an absorptive reaction can indicate that the dust is relatively harmless, while a proliferative response would indicate the dust to be definitely harmful. The dusts producing an inert reaction have been considered as less hazardous than those producing a proliferative reaction, and more dangerous than those of the absorptive group. The intraperitoneal method of studying the physiological action caused by dusts is not applicable to highly toxic material, a sublethal dose of which is too small to be grossly visible in the peritoneal tissue, or to dusts that are readily soluble. The following dusts have been examined by this method and the results, with pertinent identifying data, are given below. DUSTS CAUSING AN ABSORPTIVE REACTION Caleite.--A pure mineral dust. Chemical analysis: Acid insoluble matter, 0.0 percent; silica, 0.0 percent. Petrographic examination: A calcite of high purity. CaiciU.--A pure mineral dust. Chemical analysis: Acid insoluble matter, 0.1 percent, all of which was silica Petrographic examination: A calcite of high purity. Precipitated calcium carbonate.--A chemical byproduct. An industrial dust. Chemical analysis: Silica, 0.4 percent; calcium carbonate, 87.9 percent; magnesium carbonate, 10.1 percent; magnesium oxide, 0.1 percent; iron and aluminum oxides, 0.6 percent. Petrographic examination: Precipitated calcium carbonate, about 98 percent; crystals, probably sodium carbonate, about 2 percent. Gypsum.--The uncalcined, natural mineral An industrial dust. Chemical analysis: Silica, 1.3 percent; calcium sulfate, 97.1 percent. Petrographic exam ination: Gypsum, about 70 percent; calcite, about 30 percent. < Dreessen. W. C., DallaVaile. J. M.. et al.: A study at asbestosis is the asbestos textile Industry. Pub. Bealth Bull. No. 241. U. S. Government Printing Office. 1938. ` Sayers, R. R., Bloomfield, ]. I., et al.: Antbracosilicosis among bard-coal miners. Pub. Health Bull. No. 221. U. S. Government Printing Office, 193S. ' 1 Flinn. R. B.. Dreessen, W. C., et al.: Silicosis and lead poisoning among pottery workers. Pub. Health Bull. No. 244. U. S. Government Printing Office. 1939. 1 Dreessen. W. C., DallaValle. J. M.. et al.: Pneumoconiosis among mica and pegmatite workers. Pub. Health Bull. No. 230. U. S. Government Printing Office, 194C. - Easom. H. F., Trice, M. F.and Carpenter. C. C.: A study of the effects of exposure to dust in the mining and milling ol pyrophyllite. Report, North Carolina State Board of Health. February 1939. ' Dreessen. W. C., and DallaValle, J. M.: Effects ol exposure to dust in two Georgia talc mills and mines. Pub. Health Rep., SO: 131-143 (February 1,1933) (Reprint No. 1609). 4 REACTIONS TO INDUSTRIAL DUSTS Limestone.--An industrial dust. Chemical analysis: Silica, 1.5 percent; calcium oxide, 54.4 percent; magnesium oxide, 0.4 percent; iron and aluminum oxides, 0.4 percent. Petrographic examination: Irregularly rounded calcite. No impurities noted. Limestone.--An industrial dust. Chemical analysis: Silica, 2.73 percent; calcium carbonate, 95.21 percent; magnesium carbonate, 1.17 percent. Petro graphic examination: A dolomitic limestone. No impurities observed. Limestone.--An industrial dust. Chemical analysis: Acid insoluble matter, 7.2 percent; silica, 5 percent. Petrographic examination: Only an infrequent quartz crystal was noted. A high calcium carbonate content. Limestone.--An industrial dust. Chemical analysis: Silica, 11.7 percent; calcium carbonate, 81.7 percent; magnesium oxide, 3.4 percent; ferric oxide, 1.4 percent; aluminum oxide, 1.5 percent. Petrographic examination: About 10 percent quartz and about 90 percent calcite. Portland cement.--An industrial dust. Chemical analysis: Silica, 21.1 percent; calcium oxide, 74.4 percent; magnesium oxide, 2.8 percent. Petrographic exami nation: Normal portland cement. Pyrolusite.--An industrial dust. Chemical analysis: Manganese, 54.9 percent. Petrographic examination: No quartz observed. This material was much more slowly absorbed than the others given here. DUSTS CAUSING A PROLIFERATIVE REACTION Bisque ware.--An industrial dust. Ground semivitreous pottery bisque ware, fired at a relatively low temperature. Chemical analysis: Silica, 72.0 percent. Petrographic examination: Quartz, about 40 to 50 percent. The remainder is semifused clay and feldspar. Chert.--An industrial dust. Chemical analysis: Total silica, 76.1 percent. Petrographic examination: Quartz and chert, about 60 percent (about 25 percent of the silica is normal quartz). Calcite, about 40 percent. Diatomite.--An industrial dust. Chemical analysis: Silica, 92.5 percent; aluminum oxide, 3.5 percent; ferric oxide, 1.5 percent; calcium oxide, 0.4 percent; magnesium oxide, 0.7 percent. Petrographic examination: Pure diatomite. No quartz or calcite present. Greenware.--An industrial dust. Ground semivitreous, unfired pottery ware. Chemical analysis: Silica, 69.0 percent. Petrographic examination: Quartz, about 50 percent; feldspar, about 15 percent; clay, about 35 percent. Greenware.--An industrial dust. Ground vitreous, unfired pottery ware. Petrographic examination: Higher quartz and less feldspar than the above. Clay, about the same amount. Porcelain enamel frit.--An industrial dust. Chemical analysis: Silica, 35 to 50 percent; the remainder is oxides of antimony, zinc, and aluminum, and fluorides of sodium, aluminum, and caloium. Analysis varies within the above silica limits. Quarts.--A pure mineral dust. Chemical analysis: Silica, 99.4 percent. Petro graphic analysis: Normal crystalline quartz of high purity. Quarts.--A pure mineral dust. Chemical analysis: Silica, 99.3 percent. Petrographic examination: Normal crystalline quartz of high purity. Quarts.--An industrial dust. Chemical analysis: Silica, 99.1 percent. Petro graphic examination: Normal quartz. ' Quarts.--An industrial dust. Petrographic examination: Normal crystalline quartz of high purity. Quarts.--An industrial dust. Identical with the above sample but treated with 0.6 percent crude pine fatty acids. REACTIONS TO INDUSTRIAL DUSTS 5 Quartz-aerieite.--The source of this dust is not known. Chemical analysis: Total silica, 81.04 percent; calcium oxide, 0.30 percent; magnesium oxide, 0.45 percent; sodium oxide, 0.10 percent; potassium oxide, 0.98 percent; iron oxide, 0.25 percent; aluminum oxide, 14.26 percent; total water, 2.61 percent. Petro graphic examination: Quartz, about 50 percent; muscovite (variety, sericite), about 45 percent; fibrous sericite, less than 5 percent. Tripoli.--An industrial dust. Chemical analysis: Total silica, 98.9 percent; calcium oxide, 0.2 percent; magnesium oxide, 0.1 percent; iron and aluminum oxides, 0.3 percent Petrographic examination: Chalcedonic silica (crystalline aggregates) with an occasional crystal of normal quartz. DUSTS CAUSING AN INERT REACTION Afumt'num.-i-Pure aluminum bronzing powder of the finest grade. Chemical analysis: Aluminum oxide, 11.0 percent. Alundum.--An industrial dust. Chemical analysis: Silica, 4.6 percent; aluminum oxide, 88.4 percent; ferric oxide, 6.9 percent. Petrographic examina tion: Well crystallized, artificial alumina. Aabeatoa (amosite).--An industrial dust. Chemical analysis: Total silica, 48.31 percent; calcium oxide, 0.48 percent; magnesium oxide, 0.66 percent; sodium oxide, 0.72 percent; potassium oxide, 0.02 percent; iron oxide, 44.22 per cent; combined oxides, 46.37 percent; total water, 3.62 percent. Petrographic examination showed predominating individual fibers and about 1 or 2 percent of dolomite. Aabeatoa (chrysotile).--An industrial dust. Chemical analysis: Total silica, 37.52 percent; calcium oxide, 2.00 percent; magnesium oxide, 36.85 percent; sodium oxide, 0.54 percent; potassium oxide, 0.08 percent; iron oxide, 7.70 percent; combined oxides, 10.30 percent; total water, 12.86 percent. Petrographic ex amination: Serpentine, in part chrysotile, about 85 percent; dolomite, about 5 percent; magnetite and (or) chromite, about 5 percent; talc, less than 5 percent. Aabeatoa (crocidolite).--An industrial dust. Chemical analysis: Total silica, 50.86 percent; calcium oxide, 0.68 percent; potassium oxide, 0.08 percent; iron oxide, 38.33 percent; combined oxides, 39.03 percent; total water, 5.02 percent. Petrographic examination showed fibrous material only. * Anthroeite cool.--An industrial dust. Chemical analysis: Ash, 12.6 percent; silica, 6.6 percent. Petrographic examination: Coal about 95 percent; inorganic material, about 5 percent. About 60 percent of the inorganic material is quartz; about 40 percent is calcite, with an occasional crystal of rutile. Anthracite coal.--An industrial dust. Chemical analysis: Ash, 16.0 percent; silica, 8.6 percent. Petrographic examination: Coal, about 95 percent; inorganic material, about 5 percent. About 95 percent of the inorganic material is quartz; about 5 percent is calcite, siderite, limonite, and rutile. Bentonite.--An industrial dost. Petrographic examination: Clay, variety montmorillonite, about 97 percent; feldspar, about 2 percent; quartz, none observed. Biaque ware.--An industrial dust. Ground vitreous pottery bisque ware, fired at a relatively high temperature. Petrographic examination: Quartz, about 30 to 40 percent. The particles are wholly or partially covered by the glass phase. This is absent in the semivitreous bisque ware. Bituminous coal.--An industrial dust. Chemical analysis: Ash, 8.5 percent; silica, 0.8 percent. Petrographic examination: Mineral content (calcite), about 1 to 2 percent. 0016  v> REACTIONS TO INDUSTRIAL DUSTS Bituminous coal.--An industrial dust. Chemical analysis: Ash, 8.0 percent; silica, 3.5 percent. Petrographic examination: Mineral content (quartz, calcite, clay), between 1 and 3 percent. Calcium phosphate.--An industrial dust. Chemical analysis: Calcium phos phate, 75.38 percent; calcium carbonate, 3.98 percent; calcium fluoride, 0.80 percent; magnesium carbonate, 0.51 percent; iron oxide, 3.08 percent; aluminum oxide, 3.12 percent; free silica, 2.70 percent; combined silica, 1.87 percent. Petro graphic examination: Earthy phosphates (not apatite), about 97 percent; normal and chalcedonie quartz, about 3 percent. Chromite.--An industrial dust. Chemical analysis*. 8iliea, 7.8 percent; chromic oxide, 25.0 percent. Petrographic examination: Quartz, less than 5 percent. Diamond dust.--An industrial dust. Pure borts diamond dust used as abrasive. Petrographic examination confirms identity. . Feldspar.--Chemical analyses: Total silica, 65.9 percent; calcium oxide, 0.81 percent; magnesium- oxide, 0.10 percent; aluminum oxide, .19.55 percent; iron oxjde, 0.28 'percent; potassium oxide, 8.98 percent; sodium oxide, 3.18 percent. Petrographic examination: Feldspar (plagioclase-microcline), about 95 percent; normal quartz, about 5 percent. . . 'FyM.er's. cortA.-r-An industrial dust. Filtral clay. Chemical analysis: Silica, 55.7 percent; freq silica (estimated), .1.0 percent; water, 15.9 percent. Petro graphic examination: Clay and residual decomposing feldspar, about 95 percent; quarts, less than 1 percent; gypsum, less than 5 percent. : . , Fuller's earth.--An industrial dust.. Chemical analysis: Silica, 56.4 percent; free silica (estimated), 7.0 percent; water, 8.5 percent. .Petrographic examination: Clay and decomposing feldspar, about 90 to 95 percent; quarts, about 5 to 10 percent.,. - ,_ '' . ... .... ' Fuller's sartfu--An industrial dust. Chemical analysis: Slice, 57.9 percent ferric oxide* 2.5 percent; aluminum oxide, 13.1 percent; calcium oxider2.9 percent magnesium oxide, ,8.5 peroent; water, 6.7 percent. Petrographic examination: Clay-like masses, . rounded and. irregular, about .70 percent; quarts, about 15 percent; dolomite, about 15 percent. ....... .. Fuller's earth.--Ah industrial dust,,..Filtral day., Chemical analyse: Silica, 62.1 percent;^ee silica (estimated), 3.0 percent; water, 14.9 percent. Petro graphic examination: Clay and residual decomposing feldspar, about 98 percent; ^quartz, 1 to 2 percent; feldspar, an occasional fragment. . ^^ , / Glass trod.--An industrial duet.' Finely ground sample of commercial hard / glass wool was used. No chemical, or petrographic examinations were thought I :. ______ ,,------' ' V___ Hemarite ^Qewelers'.rouge)..--An mdustrial dust. Chemical analysis: Totaf silica,. T.5 percent; iron, oxide, .98.3 percent. Petrographic examination showed no impurities. ,__ . . , Kaolin.--An 'industrial^dust. , Petrographic examination: China clay and hydromiga predominant; quarts and feldspar, a trace. . 'Lanthanum sublimate.--An industrial dust. From the burning of white flame electrodes/^ Chemicalanalysis: T-anthanuTn, 40.0 percent. Petrographic examina tion: Particles too small to identify. ... Mica.--An industrial dust. Chemical analysis: Silica, 46.92 percent; magne- aium oride, 0.86.percent; aluminum oxide, 34.95 percent; ferric oxide, 2.65 per . cent;, potassium, oxide, 9.54 percent; sodium oxide, 1.02 percent; manganese " gioride, trace. ' Petrographic examination: Mica, both as plates and fibers, platee predominating, about 98 percent. A very small amount of quartz and feldspar. -a Precipitator an.--An industrial dust. Chemical analysis: Total silica, 49.86 percent; calcium oxide, 6.03 percent; magnesium oxide, 3.01 percent; iron and u-1 js mt? -rdf. i REACTIONS TO INDUSTRIAL DUSTS 7 aluminum oxides, 40.46 percent. Petrographic examination: Loosely consoli dated, white, soft, grit-free ash, about 40 percent; partly rounded aggregates of semifused ash, about 45 percent; smooth fused glass globules, about 10 percent; normal quartz fragments, about 5 percent; unburned coal, less than l percent. Precipitator ash.--An industrial dust. From the boiler plant of a coal com pany. Chemical analysis: Silica, 48.2 percent; aluminum oxide, 29.3 percent; ferric oxide, 8.5 percent; calcium oxide, 2.1 percent; magnesium oxide, 0.1 per cent; organic matter, 8.6 percent. Petrographic examination: Predominantly spherulized glass, some coal fragments, and a trace of quartz. Precipitator ash.--An industrial dust. Chemical analysis: Silica, 48.3 percent; aluminum oxide, 29.4 percent; ferric oxide, 8.6 percent; calcium oxide, 1,8 per cent; magnesium oxide, 0.4 percent; organic matter, 8.7 percent. Petrographic examination: Predominantly semivitrified ash particles, some spheres, coal, and a trace of quartz. - Precipitator ash.--An industrial dust. Chemical analysis: Total silica, 44.7 percent; moisture, 0.1 percent. Petrographic examination: Mostly spherical fused-glass particles, with some semifused masses of crystallites, quartz, possibly calcite and coal fragments. Precipitator ash.--An industrial dust. Lamphouse deposit from the burning of carbon arcs. Chemical analysis: Bare earth oxides (cerium group), 70.7 per cent; ferric oxide, 0.8 percent; magnesium oxide, 0.5 percent; moisture, 9.8 per cent; silica, none. Petrographic examination: Inorganio material, rudely rounded, about 5 percent of opaque carbonaceous material and no quartz. Precipitator ash.--An industrial dust. Condensate from the flue system from burning of carbon arcs. Chemical analysis: Rare earth oxides (cerium group), 59.5 percent; silica, 1.0 percent; ferric oxide, 4.1 percent; magnesium oxide, 0.9 percent; calcium oxide, 0.6 percent; ignition loss, 18.4 percent. Petrographic examination: No quartz or calcite, otherwise similar to preceding sample. Pyrophyllite.--An industrial dust. No chemical analysis, obtained. Petro graphic examination: Predominantly pyrophyllite, with a small amount of rutile and some quartz. The quantity of quartz was hard to estimate. Rock wool.--An industrial dust. A finely ground sample of commercial, insu lating rock wool. ^ Selenium.--An industrial dust. Chemical analysis: Selenium, 98.8 percent: tellurium, 0.01 percent; ash, 1.16 percent. Selenium.--A chemically prenared sample of highest purity. Sericite.--A pure mineral dust. Chemical analysis: Total silica, 51.74 percent; calcium oxide, 0.61 percent; magnesium oxide, 1.74 percent; sodium oxide, 3.40 percent; potassium oxide, 4.48 percent; iron oxide, 5.83 percent; combined oxides, 31.82 percent; total water, 6.26 percent. Petrographic examination: Sericite and feldspar residues (fibrous sericite predominates), about 95 percent; quartz, less than 5 percent. * Shale.--An industrial dust. Chemical analysis: Silica, 61.0 percent; aluminum oxide, 12.4 percent; calcium oxide, 4.5 percent; ferric oxide, 5.0 percent; magne sium oxide, 1.3 percent; sodium oxide, 2.3 percent; potassium oxide, 1.5 percent; moisture, 10.3 percent. Petrographic examination: About 35 percent quartz. The majority of the particles appear to be coated with clay. . Silicon carbide.--Pure manufactured silicon carbide. Chemical analysis: Silicon, 67.5 percent. Petrographic examination showed no impurities. Soapstone.--An industrial dust. Chemical analysis: Total silica, 49.9 percent; calcium oxide, 1.7 percent; magnesium oxide, 26.2 percent. Petrographic exam ination: Talc, as plates or fibrous splinters, about 65 percent^hMmolite, as long fibrous crystals, about 30 percent; dolomite, about 5 percent. ::: -m ffft $48 8 reactions to industrial dusts Soapstone.--As industrial dust. Chemical analysis: Total silica, 36.8 percent; calcium oxide, 5.0 percent; magnesium oxide, 22.7 percent. Petrographic examination: Talc, about 55 percent; dolomite, about 30 percent; tremolite, about 15 percent. No quarts observed. Talc.--An industrial dust. Chemical analysis: Total silica, 49.0 percent;' calcium oxide, 8.8 percent; magnesium oxide, 22.6 percent. Petrographic examination: Tremolite, about 60 percent; talc, about 40 percent. Talc.--An industrial dust. Chemical analysis: Total silica, 56.54 percent; calcium oxide, 6.25 percent; magnesium oxide, 30.74 percent; calcium silicate, 11.00 percent; calcium carbonate, 1.88 percent; iron and aluminum oxides, 1.04 percent; ignition loss, 4.60 percent. Petrographic examination: Talc, mostly fibrous, about 75 percent; tremolite, partly altered to talc, about 25 percent; calcite and (or) dolomite, about 1 percent. Titanium oxide.--An industrial dust. A finely divided high purity sample. Sodium silicate.--A laboratory prepared sample containing 1 part sodium oxide to 3.1 parts silica. Higher ratios of sodium oxide kill the animals. Trap rock.--An industrial dust. Chemical analysis: Silica, 51.7 percent; aluminum oxide, 16.0 percent; ferric oxide, 2.0 percent; ferrous oxide, 9.9 percent; calcium oxide, 10.0 percent; magnesium oxide, 6.2 percent. Petrographic examination: Feldspar, some slightly decomposed, about 45 percent; pyroxene, about 45 percent; rpagnetite, about 10 percent; biotite, aboutrl percent. Volcanic ask.--An industrial dust. Chemical analysis: Silica, 54.4 percent; aluminum oxide, 1-4.5 percent; ferric oxide, 3.8 percent; magnesium oxide, 2.6 pefcent; calcium oxide, 0.7 percent; ash, 78J2 percent. Petrographic examination: Fine volcanio ash partially altered to montmorillonite. No quarts observed. Volcanic ash.--A specially treated sample. Chemical analysis: Silica, 74.3 percent; mixed oxides, 16.8 percent; ferric oxide, 2.2 percent; calcium oxide, 0.5 percent; magnesium oxide, 2.2 percent. Petrographic examination: Glass only. No quarts or calcite observed. SUMUABT AND CONCLUSIONS A definite quantity of dust injected into the peritoneal cavity of a guinea pig produces one of three types of reaction. It disappears, causes proliferation of the peritoneal tissue, or remains as an inert foreign body. These reactions may be used as a basiB for the biological classification of industrial dusts, and seem to indicate that some rela tionship exists between the type of reaction produced in the peritoneal tissue by a dust and fhe ability of this dust to produce a characteristic type of pneumoconiosis. An absorptive reaction may indicate that a dust is relatively harmless, while a proliferative reaction, characteristic of quartz, may be associated with the ability to produce pulmonary fibrosis. Dusts of the inert group, that is, those that show a tendency to remain in the tissues, should be considered as potentially harmful, but not so dangerous as those causing a proliferative response. With this biological method of classification, which in a number of instances has been correlated with clinical observations and industrial surveys, it is quite possible to determine the pneumoconiotic poten tialities of a djist in a relatively short time, usually 60 days. 61 661 0619 REACTIONS TO INDUSTRIAL DUSTS 9 ACKNOWLEDGMENTS Acknowledgment is made of the kindness of Mr. W. A. Selvig of the United States Bureau of Mines and of Associate Chemist F. H. Goldman of the United States Public Health Service for the chemical analyses of the dusts used in these experiments. The petrographic examinations were made by Dr. Alton Gabriel of the United States Bureau of Mines and Dr. F. H. Goldman. Acknowledgment is also made to Technical Editor T. I. Edwards for assistance in preparing this report and to Medical Technician E. C. Thompson for technical aid. O : 01 501 0020 Public Health Reports sovolume FEBRUARY 14, 1941 ntjmbeb t IN THIS ISSUE Summary of Current Prevalence of Communicable Diseases The Response of Peritoneal Tissue to Industrial Dusts Immunologic Study of Australian and American "Q" Fever Studies of Lymphocytic Choriomeningitis Virus in Mice The Effect of Urea on the Bacterial Assay of Riboflavin 021 FEDERAL SECURITY AGENCY UNITED STATES PUBLIC HEALTH SERVICE Thokas Par&an, Surgeon General DIVISION or SANITART REPORTS AND STATISTICS Chaws V. An*, Auldaat 3*rf0% OntTil, CUtf Dbiiiou The Public Health Reports, first published in 1878 under authority of an act of Congress of April 29 of that year, is issued weekly by the United States Public Health Service through the Division of Sanitary Reports and Statistics, pursuant to the following authority of law: United States Code, title 42, sections 7, 30, 93; title 44, section 220. It contains (1) current information regarding the prevalence and geographic distribution of communicable diseases in the United States, insofar as data are obtainable, and of cholera, plague, smallpox, typhus fever, yellow fever, and other important communicable diseases throughout the world; (2) articles relating to the cause, prevention, and control of disease; (3) other pertinent information regarding sanitation and the conservation of the public health. The Public Health Reports is published primarily for distribution, in accord ance with the law, to health officers, members at boards or departments of health, and other persons directly or indirectly engaged In public health work. Articles of special interest are issued as reprints or as supplements, in which forms they are made available for more economical and general distribution. Requests for and communications regarding the Public Health Reports, reprints, or supplements should be addressed to the Burgeon General, United States Public Health Service, Washington, D. C. Subscribers should remit direct to the Superintendent of Documents, Washington, D. C. Librarians and others should preserve their copies for binding, as the Public Health Service is unable to supply the general demand for bound copies. Indexes will be supplied upon request. UNITED STATES GOVERNMENT PRINTING OITICE. WASHINGTON I IMI For hIi bf tb Sopcfinuadut of Dtnmata* Wuhlaftoit D. G. Prkt ft cuta. Bnbecrtpfbin price CLftO a fmt ao #*'5*1*022 CONTENTS Prevalence of communicable diseases in the United States, December 29, 1940-January 25, 1941 The response of peritoneal tissue to industrial dusts 264 Immunological relationships between the rickettsiae of Australian and American "Q" fever 272 The inhibiting effect of urea on the microbiological assay of riboflavin.. Studies on the natural history of the virus of lymphocytic choriomeningitis in mice 285 A note on modified radio pratique in Guayaquil 292 Notifiable diseases in the United States, 1939. Morbidity and mortality summaries for certain important communicable diseases______________ Court decision on public health 300 Deaths during week ended February 1, 1941: Deaths in a group of large cities in the United States______________ Death claims reported by insurance companies___ __________ ______ Pit* 259 282 293 300 300 PREVALENCE OP DISEASE United States: Reports from States for week ended February 8,1941, and comparison with former years 301 Weekly reports from cities: City reports for week ended January 25, 1941_____________ Foreign reports: Canada--Provinces--Communicable diseases--Week ended January 4, 1941.................................................................................................. Cuba--Provinces--Notifiable diseases--4 weeks ended December 7, 1940...................................................................................................... Jamaica--Communicable diseases--4 weeksended January 18, 1941. Venezuela--Caracas--Poliomyelitis 309 Yugoslavia--Notifiable riinriMrn - 1 weeks ended December 1, 1940 __ Reports of cholera, plague, smallpox, typhus fever, and yellow fever received during the current week-- Smallpox 309 305 308 308 308 309 m Public Health Reports Vol. 56 FEBRUARY 14, 1941 No. 7 PREVALENCE OF COMMUNICABLE DISEASES IN THE UNITED STATES December 29, 1940-J*nu*ry 25, 1941 The accompanying table (table 2) summarizes , the prevalence of nine important communicable diseases, based on weekly telegraphic reports from State health departments. The reports from each State are published in the Public Health Reports under the section "Preva lence of disease." The table gives the number of cases of these dis eases for the 4-week period ended January 25, 1941, the number re ported for the corresponding period in 1940, and the median number for the years 1936-40. DISEASES ABOVE MEDIAN PREVALENCE Influenza.--The number of cases of influenza continued to increase during the first 3 weeks of the 4-week period ended January 25, but decreased considerably during the fourth week. The number of cases reported weekly was as follows: Week ended January 4,, 12,905, January 11, 89,828, January 18, 120,006, and Januarf%5, 96,652 cases. The total of 383,630 cases was the highest reported for this period since 1929, when a total of approximately 425,000 cases oc curred during this period. During the 1932-33 epidemic there were approximately 144,000 cases reported for this period. The number of cases was almost seven and one-half times the number recorded in 1940 and more than 30 times the 1936-40 median figure for this period. The current epidemic started in the Mountain and Pacific regions and spread rapidly into the southern areas. For the current period 200,218 cases, or more than 50 percent of the total, were reported from the South Central region, and more than 30 percent from the South Atlantic region (114,502 cases). States in those regions reporting the highest incidence were: Texas (109,820 cases); Kentucky (20,667); Alabama (19,188); Virginia (32,412); South Carolina (28,002); Georgia (25,523); and West Virginia (23,354). Increases were also noted in the New England and North Central regions, but the incidence in those regions has been low as compared 2S5759*--tl----- 1 (259) OlfW>25' February 14.1941 260 with the southern and western regions. Maine with approximately 5,000 cases, New Hampshire with about 2,000, and Connecticut with 2,708 cases were mostly responsible for an excess of cases in the New England region; Ohio reported 6,895 of approximately 10,000 cases occurring in the East North Central region, and Kansas reported 8,406 of the 12,169 cases reported from the West North Central region. Further increases may be expected in those regions, as the maximum incidence up to that date was reported during the week ended January 25. In the Mountain and Pacific regions the peak was reached during the week ended December 21 with approximately 27,000 reported cases, while in the South Central regions the maximum weekly inci dence was reported during the week ended January 11, and it is probable that the week ended December 25 will be the peak week in the South Atlantic region. Mortality from all causes for the total number of cities reporting shows some excess during this period, the rate for January being 13.7 per 1,000 compared with an average rate for the years 1938-40 of 13.1 per 1,000. This excess in mortality from all causes is a reflection of the current influenza epidemic. The death rate for pneumonia as reported to the Public Health Service is below the average of the previous 3 years for January, while the death rate for influenza is well above the average rate for the 3 previous years. Mortality from all causes is further analyzed in table 1, where rates are shown for the 4 weeks of January for nine geographic sec tions of the United States. In the Pacific section where the current influenza epidemic first appeared, mortality from all causes was some what above normal during December (not shown in the table), and has contiffted slightly above normal during January. In the Moun tain and the two West Central sections, mortality from all causes was definitely above normal during the first week in January and has continued to be slightly above normal in the later weeks of Jan uary. In the East South Central section, mortality from all causes was slightly above normal during the second and third weeks of January. In the East North Central, Middle Atlantic, and South Atlantic sections there has also been only a slight increase in mor tality from all causes, occurring mainly in the last week of January. In the New England States mortality from all causes has been higher than average throughout January, with a marked increase in the rates for the latter half of the month. Later reports (week ended February 1) indicate a still further decline in the number of cases in practically all sections of the country. For the country as a whole, the cases totaled approximately 73,000, as compared with 96,652 cases for the week ended January 25 and approximately 120,000 for the week ended January 18. 01 0026 261 February 14, 1WI Table 1.--Mortality from all causes in cities in 9 geographic sections of the United States for the 4 weeks of January 1941 compared with an average of the S preceding years 1 Death rate per 1,000 (annual basis) Jan. 4 Jan.11 Jan. IS Jan. 29 All dtles reporting: Average. 1938-40--------------------------------------------------------------------------------------pacific: Average, l#3S-fO--------------------------------------------------------------------------------------Mouauua: Average. 1938-40----------------------------------------------------------------------- --------------West North Central: Average* 1838-40....-...----.--....-^--.----.--..-....--. West South Central: Average. 1938-40----------------------------------------------------------- ---------------------------East South Central: Average. 1938-40 But North Central: 1041 ................. ...___________________________ _ Average. 1938-40_____________________________ Middle Atlantic: 1041 ......................... ............ ................................ ..................... Average. 1938-40--------------------------------------------------------------------------------------South Atlantic: 1041 . ........................ ................... .................................................. Average. 1938-10______ ______________________ _________ New England: 1941 . , . . _____ _______ ___ _______ . . . Average. 1938-40----------------------------------------------------------- 12.9 13.1 13.8 13.4 21.5 15.3 15.0 13.4 30.7 17.8 14.1 18.1 n.i 11.8 12.3 13.1 111 14.8 14.8 1X8 117 111 1ft. 8 14.0 lft.7 1X3 111 1X2 1X3 1X3 113 115 11.8 111 113 1X8 14.9 14.5 I6u4 111 115 12.9 117 14.0 17.4 115 119 118 IX T 1X7 115 14.5 11.3 11.4 112 119 14.4 14.4 19.8 115 14. ft 112 114 lift 113 14. ft 14.1 lift 17.9 17.3 17.4 lift 1X6 11.2 14.4 112 110 14.0 20.8 14.8 i Based on data reoeived from the Bureau of the Census. Measles.--The number of cases (40,419) of measles reported for the current period was more than two and one-half times the number reported for the corresponding period in 1940 and more than twice the 1936--10 median number of cases for this period. Excesses over the seasonal expectancy were reported from the Middle Atlantic, East North Central, and East South Central regions, but in all other regions the incidence was relatively low. In the Middle Atlantic region the number of cases was more than three and one-half times the normal expectancy, and in the East North Central region the number was almost six times the median figure for the period. In the Pacific region, where the disease was unusually prevalent at this time last year, the number of cases was less than one-fourth of last year's incidence, as well as of the 1936-40 median which is represented by the 1940 figure. Poliomyelitis.--While the incidence of poliomyelitis declined still further during the current period, the number of cases (170) reported was the highest recorded since 1931 when the cases for this period totaled 194. The disease was most prevalent in the Middle and South Atlantic regions and in the North Central regions. In the Edit North Central region, Wisconsin reported 24 cases, Ohio 14, and Illinois 11 cases; Florida (7 cases) and West Virginia (6 cases) reported the largest .1 01 501 0027 February 14. 1941 262 numbers of cases in the South Atlantic region and New York, in the Middle Atlantic region, reported 19 cases. No more than 5 cases were reported from any other State. A further decline in this disease may be expected as the lowest incidence is usually reached during the months of April and May. Whooping cough.--There were a few more cases of whooping cough than might normally be expected, the cases (16,857) reported for the current period being about 60 percent above last year's figure for this period and almost 10 percent above the 1938-40 median incidence. Each region except the Mountain contributed to the excess incidence. Table 2.--Number of reported caeca of 9 communicable diseases in the United States during the 4-veek period Dec. 99, 1940-Jan. 95, 1941, the number for the corre sponding period in 1940, and the median number of cases reported for the corre sponding period 1936-40 Division United States-------------------------New England_____________ Middle Atlantic___________ East North Central West North Central_______ South Atlantic___ ________ East Sooth Central_______ West Sooth Central_______ Mountain________________ Pacific_____________ ___ __ Cor- 8-year Cur- 8-year Cor- 5?aar rent 1940 medi- rent period an period 1940 medi- rent 1M ta period medi' an Diphtheria Tnflnnw 1 Measles* 1,220 1*829 2491 382630 82889 12763 40.419 12638 12 801 9 33 33 10.081 ISO 230 368 1.430 124 185 US 2030 2383 2904 155 17.990 1.288 4.863 179 U1 317 10)012 4.893 621 12144 2.371 2371 m 119 223 12.169 2079 919 1.473 1,976 1.978 230 420 814 114.803 22134 2419 2171 384 2,776 109 174 208 82709 1278 Z284 1.149 421 421 tt232 297 877 147.309 20.968 3.908 324 883 989 73 >3 21*699 2.383 781 2081 1.126 1.390 77 112 184 12849 2143 644 908 4,426 4.428 United States-------------------------New England____ ___ __ __ Middle Atlantic___________ East North Central________ West North Central_______ Sooth Atlantic___ ________ East Sooth Central________ West Sooth Central_______ Mountain________________ Pacific____________________ Meningococcus meningitis 163 129 377 10 7 11 29 83 62 IS 21 43 S 9 36 34 20 77 32 21 66 22 3 23 4 8 17 16 7 IS Poliomyelitis Scarlet (ever 170 131 14 23 13 60 16 17 20 2B IS 11 10 11 14 7 14 12 42 83 12874 12487 23.617 1 779 917 1.661 8 2314 4.190 4.828 16 4.229 5,490 2142 7 1.200 1,891 2678 16 uni 1,287 1.183 10 688 629 620 9 332 833 711 3 342 360 760 13 369 981 1,481 United States________________ New England_____________ Middle Atlantic____ _____ _ East North Central_______ West North Central..___ _ Sooth Atlantic East Sooth Central....__ _ West South Central_____ _ Moontain________________ Pacific___________________ Smallpox Typhoid and para typhoid (aver Whooping cough * 190 320 1,144 000 000 64 39 194 76 122 430 3 8 11 506 9 47 47 23 64 166 8 20 120 312 3aj 45B 12887 10,403 '16,918 9 19 17 1,351 1.300 1.500 42 67 66 4. 481 3,463 2463 46 43 46 2647 1,869 2,294 28 16 39 947 478 475 48 35 89 2,693 833 2164 26 12 38 466 322 322 66 74 101 868 362 469 22 33 26 560 713 713 23 IS 82 1,642 876 876 Mississippi. New York, and Pennsylvania excluded; New York City included, i Mississippi excluded. * Three-year (1938-40) median. 01 501 0028 263 February H. 1<1 DISEASES BELOW MEDIAN PREVALENCE Diphtheria.--For the 4 weeks ended January 25 there were 1,220 cases of diphtheria reported, as compared with 1,829, 2,491, and 2,761 cases for the corresponding period in 1940, 1939, and 1938, respectively. The situation was favorable in all sections of the country. In the West North Central region the incidence was slightly higher than during the corresponding period in 1940, but the number of cases was still well below the 1936--40 median incidence for this period. For the country as a whole the number of cases was the lowest on record for this period. Meningococcus meningitis.--For the current period, there were 163 cases of meningococcus meningitis reported, representing an increase of more than 25 percent over the incidence for the corresponding period in 1940. The incidence was, however, less than 50 percent of the 1936-40 median figure for this period. Regions along the North and South Atlantic Coast and the West South Central and Pacific regions reported excesses during the current period over last year; the Middle Atlantic, East North Central, and Mountain regions reported fewer cases, and in the West North Central and East South Central regions approximately the same incidence was recorded as for last year. In most regions, however, the number of cases was below the preceding 5-year median. This disease has stood at a relatively low level since 1936 when 668 cases were reported for this period; the current incidence represents the first increase over a pre ceding year's incidence during this period since that year. Scarlet fever.--For the country as a whole, the incidence (12,674 cases) of scarlet fever for the 4-week period under report was approxi mately 75 percent of that reported for the corresponding period in 1940 and about 50 percent of the 1936-40 median figure for this period. In the South Atlantic and East South Central regions the incidence stood at about the normal seasonal level; but all other regions reported decreases from last year's figures, as well as very significant declines from the median figures for this period. Smallpox.--The number of reported cases (190) of smallpox was the lowest on record for this period. Of. the total number of cases, Minnesota reported 30, Wisconsin 29, Colorado 23, and Iowa and Michigan 21 each. About two-thirds of the cases were reported from those five States. This disease has been on a steady decline since 1938 when 2,435 cases were reported for the period corresponding to the one under consideration. Typhoid, fever.--The number of cases of typhoid fever reported*for the current period was 312, only slightly less than the number Reported for the corresponding period in 1940, but about 30 percent lower than the 1936-40 median incidence for this period. In the East North 01 501 0029 February 14, 1941 264 Central and Mountain regions the incidence was about normal but all other regions reported a relatively low incidence. MORTALITY, ALL CAUSES The average mortality rate from all causes in large cities for the 4 weeks ended January 25, based on data received from the Bureau of the Census, was 13.7, as compared with 12.8 in 1940 and on average of 13.1 for the corresponding period in the years 1938-40. By weeks for the current period the rates were 12.9, 13.7, 13.5, and 14.6, respec tively. .The cause of the increase in the death rate is apparently influenza; further discussion is found under that subject. THE RESPONSE OF PERITONEAL TISSUE TO INDUSTRIAL DUSTS 1 By John W. Miller, Pathologist, and R. R. Saters,* Senior Surgeon, United States Public Health Service The reaction of the peritoneal tissue to injected dusts has been described in previous reports1 and attention has been called to the possibility of using the results of such a biological response to predict the pneumoconiosis-producing potentialities of industrial dusts. From time to time, minor modifications in the method of introducing the dusts into the animals have been made to simplify the procedure without altering the results. As now practiced, the test is briefly as follows: Two cubic centi meters of a 5-percent suspension of air-elutriated (or 325-mesh screened), heat-sterilized dust in sterile, physiological saline solution is injected into the peritoneal cavities of a number of guinea pigs. Animals are killed and examined 14, 45, and 90 days after injection (in earlier experiments at intervals up to 1 year). The nodules produced by the dust on the anterior abdominal walls or in the omentum at the various intervals are compared. The gross appearance is usually sufficient for interpretation of results. Three general types of reaction are produced by the various dusts. These have been designated as absorptive, proliferative, and inert. Dusts of the absorptive group produce nodules which progressively decrease in size as the interval between injection and examination increases. Eventually the dust disappears from the peritoneal tissue.* i 1 From the Division of Industrial Hygiene, National Institute of Health. i Director of the Bureau of Mines. > Miller. J. W.. and Sayers. R. E-: The response of peritoneal tissue to dusts introduced as foreign bodies. Pub. Health Rep.. 49: 80-89 (January 19, 1934) (Reprint No. 1606). J. Am. Med. Assoc., 103 : 907-912 (Sep tember 21 1934). Am. J. Pub. Health, 26:432-436(April 1933). Pub. Health Rep., 91:1677-1689 (Decem ber 4. 1936) (Reprint No. 1787). Miller, J. W,, and Sayers. R. R.: Microscopic appearance of experimentally produced dust noddies in the peritoneum. Pub. Health Rep., 90: 1619-1628 (November 13, 1933) (Reprint No. 1717). 01 501 0030 265 February 14,1941 Microscopically, a typical early nodule consists of a mass of the dust mixed with fine, granular, necrotic material. A zone of fibroblasts with an occasional macrophage surrounds this more or less centrally placed mass. With time the necrotic material becomes less and finally disappears. Brown pigment particles, apparently of endogenous origin, are usually found rather early, and in an experiment of a year's duration are the only evidence that the dust was introduced into the peritoneal cavity. Dusts causing a proliferative type of reaction produce nodules which progressively increase in size as the interval between injection and examination increases. The maximum growth, a 0.1-gm. dose for each guinea pig, is reached in about 90 days. Microscopically the nodules 7 days after injection are similar to those produced' by the dusts of the absorptive group. As the process continues, the fibro blasts in the cellular zone about the central mass of dust and necrotic material are largely replaced by macrophages which are usually filled with dust particles. This is most marked in the 30-day series. Later, the engulfed dust particles appear to decrease in numbers and fibroblasts and adult connective tissue cells predominate. The area of necrotic material persists throughout the duration of the test. After 90 days fat cell formation in the cellular zone and calcification of the necrotic material is noted. All of the dusts classified in this group studied thus far are various forms of naturally occurring silica. The nodules produced by the inert group of dusts are, in the early stages, grossly similar to those of the other two groups. As the interval between injection and examination increases the nodules become flattened with irregular edges, and numerous dispersed par ticles are present in the adjacent peritoneum. These are often found a considerable distance from the original nodules. The amount of dust found in the peritoneal cavity 1 year after injection is essentially the same as noted in 7 days. Histologically, the fibroblast is the early predominating cell. An increase in macrophages is noted at the 30-day interval and eventually fibrous tissue and accompanying fat cells predominate. No necrosis is noted at any interval in the entire process. The response is characteristic of that caused by a nonirritat ing foreign body. It has been possible to correlate the response of peritoneal tissue to certain dusts with the results of X-ray examination or of post-mortem study of workers exposed by inhalation to high concentrations of the same dusts for protracted periods of time. These records are far from complete, because medical and roentgenographic surveys are available for only a limited number of the dusty trades. Neverthe less, the preliminary results of such comparisons can be summarized: (a) No cases of pneumoconiosis have been reported and confirmed among workers exposed solely to dusts of the absorptive group; (b) all 01 501 0031 February 14,1Ml 266 of the dusts so far examined that fall into the proliferative group are known to produce a nodular, pulmonary fibrosis (silicosis); (c) pneu moconioses caused by dusts of the inert group (asbestos,* anthracite mine dusts,5 bisque ware,* mica,7 pyrophyllite,5 and talc ) have been reported as a result of X-ray examination of industrial workers. 'Where autopsy material is available, certain of the dusts of this group are known to produce a diffuse, interstitial, pulmonary fibrosis, or a mixed nodular and diffuse fibrosis, such as is produced by anthracite coal containing free silica. Interpretation of the response produced by a dust in the peritoneal tissue in animala can be used as an index to determine the potential harmfulness of an industrial dust to which workers are exposed. Thus, an absorptive reaction can indicate that the dust is relatively harmless, while a proliferative response would indicate the dust to be definitely harmful. The dusts producing an inert reaction have been considered as less hazardous than those producing a proliferative reaction, and more dangerous than those of the absorptive group. The intraperitoneai method of studying the physiological action caused by dusts is not applicable to highly toxic material, a sublethal dose of which is too small to be grossly visible in the peritoneal tissue, or to dusts that are readily soluble. The following dusts have been examined by t.hia method and the results, with pertinent identifying data, axe given below. DUSTS CAUSING AN ABSORPTIVE REACTION Colette.--A pure mineral dust. Chemical analysis: Acid insoluble matter, 0.0 percent; silica, 0.0 percent. Petrographic examination: A calcite of high purity. Colette.--A pure mineral dust. Chemical analysis: Acid insoluble matter, 0.1 percent, all of which was silica. PetrogTaphic examination: A calcite of high purity. Precipitated calcium carbonate.--A chemical byproduct. An industrial dust. Chemical analysis: Silica, 0.4 percent; calcium carbonate, S7.9 percent; magrimriiim carbonate, 10.1 percent; magnesium oxide, 0.1 percent; iron and aluminum oxides, 0.6 percent. Petrographic examination: Precipitated calcium carbonate, about 98 percent; crystals, probably sodium carbonate, about 2 percent. Qyptum.--The uncalcined, natural mineral. An industrial dust. Chemical analysis: Silica, 1.3 percent; calcium sulfate, 97.1 percent. Petrographic exam ination: Gypsum, about 70 percent; calcite, about 30 percent. Draom, W. 0., DaHaVaUe, 1. M., et il.: A stndy et eebestosla hi the asbestos textile Industry. Fob. Health Boll. No. Ml. U. S. Government Printing Office, 1938. ' Baras, R. IL, BloomHeld, J. I., et el.: Anthncosillcosls among hard-coal miners. Pub. Health Bull. No. 231. U. B. Government Printing Offioe. 1936. PUnn, R. H., Draessen, W. O., et aL: Silicosis and lead poisoning pottery workers. Pub. Bull. No. 244. U. S. Government Printing Office, 1939. ' Dreessen, W. O., DeliaVeUe, I. M., et a].: Pneumooonlcsls among mica and pegmatite workers. Pub. Health Bull. No. 230. U. 8. Government Printing Office. 1940. ' Eaaom, H. P.. Trice, M. ?., and Carpenter. O. O.: A study of the effects of exposure to dust in the and vnfisng of pyrophyllite. Report, North Carolina State Board of Health. February 1939. i Dreeaaen, W. C., and DallaValle, J. M.: Effects of exposure to dust In two Georgia talo mills and mines. Pub. Health Rep., 30: 131-143 (February 1, 1933) (Reprint No. 1369). 01 501 0032 267 February 14,1941 Limestone.--An industrial dust. Chemical analysis: Silica, 1.5 percent; calcium oxide, 54.4 percent; magnesium oxide, 0.4 percent; ironand aluminum oxides, 0.4 percent. Petrographic examination: Irregularly rounded calcite. No impurities noted. Limestone.--An industrial dust. Chemical analysis: Silica, 2.73 percent; calcium carbonate, 95.21 percent; magnesium carbonate, 1.17 percent. Petro graphic examination: A dolomitic limestone. No impurities observed. Limestone.--An industrial dust. Chemical analysis: Acid insoluble matter, 7.2 percent; silica, 5 percent. Petrographic examination: Only an infrequent quartz crystal was noted. A high calcium carbonate content. Limestone.--An industrial dust. Chemical analysis: Silica, 11.7 percent; calcium carbonate, 81.7 percent; magnesium oxide, 3.4 percent; ferric oxide, 1.4 percent; aluminum oxide, 1.5 percent. Petrographic examination: About 10 percent quarts and about 90 percent calcite. Portland cement.--An industrial dust. Chemical analysis: Silica, 21.1 percent; calcium oxide, 74.4 percent; magnesium oxide, 2.8 percent. Petrographic exami nation: Normal portland cement. Pyrolusite.--An industrial dust. Chemical analysis: Manganese, 54.9 percent. Petrographic examination: No quartz observed. This material was much more slowly absorbed than the others given here. DUSTS CAUSING A PROLIFERATIVE REACTION Bisque ware.--An industrial dust. Ground semivitreous pottery bisque ware, fired at a relatively low temperature. Chemical analysis: Silica, 72.0 percent. Petrographic examination: Quartz, about 40 to 50 percent. The remainder is semifused clay and feldspar. Chert.--An industrial dust. Chemical analysis: Total silica, 70.1 percent. Petrographic examination: Quartz and chert, about 60 percent (about 25 percent of the silica is normal quarts). Calcite, about 40 percent, Dxatomite.--An industrial dust. Chemical analysis: Silica, 92.5 percent; aluminum oxide, 3.5 percent; ferric oxide, 1.5 percent; calcium oxide, 0.4 percent; magnesium oxide, 0.7 percent. Petrographic examination: Pure diatomite. No quartz or calcite present. Greenware.--An industrial dust. Ground semivitreous, unfired pottery ware. Chemical analysis: Silica, 09.0 percent. Petrographic examination: Quartz, about 60 percent; feldspar, about 16 percent; clay, about 35 percent. - Greenware.--An industrial dust. Ground vitreous, unfired pottery ware. Petrographic examination: Higher quartz and less feldspar than the above. Clay, about the same amount. Porcelain enamel frit.--An industrial dust. Chemical analysis: Silica, 35 to 50 percent; the remainder is oxides of antimony, zinc, and aluminum, and fluorides of sodium, aluminum, and calcium. Analysis varies within the above silica limits. Quarts.--A pure mineral dust. Chemical analysis: Silica, 99.4 percent. Petro graphic analysis: Normal crystalline quartz of high purity. Quarts.--A pure mineral dust. Chemical analysis: Silica, 99.3 percent. Petrographic examination: Normal crystalline quartz of high purity. Quartz.--An industrial dust. Chemical analysis: Bilica, 99.1 percent. Petro graphies examination: Normal quartz. Quarts.--An industrial dust. Petrographic examination: Normal crystalline quartz of high purity. Quarts.--An industrial dust. Identical with the above sample but treated with 0.6 percent crude pine fatty acids. February 14, lSU 268 Quartz-sericite.--The source of this dust is not known. Chemical analysis: Total silica, 81.04 percent; calcium oxide, 0.30 percent; magnesium oxide, 0.45 percent; sodium oxide, 0.10 percent; potassium oxide, 0.98 percent; iron oxide, 0.25 percent; aluminum oxide, 14.26 percent; total water, 2.61 percent. Petro graphic examination: Quarts, about 60 percent; muscovite (variety, sericite), about 45 percent; fibrous sericite, less than 5 percent. Tripoli.--An industrial dust. Chemical analysis: Total silica, 98.9 percent; calcium oxide, 0.2 percent; magnesium oxide, 0.1 percent; iron and aluminum oxides, 0.3 percent. Petrographio examination: Chaicedonic silica (crystalline aggregates) with an occasional crystal of normal quartz. OUSTS CAUSING AN INBBT ABACTION Aluminum.--Pure aluminum bronzing powder of the finest grade. Chemical analysis: Aluminum oxide, 11.0 percent. Alundum.--An industrial dust. Chemical analysis: Silica, 4.6 percent; aluminum oxide, 88.4 percent; ferric oxide, 6.9 percent. Petrographic examina tion: Well crystallized, artificial alumina. Asbestos (amonte).--An industrial dust. Chemical analysis: Total silica, 48.31 percent; calcium oxide, 0.48 percent; magnesium oxide, 0.66 percent; sodium oxide, 0.72 percent; potassium oxide, 0.02 percent; iron oxide, 44.22 per cent; combined oxides, 46.37 percent; total water, 3.62 percent. Petrographic examination showed predominating individual fibers and about 1 or 2 percent of dolomite. Asbestos (chrysotile).--An industrial dust. Chemical analysis: Total silica, 37.52 percent; calcium oxide, 2.00 percent; magnesium oxidie, 36.85 percent; sodium oxide, 0.54 percent; potassium oxide, 0.08 percent; iron oxide, 7.70 percent; combined oxides, 10.30 percent; total water, 12.86 percent. Petrographic ex amination: Serpentine, in part chryBOtile, about 85 percent; dolomite, about 5 percent; magnetite and (or) chromite, about 5 percent; talc, less than 5 percent. Asbestos (crocidolite).--An industrial dust. Chemical analysis: Total silica, 50.86 percent; calcium oxide, 0.68 percent; potassium oxide, 0.08 percent; iron oxide, 38.33 percent; combined oxides, 39.03 percent; total water, 5.02 percent. Petrographic examination showed fibrous material only. Anthracite coal.--An industrial dust. Chemical analysis: Ash, 12.6 percent; silica, 6.6 percent. Petrographic examination: Coal about 95 percent; inorganic material, about 5 percent. About 60 percent of the inorganic material is quartz; about 40 percent is calcite, with an occasional crystal of rutile. Anthracite coal.--An industrial dust. Chemical analysis: Ash, 16.0 percent; silica, 8.6 percent. Petrographic examination: Coal, about 95 percent; inorganic material, about 5 percent. About 95 percent of the inorganic material is quartz; about 5 percent is calcite, siderite, limonite, and rutile. Bentonite.--An industrial dust. Petrographic examination: Clay, variety montmorillonite, about 97 percent; feldspar, about 2 percent; quartz, none observed. Bisque ware.--An industrial dust. Ground vitreous pottery bisque ware, fired at a relatively high temperature. Petrographic examination: Quartz, about 30 to 40 percent. The particles are wholly or partially covered by the glass phase. This is absent in the semivitreous bisque ware. Bituminous coal.--An industrial dust. Chemical analysis: Ash, 8.5 percent; silica, 0.8 percent. Petrographic examination: Mineral content (calcite), about 1 to 2 percent. 269 February 14.1941 Bituminous coal.--An industrial dust. Chemical analysis: Ash, 8.0 percent; silica, 3.5 percent. Petrographic examination: Mineral content (quartz, calcite, clay), between 1 and 3 percent. Calcium phosphate.--An industrial dust. Chemical analysis: Calcium phos phate, 75.38 percent; calcium carbonate, 3.98 percent; calcium fluoride, 6.80 percent; magnesium carbonate, 0.51 percent; iron oxide, 3.08 percent; aluminum oxide, 3.12 percent; free silica, 2.70 percent; combined silica, 1.87 percent. Petro graphic examination: Earthy phosphates (not apatite), about 97 percent; normal and chalcedonic quartz, about 3 percent. Chromite.--An industrial dust. Chemical analysis: Silica, 7.8 percent; chromic oxide, 25.0 percent. Petrographic examination: Quartz, less than 5 percent. Diamond dust.--An industrial dust. Pure borts diamond dust used as abrasive. Petrographic examination confirms identity. Feldspar.--Chemical analysis: Total silica, 65.9 percent; calcium oxide, 0.81 percent; magnesium oxide, 0.10 percent; aluminum oxide, 19.55 percent; iron oxide, 0.28 percent; potassium oxide, 8.98 percent; sodium oxide, 3.18 percent. Petrographic examination: Feldspar (plagioclaae-microcline), about 95 percent; normal quartz, about 5 percent. Fuller's earth.--An industrial dust. Filtral clay. Chemical analysis: Silica, 55.7 percent; free silica (estimated), 1.0 percent; water, 15.9 percent. Petro graphic, examination: Clay and residual decomposing feldspar, about 95 percent; quartz, less than 1 percent; gypsum, less than 5 percent. Fuller's earth.--An industrial dust. Chemical analysis: Silica, 56.4 percent; free silica (estimated), 7.0 percent; water, 8.5 percent. PetrogTaphic examination: Clay and decomposing feldspar, about 90 to 95 percent; quarts, about 5 to 10 percent. Fuller's earth.--An industrial dust. Chemical analysis: Silica, 57.9 percent; ferric oxide, 2.5 percent; aluminum oxide, 13.1 percent; calcium oxide, 2.9 percent; magnesium oxide, 8.5 percent; water, 6.7 percent. Petrographic examination: Clay-like masses, rounded and irregular, about 70 percent; quartz, about 15 percent; dolomite, about 15 percent. Fuller's earth.--An industrial dust. Filtral clay. Chemical analysis: Silica, 62.1 percent; free silica (estimated), 3.0 percent; water, 14.9 percent. Petro graphic examination: Clay and residual decomposing feldspar, about 98 percent; quartz, 1 to 2 percent; feldspar, an occasional fragment. Glass wool.--An industrial dust. Finely ground sample of commercial hard glass wool was used. No chemical or petrographic examinations were thought necessary. . Hematite (jewelers' rouge).--An industrial dust. Chemical analysis: Total silica, 1.5 percent; iron oxide, 98.3 percent. Petrographic examination showed no impurities. Kaolin.--An industrial dust. Petrographic examifiation: China clay and hydromica predominant; quartz and feldspar, a trace. Lanthanum sublimate.--An industrial dust. From the burning of white flame electrodes. Chemical analysis: Lanthanum, 40.0 percent. Petrographic examina tion: Particles too small to identify. Mica.--An industrial dust. Chemical analysis: Silica, 46.92 percent; magne sium oxide, 0.86 percent; aluminum oxide, 34.95 percent; ferric oxide, 2.65 per cent; potassium oxide, 9.54 percent; sodium oxide, L02 percent; manganese dioxide, trace. Petrographic examination: Mica, both as plates and fibers, plates predominating, about 98 percent. A very small amount of quartz and feldspar. Precipitator ash.--An industrial dust. Chemical analysis: Total silica, 49.86 percent; calcium oxide, 6.03 percent; magnesium oxide, 3.01 percent; iron and February 14,1M1 270 aluminum oxides, 40.46 percent. Petrographic examination: Loosely consoli dated, white, soft, grit-free ash, about 40 percent; partly rounded aggregates of semifused ash, about 45 percent; smooth fused glass globules, about 10 percent; normal quartz fragments, about 5 percent; unburned coal, less than 1 percent. Precipitator ash.--An industrial dust. From the boiler plant of a coal com pany. Chemical analysis: Silica, 48.2 percent; aluminum oxide, 29.3 percent; ferric oxide, 8.5 percent; calcium oxide, 2.1 percent; magnesium oxide, 0.1 per cent; organic matter, 8.6 percent. Petrographic examination: Predominantly spherulized glass, some coal fragments, and a trace of quartz. Precipitator ash.--An industrial dust. Chemical analysis: Silica, 48.3 percent; aluminum oxide, 29.4 percent; ferric oxide, 8.6 percent; calcium oxide, 1.8 per cent; magnesium oxide, 0.4 percent; organic matter, 8.7 percent. Petrographic examination: Predominantly semivitrified ash particles, some spheres, coal, and a trace of quartz. Precipitator ash.--An industrial dust. Chemical analysis: Total silica, 44.7 percent; moisture, 0.1 percent. Petrographic examination: Mostly spherical fused-glass particles, with some semifused masses of crystallites, quartz, possibly calcite and coal fragments. Precipitator ash.--An industrial dust. Lamphouse deposit from the burning of carbon arcs. Chemical analysis: Rare earth oxides (cerium group), 70.7 per cent; ferric oxide, 0.8 percent; magnesium oxide, 0.5 percent; moisture, 9.8 per cent; silica, none. Petrographic examination: Inorganic material, rudely rounded, about 5 percent of opaque carbonaceous material and no quartz. Precipitator ash.--An industrial dust. Condensate from the flue system from burning of carbon arcs. Chemical analysis: Rare earth oxides (cerium group), 59.5 percent; silica, 1.0 percent; ferric oxide, 4.1 percent; magnesium oxide, 0.9 percent; calcium oxide, 0.6 percent; ignition loss, 18.4 percent. Petrographic examination: No quartz or calcite, otherwise similar to preceding sample. Pyrophyllite.--An industrial dust. No chemical analysis obtained. Petro graphic examination: Predominantly pyrophyllite, with a small amount of rutile and some quartz. The quantity of quartz was hard to estimate. Rock wool.--An industrial dust. A finely ground sample of commercial, insu lating rock wool. Selenium.--An industrial dust. Chemical analysis: Selenium, 98.8 percent; tellurium; 0.01 percent; ash, 1.16 percent. Selenium.--A chemically preDared sample of highest purity. Sericite.--A pure mineral dust. Chemical analysis: Total silica, 51.74 percent; calcium oxide, 0.61 percent; magnesium oxide, 1.74 percent; sodium oxide, 3.40 percent; potassium oxide, 4.48 percent; iron oxide, 5.83 percent; combined oxides, 31.82 percent; total water, 6.26 percent. Petrographic examination: Sericite and feldspar residues (fibrous sericite predominates), about 95 percent; quartz, less than 5 percent. Shale.--An industrial dust-. Chemical analysis: Silica, 61.0 percent; aluminum oxide, 12.4 percent; calcium oxide, 4.5 percent; ferric oxide, 5.0 percent; magne sium oxide, 1.3 percent; sodium oxide, 2.3 percent; potassium oxide, 1.5 percent; moisture, 10.3 percent. Petrographic examination: About 35 percent quartz. The majority of the particles appear to be coated with clay. Silicon carbide.--Pure manufactured silicon carbide. Chemical analysis: Silicon, 67.5 percent. Petrographic examination showed no impurities. Soapstone.--An industrial dust. Chemical analysis: Total silica, 49.9 percent; calcium oxide, 1.7 percent; magnesium oxide, 26.2 percent. Petrographic exam ination: Talc, as plates or fibrous splinters, about 65 percent; tremolite, as long fibrous crystals, about 30 percent; dolomite, about 5 percent. 271 February 14.1*41 Soapstone.--An industrial dust. Chemical analysis: Total silica, 36.S percent; calcium oxide, 5.0 percent; magnesium oxide, 22.7 percent. Petrographic examination: Talc, about 55 percent; dolomite, about 30 percent; tremolite, about 15 percent. No quartz observed. Tale.--An industrial dU6t. Chemical analysis: Total silica, 49.0 percent; calcium oxide, 8.8 percent; magnesium oxide, 22.6 percent. Petrographic examination: Tremolite, about 60 percent; talc, about 40 percent. Talc.--An industrial dust. Chemical analysis: Total silica, 56.54 percent; calcium oxide, 6.25 percent; magnesium oxide, 30.74 percent; calcium silicate, 11.00 percent; calcium carbonate, 1.88 percent; iron and aluminum oxides, 1.04 percent; ignition loss, 4.60 percent. Petrographic examination: Talc, mostly fibrous, about 75 percent; tremolite, partly altered to talc, about 25 percent; calcite and (or) dolomite, about 1 percent. Titanium oxide.--An industrial dust. A finely divided high purity sample. Sodium silicate.--A laboratory prepared sample containing 1 part sodium oxide to 3.1 parts silica. Higher ratios of sodium oxide kill the animals. Trap rock.--An industrial dust. Chemical analysis: Silica, 51.7 percent; aluminum oxide, 16.0 percent; ferric oxide, 2.0 percent; ferrous oxide, 9.9 percent; calcium oxide, 10.0 percent; magnesium oxide, 6.2 percent. Petrographic examination: Feldspar, some slightly decomposed, about 45 percent; pyroxene, about 45 percent; magnetite, about 10 percent; biotite, about 1 percent. Volcanic ask.--An industrial dust. Chemical analysis: Silica, 54.4 percent; aluminum oxide, 14.5 percent; ferric oxide, 3.8 percent; magnesium oxide, 2.6 percent; calcium oxide, 0.7 percent; ash, 78.2 percent. Petrographic examination: Fine volcanic ash partially altered to montmorillonite. No quarts observed. Volcanic ash.--A specially treated sample. Chemical analysis: Silica, 74.3 percent; mixed oxides, 16.8 percent; ferric oxide, 2.2 percent; calcium oxide, 0.5 percent; magnesium oxide, 2.2 percent. Petrographic examination: Glass only. No quartz or calcite observed. SUUUABT AND CONCLUSIONS A definite quantity of dust injected into the peritoneal cavity of a guinea pig produces one of three types of reaction. It disappears, causes proliferation of the peritoneal tissue, or remains as An inert foreign body. These reactions may be used as a basis for the biological classification of industrial dusts, and seem to indicate that some rela tionship exists between the type of reaction produced in the peritoneal tissue by a dust and the ability of this dust to produce a characteristic type of pneumoconiosis. An absorptive reaction may indicate that a dust is relatively harmless, while a proliferative reaction, characteristic of quartz, may be associated with the ability to produce pulmonary fibrosis. Dusts of the inert group, that is, those that show a tendency to remain in the tissues, should be considered as potentially harmful, but not so dangerous as those causing a proliferative response. With this biological method of classification, which in a number of instances has been correlated with clinical observations and industrial surveys, it is quite possible to determine the pneumoconiotic poten tialities of a dust in a relatively short time, usually 60 days. Oi 501 0037 February 14,1841 272 ACKNOWLEDGMENTS Acknowledgment is made of the kindness of Mr. W. A. Selvig of the United States Bureau of Mines and of Associate Chemist F. E. Goldman of the United States Public Health Service for the chemical analyses of the dusts used in these experiments. The petrographic examinations were made by Dr. Alton Gabriel of the United States Bureau of Mines and Dr. F. E. Goldman. Acknowledgment is also made to Technical Editor T. I. Edwards for assistance in preparing this report and to Medical Technician E. C. Thompson for technical aid. IMMUNOLOGICAL RELATIONSHIPS BETWEEN THE RICK ETTSIAE OF AUSTRALIAN AND AMERICAN "Q" FEVER By Ida. A. Bengtson, Senior Bacteriologist, National Institute of Health, United States Public Health Service INTRODUCTION . The relationship between Australian "Q" fever and a disease caused by an infectious agent isolated from ticks in Montana was first considered by Dyer (1) in a description of a human case of a disease probably contracted as a result of a laboratory infection by a member of the staff of the National Institute of Health while on a visit to the Rocky Mountain Laboratory of the United States Public Health Service at Hamilton, Mont. The source of the infection was problematical, although the subject had handled cultures and n.nima.ls infected with a filter-passing agent which had been isolated at the laboratory by Davis and Cox () in 1935 from the wood tick Dermacentor andersoni. The organism concerned, as described by Cox (S), was a minute pleomorphic organism resembling the nckettsiae mor phologically and in staining reactions, and in the intracellular and also extracellular occurrence of the organism in the affected tissues of laboratory animals. The infectious agent had been shown to be filterable through both Berkefeld N and W filters. In a later publi cation Cox (4) designated the new rickettsia as Rickettsia diaporica. In experiments to determine the nature of the infectious agent it was found by Dyer at the National Institute of Health that cross immunity tests between the virus from patient X which had been established in guinea pigs, and typhus, both epidemic and endemic, and Rocky Mountain spotted fever were negative, while five guinea pigs recovered from a strain of "Q" fever previously furnished to the National Institute of Health by Dr. Burnet of Australia were immune to the "X" strain of Dyer. i 01 501 0038 273 February IV 1W1 "Q" fever was described by Derrick (5) in 1937 as a new disease occurring in Australia. It affected principally meat workers and dairy farmers. It was distinguished from typhus by the absence of a rash and by a negative Weil-Felix reaction. The outstanding symp toms were fever and headache, and no fatalities occurred. Burnet and Freeman (6) described a rickettsial organism present in sec tions and smears of infected mouse spleens and livers. Emulsions of the organism were agglutinated by the serum of patients having the disease, and sera from convalescent patients protected laboratory animals against the disease. It was assigned the name Rickettsia bumeti by Derrick (7). . Further cross-immunity and protection tests were later reported by Dyer (8). In the cross-immunity tests the strains used were: A "Q" fever strain received from Dr. Burnet in the form of two infected mouse spleens and subsequently maintained in mice and guinea pigs; the X strain of Dyer; a strain of endemic typhus and one of epidemic typhus, and two strains of Rocky Mountain spotted fever (the Bitterroot strain and an eastern spotted fever strain isolated from a case of the disease in Maryland). There was com plete cross-immunity between the Q and X strains. There was no cross-protection between the X strain and the typhus and spotted fever strains, and none between the "Q" fever and spotted fever strains. There was a suggestion of immunity against the Q strain by the typhus strains, though the reverse was not true. In the pro tection tests definite protection against the X virus was shown with X serum and "Q" fever serum, while no protection was afforded against either by spotted fever serum. Burnet and Freeman (3) also compared the Australian Q virus and the American X virus. They call attention to the more acute infection of guinea pigs by the American X strain, with shorter incu bation period and death of the animals injected with the larger doses, the fibrinous exudate on the spleen, and congestion and partial con solidation of the lungs. Both were found virulent for monkeys, the X strain being found to be considerably more virulent. The higher virulence of the X strain was shown by the development of "foci" on the infected chorioallantoic membrane of chick embryos, whereas these were absent in embryos infected with the Q strain. , A complete cross-immunity in guinea pigs was obtained with the two strains; similar results were also obtained in agglutination tests with human, monkey, bandicoot, rabbit, and mouse sera against emulsions of rickettsiae from spleens of mice infected with both the Q and X strains. 01 501 0039 February 14.1941 274 EXPERIMENTAL In an effort to elucidate further the relationship of the Australian and American diseases agglutination and agglutinin absorption tests were performed. Tests were also made with filtrates to determine whether a precipitin reaction could be demonstrated. Two human sera were used, several rabbit immune sera against the X and Q strains, guinea pig and mouse sera, and also some specimens of sera received from Dr. Burnet of Australia, including sera from two convalescent patients and from two bandicoots. The antigens were prepared principally from infected mouse spleens and livers, but yolk sac material of infected chick embryos was also used. The infection was established in mice by the intraperitoneal inoculation of 0.5 cc. of 10-percent suspensions of the spleen or liver of infected guinea pigs. Transfers were made at weekly intervals, using spleens or livers showing the largest number of rickettsiae. Usually two or three passages were necessary before the rickettsiae were present in sufficient numbers to warrant the preparation of the suspensions. It was found that the number of rickettsiae could be increased in a shorter length of time by the inoculation of mice with infected yolk sac material. In general, infection with a larger number of rickett siae was established in a shorter time in the case of the X strain than with the Q strain;-this was to be expected in view of the greater virulence of the X strain. The infected mouse spleens and livers were ground in mortars with alundum, and 10-percent suspensions were prepared by the addition of buffered salt solution adjusted to pH 7.0. The method of L4on (10) was used in the separation of the tissues from the rickettsiae. After a preliminary centrifugation at 1,000 r. p. m. for 5 minutes to precipi tate the alundum and larger particles of tissue the supernatant fluid was centrifuged at 3,500 r. p. m. for 1J{ hours. The supernatant fluid from this centrifuging was retained for further centrifugation and for filtration. The majority of rickettsiae were precipitated by this method, but a few could be precipitated by added centrifugation at a high speed using the angle centrifuge at a speed of 10,000 r. p. m. The precipitate was suspended in buffered salt solution at pH 7.0 and 0.5 percent glacial acetic acid was added, drop by drop, to a pH of 5.1 to 5.2 after the temperature had been brought to 35 to 40 C. A light centrifugation for 4 to 5 minutes served to precipitate the proteins, leaving the rickettsiae in the supernatant fluid with very little tissue. The suspensions were again centrifuged at 3,500 r. p. m. for 1% hours to precipitate the rickettsiae and taken up in appropriate amounts of buffered salt solution and centrifuged lightly to pre cipitate any large particles. In some cases the reaction was adjusted with N/lO NaOH to pH 7.0 without recentrifugation. 01 501 0040 275 February 14.141 Silica standards were used for adjusting the turbidity of the anti gens and tests were carried out with suspensions with turbidities corresponding to 300 and 150 parts per million. Suspensions were also prepared from infected yolk sac from chick embryos, employing the method described above, but more difficulty was experienced in obtaining pure suspensions with this material. As to the relative virulence of infected mouse spleen and infected yolk sac, the mouse spleen was found at times to be infective in a titer of 1 X 10~u, which is the same as reported by Cox for yolk sac material. For the immunizations of rabbits purified suspensions of the rick ettsiae killed by the addition of 1/10,000 merthiolate were injected intravenously. Sera of rather good titer were obtained after two intravenous inoculations of 1 cc. of suspenions 2 days apart, followed by another inoculation of 2 cc. in a month, and bleeding in 2 weeks. Other rabbits were given a series of 6 inoculations at weekly inter vals, without raising the titer. Another set of rabbits received inocu lations with increasing amounts on 2 successive days each week for 8 weeks and in these somewhat higher titers were obtained in the case of the X serum but not of the Q serum (table 1). AGGLUTINATION TESTS Simple agglutination tests were performed with human sera and with sera of experimental animals as shown in table 1. The turbidity of the antigen was equivalent to 300 parts per million. Incubation was at 45 C. for 2 hours, after which the tubes were kept overnight at ice-box temperature. Table 1.--Agglutination of Q and X antigens by animal and human sera Seram dilutions Con trol (no uo 1:20 1:40 1:80 1:160 1:330 1:640 seram) X rabbit seram 1: > X antisen___ _ 4 4 4i 4 4 4 2 q antigen____ ,, ________ --................ 3 3 4 4 4 2 X rabbit seram A- > X antigen ... 4 4 4 4 4 4 3 Q antigen 4444 4 4 3 Q nbbit seram 1: X antigen______ ________________________ 4 4 4 4 4 4 3 Q antigen 4444 4 4 3 Q rabbit seram 4:1 X antigen 4444 4 3 2 Q antigen................ ...... ................ ......... 4 4 4 4 4 3 1 X guinea pig seram 397: * X antigen ___________________________ 3 3 3 3 3 2 1 Q antigen______________________________ 3 3 3 3 3 2 1 X guinea pig seram 413: > X antigen............................................ . 3333 3 3 1 Q antigen................... -- ___ ____ ____ 3 3 3 3 3 2 1 Q guinea pig seram 388: > X antigen 4444 4 3 1 Q antigen____ 4444 4 3 1 Sea footnotes st end of table. 285789*--11----- 2 ( ( 01 501 0041 February 14.1941 276 Table 1.--Agglutination of Q and X antigens by animal and human sera--Contd. Serum dilations Con trol (no lao 1:30 1:40 1:80 1:160 1:320 1:640 serum) X mouse rerum 18 (3): X antigen--------------------------------------------- 2 2 1 0 Q antifen________ _____________________ 2 1 1. 0 0 0 0 0 0 0 X mouse serum 18 (S-S); < X antigen_________________ 221 1 Q antigen........... ......................... ............... 2 2 2 1 0 0 0 0 0 0 Human serum A:' X antigen___ _____ __________ _______ 2 2 1 0 Q antigen---------- --------------------- ------------- 2 2 1 0 0 0 0 0 0 0 Human serum B: * X antigen 2 100 0 0 0 Q antigen_________ ____________________ 2 1 0 0 0 0 0 Hitman serum MacArtbur: * X antigen______________________________ 3 2 2 2 1 0 0 Q antigen 222 1 1 0 0 Bandicoot 11B:' X antigen 2100 0 0 0 Q antigen... ______________________ 2 1 0 0 0 0 0 Bandicoot 129: r X antigen_____________________ ----------- 1 2 2 2 2 1 0 Q antigen_____ _________________________ 2 2 2 2 1 0 Q Normal rabbit serum: X antigen 0000 0 0 0 Q antigen________ _____________________ 0 0 0 0 0 0 0 Normal horse serum: X antigen______________________________ 0 0 0 0 0 0 0 Q antigen____ 0000 0 0 0 1 Rabbits received 3 intravenous inoculations of rlekettsia suspension. ' Rabbits received 16 intravenous inoculations of rickettsia suspension. 1 Quinta pics received 2 inoculations of 1 oe. of X vaccine a week apart and were tested for Immunity 16 days later by inoculation of 1 ee. of a 10-percent suspension of Infected guinea pig spleen. * Mice inoculated intraperitonoelly with 0.3 cc. of a 10-percent suspension of infected mouse spleen. * Five months after onset of Illness. * Thirteen days after onset of Hinton (specimen received tram Dr. Burnet). 1 Specimen received from Dr. Burnet. In another test an anti-X serum and an anti-Q serum were tested against two other lots of X and Q antigens. In this test the antigens were made up to a turbidity of 300 parts per million and to 150 parts per million with the result shown in table 2. Table 2.--Agglutination of Q and X antigens (of varying turbidity) by anii-Q and anti-X raobit sera .01 501 00*2 277 February 14.1041 While the results obtained with the more dilute antigens were clear-cut it would not seem advisable to use as dilute a suspension as this in diagnostic tests with unknown sera. The results of the simple agglutination test show the close relation ship between the two rickettsiae, there being practically no differ ence in the results obtained, confirming the findings of Burnet and Freeman (9). ' AGGI/UTININ ABSORPTION TESTS Agglutinin absorption tests were performed with absorbed X and Q serums against both X and Q antigens. The antigens were concen trated by subjecting 15 cc. of each suspension of a turbidity corre sponding to 300 parts per million to high speed centrifugation for 30 minutes at approximately 10,000 r. p. m.; the supernatant fluid was removed and the precipitated rickettsiae suspended in 2 cc. of the 1:10 dilution of the corresponding serum. This suspension was placed in a 45 water bath for 2 hours and then centrifuged at a speed of 2,500 r. p. m. for 15 minutes to precipitate the agglutinated rickettsiae. The absorbed sera were tested against both the X and Q antigens of a turbidity of 300 parts per million with the results shown in table 3. Tabu 3.--Agglutinin absorption test Seram dilations 1:20 1:40 ISO 1:1 1:320 Control (no 1*40 serum) Absorbed X senna: X antigen 444 3 I 0 Q antigen _______________________ __ 4 4 4 1 0 0 Absorbed Q serum: X antigen--------------------------------------------------- 1 0 0 0 0 0 Q antigen____________ . 000 0 0 0 0 0 The results against the X and Q antigens were similar with both absorbed sera. In the case of the Q serum the X and Q agglutinins were both absorbed and no agglutination wa^obtained against either antigen. With the X serum, however, it was necessary to repeat the absorption process twice, after which no agglutination was obtained against either antigen, as shown in table 4. Table 4.--Agglutinin absorption test with absorbed X serum Serum dilutions 1:20 1:40 ISO 1:1 1:320 1*40 X antigen_____________________ __________________ 0 0 0 0 0 0 Q antigen 0 0 0 0 kJL J> 01 501 0043 February 14.1M1 278 The results of the agglutinin absorption tests are therefore further evidence of the identity of the two organisms. TESTS FOB PRECIPITIN REACTIONS Berkefeld N filtrates.--The supernatant fluids from the centrifuga tion of the 10 percent suspensions of mouse spleen and livers at 3,500 r. p. m. for IK hours were used for precipitin tests. These supernatant fluids were first filtered through Berkefeld N filters. It might be expected that such filtrates, while perfectly clear, would still contain a sufficient number of rickettsiae to cause agglutination. The results obtained are shown in table 5. In these tests an X serum with an agglutination titer of 1:640 and a Q serum with an agglutination titer of 1:320 were used. The concentrations of the serum and antigen were both varied in order to obtain information as to the most suitable dilution to use. A control test was made with normal rabbit serum. As shown in the protocol of the test, a rather definite precipitate was formed, particularly in the lower dilutions. This was especially true of the X serum when tested against the Berkefeld N filtrates of the X and the Q supernatant fluids. The amount of the precipitate with the Q serum was decidedly less. Though the precipitate was definite and the supernatant fluid dear, the amount of precipitate formed was much smaller than in the agglutination test but somewhat greater in the case of the X serum than might perhaps be expected from residual rickettsiae in the filtrate. A further test was made with the same filtrates passed through collodion membranes of a pore size of 0.4m.1 Burnet and Freeman (6) reported that the Q rickettsiae are not completely held back by gradocol membranes of 0.7m average pore diameter but that small amounts passed through these membranes, as shown by inoculation and im munity tests on guinea pigs. Since the material used in the tests described bad been treated with 1/10,000 dilution merthiolate it was necessary to test fresh material with the same pore-size filters to determine whether anjs of the infectious material passed through the filter. Suspensions of the fresh X material consisting of spleens and livers of infected mice were prepared as before and subjected to filtra tion through Berkefeld N filters before passing through the collodion membranes of the same pore size as was used for the filtrates under test. Infection occurred in guinea pigs with the Berkefeld filtrate as well as with the collodion filtered material, showing that some of the infectious agent was still present. . 1 Tbe writer Is indebted to I>r. Evelyn B. TOden tor the preparetion of tbe ooUodton membranes. 501 0044 279 February U. I#41 Table 5.--Test* for precipitin reactions (Berkefeld S filtrates) Antigen dilutions Control 1:2 1:4 1:8 1:18 1:33 1:64 1:128 serum) X antigen X iramwu rabbit serum Senna dilations: l'l __... . ......................... 44322 1 1 1:4.................. .............................. 3 2 2 2 2 1 0 1:8. 2 3 1 1 1 0 0 1:16. 1 000 0Q0 1:32 0 0 0 0 0 0 0 0 Q antigen Serum riflntVvM; 1 '2 4 4 4 3 3 2 1 1:4. 3 3 3 3 3 3 1 1:8. 3 3 2 2 1 0 0 1:16. 223 1 0 00 1:32.-------- ------------------------------ 2 1 1 0 0 0 0 u X antigen Q immune nbbtt mum Seram dflatioas: 1:2___________________ 221 I 000 1:4. ------------------------------------ 1 1 0 0 0 0 0 1:8. '. 0000 0 00 1:16 0 0 0 0 0 0 0 1:32----- ------ ------------------ --- 0000 000 Q antigen Seram dilations: 1'? ,, . . __ 2 2 2 1 1 00 1:4 1 1 1 0 0 0 0 1:8. ................. .......................... 1 0 0 0 0 0 0 1:18 ......................................... 0 0 0 0 0 0 0 1:32 0 0 0 0 0 0 0 Normal rabbit serum X antigen Seram dilations: 1 *? i 1 1 000 000 1 0 0 0 0 0 0 lrft _ . .. . __ ... 000 0 000 1:16..... ........................... ......... 0 0 0 0 0 0 0 1:32---------------------------------------- 0 0 0 0 0 0 0 Q antigen Seram dilations: 1:2. .. ...__....... ___ _____ 1 0 0 0 0 0 0 1:4_______________________ . 0 Q 0 0 0 0 0 1:8 . ___________ 000 0 0 0 0 1:18____ __________________ 0 000 00 0 1:33_______ _______ _______ 0 0 0 0 0 0 0 01 501 004*5 February w. 1M1 280 However, the results obtained in the test with the immune sera were practically negative, as shown in table 6, indicating that under the conditions of the experiment precipitin was not present in the immune sera. It is possible that evidence of the presence of this antigen might be obtained by immunization of rabbits with Berkefeld filtrates of infected material. In any case, however, the results ob tained with filtrates serve to establish further the identity of the two rickettsiae. Table 6.--Tests for precipitin reactions, X immune rabbit serum, and collodion membrane filtrates DISCUSSION The close immunological relationship of the Q and X strains of rickettsiae is indicated by the tests described. This affords added evidence of the identity of the Australian and the American diseases as shown by the cross-immunity and protection tests in laboratory animals described by Dyer (1, 8) and by Burnet and Freeman (9). As has been pointed out by Burnet and Freeman (9) and as has also been observed in this laboratory the virulence of the Xstrainis decidedly greater than that of the Q strain from Australia. This is reflect ed in the greater ease with which the disease may be established in mice, with correspondingly larger numbers of rickettsiae, as well as in the more pronounced effect in guinea pigs, with a high mortality where large doses of infected mouse spleens or livers are inoculated. However, it is well known that in a number of other disease entities there may be a variation in the virulence of strains. This is particu larly true of Rocky Mountain spotted fever, a much higher mortality in laboratory animals being associated with the Bitterroot type first described in the western part of the country than with certain other strains. Also it is well known that there may be fluctuations in the virulence of a particular disease at different periods; smallpox is a nota- 01 501 0046 281 February a 1M1 ble example. It is possible that the virulence of the Australian "Q" fever might differ from the similar disease in this country as a result of the modification of the virus in a host species or in an insect vector. The increased virulence of the X virus for the guinea pig after mouse passage, and the increased virulence for the mouse after chick embryo yolk sac passage afford concrete examples of such a change. In view, therefore, of the practical identity of the results in the serological tests, using both human and experimental animal sera, and of the results obtained in cross-immunity and cross-protection tests in ani mals, and of the clinical symptoms of the two diseases as pointed out by Dyer, it would appear justifiable to consider the Australian and the American types as one and the same. ' SUMMARY Agglutination and agglutinin absorption tests afford evidence of the identity of the rickettsiae which are the etiological agents of Australian "Q" fever, a disease affecting principally abattoir workers in that country, and a similar disease which occurred as the result of a probable laboratory infection in a member of the staff of the National Institute of Health. Further evidence of the identity of the two organ isms has been shown in tests with immune and convalescent sera and Berkefeld N filtrates and ultrafiltrates, though this test was not shown to be that of a true precipitin reaction. REFERENCES (1) Dyer, R. E.: A filter-passing agent isolated from ticks. IV. Human infec tion. Pub. Health Rep., 53 : 2277-2282 (Dec. 30, 1938). () Davis, Gordon E., and Cox, Herald R.: A filter-passing infectious agent isolated from ticks. I. Isolation from Dermacentor andertoni, reaction in animals, and filtration experiments. Ibid., 53 : 2259-2267 (Dec. 30, 1938). (5) Cox, Herald R.: A filter-passing infectious agent isolated from ticks. III. Description of organism and cultivation experiments. Ibid., 53 : 2270 2276 (Dec. 30, 1938). (4) Cox, Herald R.: Studies of a filter-passing infectious agent isolated from ticks. V. Further attempts to cultivate in cell-free media. Suggested classification. Ibid., 54: 1822-1827 (Oct. 6, 1939). (5) Derrick, E. H.: "Q" fever, a new fever entity: Clinical features, diagnosis, and laboratory investigations. Med. J. Australia, 2: 281-299 (Aug. 21. 1937). (5) Bumet, F. M., and Freeman, Mavis: Experimental studies on the virus of "Q" fever. Ibid., 2: 299-305 (Aug. 21, 1937). (7) Derrick, E. H.: Rickettsia bumeti: The cause of "Q" fever. Med. J. Austra lia, 1: 14 (Jan. 7, 1939). (8) Dyer, R. E.: Similarity of Australian "Q" fever and a disease caused by an infectious agent isolated from ticks in Montana. Pub. Health Rep.,' 54: 1229-1237 (July 7, 1939). (9) Burnet, F. M., and Freeman, Mavis: A comparative study of rickettsial strains from an infection of ticks in Montana (United States of America) and from "Q" fever. Med. J. Australia, 2: 887-891 (Dec. 16, 1939). (10) L4on, A. P. de: M6todo para purificar la vacuna contra el tifo. Bol. del Inst. de Higiene, Departamento de Salub., Mexico, 2: 368 (1936). (If) Cox, Herald R.: The cultivation of Rickettsia diaporica in tissue culture and in the tissues of developing chick embryos. Pub. Health Rep., 54: 2171 78 (Dec. 8,1939). 6l 501 0047 February 14.1M1 282 THE INHIBITING EFFECT OF UREA ON THE MICROBIOLOGICAL ASSAY OF RIBOFLAVIN By Harris Isbell, Patted .Assistant Surgeon, J. G. Woolet, Baeleriologitt, and H. F. Fraser, Patted Assistant Surgeon, Untied States Public Health Service Fraser, Topping, and Isbell (1) applied the microbiological method of Snell and Strong () to the assay of riboflavin in the urine of normal and riboflavin-deficient dogs and rats. They found that the addition of increasing amounts of certain urines of low riboflavin content to the assay tubes produced a progressive diminution in the value of riboflavin found per milliliter of urine. A similar effect has been noted in the assay of human urines of low riboflavin content. Three typical examples of the inhibiting action of human urine are presented in table 1. ' Table 1.--Inhibitory effect of urine on the microbiological assay ofriboflavin In an effort to determine the cause or causes of the inhibitory effect of urine on the microbiological assay certain quantitatively important constituents of urine were studied for their inhibitory action on acid production by Lactobacillus casei. Definite quantities of the pure compounds were added to tubes containing known amounts of riboflavin. The quantities added were chosen to cover and exceed the range over which the ions comprising the compounds, or the compounds themselves, occur in human urine. NaCl in amounts from 10-250 milligrams, N&gS04 in amounts from 10 to 200 milli grams, KC1 in amounts from 10 to 100 milligrams (NH4)jS04 and NEL,C1 in amounts from 10 to 200 milligrams were tested. No diminu tion in the assay values was noted with any of these salts over the ranges used. Some increase in the assay values was found with all the salts at levels of 80 milligrams or more per tube. Addition of increasing amounts of urea to the tubes produced a progressive decrease in the assay values from approximately 20 per cent at the level of 20 milligrams of urea per tube to 80 to 100 percent at the level of 80 milligrams. Table 2 shows the mean values of ribo flavin found by assay in the presence of varying amounts of urea. 01 501 0048 283 February U. 11HI Table 2.--Effect of urea on mierobiobjgical assay of riboflavin 1 Micro(trams riboflavin added to tube Micrograma riboflavin found in presence of urea Milligrams urea added to lube 10 30 30 40 00 80 a os a 045 a cm 0.04 0.035 ao2 aoo .075 .06 .05 .04 .01 .02 .00 .1 .09 .08 .07 .06 .05 .04 .IS . .14 .13 .11 .09 .08 .055 .2 .19 . 1GS .15 .135 .12 .2 .195 .16 .3 .25 .34 .21 .173 > Each value la aa avenge of S to 8 duplicate determination!. From the data given in table 2 the partial regression equation (3), X=0.000824Y+1.21Z- 0.017,* was calculated where X represents the micrograms of riboflavin actually present in the tube, Y the milligrams of urea present, and Z the amount of riboflavin apparently present as determined by assay. Since the equation was derived from data based on the depressing action of a pure solution of urea, it was necessary to determine whether or not urea accounted for all the inhibiting effect of urine. Specimens of urine exhibiting the inhibitory phenomenon were therefore assayed, the amount of urea per milliliter of urine determined by the method of Van Slyke and Cope (4),* and the values obtained corrected by the use of the regression equation. Known amounts of riboflavin were added to the same urines, assays performed, the values corrected by use of the regression equation, and the percentage recovery of added riboflavin calculated. Table 3 gives the results obtained with 5 typical urines at varied levels of both urea and riboflavin. One hundred and thirty-six determinations on 24 separate urines gave an average recovery of added riboflavin of 103 percent with a variation of 87 to 118 percent. In 48 other determinations on 8 urines, known amounts of ribo flavin were added to tubes containing 0.5 to 1.0 milliliter of urine. The urines used contained less than 20 milligrams of urea per milliliter of urine. The tubes were assayed, the value of riboflavin per milli liter of urine obtained by difference, and the results obtained compared with those found by using the correction formula. The average values found were identical in all cases.* 1 i standard error ot estimate.. 1 The method was slightly modified from the procedure described by Van Slyke and Cope In that tbe urine was diluted 1-60 or 1-100 instead ot to a value calculated from tbe per mlnnte urine volume and read against tbe standard of 0.2 milligrams nitrogen. Instead of against a blood filtrate. 01 501 0049 February 14.1M1 284 Table 3.--Recoveries of riboflavin added to urine Urine No. Ml. urine added Me. ores added by urine Micrograma ri boflavin added by urine Micro grams ri Total ri boflavin boflavin add'd es present in pore 30- tsbe lutioo Microfrram.1 ri boflavin actually found Mtcro- grams ri boflavin by oorrectlon form Percent recov ery ula rv_.. _______________ 2.0 15. S 2.0 15. S 3.0 23.7 2.0 217 4.0 3L0 V----------------------------------- 2L0 214 3.0 34.1 4.0 418 VI_________ _________ vn.......................... vm_____________ 10 313 10 3fs3 10 313 4.0 414 10 413 4.0 71*5 LO 23 10 46 100 .06 .00 .00 .12 .04 .06 .06 .046 .046 .046 .06 .133 .18 .01 .14 103 .1 .05 .1 .06 .1 .16 .2 .i .13 .2 .i .05 .06 .05 .1 an .10 .14 .10 .17 . .14 .21 .28 .146 .106 .246 .18 .185 .23 .12 .24 0.09 .15 .12 .16 .13 .13 .17 .10 .13 .17 .206 .133 . 137 .171 .12 .21 &1 .13 .14 .18 .15 .14 .21 .24 .16 .2 .235 .19 .103 .24 .14 .25 00 MO 100 94 00 100 100 87 110 94 06 118 10S 104 m 104 DISCUSSION The excellent recoveries of added riboflavin from urines exhibiting the depressing effect are strong evidence that urea accounts for most, if not all, of the inhibiting action of urine. The results given also prove that the regression equation may be used to obtain the true amount of riboflavin present in a urine exhibiting the depressing phenomenon. The equation need not be applied unless 20 milli grams or more of urea are present in each tube. The regression equation applies best between the levels of 20 to 60 milligrams of urea and in the presence of 0.075 to 0.2 micrograms of riboflavin. If desired, tho use of the regression equation may be avoided altogether by adding known quantities of riboflavin to tubes containing 0.5 to 1.0 milliliter of urine and obtaining the values per milliliter of urine by difference. _ The stimulation observed with various inorganic salts at levels of 80 milligrams or more should not introduce appreciable error since the amounts required to produce the stimulation do not ordinarily occur in human urine (5). SUMMARY _ The inhibiting effect of urines of low riboflavin content on the microbiological assay for riboflavin according to the method of Snell and Strong is demonstrated. Methods for correcting the error due to the inhibiting effect of urea are presented. REFERENCES (1) Fraser, H. F., Topping, N. H,, and Isbell, H.: The bacterial assay of ribo flavin in the urine and tissues of normal and depleted dogs and rats. Pub. Health Rep., 55: 280 (1940).. 501 0050 285 February 14,1941 {2) Snell, . E., and Strong, F. M.: A microbiological assay for riboflavin. Ind. and Eng. Chem., 11: 346 11939). (3) Fisher, R. A.: Statistical Methods for Research Workers, 6th ed. Oliver and Boyd, Edinburgh and London (1936). (4) Van Slyke, Donald D., and Cope, C. L.: A simplified colorimetric determina tion of blood urea clearance. Proc. Soc. Exp. Biol, and Med., 29: 1169 (1932). (5) Bodansky, M.: Introduction to Physiological Chemistry. Ind. ed. John Wiley and Sons, New York (1930). STUDIES ON THE NATURAL HISTORY OF THE VIRUS OF LYMPHOCYTIC CHORIOMENINGITIS IN MICE By Victor H. Haas, Passed Assistant Surgeon, Division of Infectious Diseases, National Institute of Health, United States Public Health Service The virus which produces lymphocytic choriomeningitis in man occurs spontaneously in domestic mice (Mus muscvlus), and this rodent infection is connected epidemiologically with human cases (Armstrong). The studies here reported deal with the behavior of the infection in mice. Spontaneous infection in white mice was studied intensively by Tr&ub, who found that less than 20 percent of the naturally infected animals showed symptoms, although virus was present in practically every organ of the infected mice, as well as in blood, urine, and nasal secretions. Infection spread among mice in two ways--transmission from mother to offspring in utero, and from infected to noninfected mice hy contact. Mice infected in utero or in extreme infancy often retained virus for long periods, but when mice were infected after reaching maturity, virus was recoverable for only a short period. Exposure to the virus produced strong immunity in mice, regardless of whether the animal in question continued to harbor demonstrable virus or not. The present report is essentially a confirmation of Traub's thorough studies, with some extensions consequent to a somewhat different approach. METHOD or STUDY Except where otherwise mentioned, these studies were made on albino mice of the National Institute of Health "Swiss" stock. Usually mice were kept in glass battery jars; where more than 6 mice were used at a time, large glass cages with screen tops were employed. Two strains of virus were used, one recently isolated from a human case of choriomeningitis, and the other originating in naturally in fected house mice. The two strains behaved similarly. To determine whether mice under study had contracted infection, the usual method was to test their ability to withstand intracerebral 01 501 0051 February M. 1M1 286 inoculation with 10-15 M. L. D. of the stock virus; along with each group of mice thus tested, from 5 to 15 fresh mice were inoculated in the same manner, in order to make certain that the virus used in the immunity test actually produced the disease in animals known to be nonimmune. In some cases, mice were sacrificed and active virus was recovered from their viscera. In this report the term "natural infection" refers to infection con tracted in utero or by contact with infected mice, as distinguished from infection by inoculation. NATURE OF THE INFECTION IN MICE Symptoms in naturally infected mice were extremely mild or en tirely inapparent, as shown by the following examples: 1. Seven naturally infected house mice kept in the laboratory for over 5 months showed no evidence of illness, though virus was re covered from their blood and feces during this period. Thirty-six white mice infected by cage contact with the 7 house mice also showed no symptoms. 2. In a series of experiments, 66 fresh white mice were placed in jars with infected white mice for periods of 12 to 28 days; over half became infected through this contact, and there were 4 deaths, pre sumably incidental, since in another series of tests, where no trans mission of infection occuned in mice kept under the same conditions, there were 24 deaths among 117 animals. Mice from infected litters seemed to mature less rapidly than did normal mice, though this is only an impression, as no weights were kept. TRANSMISSION AND SURVIVAL OF INFECTION Transmission in vtero.--Infection of mice in vtero was accomplished in two ways: (1) Pregnant mice inoculated before delivery produced infected litters in many instances; the route of inoculation of the mother was not important. (2) Mice were inoculated intranasally 1 or 2 days after birth; when the females matured and were bred, they tended to produce infected offspring. Mice infected in vtero transmitted the virus to their descendants in many, instances, as is shown in table 1. That infection of these off spring was not due to chance spread of virus in the laboratory appears later, in table 3, where it is shown that litters boro to mice inoculated after reaching adulthood, but before becoming pregnant, failed to become infected. Since infected mice were usually detected by immunity tests, it is necessary to show that it was actual infection and not merely immunity that was passed on from mothers to offspring. This is indicated by the following observations: 01 501 0052 287 February It. 1W1 1. One mouse from each of 4 litters, removed two or three genera tions from inoculated ancestors, was killed and found to contain virus by inoculating an emulsion of its spleen and liver into fresh mice; the Utter mates of these infected mice were at the same time found to be immune by the usual test. On the other hand, one mouse from each of two other Utters yielded no virus, and the Utter mates of these mice did not survive the immunity test. 2. Five mice infected in viero were killed from 107 to 216 days after birth and found still to harbor Uving virus.1 3. Virus was recovered from a pooled sample of feces from 5 mice infected in viero; the mice were 107 days old at the time of this test. 4. Twenty-one mice infected in viero transmitted infection to fresh mice kept in jars with them for periods of 12 to 28 days. Table 1.--Transmission of virus to descendants of mice inoculated during pregnancy or during infancy Descendants of Inoculated female mloe M mloe Inoculated 1 to 11 days 21 mk* InnralatM lntrazuulfr before delivering young within 1 to 2 dap of birth Total born Number In fected Total bom Number In fected Litters Mloe Litters Mice Litters Mice Litters Mloe First generation Second generation... .. .. Third generation_________________ 1a4 14 94 limft 10 10 u 3t4t 57 ITt 0) &: 0) 15 9 57 60 0) Btndiea on the group Infected by inoculation In infancy wen not carried beyond two generations of offsprtxut. The prolonged survival of the virus in mice infected in viero is indicated by these observations. Another example of this survival appears in the abiUty of females to transmit infection to successive Utters in the same generation. This is shown in table 2. Tabu 2.--Transmission of infection by mice to multiple litters Offspring of i mice Infected in utero or early Infancy, which gave birth Ntunber mice Namter mice to more than 1 Utter each mutters Infected First Utters.____ Second Utters____________________ ___________ Third Utter . __ ________ ____________ a 40 >33 22 > Offspring of ( mice. Two mica produced Infected first Utun bot failed to Infect their second Utters. In contrast to mice infected in viero or early infancy, animals inoc ulated after reaching maturity (i. e., 3 weeks or older) did not transmit infection to their offspring, provided they were not pregnant at the time of inoculation or did not become so shortly thereafter. This appears in table 3. 1 These mice bad been Inoculated with tbe rtock Tints when they wan 1 month old. In order to test their Immunity. Experience with this strain of Tims has Indicated that In the malority of it lg not reooTarable from Inoculated mloe for longer than a few weeks after Injection, and therefon eoold not bare been reeponsible for the remits obt&lned heie. ' 01 501 0053 February 14.1941 288 Table 3.--Failure o} mice inoculated after reaching maturity to transmit infection to their offspring Offspring Min inoculated during adult life and subsequently producing . offspring Number born Number infected Listen Mice Litters Mice 33 females Inoculated 34 to 149 days before giving birth to young. as 143 Nono None 14 males inoculated 23 to 93 days before siting offspring............. 8 30 Nono None One female, not included in table 3, produced infected offspring 31 days after being inoculated; apparently enough virus survived to infect the offspring conceived shortly after inoculat:on. In further contrast to mice infected in uiero or early infancy, adult mice inoculated while pregnant did not transmit the virus to offspring conceived after the birth of those carried at the time of inoculation. Three mice inoculated during pregnancy and giving birth to infected litters subsequently produced additional offspring to the total of 16, none of which were infected. Most of the second and third generations of infected mice were obtained by breeding infected males with infected females. In three instances, however, naturally infected females produced litters sired by uninfected males. Two of these litters were infected, indicating that virus passed from infected mothers to offspring regardless of the status of the male parents. On the other hand, when infected males were bred to uninfected females, the offspring were not infected, as indicated by the following summary: 11 infected males were bred with 19 uninfected females; 13 litters resulted, comprising 74 mice; 12 of these litters, comprising 69 mice, were uninfected. One litter of 5 mice was immune when tested, and it is probable that these particular mice acquired infection through contact with the infected father, a circumstance generally prevented by removing the male before the young were delivered. A second uninfected female in the same jar at the time this litter was boro later produced an uninfected litter, contact between this litter and the father having been avoided. Transmission by contact.--Mice infected in utero or in infancy trans mitted infection to others placed in contact with them. This is shown in table 4. In one of the tests in which white mice were infected through contact with the gray mice, virus was recovered from a contact as early as the sixth day. In addition to the examples of contact infection given above, there were four litters inoculated intranasally on the first or second day after birth and allowed to remain with the mothers for .a month. At the end of this period all the mothers were immune. ' 01 501 0054 289 February M. 1941 Table 4.--Transmission of virus by mice infected in utcro or infancy to mice placed in contact with them Infected mice with which flesh mice were io contact Length of contact (days) Fresh mice Number Number used Infected 32 white mice infected in utcro ted early Infancy .................... 6 to 28 13 to 28 i47 `M 36 35 i ft different test!. 1 IB diflerent tests. * These mice were all St least l month old when used (or then tests. Mice which became infected after reaching their maturity (i. e., 3 weeks or older) rarely transmitted the virus to contacts, in contrast to mice infected in utero or in infancy. This was true regardless of whether the adult mice had been infected by inoculation or by having been themselves in contact with mice capable of transmitting infection. The experiments establishing these statements are summarized in table 5. Table 5.--Failure of mice infected after reaching maturity (t. e., S weeks or older) to transmit virus to fresh mice placed in contact with them Mice infected by Inoculation or by contact after reaching maturity, and then nlaeed'in contact with treah mice Length of contact (days) Fresh mice Number Number used infected 25 white mice infected through contact with natnnDy infected miee.. 73 white mice infected by inoculation (Terioto routes). _________ Total _________________ ___________________ _________ IS to 31 8to 37 150 195 145 2 1 3 i io different tests. > 2 different tats. The mode of spread of contact infection among mice was investigated by the following experiments: 1. Sex.--Semen taken from infected males and instilled into the vaginae of 12 females infected 9 of them; the females eventually pro duced 8 litters, comprising 51 mice, none of which were infected. Experiments on contact infection indicated that sexual contact was not necessary for transmission of the virus: 6 females infected 8 out of 17 males; 5 males infected 9 out of 16 females; 2 males infected 3 out of 5 males; 4 females infected 9 out of 16 females. 2. Feces and urine.--Traub found the virus in urine of infected mice but was unable to infect mice by placing them in cages heavily contaminated with such urine. During the present studies, virus was recovered from two pooled samples of feces collected, respectively, from 3 and 5 infected mice. The experiments summarised below, dl 501 0055 February 14,1M1 290 however, indicate that feces and urine were not essential for trans mission of the infection among mice: (a) Ten fresh mice were put into a glass cage which had been inhab ited for 22 days by infected mice, and which had not been cleaned in any way. After 16 days in this cage the fresh mice were found to be nonimmune; the infected mice had transmitted infection to 18 fresh mice during their occupancy of this cage. (b) Each of five jars was divided into an upper and a lower compart ment by a horizontal screen. In each of three jars an infected mouse was kept in the bottom compartment and two fresh mice in the top; in the other two jars the position of the mice was reversed. Mice in the lower compartment were exposed to urine and feces falling through the screen from those above, but mice in the upper section were not exposed to these excreta. The test lasted a month, and the result was that one fresh mouse in each jar was found to have become infected. In other words, mice not exposed to feces and urine were infected as readily as those so exposed. It must be concluded from these experiments that neither sexual contact nor feces and urine were essential in the spread of contact infection among mice. Since ectoparasites were not present in the cages where such spread occurred, it appears that nasal discharges or saliva were the likely means of disseminating the virus. Quite possibly both are important; Traub found abundant virus in nasal washings, and nose-to-nose contact among mice is common. In some instances, however, fighting results in infliction of numerous wounds, and during these studies virus was recovered from 2 badly bitten mice. Survival of the virus.--The observations already discussed suggest that virus survived for long periods in mice infected in utero or in early infancy, whereas in mice infected after reaching maturity active infection tended to be demonstrable only for a short while. This contrast between mice infected at different stages of life is further emphasized by the following experiment: Five fresh mice were placed in a cage with 3 infected mice, 1 of which had been infected in utero and 2 on the day of birth. After 23 days in the cage, all the mice were given the usual immunity test, which they survived; 35 days after this test all were killed and tested for virus. The mouse infected in vitro, which was 216 days old when killed, yielded active virus, as did one of those infected on the day of birth, 185 days before; the other mouse infected on the day of birth, 148 days previously, yielded no demonstrably active virus, nor did any of the 5 mice which had developed an immunity, following con tact with the infected animals.'* * Mice inoculated inttacerebrnlly with spleen emulsions of these five mice failed to develop any signs of choriomeningAs; the mice inoculated with such an emnltlnnf mm one of theaa flea mioe later survived an immunity test with the stock vims, indicating that In this one vims TMv have been present in very small amount or in a condition not sufficiently active to produce delectable disease. 01 501 0056 291 February 14,1941 It appears that there was a basic difference between the nature of infection established in utero or in very young mice and that intro duced into mice already mature, and this difference was indicated by the ability of mice infected in utero or in infancy to retain the virus and to transmit infection to offspring and contacts, while the others did not. . SUMMARY Infection of white mice by the virus of choriomeningitis, when acquired in utero or by contact, was generally of an inapparent type. Mice infected in utero or early infancy tended to retain active virus for long periods, probably in some instances for life, and to transmit infection to offspring and contacts. Infection passed from infected mothers to offspring whether the fathers were infected or not, but it did not pass from infected fathers to offspring through uninfected mothers. Mice infected after reaching maturity did not transmit infection to their offspring, except for females pregnant at time of inoculation, and rarely infected contacts. Active virus was not generally demon strable in such mice except for short periods after exposure or inoculation. Transmission of infection from naturally infected mice to fresh contacts occurred when exposure through sexual contact, urine, and feces were eliminated, infection in such instances apparently being conveyed by nasal secretions or saliva. These observations ore in agreement, in the essential points, with those previously reported by Traub. The behavior of this virus in mice is particularly interesting because of two underlying facts: First, the continuous propagation of an infection that is inapparent, or nearly so; and second, the basic difference in response to infection shown by very young mice as com pared to the response of mice subjected to infection after reaching maturity. ACKNOWLEDGMENT Acknowledgment is made to Senior Surgeon Charles Armstrong for advice and suggestions, as well as for provision of many of the physical materials used in these studies. REFERENCES Armstrong, Charles: Studies on choriomeningitis and poliomyelitis. Trans, and Studies of the College of Physicians of Phiia., 4th Series, Vol. 8, No. 1 (April 1940). Traub, Erich: An epidemic in a mouse colony due to the virus of lymphocytic choriomeningitis. J. Exp. Med., 63:533 (1936). 285759*--41------8 01 501 February^!.1M1 292 Traub, Erich: Persistence of lymphocytic choriomeningitis virus in immune animals and its relation to immunity. Ibid., 63:847 (1936). --------------- : The epidemiology of lymphocytic choriomeningitis in white mice. Ibid., 64:183 (1936). ----------------: Immunization of guinea pigs with modified strain of lymphocytic choriomeningitis virus. Ibid., 66:317 (1937). _ Factorsi finf'luenc'ing persi'stence o~f c'horiomeningitis virus in blood of mice after clinical recovery.' Ibid., 68:229 (1938). --------------: Epidemiology of lymphocytic choriomeningitis in a mouse stock observed for 4 years. Ibid., 69:801 (1939). A NOTE ON MODIFIED RADIO PRATIQUE IN GUAYAQUIL By Robert OlESEH, Medical Director, United Statu Public Health Service Radio pratique was inaugurated at the port of New York on Feb ruary 1, 1937, and has been in successful operation since that time.1 This procedure is also practiced in Boston, New Orleans, New York, Los Angeles, and San Francisco. In United States ports only passenger vessels with accredited ship's doctors are eligible for radio pratique. However, in Canada cargo as well as passenger vessels are accorded this privilege even though a physician is not a member of the crew. Radio pratique, as adminis tered at William Head quarantine station, 'Victoria, British Columbia, has been described by Dr. H. B. Jeffs.2 Experience with radio pratique for freighters has been entirely satisfactory in Canada. Radio pratique principles have now been extended to other coun tries, Ecuador being the latest to make use of this practical modifica tion of maritime quarantine. According to recent information the following procedure is in effect for southbound vessels arriving in Guayaquil: 1. Within 24 hours prior to arrival the ship's doctor shall send a radio message to the quarantine officer advising that there is no illness of any kind on board and that all passengers have been vaccinated against smallpox. 2. Upon arrival in port the vessel will be boarded by the quaran tine officer who will require a copy of the radiogram signed by the master and the ship's doctor. 3. The ship's doctor must also present a vaccination certificate for each person who lands in Guayaquil. 4. Having obtained these documents the quarantine officer may allow the other port authorities to board the vessel without further __ formality. , '5. Pratique will be withheld and customary inspection made under the following circumstances:* i i Akin, C. V.: PraUeoy by Wlrelees In Lien of Quarantine Inspection for Paasanger VesaeJa. Fob. Health Rej*. U: SOT (Apr. fj. 1937). i Bulletin of tbe International Office of Public Health, Sli 1581 (September U39). t ^ ' f `t 01 501 0058 293 Sebruary 14.1941 (o) If the radiogram is not confirmed. (6) If the vaccination certificates are not in order. (c) If illness has occurred after the radiogram was sent. Cargo vessels are not included in this procedure. Steamship companies estimate that a considerable saving of time will be effected at Guayaquil by this utilization of radio messages prior to the arrival of vessels in port. Comment.--It has been found, as the result of actual practice and careful observation, that the public health has not been imperiled by radio pratique and that this modification of maritime quarantine is helpful in expediting commercial activities. With the leadership already provided in several countries it may be expected that the measure will be adopted even more widely. NOTIFIABLE DISEASES IN THE UNITED STATES, 1939 Morbidity and Mortality Summaries for Certain Important Commnnicable Diseases The United States Public Health Service has recently issued a tabular morbidity and mortality compilation, by States and by months, for the notifiable diseases as reported by the State health officers in 1939.1 A summary of this compilation is presented here, together with case and death rates, case fatality rates, and, in some instances, the estimated expectancy based on figures for recent pre ceding years. For certain diseases, some States do not report cases, or the case reports are manifestly incomplete. In such instances groups of States with the most satisfactory morbidity reports are treated separately in order to arrive at more nearly accurate case and case fatality rates, while the totals for the larger group of States include the deaths as cases in States which reported fewer cases than deaths. Case fatality rates are not computed, however, on such totals. The mortality figures may be considered as approximately correct, although they will not agree in all instances with the final figures of the Bureau of the Census. The estimated expectancy, given for some of the diseases, represents an attempt to ascertain from the experience of recent years the num ber of cases of a disease that might normally have been expected in 1939. In comparing the numbers of cases reported in 1939 with the esti mated expectancy, or with figures for preceding years, it should be borne in mind that there has been a gradual improvement in the > Tbe Notifiable Diseases--Prevalence in States. 1939. Supplement No. 163 to tbe Public Health Reports. Government Printing Office. Washington. 1941. . 01 501 0059 Feb.-airy 14,1M1 294 reporting of notifiable diseases and that the population has increased. A large increase, however, especially in the case rate, is likely to represent an actual increase in the prevalence of the disease. The populations given for groups of States, used in computing case and death rates, were estimated as of July 1, 1939, by the Public Health Service, and are based on the populations for 1930 and preliminary figures for 1940 populations as published by the Bureau of the Census. CRBHKTOX tS>* 47 8tatu: Cues reported, 1839 (popatetloD 130473,000)._______ Bsttmatad expectancy baaed on yeare 1833-38...--------------- Cases per 1400 Inhabitants, 1938------ -------------------- ---- Ceaes par 1,000 inhabitants, estimated expectancy------------- Deaths registered, 1930_________________________________ Deaths per 1400 Inhabitants. 1839.......................................... Cases reportsd tor each death registered, 1839--................ 4B States: ` . Cases reported, 1939 (population 130,783.000).------ ------------- Casea par 1400 Inhabitants. 1939________--......... --------- 338.486 331.319 L 984 3.039 110 0.001 2.330 . 238,746 . 1.979 47 Stntaa: > Cases reported, 1939 (population 130478,000)... __________ Estimated expectancy baaed on yean 1933-38.... Cases per 1400 Inhabitants. 1939_________ Cases per 1,000 Inhabitants, estimated expectancy- Deaths reclstered, 1939----- Deaths per 1400 Inhabitants. 1939-------------------- Cases reported tor eacb death registered. 1939-- 48 Cases reported. 1439 (population 130,763,000)__________ ______________ ______ _____________ Caaea per 1400 inhabitants. 1930---------------- ----- ----------------________ _______ ____ __________ 24.048 38.269 0.183 0.301 1022 24.033 a 184 8WHBT OKOXmtO <37b) 33 States:' Cases reported. 1939 (population 107488400). Cases per 1400 Inhabitants, 1939..--------------Deaths reclstered. 1939_________ _ Deaths per 1400 Inhabitants, 1939.. Casss reported tor each death reclstered, 1939.. 39 States: i Cases reported. 1989 (population 138.883,000).-- Deaths registered. 1939_________ ____ ________ Deaths per 1400 Inhabitants, 1930____________ 47 States:' Deaths reclstered, 1939 (population 130478,000)____ Deaths pet 1,000 Inhabitants, 1999------------------------ 2.981 a 028 220 0.002 14 >3.039 278 0.002 0.032 DTSXHTXBT tlliCTM.tlT) (370) 818tates: Cases reported, 1938 (population 101,478,000)-------------------------------------------------------------------- 21,137 Cases per 1400 Inhabitants, 1939---------------------------------------------------------------------------------- 0.308 Deaths registered, 1939__________________________--------------- --________________________ 831 Deaths per 1400 Inhabitants. 1939--------------------------------------------------------- -- a 008 Cnee reported tor each death registered. 1939---------------------------------------------------------------- - 23 41 Statu:1 Cases reported. 1939 (population 133,719,000)_____________________________________________ * 31,327 Deaths registered, 18391____ 1,021 Deaths par 1,000 inhabitants, 1939_______________________________ 0.008 48 Statu: _ Deaths reclstered. 1939>Cpopalatlon 128482,000)__________________________________________ 1,046 Deaths per 1.000 inhabitants, 1939 0.008 ncDuuns, monne oa Lxmaaoic on 29 8tatu: > Cases reported. 1939 (population 81.496.000) Cesee per 1.000 Inhabitants. 1939 Deaths registered, 1939---------------------------------------- --------------------------------------------------------- Deaths per 1,000 inhabitants, 1939._________ ____________________________________________ Cases reported tor each death registered. 1939 47 Statu: > Cases reported. 1939 (population 130,273.000)________________________________________ ____ Deaths registered, 1939__________ ______________________________________________________ Deaths per 1,000 Inhabitants, 1939__________________________________________________ ____ 787 0.010 363 0.004 2.168 > 1,069 643 0.003 Figures tn parentheses in the subheadings are disease title numbers from the International List of Causes of Death. 1938. > The District of Columbia is also included but not counted as a State. > Includes the number o( deaths used as cases when no cases are reported, or when the reported number of cases is less tban the number of deaths. 01 501 0060 295 February 14,1M1 OOXOUBEA (23) 48 States: t Cases reported, 1939 (population 130,763,000)___________ Cases per 1,000 inhabitants. 1939____ __________________ 178,343 1.364 OTltlSU (33) 42 States:> Cases reported. 1939 (population 101,802,000)_______________ Cases per 1,000 Inhabitants. 1939________________ _ . ...... Deaths registered, 1939______________________ - __ ___ Deaths per 1.000 inhabitants, 1939________________________ Cases reported (or each death registered. 1939______________ 47 States:* Cases reported. 1930 (population 130*273.000).______ _____ __ Deaths registered. 1939.................................. ............ ............ .. Deaths per 1.000 inhabitants, iq ,____ ______ 48 States: i Cases reported, ioao ..................... ...r,,r..... .....................-r--^ OS) 40 States: Cases reported. 1939 (population 125.977.000)..... Cases per 1,000 inhabitants, 1939... Deaths registered, 1939.................... Deaths per 1.000 inhabitants, 1939.. Cases reported (or each death registered. 1939................... 40 States: * Cases reported, 1939 (population 128,827,000). Deaths registered, 1939.................... Deaths per 1.000 inhabitants, 1939.. 47 States: * Deaths registered, 1939 (population 130,275400). Deaths per 1,000 inhabitants, 1939.M....M...... 273.303 - 2.708 .. 19.724 ~ a 194 .. 13.988 ..*277.813 .. 21.834 .. a 188 ...277.818 82,654 1.749 0.014 47 *82.833 1.750 a 014 2.750 0.0L3 MEASLES (3ft) 47 States: * COM3 reported, 1939 (population 130473,000)______________________ ______ ________________ 403.037 Cases per 1,000 Inhabitants, 1909-----------------------------------------------.......__ _ 3. 094 Deaths registered, 1939_____ ____ 1.171 Deaths per 1.000 inhabitents, 1930______________________________________________________ 0.009 Csses reported (or each death registered. 1939 344 48 States:' Cases reported, 1939 (population 130,763,000) 403.317 Cases per 1.000 Inhabitants, 1909_________________________ 3.084 Mixraoms, hxmihcococcus <e> 43 States:" Cases reported. 1939 (population 128,024.000) Estimated expectancy based on years 1933-38------------------------------Cases per 1,000 inhabitants, 1939___ _____ _______________________ Cases per 1,000 Inhabitants, estimated expectancy_________________ Deaths registered, 1939._________ ______________________________ Deaths per 1,000 Inhabitants, 1939_________________________ _____ Casea reported (or each death registered. 1939_____________ _______ 47 States:1 Cases reported. 1939 (population 130.275,000) Deaths registered. 1939__________ ______________________________ Deaths per 1,000 Inhabitants, 1939 48 States:' Cases reported, 1939___________________________________________ 1,970 3.611 a 015 0.029 694 a 005 2.839 ' 1,991 a 713 005 >1.993 mmrs (mo 40 States: Cases reported, 1939 (population 98J06.000)______________________________________________129,714 Estimated expectancy based on yean 1933-38113,385 Casee per 1,000 Inhabitants, 1939_______________________________________________________ 1.319 Cases par 1,000 inhabitants, estimated expectancy 1.198 Deaths registered. 1939---------------------------------------- 70 Deaths per 1,000 Inhabitants, 1939__ ___________________________________________________ 0.001 Csses reported lor each death registered, 1939 1.853 44 StfttAK Cases reported. 1939 (population 109448,000)* 129,731 Deaths registered, 1939______ 87 Deaths per 1,000 inhabitants, 1939 0.001 47 States: Csses reported, 1939*131.S26 ' The District o( Colombia is also Included but not coanted as a State. : Includes the number o( deaths used as cases when no cases ere reported or wnen the reported number o( senes is less then the number of deaths. 01 501 0061 Tebnury 14,1M1 296 ULLAGE! (0) 18 6UtMt Cues reported. IBM (population 484112310)_____________ Casa par ljoao inhabitants, 1030------- ---------------- ------- Deaths registered, 1839__________ ______ , - - Deaths per 1J00 Inhabitants, 1039- - ... -- Cases reported tor etch death registered, ioso -- H States:1 Cases reported, 1839 (popelatlnn 133,318,000)__ Deaths registered, 1039 -- Deaths par WOO ia9 47 States:1 Deaths registered, 1839 (population 130,2?WOO) Deaths per WOO Inhabitants. 1939_______ ___ . 10.200 . 0.209 . 1.925 . 0.039 . 3.299 .MQ.717 .. 2.442 0.020 . 1442 . 0.010 nrtPMOtnu tux nass uor-toei 39 States:1 Cases repotted, 1939 (population Ml,Martin) . . ...---------------- Csaes par WOO Inhabitants, ibm------------ ------- . --- Deaths registered. 1939__________ -------------------------- Deaths per WOO Inhabitants, 1939__________ - Cases repotted ter each death reclttcred, 1839___________________ 47 States:1 Deaths registered. 1939 (population 130,773^00)__________ ______ Deaths per 12100 Inhabitants, 1939 . ...........................- 48 States:1 Cases reported, 1939.._______________ _______ _________ ---- 121.237 1.332 81534 0.880 1307 - 77.802 .. 0.390 147,838 rouoirfzuBa as> 47 States:1 Cases repotted, 1939 (population 130,273.000)........ ............. -- Estimated expectancy baaed on yeare 1933-38__________ _ Panoj per ^ Cases per 12)00 Inhabitants, estimated expectancy -.......... Pfattit MbtOBde 1930 ..-------------------r- Deaths pet 12)00 inhabitants, 1030--------------- -------------------- Cases reported for sseb death registered, 1030.........--........ 4S States.-' Cases reported. 1939 (population 130,7032100)______________ Casee per WOO Inhabitants. 1939_____________________ ___ 7, ddV 1726 0.058 0.020 750 0.006 0.708 7.343 0.056 Knur mu at) 47 States:1 Cases reported, 1930 (population 13127320).................... Estimated expectancy based on yeam 1933-38....... --___ ___ Ceaes per 120 Inhabitants, 1939_________ _____ _________ Cases per 1.000 Inhabitants, estimated expectancy_________ Deaths registered, 1939_____________________....____ ____ Deaths per WOO inhabitants. 1039______________________ Casee reported tor eech death registered. 1939____________ 48 States:1 - Cases reported. 1339 (population 130,70320)______________ Cases per 120 Inhahitents. 1939________________________ . 101733 . 207,103 1.243 1.030 833 . 0.007 190 161897 L246 sxrnc sou thsoat ciisb> S3 States: Cases reported. 1039 (population 85X8020)___________________ Cases per 120 Inhabitants, 1330_____________________________ Deaths registered. 1939.................. ................... -- Deaths per 120 inh,,hitwf iq?q . ............. ... . Cases reported In each death registered. 1933 43 States:1 Cases repotted. 1333 (population 119X0120)__________________ Deaths registered. 1939 Deaths per 120 Inhabitants. 1939___________________________ 48 States:1 ' Cases reported. 1939 8,338 0.100 1,262 0.015 6.765 >9.227 1.051 0.016 10,758 OtAUTOX IM> 47 States:1 Casas reported. 1933 (population 130X75.000)____________________ Estimated expectancy, based on yean 1932-38__________________ Cases per 120 inhabitants. 1930 Cases per 120 inhabitants, estimated expectancy_______________ Deaths registered. 1939_____________ __________ ______________ Deaths per 120 inhabitants. 1939__ _______ ___________________ Cases reported (or each death registered. 1939___________________ 48 States:1 Cases reported. 1939 (population 130,76320)____________________ Cases per 120 Inhabitants, 1939___________ ___________________ 9.877 7.083 0.076 0.036 39 a 0003 233 8,877 0.076 1 Tbe District of Colombia Is also included bnt not ooonted as a State. Includes tbe number of deaths used as cases when do cases ere reported or when the reported number of cases is less than the number of deaths. < Includes 7,484 cases of lobar pneumonia only. 01 501 0062 297 February U. l&ii srwnus <30) 48 StAttfS* ( Cases repotted. 193# (population 130.7S3.000)------------- ----------- ------------------------------------------ 485. nfij Cases per 1,000 inhabitants, ________________________________________ 1709 TPBUCCLOSa ULU. TOEMSl US-X3> 37 States:' Cases reported, 1939 (population 103,700,000)_________ _______------------------------------------------ 92.293 Cases per 1.000 Inhabitants, 1939------------------------------------------------------------------------------------- 0.890 Deaths registered, 1939__________________________ __________ _________ ___ ______________ 47.828 Deaths perl. 000 inhabitants. 1039 0.461 Cases reported lor each death Mistered, 1138...... ...................... ....................... ......................... L 930 45 States:* Cases reported. 1939 (population 12W9M00)_____________________________________________ >102.775 Deaths registered, 1939..____ ______________________________________________________ ____ 88.313 __ Deaths per 1,000 Inhabitants. 1039_____________________ __________ a 468 *~~47 States: ` Deaths registered. 1939 (popnlaton 130,273,000)____________ ______________________________ 61.319 Deaths per U000 Inhabitants. 1939______________________________________________________ 0.471 n7Bg>coioais (usnataToar smut) os> 21 States:' Cases reported. 1939 (population 63.639,000)__ Cases per 1.000 Inhabitants, 1939___ Deaths registered, 1939-. Deaths per 1,000 Inhabitants, 1939_ Cases reported lor each death registered, 1939.. 46 States:' CDaes&etsbsreRpooirstetedr,ed19,39 (population 129,632,000).. Deaths per UXX) Inhabitants, 1939____ 48 States:' Cases reported, 1939________________ 32.388 0.831 37,373 0.430 1.933 >81.481 88.941 0.433 ' SI, 998 rtbod rrru a) hip rsJUTtraotp rmi w 47 States:' Cases reported. 1939 (population 130.275,000)______________ _ . - - . Estimated expoctancy based on years 1833-38 Cases per 1,000 Inhabitants, 1939....................... .................................... Cases per 1.000 Inhabitants, estimated expectancy__________________ 'Pfiithi Tfg**t*|,6d. 1039________ __________ ______ Deaths per 1,000 Inhabitants, 1939-I--1II-I______________ ____ __ ~ Cases reported (or each death registered, 1939______________________ 48 8tates:> Cases reported, 1939 (popnlation 130,763,000)___ ______________ _____ Cases per 1,000 inhabitants, 1939________________________________ ... 13.088 18.879 0.100 0.147 1.987 0.018 6.837 13,069 0.100 srHoonxo comm (9> 47 States:' Cases reported, 1939 (population 130,273.000) is), 046 Estimated expectancy based an yean 1933-38______________ 199.896 Cases per 1,000 inhabitants, 1939____________ ____________ i. 408 Cases per 1.000 inhabitants, estimated expectancy_______ _ i. 374 Deaths registered. 1939._____________ ___________________________________________________ Deaths per 1,000 inhabitants, 1939______________________________________________________ Cases reported (or each death registered, 1939____________________________________________ 48 States:1 Cases reported, 1939 (popnlation 130,763/100)_____ _____ _______________ _183.188 Cases per 1/XX) inhabitants, 1939 3.008 a 023 61 1.401 ' The District of Colombia Is also included bat not aoanted as s State. ' Includes the nnmber c4 deaths used as cases when no cases are reported, or whan the reported number ol ceses is leas than the nnmber at deaths 01 501 0063 Tebroary 11.1M1 298 Bs=!SSiissIiHIs=rI!3aKsiiI ill RSSs S'rS?- -g2"lSrf5r" Total Cases reported, 1939, by monthi A p ril *1 rRSRsa2SiIs5aS"'SiisslB8S iaf g* j-W V v 2- ~*r A -^riaSSSs5SSs2ir"SI5ISiaRi SSS sf - "g =g= "raaSSSiSSSiRaSS-sSsSSSSssS Ssi o' v v mv v w v vv v vgv October i| **SsS2SSSsS=SISsS''sis=SSs852 Ssi 1 K K *< cf VfC d dd d ^50 a *SslaSSS2S5I21I5"iSI=2ss852 Si 0 V V V VVV MW V >V V Wg < HK -gSi58sgiisiS5Si-8sS2S8|S| gs= V V V Mjf WV V aV V rfjV *'8"s2s2s5as82S28l"512ISisSs S53 *% d d dd^ ddd d dd d d^d *r,8s85s5s55iii3S'aS321s:IS8 22 i g J * =** S-= Sgg "c2Ssr5821SS!ssI";S8sskbSs SS3 ft - g-g 2-ft ggg I tf *"-g2=81SSSSSg5SS|--sgssssasg 51= g- g**S a ggg Is -g-52css!=|g5gRi""=8gS|=gsg gas g- 2-s g g a--w ggg -rSS2S8B255sSSBr"28lSSi=la =5= I 5 s'-g g a tf--w 2ss 2228a,0522225;822?i5523g3g2gS5 225 Number ol Stales iiyii! ii iiurnyyi \ Sm i if! i LI y s | i! N y| It i i illiliyi]i i: i:!: jigsiiiliisnsi: = i=si|n mi !:i liji -IS- liiiSSiiiiiliilil! iaas2SSSSi^aIaaB^^^He3> S 01 501 0065 299 9 0-t'c*eirMsiaKnMe*wf*oaiNng = SJS5S5ag^sr5SSr"SSTMSS?iS=2i ~ " s-'-' r'R" E3"r e* ** e . February H. 1941 Total Decem ber Novem ber Death refisttred, 1939, by monthii Usassgsss^ftas'--sa sssss^s -- >" w ift 82S2S5s53*SB8--83"=BSasa8 M O" -- a r- e* eu <0 W October iss gs-sssg *" i *" VV " is e*m sssassgssj-gcs^^s 3g-=sss S3 I1 e- S,, ag-SBg2!5SR2gg-S*" =S"a--8 <3 i 1 eafe 5gSSSgSS*Sg2S5e,|5=g22g 3frt *" er " w -* SSSaag5S39*=5-Sg"Sg*S2=g i < v Januery K assssgsssss&ft-ssg^gg-g^sg m s r <5r mo SSsS2SS5S<>SRe*,!,&fe*,ag*S'0,pg I * eO V * a s aB^s*sai-s^s--s^s--*ss* -softsas^-an mS s sea-si s Is !gNafnr>oo S-- Sgc3 gs* jg oI-E -8 n 1 V * i ao >Anse(*eaOKe !en0Nfa(( teeB non e> gj. t " - J V ~ eN>*Nr>eiorf**i,>Kr>NNi>er*rNi*eHt-NN !o^-*i1a3 0g Disease ii i ii ii< iiiti ttii><it>t,ai>**ii i : i t! : t ii <?n : ! lit* i^ a 1 i a in > a :i !i t ii ii i i i*a :i t i* a i <l^;s a a a iO :i :i aa i a 'a ` l5 aisw< i |* aa eaaira *> t t 4 ij; t e e t , iQ a > aa aaaiaa * Mr a *a,* * a,a ,' i* a-* a a 1a a a a 1 * a a a a a * * ^ a a a < 1 i3 a a^ > as a i3 i a a , a<^" " a 2 a $5!!! r (si i : :cRrs : : :si---=o : : ;ilcg : : :-JsS3 : esa*.- : : : : ; :S :8 :S := :g : : : : : ;2 ; rs u : :5 :fi ':2s 'ufigt?, *:w:s3j ;^sl3g2 C* ' S si `.2 : t i o * `Q>SJi a* i, i~a. "s * 2 * aft w Ui l1 j ^11-s s If ' 9 s3 wl5OSSS&ixi>52 so "|Ia=ct |3^3 t*= sO.Ulliili . * 1=qJ1o3 tbg-*C,cSiciRS--ewvS--s>S(3^2S|f|l2Bo&a<---S3=ftS-s-Ss-ajgciag"|c' S5iJ.fi ^SaQa-C 1 2 3 3 3 >a>aBr 3?^&*e-er*P^ *35 at, ? is til i i!**51 Ifyi j Slalf ! fe*so-co:io5fa= 4^s i!o|B^**a13 D^|Q3aft_*.^a- 305 S5 ~S' 3 iljjs = oa2Sl i ?rli5 I SSBo2b. Num ber ot ! Statee1 1 February It. 1941 300 COURT DECISION ON PUBLIC HEALTH Trichinosis held compensable under workmen's compensation act.-- (Massachusetts Supreme Judicial Court; Destefano v. Alpha Lunch Co. of Boston, Vaida v. Same, 30 N.E.2d 827; decided January 3, 1941.) In actions for breach of the implied warranty of fitness of food under a Massachusetts statute it appeared that the plaintiffs worked for the defendant company in one of its restaurants. Each plaintiff took two meals a day, except Sunday, at the restaurant, the meals forming part of the pay. Both plaintiffs became ill with trich inosis and testified that, during the 2 weeks preceding the onset of the disease, they ate pork and other products of the pig at the defendant's restaurant and nowhere else. The defendant was insured under the workmen's compensation act and the plaintiffs had made no reserva tion of common law rights under that act. The supreme court took the view that what happened to the plain tiffs constituted a "personal injury" within the workmen's compensa tion act. "It differed from the inhalation of germs of disease, illustrated by Smith's Case, Mass., 30 N.E.2d 536.1 It resembled more the cases of poisoning therein cited, and Osterbrink's Case, 229 Mass. 407, 118 N-E. 657, where the employee drank muriatic acid by mistake for water." Also the court was of the opinion that such personal injury arose out of and in the course of the plaintiffs' employment. "Since the injury was compensable under the workmen's com pensation act, it will not support an action against the employer at law, whether in tort or in contract, or whether or not based upon a statute. * * *" The action of the court below in ordering judgment for the defendant was sustained. DEATHS DURING WEEK ENDED FEBRUARY 1, 1941 [From the Weekly Health Index. Issued by the Bureau of the Census, Department of Commerce] Week ended Feb. 1.1M1 Correspond ing week. 1940 Data from 88 large cities of the United States: Total ..................................... Deaths under 1 year of age_______ _________ ______ .____ __ ___ ATorsgft for 3 prior ............................................ ...................... Deaths under 1 year of age, first & weeks of year Data from industrial Insurance companies: Policies in fort*........ .. . - .................................... .... Number of death claims_________ ______________________________ . Death claims per 1.000 policies in force, annual rate______________ . Death claims per 1,000 policies, first 5 weeks of year, annual rate 10,112 9,586 40,361 668 657 2,816 64.727.301 14,790 11.0 10.6 10.163 48,141 577 2,780 M, 327.780 13,817 10.9 10.4 > See Public Health Beports, January 31,1M1. p. 1B7. 01 501 0066 PREVALENCE OF DISEASE No Health department. State or local, can ejfedisely prevent or control dieeaee without knowledge of imm, where, and under what conditions cases are occurring UNITED STATES REPORTS FROM STATES FOR WEEK ENDED FEBRUARY 8, 1941 SnilUB*17 For the third successive week the incidence of influenza has recorded a decrease, with a total of 38,241 cases reported by the State health officers, as compared with 72,578 cases for the preceding week. The decline is noted for all geographic areas except the Pacific, where California reported 1,387 cases, as compared with 1,149 last week. It appears likely, however, that this increase may be attributed to delayed reports. West Virginia, with 6,046 cases; Virginia, with 6,976; and Texas, with 4,580, reported the highest incidence for the current week, although a sharp decline from the preceding week occurred in each of these States. Of the other eight communicable diseases, only measles, polio myelitis, and whooping cough were above the 5-year (1936-40) median expectancy. Also, the cumulative totals of these diseases for the first 6 weeks of the current year were above the cumulative me dians. The number of cases of measles reported for the current week is approximately two and one-half times the 5-year median, while whooping cough was only slightly above the expectancy. The 29 cases of poliomyelitis (as compared with a 5-year median of 18) ex ceed the number reported for the corresponding week in any of the preceding 5 years. The cases were scattered, with only three States reporting as many as 3 cases. Of 58 cases of smallpox, 25 cases were reported in the East North Central States (12 in Wisconsin and 8 in Michigan). One case of tularemia each was reported in Maryland, North Carolina, and South Carolina; and of 24 cases of endemic typhus fever, 14 were reported in Georgia. For the current week the Bureau of the Census reports 10,214 deaths in 88 major cities of the United States, as compared with 10,112 for the preceding week and a 3-year (1938-40) average of 9,525 for the corresponding week. The current figure is 689 above the 3-year average as compared with a similar excess of 526 for the preceding week. (301) 01 501 0067 February 14, 1941 302 Telegraphic morbidity reports from State health officers for the week ended February S, 1941, and comparison with corresponding week of 1940 and 5-year median In these tables a tero indicates a definite report, while leader simply that, although none wen reported, eases may have occurred. Division and State Diphtheria TnflnkT}m Measles Meningitis, me ningococcus Week ended-- Feb. Feb. 8. 10. 1941 1040 Me dian 1936 40 Week ended-- Feb. Feb. 8. 10. 1941 1040 Me dian 1936 40 Week ended-- Feb. Feb. 8. 10. 1941 1940 Me dian 1936 40 Week ended-- Feb. Feb. 8. 10. 1841 1940 Me dian 1936 40 KIV SNO. Maine................... ............ New Hampshire Connecticut____ _______ KID. AIL. 0 1 3 63 1 3 70 200 155 0 0 0 (c0 5 1 * 8 52 44 0 0 0 C c 0 20 10 a 27 c 1 33 433 272 435 \ 0 0 1 1 10 0 111 99 o o a a 1 317 2 4 30 177 177 0 0 0 New York____________ ii 22 34 1427 38 '60 3,088 287 673 1 0 4 New Jersey u 8 11 1.158 28 29 844 66 6fl 2 c 1 25 24 44 2.818 8C 170 3 Z. NO. CZN. Ohio................................. 10 15 20 883 22 20 1,838 22 24 3 1 3 Indiana__________ _____ 11 18 39 173 90 32 183 6 14 0 0 4 Illinois________________ 19 3C 32 195 134 134 1,831 30 36 1 0 4 Michigan * i 9 12 155 11 3 1.320 231 251 0 0 1 Wisconsin________ _____ 0 4 3 718 77 65 5S5 182 182 1 01 . NO. CZN. Minnesota_____________ 3 3 3 838 1 1 6 359 120 2 0 1 Iowa ________________ 13 3 6 396 25 8 130 97 55 0 1 1 Missouri_______________ 4 10 10 68 33 182 74 5 10 1 0 1 North Dakota................. .0 3 2 84 81 13 11 13 13 0 0 0 South Dakota 1 1 1 2a 4 4 18 7 4 0 0 0 Nebraska 1 0 3 14 3 2 6 31 22 0 Q 0 Kansas.______ _______ * 10 11 340 101 68 174 301 20 3 1 1 80. ATL. DoIawata.......... . .... .. 1 0 0 10 6D 24 o Maryland 1_______ ...... < 7 9 351 2S3 103 61 4 112 0 2 2 Dist. o( Col________ ____ 0 0 6 79 10 5 14 2 11 0 1 1 Virginia____ _____ ___ 6 12 22 6,976 2,882 498 42 99 1 2 10 West Virginia1........... . 3 11 11 fly 046 400 iti 125 15 15 0 4 3 North Carolina................ 16 25 24 590 121 67 182 107 107 0 1 2 South Carolina1 7 3 3 3060 3331 1,000 47 6 23 2 2 2 Georgia1______________ 7 11 3509 728 490 202 76 76 2 0 1 Florida.................. 4 4 9 387 50 4 21 41 41 0 0 0 Z. SO. CZN. Kentucky_____________ 11 10 9 246 86 86 203 35 70 3 0 6 Tennessee... 10 9 13 3003 424 176 99 M 64 3 2 4 Alabama1____ _________ 6 5 8 3,481 530 334 476 73 73 5 2 2 Mississippi *............... 246 3 w. SO. CZN. Arkansas______ ________ 12 8 8 767 1.608 S3 83 4 4 0 0 1 Louisiana > 5 11 11 218 360 44 7 15 15 2 0 0 Oklahoma_____________ 15 8 a 657 664 283 11 4 15 0 1 1 Texas1............................. 36 51 51 4.580 4.437 940 213 270 167 6 3 5 MOUNTAIN Montana................ 10 1 1 116 7 7 8 28 20 0 0 1 21 1 fl 6 25 iftl 0 2 1 189 4 14 Colorado_____________ __ 9 9 9 311 26 85 321 XL o Now Mexico............. Arizona.................. TJtah > . . * 1 2 20 3 9 7 7 721 9 29 4 281 297 173 80 13 13 0 66 125 190 81 0 0 0 0 0 0 Nevada____ ____________ 0 oo PACIFIC Washington............. 0 3 2 52 35 4 70 676 182 0 0 1 Orceon 8 2 2 54 107 76 325 247 34 0 0 0 California.. ............. 18 22 2! 1.387 1.499 322 101 433 433 3 1 1 Total 317 378 491 38.241! 16.583 4.577116.664 5.083 6.519 46 35 89 6 weeks________________ 2.840 2,628 3, 574)494, 449182,18C|20,877 70.927j25.982 31. $71 264 188 552 * See footnotes at end of table. 01 501 0068 303 February u, imi Telegraphic morbidity reports from State health officers for the week ended February 8, 1941, and comparison with corresponding week of 1940 and 5-year median--Con. ` PoliomyeiHtts Scarlet lever Smallpox Typhoid and para typhoid fever Division and State Week ended Pab. Pabv 8. 10, 1941 1M0 Modian 1936 40 Week ended Feb. Feb. 8. 10. 1941 1940 Weekended Median 1936 Feb. Feb. 40 8. 10. 1941 1940 Week ended Median 1936 Feb. Feb. 40 8. 10, 1941 1940 Me dian 1936 40 HIV XNO. Maine....... ...... New Hampshire-------- Vermont.................. ....... Massachusetts_________ Rhode Island___ . ft 0 0 0 0 0 0 0 1 0 0 19 28 0 447 0 4 9 16 0 143 134 250 0 1ft 12 30 0 0 0 0 0 00 0 ft 0 ft 00 0 ft ooc 1 o 0 0 2 0 0 \ Connecticut......^.--. 0 0 0 43 90 97 0 0 0 i 5 1 KD. ATX. New York_____________ 0 2 1 380 965 690 0 0 o 5 g New Jersey___ _________ Pennsylvania.____ 0 1 0 0 0 80S 333 17a 0 348 370 473 0 0 0 0 0 0 0 0 2 8 1 8 X. XO. CBN. Ohio__ ______ _ . Indiana........ .................. 0 0 I 0 1 388 277 313 0 145 221 SI 5 0 0 6 3 6 1 4 0 1 1 flUnnfr._, Michigan > . ... Wisconsin_________ _ 3 1 I 0 1 1 0 iM 583 622 0 1 142 381 497 8 0 10A 150 298 12 2 11 23 55 8 0 0 1 0 0 2 4 1 W. XO. CXH. Minnesota__ .. .. Iowa_____ _ __ Missouri___________ ________ North Dakota................. .. 10 54 30 00 0 0 0 0 49 113 ieo 46 70 183 76 91 145 16 28 38 6 3 S 0 58 9 33 2 17 02 o o 0 o o 1 1 ftSouth Dakota....________ Nahreaka Kazms........___, _ 0 0 0 0 0 0 0 0 0 17 39 90 as 20] S3 ?a 75 209 0 0 0 46 05 1 10 1 o 0 o 0 0 0 SO. ATXte ftDelaware______________ 000 7 10 7 0 0 Q o o ftMaryland *________________ Dlst. of Ool________________ 1 0 0 0 0 0 83 62 63 9 21 18 0 0 0 0 0 2 1 2 1 o Vtninia____________________ Waft Virginia___________ North Carolina................ 0 3 3 0 0 0 0 0 0 47 28 40 30 77 50 48 S3 S3 0 0 0 0 0 0 ft 0 0 4 2 2 1 o 3 South Carolina >__________ 0 0 0 63300 00 3 3 Georgia___________________ Florida_____________________ 0 a 2 0 0 0 21 35 19 a 11 10 0 0 2 0 0 0 Q 0 2 3 8 2 S.80.CXX. Kentncky . . Tennessee. .............. 0 0 0 0 1 S3 94 68 0 103 64 44 0 0 0 1 0 1 4 2 3 o 2 Alabama*__________________ Mississippi *_______________ 0 1 3 2 1 I 14 13 22 S38 0 1 0 ft 1 0 1 Q 3 1 2 i W. 80. CXX. Arkansas .. Louisiana1...................... Oklahoma_________________ Texas *................................ 1 00 9 3 15 2 3 2 2 2 * 000 4 13 13 2 0 0 3 2 5 1 1 I 18 31 31 l 1 2 0 1 3 1 1 1 75 75 89 5 1 5 10 3 3 MOUNTAIN Montana.______ _______ 0 0 0 25 S3 53 1 0 11 1 0 1 Idaho...... .... .... 0 l0 16 42 36 1 1 20 1 1 Wyoming.. ________ 000 8 4 12 0 0 4 0 0 0 Colorado___ __________ New Mexioo______ ____ 0 0 0 37 59 59 0 13 13 0 0 ft 1 00 4 13 25 0 0 0 3 3 3 Arizona Utah *________ 000 1 00 7 13 s 2 1 0 1 0 0 7 31 31 0 0 0 0 0 0 Nevada_____ ________ 0 0o o TACTIC Washington Oremn............................. California_______ ______ 0 0 0 0 0 0 24 59 62 18 22 45 0 0 3 0 1*2 Q 1 3 1 2 2 2 105 140 200 0 1 11 5 10 2 1 4 Total------------ ------ 21 18 3.466j 4.5831 A 146 58 63 371 60 72 87 t weeks________________ 317 203 124 19.470125. Ml <35.037 304 453 1,828 445 475 661 See footnotes at end of table. 91 501 0069 February 14, 1941 304 Telegraphic morbidity reports from State health officers for the week ended February 8, 1941, and comparison with corresponding week of 1940 and 5-year median--Con. Whooping cough Whooping cough Division and State Weekended Feb. 8. 1941 Feb. 10. 1940 Division and State Weekended Feb. 8. 1941 Feb. 1ft 1940 NBW SNO. Maine................................ ... Maiwichnytta______________ Rhode Island Connecticut_______ ......... MID. ATXca New Jersey Pennsylvania..... X. NO. CStf. Ohio ............................ ...... Indiana Illinois____ ________________ Michigan*..._____ _______ Wisconsin W, NO. CBN. Minnesota___________ __ ___ North Dakotaa.....M..M.... South Dakota______________ Nebraska_____________ __ ITmus.................................... ... .. SO. ATI. Maryland 1_________________ Dist. ot CoL._______________ West Virginia *_____________ North Carolina-------------------South Carolina1____________ 8 2 8 272 6 83 337 102 428 341 9 107 175 180 88 39 33 18 8 15 70 8 94 5 232 102 302 61 so. atl--continued 77 4 47 FlnrirU . 144 13 X. SO. CBN. 64 Kentucky_________________ Tennessee > laham* 1 . ... 394 M(ri4ippf * ____ ________ 95 341 XT. SO. CBN. Arkansas 02 Louisiana1.............................. 46 Oklahoma__________________ 80 Texas > 115 93 MOUNTAIN Montana................................. Idaho____ _________________ Wyoming 25 Colorado__________________ 10 15 18 Otah -------------------------------11 Nevada 4 55 FACme Wohfngtnn 9 165 California 15 57 Total , ,............ . . 8 78 8 weeks____________________ 8 15 38 17 18 38 80 73 41 49 7 28 8 19 31 4 343 118 71 14 5 9 59 20 13 37 5 20 74 883 0 . _ ______ 123 13 424 4.392 25.434 19 36 154 3,230 16,720 * New York City only. 1 Period ended earlier than Saturday. > Typhus lever, week ended Feb. 8,1M1, 24 eases as follows: South Carolina, 5; Georgia, 14; Alabama, 2; I Anisia?^ 2; Texas, 1. Approximately 1,000 delayed reports tor November and December included. 01 501 0070 305 February 14,1841 WEEKLY REPORTS FROM CITIES City reports for ueek ended January S5, 1941 This table summarizes the reports received weekly from a selected list of 140 cities (or the purpose of showing a mas section of the current urban incidence of the communicable diseases listed in the table. State and city Dlphcaaea Cases Deaths Menales case* Pneodeaths Scar* let fever cases Small- Tuber POZ culosis cases deaths Ty phoid fever cases Whoop ing cough cases Deaths, all causes Data for 00 cities: 6-rear average.. Current week >. 163 le347 67 fir 012 138 2 fisa 933 1,728 202 6,306 738 1,129 36 366 4 376 18 1,119.. 12 1,202.. Maine: Portland New Hampshire: Concord M Manchester___ NiShnt __.r. . Vermont: Bane........ ........ Burlington____ Rutland Massachusetts: Boston__ ...... Fall River_____ Springfield..... Worcester. Rhode Island: Pawtucket____ Providence____ Connecticut: Bridgeport____ Hartford New Haven___ New York: Bntfriw ___ _ New York_____ HlXhwTM_____ Syracuse New Jersey: Camden______ Newark_______ Trenton____ ... Pennsylvania: Philadelphia... Pittsburgh..... Reading---------Scranton... . 01 0 Q ... 0 6s 0 0 0 __ 01 0 0 0 13 0s 0 80 0 22 0 30 17 0 0 .--..2.2.2. 0 12 0 41 0e 1 SO 0 66 1 o 1 X64 ooo 1 3 0 X 13 oo07 0 400 0000 fi 88 a 102i 1 3 1 10 0 63 6 21 0000 3 1 11 0 l 1 t8 0161 30 17 6 27 13 31 10 1,248 m 230 0 fi 4 3 0033 2 24 2 4 0 122 17 20 2 2 6 66 7 773 81 0 228 1 60 100 29 6 60 o o 0 0 o 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 Q 0 Ohio: Cincinnati__ Cleveland_____ 0 43 1 437 1 28 3 447 n 17 Colnrobnr___ X6 6 10 6 Toledo TiutUim: 02 1 i7 Anderson........ 0 ___ 002 Fort Wayne___ Indianapolls___ Mtmde_______ 0 3 __ 0. 0u 3 2 6 30 X ii X South Bend___ 0 022 Terre Haute___ 0 1 mtnols: 001 Alton_____ ___ 01 10i Chicago___ ___ Elgin-------------- 10 4fi 0 _____ a 000 01 7 4 Moline Springfield. 0 .... 0 0 0 4 1 0fi Michigan: Detroit________ 4 86 8 777 17 Flint................. 0 2 18 7 Grand Raplda_ 0 X01 Wisconsin: Kenosha______ 0 .... 0 80 Madison Q .... 0 2 0 Milwaukee____ Racine______ _ ......0. ...... 0 ______ IS ______ 6 _____ Superior ____ 0 0 00 14 28 8 7 0 1 18 fi 0 0 4 270 1 0 8 82 ii l l 88 3 0 0 0 0 0 o 0 0 0 0 0 0 0 0 0 0 o 0 0 0 0 6 > Figures for Bern, Racine, and Boise estimated; reports sot reoelved. o o 1 0 0 1 0 a o 3 0 1 0 6 83 0 0 a 10 0 28 0 1 8 8 s 4 0 \ a i 0 o 0 48 0 0 0 10 0 0 0 0 0 o o 16 o o 349 04 0 1 63 lo oo o6 00 o1 1 26 04 49 0 16 IM 1 139 1,603 0 8 74 0 3 44 0 3 47 D 7 137 0 1 60 0 70 701 0 40 226 0 16 33 0 2 146 0 63 316 0 1 2931 104 91 0 0 20 o 6 16 131 0 0 13 0 0 38 00 12 00 9 3 03 803 0 0 21 0 0 16 1 2 28 0 119 806 0 16 36 00 01 0 64 9 10 96 0i 8 01 501 0071 February *4. icn 306 City reports for trerk ended January 25, 194i--Continued State ud city Diph- Induenta therm cases Cases Deaths PneJ ?"r' Mea sles moniai , ,, cases Small Tuber-! To pox rulosis: cases deaths, c[ais!e"s Whoopin? couch cases Deaths. all causes Minnesota: Duluth....... ...... Minneapolis___ St. Paul Iowa: Cedar Rapids.. Davenport.___ Dm Moines___ Stoux City____ Waterloo______ Missouri: Kansas City___ St. Joseph St. Louis North Dakota; Grand Forks... Minot South Dakota: Aberdeen Sioux Falls Nebraska: Lincoln_______ Omaha Kansas: Lawrence Topeka _____ . Wichita 03 0 13 0 0 3. 0 0 0i Q 1 31 0 0 0 0 0 1 0 0r o 13 0 0 2 0 1 0 0 3 21 1 60S 1 8 0 2 0 13 112 2 2 5 6 0 4 0 3 69 1 40 0 o 0 20 o 1 0 0 0 11 0 6 0 l 2S 0 3o o g 1 2o Q S 3 12 12 3 3 0 a 113 0 0 9 0 0 0 0 2 77 9 26 19 0 7 1 14 270 0ooq00 0 0o o 1 oo Q o o 0 2o o 0001 000 o 0 7 0 10 o 1 1 0 10 3 0 l 0 0 63 0 100000 o 20 o 1 o o 1 23201 0 0 15 3 32 Delaware: Wilmington___ Maryland: 0 0 4 6 l 0 0 0 - 42 Baltimore......... Cumberland... 2 105 01 o 5 5 16 33 0 10 0 60 270 0 20000 0 o 9 0oooo Dbt. of Col.: Washington__ _ Virginia: Lynchburg____ I 108 0 2 5 14 11 0 9 0 0 *> l 1 o 7 171 Norfolk............. Roanoke West Virginia: 0 260 o 0 ____ 1 351030 72 3 37 0 26 4 I 0 0 0 23 26 Charleston____ 0 19 151 1000 0 10 Huntington___ WWiinff........ 0 o 0 0o 2o2 o o North Carolina: Oastoma____ _ 03 0 o0 o Raleigh_______ Wilmington..-- 0 15 0 0 0 21 00 6 0o4oo 6 7 Winston-Salem. South Carolina: 3 18 0 1 0 1 0 2 0 27 27 Charleston____ Florence______ Georgia: 0 2,274 1 322 o 4 10 7 l 0 2 0 0 19 02 0 7 0 0 o 1 0 0 0 33 10 20 Atlanta 0 603 12 1 7 6 0 10 t Brunswick..... flkfflnnah 01 0 256 1 0 10000 7 03002 0 Florida: l 112 05 o 51 Miami Tampa 0 46 2 0 3 1 0 0 0 1 63 2 3 1 0 2 1 0 2 0 0 36 Kentucky: Ashland Covington.___ 06 12 0 200 1 0 1 0 033201 0 3 20 3 1 0 Louisville Tennessee: 0 S3 l 21 9 W 6 2 0 10 Knoxville...... 0 319 4 1 94020 0 Memphis___ _ 0 nr 0 11 0 8 4 6 7 4 0 S 1 0 13 12 Alabama: Birmingham .. Mobile....... ...... Montgomery... 1 673 1 22 0 87 8 3900 1 0 7 0300 2 0 2 40 0 1 0 0 11 22 66 58 98 73 96 33 01 501 0072 307 February 14* 1WI City report* for toeek ended January So, 19*1--Continued Sue and city Diph Influents theria cases Cases Deaths Mea sles cases Pneu monia deaths Scar let fever cases I Small- Tuber- pox culosis cases deaths Ty- IWhoopnbotd' in* fever couch cases cases Deaths, all causes Arkansas: Fort Smith Little Rock.__ Louisiana: Lake Charles__ New Orleans... Shreveport Oklahoma: Oklahoma City. Tulsa_____ Texas: Dallas............... Fort Worth___ Galveston_____ Houston San Antonio__ Montana: Great Fall. Helena___ ..... Missoula Idaho: Boise_________ Colorado: Colorado Denver Pueblo.............. New Mexico: Albuquerque__ Utah: Salt Lake City. Washington: Seattle......... .... Spokane Oregon: Portland Salem....... . California: Los Angeles___ Sacramento___ San Francisco.. 03 0 116 0 2 61 0 0 __ .. 2 07 0 1 57 1 106 1 32 0 0 0 08 0 97 0 1 5 0 01 2 0 no 0l 0 06 06 3 173 40 0 30 0 o0 0 1 2 11 0 0 2 0 0l 1 0000 5 0 34 8 0 11 2 3 03 oo 1 1 4 0 4 0 3 0 0 0 0 720 0 0 4 0 3 36 4 3 0 1 0 00 i 0000 41S2000 S072070 0ol2 o 1 0og7 o o 0 0 l 0 0 r0 1 100000 4 2 58 07 5 187 43 * 54 37 0 85 0 43 1 10 0 105 5 70 0 12 o 0222 o 1o 3 6 9 8 0 3 Q ll 109 00 1 i 0 1 0 2 u 0 * 4 1 0 0 3 0 0 15 0 7 4 2 0 0 0 9 35 1 3430 50 8 104 2 0 00 13 2 1 0 o 1 0 2 10 45 45 1 IS 2 4 0 3 0 0 90 1 00 0 2 2 4 5 27 0 17 0 48 442 3 0 3 7 0 3 0 1 42 1 0 6 1 0 6 0 41 197 State and city Meningitis. meningococcus Cases Deaths cases State and city Meningitis, meningococcus Cases Deaths cases New York: Bnflala _ New York_____ New Jersey: Newark_______ Pennsylvania: Philadelphia. Ohio: Cincinnati TnrtUna1 Indianapolis.............. Illinois: Wisconsin: Milwaukee____ ....... i 2 1 2 0 1 1 o 1 0 1 0 1 0 o 1 o 0 Sooth Carolina: 0 1 Florida: Miami. . . . 0 Alabama: Birmingham__ 0 Louisiana: Shreveport___ .. l Texas: 0 Dallas. Oalveston____ 0 Oregon: Portland_____ 3 Los Angeles___ 0 . 1 0 1 0 0 1 1 1 Dengue fever.--Cases: Charleston* 3. C., 3. Encephalitis, epidemic or lethargic.--Cases: New York. 6. Pellagra.--Cases: Charleston, S. C., 2; Atlanta. 1; Savannah, 1. Rabies in man.--Deaths: dan Francisco, l. Typhus fever.--Cases: New York, 3; Charleston, S. C., 1; Atlanta, l; Miami, 1; Tampa, 1. 2S57590--41-------4 o 0 1 1 o 0 0 0 2 0 0 1 0 0 l 01 501 0073 FOREIGN REPORTS CANADA Provinces--Communicable diseases--Week ended January 4, 1941.-- During the week ended January 4, 1941, cases of certain communi cable diseases were reported by the Department of Pensions and National Health of Canada as follows: Diseasa Prince Edward Island Nova Scotia New Bruns wick Que bec On tario Mani toba Sas katch ewan Al berta British Colum Total bia Cerebrospinal mcningi* tis................ ................ Chickenpox. . .. . . Diphtheria____________ Dysentery____________ w* .u! 1 Pn*m*wm{& . _ __ 8carletfever___ .___ ... Typhoid and parity_jpnoid fever........... 2 12 2 M 264 1 147 0 4 30 u 3 4 18 2 78 311 3 16 2 10 438 n 21 400 7 as 40 l i S3 137 6 17 40 8 10 40 134 34 7 0 71 10 2 8 2 6 10 SO 1 32 128 1 13 10 1 1 2. 5 46 87 683 80 2 820 1,640 1 105 1,005 8 140 17 00 I o 201 7B 10 10 220 CUBA Provinces--Notifiable diseases--4 weeks ended December 7, 1940.-- During the 4 weeks ended December 7,1940, cases of certain notifiable diseases were reported in the Provinces of Cuba as follows: Disease Plnar del Rio Habana Matanaa Santa Clara Camaguey Orients Total 1 0 3 16 PhiekMfMT ... . ______ __ __ 2 l3 20 1 2 7 36 11 Malaria 87 M 2 l 7 2 72 id 22 22 22 TparihAina . .................................... Tuberculosis 3 28 33 12 27 10 28 h! Typhoid never_________________ ii 70 7 22 13 17 IN JAMAICA Communicable diseases--4 weeks ended January 18, 1941.--During the 4 weeks ended January IS, 1941, cases of certain communicable diseases were reported in Kingston, Jamaica, and in the island outside of Kingston, as follows: (308) 501 0074 309 February H. 1M1 Disease Kingston Other localities Chickenpox________________ Diphtheria_______ ______ Dysentery ____ ... Leprosy___ __________ 1 2 8 X xx 8 Disease Kingston Other localities 1 e M S 36 VENEZUELA Caracas--Poliomyelitis.--An increase in the number of poliomyelitis cases has been reported in Caracas, Venezuela (population 204,000), with 9 cases in November 1940 and 36 cases from December 1, 1940, to January 11,1941, as compared with 6 cases from January to October (inclusive) 1940. The disease, was stated to be mild, with only 4 deaths reported. YUGOSLAVIA Notifiable diseases--4 weeks ended December 1, 1940.--During the 4 weeks ended December 1, 1940, certain notifiable diseases were reported in Yugoslavia as follows: Disease Cases Deaths Disease Cases Deaths Anthrax........................................ Cerebrospinal meningitis_______ Diphtheria and crnop................... Dysentery Lethargic enoepbailtls 13 1 59 14 no 34 31M82 91 a 4 x 1-- Paratyphoid feser______________ pQUomValxtia................................ Sepais-------------------------------------- 26 8 393 T 23 438 23 1 3 g 331 REPORTS OF CHOLERA. PLAGUE. SMALLPOX. TYPHUS FEVER, AND YELLOW FEVER RECEIVED DURING THE CURRENT WEEK Non.--A cumulative table giving current Information regarding tbe world prevalence of qnarantinabie diseases appeared In tbe Public Burra Rxroars of January 31, 1M1, pages 308-210. A. similar table win appear in future Issues of tbe Puauc Bmn Rtroare for tbe last Frida; of each month. Smallpox Japan.--According to a report dated January 23,1941, an outbreak of smallpox has been reported in Japan. In Aomori Prefecture new cases increased to 36 between January 1 and 21, 1941. For the same period Akita Prefecture reported 5 cases and Tokyo Prefecture 5 cases. Three deaths had occurred. X 01 501 0075