Tularemia In Man Research Articles

Anti-Francisella tularensis DNA aptamers detect tularemia antigen from different subspecies by Aptamer-Linked Immobilized Sorbent Assay

Aptamers are powerful candidates for molecular detection of targets due to their unique recognition properties. These affinity probes can be used to recognize and bind to their targets in the various types of assays that are currently used to detect and capture molecules of interest. They are short single-stranded (ss) oligonucleotides composed of DNA or RNA sequences that are selected in vitro based on their affinity and specificity for the target. Using combinatorial oligonucleotide libraries, we have selected ssDNA aptamers that bind to Francisella tularensis subspecies (subsp) japonica bacterial antigen. F. tularensis is an intracellular, nonmotile, nonsporulating, Gram-negative bacterial pathogen that causes tularemia in man and animals. Just as antibodies have been used to detect specific targets in varying formats, it is possible that nucleic acid-binding species or aptamers could be used to specifically detect biomolecules. Aptamers offer advantages over antibody-based affinity molecules in production, regeneration and stability due to their unique chemical properties. We have successfully isolated a set of 25 unique DNA sequences that specifically bind to F. tularensis subspecies japonica. When tested in a sandwich Aptamer-Linked Immobilized Sorbent Assay (ALISA) and dot blot analysis, the aptamer cocktail exhibited specificity in its ability to bind only to tularemia bacterial antigen from subspecies japonica, holarctica (also known as palaearctica) and tularensis but not to Bartonella henselae. Moreover, there is no binding observed either to pure chicken albumin or chicken lysozyme. Thus, it appears that this novel antitularemia aptamer cocktail may find application as a detection reagent for a potential biological warfare agent like F. tularensis.

Rapid local expression of interleukin-12, tumor necrosis factor alpha, and gamma interferon after cutaneous Francisella tularensis infection in tularemia-immune mice.

Francisella tularensis LVS is an effective live vaccine strain used for cutaneous vaccination against tularemia in man. In mice, injection of LVS causes invasive disease and subsequent development of immunity that is characterized by effective control of otherwise lethal doses of the organism. In the present investigation, it is shown that LVS-immune mice controlled an intradermal infection much more effectively than did naive mice; bacterial counts in skin samples were 1.5 to 2.0 log10 lower 24 h after injection and 6 log10 lower 72 h after injection in immune mice. Moreover, in contrast to naive mice, no bacteria were demonstrated in samples from livers and spleens of immune mice. By immunohistochemistry, skin samples from immune mice showed an intense staining for interleukin-12 (IL-12) and a moderate staining for tumor necrosis factor alpha (TNF-alpha) at 24 h postinoculation, after which staining for both cytokines faded. In naive mice, the staining for IL-12 was weak at all time points and no staining for TNF-alpha was observed. No staining for gamma interferon (IFN-gamma) was observed in any group before 72 h. At that time point, skin samples from immune mice showed moderate staining and skin samples from naive mice showed weak staining. Reverse transcriptase PCR showed an induction of mRNA of the three cytokines in the skin within the first day after injection. A quantitative analysis demonstrated higher IFN-gamma and TNF-alpha mRNA levels in immune mice at 24 h postinoculation. In conclusion, immunization with F. tularensis LVS conferred a capability to respond to cutaneous reinfection, with rapid local expression of IL-12, TNF-alpha, and IFN-gamma, and this expression was paralleled by containment and mitigation of the infection. The cytokine response may be part of a local barrier function of the skin, important to host protection against tularemia.

Synchronous population fluctuations in voles, small game, owls, and tularemia in northern Sweden

1. The population fluctuations in time in northern Sweden are examined for the following species: voles, mountain hare, willow grouse, black grouse, capercaillie, hazel hen, red fox, long-eared owl, Tengmalm's owl, and tularemia. Necessary population data have been obtained from the period 1963-1975/76 as revealed by catches, literature survey, hunting statistics, bird ringing, and obligatory reporting of tularemia in man. 2. The populations of the species under consideration are found to fluctuate synchronously in time and show a 3- or 4-year cycle for the period 1963-1975. Population peaks have occurred in connection with the peak densities of voles in the winters 1963-1964, 1966-1967, 1969-1970 and 1973-1974. 3. Voles caused extensive forest damage (mainly bark-eating) in at least the latter three peak winters. From consideration of the available literature it is apparent that bark is a marginal food. Thus, increased bark-eating during peak densities of voles in winter should be interpreted as a shortage of preferred food. 4. The species studied appear to form a unit (subsystem) within the boreal forest ecosystem. This idea is supported by the connecting predatorprey relationships and the demonstrated synchronous population fluctuations. The subsystem contains herbivores, their food vegetation, and predators. Tularemia is regarded as only one among other predators on voles and mountain hares. 5. It is postulated that voles play a central role in causing the overall synchronism in the population fluctuations of the subsystem. 6. The synchronous population fluctuations described can be explained by the following model for their regulation: a) An initial decline in vole numbers is brought about by food shortage at winter peak densities. b) Predator populations (built up with the help of the rich supply of voles) cooperate with food shortage and at some critical point predators alone are able to fulfil the decrease in vole numbers. c) Because of the decrease in vole numbers the predators are forced into a decline themselves and must turn to alternative prey species. Mountain hare and gamebird populations represent a low biomass compared with vole populations and predation thus causes the decline in numbers of these small game. d) Low numbers of predators and excessive food supply then allow voles, mountain hares, and gamebirds to increase again. e) The building up of vole populations sets the stage for another increase in the number of predators and a new cycle is started.

The role of endotoxin during typhoid fever and tularemia in man. IV. The integrity of the endotoxin tolerance mechanisms during infection.

Volunteers infected with Salmonella typhosa develop a remarkable hyperreactivity to the pyrogenic and subjective toxic activities of homologous (S. typhos) and heterologous (Pseudomonas) endotoxins. The present studies quantitate this augmented reactivity and demonstrate by three differing approaches that significant tolerance to these endotoxins can be readily induced within the framework of the hyperreactive state. Thus, (a) tolerance induced before illness by repeated daily intravenous injections of the endotoxins remained demonstrable during overt illness, (b) daily intravenous injections of the endotoxins begun during overt illness evoked progressively increasing tolerance, and (c) continuous intravenous infusions of S. typhosa endotoxin during illness rapidly induced a pyrogenic refractory state. Despite unequivocal activation of the endotoxin tolerance mechanisms by any of the above methods, the febrile and toxic course of typhoid fever proceeded unabated. Similarly, in other volunteers with Pasteurella tularensis infection, continuous intravenous infusions of S. typhosa endotoxin evoked initial hyperreactive febrile and subjective toxic responses followed by rapid appearance of a pyrogenic refractory state without modification of the underlying clinical illness. These observations suggest that circulating endotoxin plays no major role in pathogenesis of the sustained fever and toxemia during typhoid fever and tularemia in man. The mechanisms responsible for the systemic hyperreactivity to endotoxin during typhoid fever and tularemia were further investigated. Low grade endotoxemia, nonspecific effects of tissue injury, impaired ability of the reticuloendothelial system to clear circulating endotoxin, and production of cytophilic antibodies capable of sensitizing leukocytes to endotoxin did not appear responsible. Inflammatory reactions to intradermal S. typhosa endotoxin increased significantly during typhoid fever. However, since no such dermal hyperreactivity developed to Pseudomonas endotoxin during typhoid fever nor to S. typhosa endotoxin during tularemia, the systemic hyperreactivity to bacterial endotoxins during typhoid fever and tularemia could not presently be ascribed to enhanced levels of acquired hypersensitivity.

Notes on Pasteurella tularensis isolated from a vole, microtus oeconomus pallas, in Alaska.

In October, 1963, during a time of abundance of microtine rodents, Pasteurella tularensis was isolated from a northern vole, Microtus oeconomus Pallas, at the Ugashik Lakes on the upper Alaska Peninsula. The morphological, cultural, and serological characteristics of this isolate are described, and comparative virulence in experimentally inoculated animals, including series of indigenous rodents, is discussed. The isolate was less virulent for rabbits and guinea pigs than was that which has been isolated previously from ticks, Haemaphysalis leporispalustris (Packard), in Alaska, and was also less virulent for these animals than was strain SCHU S4. The isolate from the vole seemed to resemble most closely the Eurasian strain of P. tularensis, as might be expected on zoogeographical grounds. A distinguishing feature of the isolate was its ability to grow readily on blood agar in the absence of cystine. The relatively high rate of subclinical tularemia in man in northern and western Alaska, as indicated by the results of serological tests, may be attributable to this organism. Water-borne bacteria may be the source of infection in man.

Insulin response during tularemia in man.

Serum insulin concentrations were measured serially in seven nondiabetic subjects following a rapid intravenous glucose load during a preinfection control period, during early clinical respiratory tularemia, and again in convalescence following therapy. Within twenty-four hours of onset of clinical illness the rate of glucose disappearance from the blood had diminished significantly (p<0.05). At the same time there was a brisk rise in insulin levels reaching higher peak concentrations and falling more slowly than the response observed during the preinfection control period. The pattern during clinical illness was different from that described after intravenous glucose loading in maturity onset diabetes or obesity and may have been influenced by glucocorticoid excess. Increased whole blood pyruvate concentrations following glucose loading during clinical illness were compatible with heightened glucocorticoid ction. The magnitude of insulin clinical illness was significantly increased (p<0.02) and was directly related to height of fever In contrast, the rate of glucose disappearance was inversely related to fever. The inverse relationship of the magnitude of insulin output to the rate of glucose reappearance suggested a peripheral inhibition of insulin action during infection. Although fever may have played a role during acute illness, the persistence of an abnormal insulin response in one patient during convalescence suggested that this change was not dependent upon fever alone. Other factors that may have contributed to the peripheral inhibition of insulin action during clinical illness are briefly discussed.

THE ROLE OF ENDOTOXIN DURING TYPHOID FEVER AND TULAREMIA IN MAN. 3. HYPERREACTIVITY TO ENDOTOXIN DURING INFECTION.

THE ROLE OF ENDOTOXIN DURING TYPHOID FEVER AND TULAREMIA IN MAN. 3. HYPERREACTIVITY TO ENDOTOXIN DURING INFECTION.

THE ROLE OF ENDOTOXIN DURING TYPHOID FEVER AND TULAREMIA IN MAN. II. ALTERED CARDIOVASCULAR RESPONSES TO CATECHOLAMINES.

THE ROLE OF ENDOTOXIN DURING TYPHOID FEVER AND TULAREMIA IN MAN. II. ALTERED CARDIOVASCULAR RESPONSES TO CATECHOLAMINES.

Infectious Diseases in a Black-Tailed Jack Rabbit (Lepus californicus melanotis, Mearns) Population in Southwestern Kansas

Brown et al. (1) reported that 105 of 120 cases of tularemia in Kansas from 1928 to 1933 were from skinning or handling wild ribbits, but of the 105 cases reported, only seven were from contact with jack rabbits. Francis (2) also lists the jack rabbit as a possible source of tularemia in man. There are several reports of the isolation of P. tularensis from the tissues of infected jack rabbits (3-8) and from ticks taken from jack rabbits (4-9). On the other hand, several investigators failed to isolate the organism from jack rabbits (9, 10) or to demonstrate any agglutinins against P. tularensis in the serum of the jack rabbits tested (8-11). Bacon and Drake (7), testing 558 jack rabbit sera, found only two positive for P. tularensis agglutinins.

Tularemia in Man from a Domestic Rural Water Supply

An explosive water-borne epidemic of tularemia in the Union of Soviet Socialist Republics in 1935 was reported by Karpoff and Antonoff (1). Over 43 cases were observed in a group of farm laborers who used water from one stream which was found to be contaminated with Pasteurella tularensis. The portal of entry of infection appeared to be the tonsils and buccal mucosa and in some cases the conjunctiva. The anginal form of the infection predominated, but typhoidal and oculoglandular forms were present. Cultures were isolated from some experimental animals injected with tissues from a patient and from others injected with water from the suspected stream. Twenty-one patients were tested after the thirty-fifth day of illness for agglutinins against P. tularensis, and all were positive. Contamination of natural waters in Montana with P. tularensis was reported by Parker, Jellison, Kohls, and Davis (2); Jellison, Kohls, Butler, and Weaver (3); and by Parker, Steinhaus, and Kohls (4). Since 1942 contamination of numerous streams at one time or another, often persisting for months, has been repeatedly demonstrated at the Rocky Mountain Laboratory. In most instances, the presence of the organism in water has been associated with the occurrence of tularemia in beavers and muskrats inhabiting the streams or ponds concerned. Many cases of tularemia have been contracted by persons who skinned or handled such diseased animals, but to the present there has been little evidence of human infection resulting from direct contact with contaminated water. The occurrence in Gallatin County, Mont., of four cases of tularemia associated with one domestic water supply under circumstances which appear to preclude other likely sources of infection is the subject of the present report. In the summer of 1949, two cases of tularemia, in which the portal of entry appeared to be the throat, were treated by one of the authors (Epler). Neither patient exhibited an external initial lesion of any kind, and neither gave a history of close contact with wild rodents,

The Effect of Aureomycin Upon Infections with Bacterium Tularense in Experimental Animals

Abstract Tularemia is an acute disease producing a mortality rate of about 5 per cent in human beings when not treated specifically. The prolonged convalescent period observed in untreated patients is most distressing. The use of streptomycin in the therapy of tularemia in man is based upon experimental results obtained from studies with mice by Heilman (1), and its efficacy has been adequately demonstrated (2). Recently a new antibiotic, aureomycin (duomycin), has been developed at the Lederle Laboratories (3), and its value as an agent in the therapy of various infectious diseases has been described (4, 5, 6). The results obtained in treatment with aureomycin of white mice, white rats and guinea pigs infected with Bacterium tularense will be presented in this paper. The data indicate that aureomycin is effective in the treatment of tularemia in these animals. Materials and Methods.

Ulceroglandular tularemia treated with streptomycin; a report of two cases.

HEILMAN'S1 demonstration of the effectiveness of streptomycin against Pasteurella tularensis in vitro and in vivo has found application in the treatment of tularemia in man. The cases presented below are considered to be of interest because they report additional experience with the use of streptomycin in the treatment of tularemia. Furthermore, they afford an interesting comparison of the effectiveness of treatment of the acute and chronic phases of the disease.Case ReportsCase 1. A 39-year-old man was hospitalized on February 14, 1947, complaining of "cold sensations," pain in the eyes and back and coughing and sneezing of 2 days' . . .

RUPTURE OF THE SPLEEN DUE TO TULAREMIA: REPORT OF A CASE

Case Reports1 November 1946RUPTURE OF THE SPLEEN DUE TO TULAREMIA: REPORT OF A CASEE. BUIST WELLS, M.D., CLIFFORD TILLMAN, M.D.E. BUIST WELLS, M.D.Search for more papers by this author, CLIFFORD TILLMAN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-25-5-852 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptINTRODUCTIONRupture of the spleen as one of the manifestations or complications of tularemia apparently has rarely if ever before been encountered. A thorough search of the literature reveals no recorded instance of this nature. A patient was recently observed at Vanderbilt University Hospital in whom this condition was found at autopsy following a clinical course in which the exact diagnosis remained obscure. Because of its unusual nature a report of this case seems justified.CASE REPORTHistory. A 41 year old white male farmer was admitted to the medical service of Vanderbilt University Hospital on December 18, 1944 with...Bibliography1. RANSMEIEREWING JCCL: The agglutination reaction in tularemia, Jr. Infect. Dis., 1941, lxix, 193-205. CrossrefGoogle Scholar2. KENNEDY JA: Pulmonary tularemia, Jr. Am. Med. Assoc., 1942, cxviii, 781-787. CrossrefGoogle Scholar3. FOSHAY L: Tularemia: A summary of certain aspects of the disease including methods for early diagnosis and the results of serum treatment in 600 patients, Medicine, 1940, xix, 1-83. CrossrefGoogle Scholar4. GOODPASTUREHOUSE EWSJ: The pathologic anatomy of tularemia in man, Am. Jr. Path., 1928, iv, 213-226. Google Scholar5. FRANCIS E: The pathology of tularemia, Natl. Inst. Health, Bull. No. 167, 1937, Washington. Google Scholar6. Intrathoracic changes in tularemia, Med. Bull. Vet. Admin., 1934, xi, 77-83. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Nashville, Tennessee*Received for publication July 31, 1945.From the Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byA Rare Case of Spontaneous Splenic Rupture Secondary to Tularemia Following a Cat BiteAcute lymphocytic leukaemia presenting as spontaneous splenic ruptureAcute Leukemia with Rupture of the Spleen as the Initial Symptom 1 November 1946Volume 25, Issue 5Page: 852-859KeywordsAutopsyMedical servicesSpleenTularemia ePublished: 1 December 2008 Issue Published: 1 November 1946 PDF downloadLoading ...

Vaccine Prophylaxis against Tularemia in Man

IT is characteristic of tularemia that most patients develop a high degree of natural resistance after infection occurs. The mortality is low. Recovery confers lifelong immunity which protects against subsequent massive exposures with an effectiveness seldom encountered in bacterial diseases. Second attacks of disease are unknown. Local reinfections occur occasionally among immunes subjected to repeated exposures to virulent strains but, as Francis first indicated, they are either asymptomatic or associated with brief and mild constitutional symptoms.' One of us has recorded apparent immunity, due to vaccination, which successfully withstood accidental massive exposures to strains of high virulence.2 Although tularemia is of minor importance as a cause of death it has considerable social and economic importance in areas of high endemicity as a cause of prolonged morbidity and disability. Its capacity to disrupt normal activities of military encampments is recognized.3 The extreme ease with which infection is acquired, and the high infection rates among butchers and market men, scientific investigators, rabbit hunters and their wives and cooks who prepare game for the table, indicate the desirability of better methods of protection than those now in use. Preliminary experiments with heat killed and formalinized Bacterium tularense * suspensions demonstrated clearly that vaccines made by these methods, from either virulent or avirulent strains, provoked severe and extensive constitutional and local reactions upon initial injection into normal individuals. Reasonably well tolerated doses were so small that several months of daily injections were required to produce agglutinin titers to 1:320, a scheme tolerable for a few laboratory workers but impracticable for large scale use. The successful efforts of Ramon and his associates to diminish primary toxicity of toxins and of various bacteria without significant impairment of their antigenicity., by various chemicals, led us to try similar methods. We established the following specifications for an acceptable vaccine:

TULAREMIC MENINGITIS

Case Reports1 March 1937TULAREMIC MENINGITISReport of Case with Postmortem Observations*EDGAR R. PUND, M.D., F.A.C.P., MILFORD B. HATCHER, M.D.EDGAR R. PUND, M.D., F.A.C.P.Search for more papers by this author, MILFORD B. HATCHER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-10-9-1390 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe histopathology of tularemia is adequately described in the literature notwithstanding the few reports of postmortem examinations. But because there are few reported necropsies the pathology of the disease is of particular interest in regard to the distribution of the lesions. Last year Bernstein was able to collect only 18 necropsies and to these he added three of his own. We have reviewed these cases and three additional reports by Beck and Merkel, Amoss and Sprunt, and Kavanaugh to determine the distribution of the lesions. This study was prompted by the occurrence of a fatal case of tularemia which was...Bibliography AMOSSSPRUNT HLDH: Tularemia: review of literature of cases contracted by ingestion of rabbit and the report of additional case with a necropsy, Jr. Am. Med. Assoc., 1936, cvi, 1078. CrossrefGoogle Scholar BARDONBERDEZ RG: Tularemia; report of a fatal case with postmortem observations, Jr. Am. Med. Assoc., 1928, xc, 1369. CrossrefGoogle Scholar BECKMERKEL HGWC: Tularemia; fatal case of the typhoid form caused by ingestion of rabbit: autopsy report, South. Med. Jr., 1935, xxviii, 422. CrossrefGoogle Scholar BERNSTEIN A: Tularemia: report of three fatal cases with autopsies, Arch. Int. Med., 1935, lvi, 1117. CrossrefGoogle Scholar BLACKFORD SD: Pulmonary lesions in human tularemia; pathologic review and report of a fatal case, ANN. INT. MED., 1932, v, 1421. LinkGoogle Scholar BOWEWAKEMAN DPDC: Tularemia and pregnancy: report of a case, Jr. Am. Med. Assoc., 1936, cvii, 577. CrossrefGoogle Scholar BRYANTHIRSCH AREF: Tularemic leptomeningitis; report of a case, Arch. Path., 1931, xii, 917. Google Scholar BUNKERSMITH CWEE: Tularemia; report of four cases, one fatal, with autopsy report, U. S. Nav. Med. Bull., 1928, xxvi, 901. Google Scholar FOULGERGLAZERFOSHAY MAML: Tularemia; report of a case with postmortem observations and a note on the staining of Bacterium tularense in tissue sections, Jr. Am. Med. Assoc., 1932, xcviii, 951. CrossrefGoogle Scholar FRANCISCALLENDER EGR: Tularemia; microscopic changes of the lesions in man, Arch. Path., 1927, iii, 577. Google Scholar GOODPASTUREHOUSE EWSJ: The pathologic anatomy of tularemia in man, Am. Jr. Path., 1928, iv, 213. Google Scholar GUDGER JR: Tularemic pneumonia; report of a case, Jr. Am. Med. Assoc., 1933, ci, 1148. CrossrefGoogle Scholar GUNDRYWARNER LPCG: Fatal tularemia: review of autopsied cases with report of a fatal case, ANN. INT. MED., 1934, vii, 837. LinkGoogle Scholar HAIZLIPO'NEIL JOAE: A case of meningitis due to Bacterium tularense , Jr. Am. Med. Assoc., 1931, xcvii, 704. CrossrefGoogle Scholar HARTMAN FW: Tularemic encephalitis, Am. Jr. Path., 1932, viii, 57. Google Scholar HARTMANBEAVERGREEN HRDCRG: The occurrence of tularemia in Minnesota in 1921: report of two cases—one fatal with necropsy report, Minnesota Med., 1933, xvi, 559. Google Scholar KAVANAUGH CN: Tularemia; a consideration of 123 cases, with observations at autopsy in one, Arch. Int. Med., 1935, lv, 61. CrossrefGoogle Scholar MASSEE JC: Tularemia in Georgia; report of a fatal case, Jr. Med. Assoc. Georgia, 1931, xx, 66. Google Scholar PALMERHANSMANN HDGH: Tularemia: report of a fulminating case with necropsy, Jr. Am. Med. Assoc., 1928, xci, 236. CrossrefGoogle Scholar PERMARMACLACHLAN HHWW: Tularemic pneumonia, ANN. INT. MED., 1931, v, 687. Google Scholar RICHMCCORDOCK ARHA: The pathogenesis of tuberculous meningitis, Bull. Johns Hopkins Hosp., 1933, lii, 5. Google Scholar SIMPSON WM: Tularemia; study of rapidly fatal case (four days, seven hours), Arch. Path., 1928, vi, 553. Google Scholar VERBRYCKE JR: Tularemia, with report of a fatal case simulating cholangitis with postmortem report, Jr. Am. Med. Assoc., 1924, lxxxii, 1577. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Augusta, Georgia*Received for publication November 19, 1936.From the Department of Pathology, University of Georgia School of Medicine, Augusta, Georgia. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byTULAREMIC MENINGITISDie psychischen Störungen bei InfektionskrankheitenDie psychischen Störungen bei Infektions- und TropenkrankheitenVeränderungen des Zentralnervensystems bei weiteren infektiösen ErkrankungenTularemic Meningism and Serous MeningitisTularämieTularemia in infancy 1 March 1937Volume 10, Issue 9Page: 1390-1398KeywordsAutopsyHistopathologyLesionsMeningitisTularemia Issue Published: 1 March 1937 PDF downloadLoading ...

Pulmonary Lesions in Human Tularemia*†

Article1 May 1932Pulmonary Lesions in Human TularemiaPathologic Review and Report of a Fatal CaseSTAIGE D. BLACKFORD, M.D.STAIGE D. BLACKFORD, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-5-11-1421 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptAlthough it is well known that tularemia is a blood-borne infection, little notice has been taken of the frequency with which it attacks the lung. Francis1reported abstracts of the twenty-four fatal human cases of which he had record up to October, 1928, and in more than one-third of these a diagnosis of intercurrent bronchopneumonia had been made. Simpson2subsequently expressed the opinion that the physical signs in many of these so-called bronchopneumonias were probably due to multiple tularemic necroses. The author3has recently published the thirteen cases which have come under his personal observation and six of these gave...References1 FRANCIS E: Symptoms, diagnosis and pathology of tularemia, Jr. Am. Med. Assoc., 1928, xci, 1155-1161. CrossrefGoogle Scholar2 SIMPSON WM: Tularemia; study of a rapidly fatal case (four days, seven hours), Arch. Path., 1928, vi, 553-574. Google Scholar3 BLACKFORD SD: Tularemia in differential diagnosis, Va. Med. Monthly, 1931, lviii, 10-13. Google Scholar4 PALMERHANSMANN HDGH: Tularemia; report of a fulminating case with necropsy, Jr. Am. Med. Assoc., 1928, xci, 236-239. CrossrefGoogle Scholar5 BARDONBERDEZ RG: Tularemia: report of a fatal case with postmortem observations, Jr. Am. Med. Assoc., 1928, xc, 1369-1371. CrossrefGoogle Scholar6 BUNKERSMITH CWEE: Tularemia; report of four cases, one fatal, with autopsy report, U. S. Nav. Med. Bull., 1928, xxvi, No. 4, 901-911. Google Scholar7 GOODPASTUREHOUSE EWSJ: The pathologic anatomy of tularemia in man, Am. Jr. Path., 1928, iv, 213-226. Google Scholar8 VERBRYCKE J.: Tularemia, with report of a fatal case simulating cholangeitis, with postmortem report, Jr. Am. Med. Assoc., 1924, lxxxii, 1577-1581. CrossrefGoogle Scholar9 FRANCISCALLENDER EGR: Tularemia; the microscopic changes of the lesions in man, Arch. Path. and Lab. Med., 1927, iii, 577-607. Google Scholar10 MASSEE JC: Tularemia in Georgia; report of a fatal case, Jr. Med. Assoc. Ga., 1931, xx, 66-67. Google Scholar11 SIMPSON WM: Tularemia; history, pathology, diagnosis and treatment, 1929, Paul B. Hoeber, New York, p. 106. Google Scholar12 STITT ER: The diagnostics and treatment of tropical diseases, 1929, Blakiston's Son & Co., Philadelphia, Pa., p. 279. Google Scholar13 FOULGERGLAZERFOSHAY MAML: Tularemia, Jr. Am. Med. Assoc., 1932, cxviii, 951-954. CrossrefGoogle Scholar14 PERMARMACLACHLAN HHWW: Tularemic pneumonia, Ann. Int. Med., 1931, v. 687-698. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: University, Virginia*From the Department of Internal Medicine, University of Virginia Hospital.†Received from publication, August 3, 1931. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byTularaemic pneumonia: Pathogenesis of the aerosol-induced disease in monkeysPLEUROPULMONARY COMPLICATIONS OF TULAREMIA: TWO REPORTS OF TULAREMIC LUNG ABSCESSESTularämieTULAREMIC MENINGITIS Report of Case with Postmortem Observations*EDGAR R. PUND, M.D., F.A.C.P., MILFORD B. HATCHER, M.D.FATAL TULAREMIA REVIEW OF AUTOPSIED CASES WITH REPORT OF A FATAL CASE*LEWIS P. GUNDRY, M.D., C. GARDNER WARNER, M.D.Atmungsorgane 1 May 1932Volume 5, Issue 11Page: 1421-1426KeywordsHospital medicineLesionsLungsNecrosisPneumoniaTularemia Issue Published: 1 May 1932 PDF downloadLoading ...

OCULAR LESIONS IN TULAREMIA

In 1911, McCoy and Chapin, 1 while investigating a fatal epidemic of what was supposed to be bubonic plague in the California ground squirrels, isolated a small, gram-negative, nonmotile and nonsporebearing pleomorphic organism, which they named Bacterium tularense , since it was found in Tulare County, California. During their investigations two of the laboratory workers contracted what was later found to be the human form of this infectious disease. These are the first proved cases of tularemia in man to be recorded. Tularemia is only secondarily a human disease, being primarily a fatal bacteremia of wild rodents. In nature it has thus far been found in the ground squirrel, wild rabbits and hares, wild rats and wild mice. It is transmitted to man by the bite of an intermediate host, by the bite of contaminated animals or by self-inoculation. The intermediate hosts include horse-flies, wood-ticks, bedbugs and fleas. In most

Tularemia*

Tularemia*

Tularemia (Francis' Disease)*†

Excerpt The history of tularemia makes fascinating study. It is, in every respect, "the first American disease." The physicians of this country should be thrilled by the thought that not only was t...