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Nephropathia epidemica (NE) in Scandinavia is a zoonosis caused by Puumala virus. The main animal reservoir is the bank vole. NE predominantly affects men. Its annual incidence varies in a cyclic fashion, with peaks occurring every third to fourth year. The clinical picture of NE in Scandinavia is similar to that of hemorrhagic fever with renal syndrome in other parts of the world, although NE generally has a milder course. The case-fatality rate is approximately 0.2%. The most common clinical findings in NE are an acute onset of symptoms, fever (greater than or equal to 38 degrees C), oliguria, headache, back pain, and polyuria. Hemorrhagic manifestations are seen in about one-third of cases, and up to 5% of patients have gastrointestinal bleeding or disseminated intravascular coagulation. Thrombocytopenia occurs in a majority of patients. In the acute phase, the glomerular filtration rate is markedly decreased and tubular dysfunction is evident. Most patients with NE recover within 6 months.
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PMID:Nephropathia epidemica (hemorrhagic fever with renal syndrome) in Scandinavia. 168 81

Leptospirosis is a zoonosis with protean clinical manifestations. Its diagnosis requires a high index of suspicion and is confirmed by isolation of the organism or, more commonly, by serologic tests. In the fall of 1987, after severe flooding, we saw 93 patients with leptospirosis, confirmed by a microagglutination test. Thirteen percent of the patients had no clinical or laboratory findings except fever and headache, but the rest had mild to severe manifestations. Jaundice, renal failure, and aseptic meningitis were not common, but pulmonary symptoms, when present, were striking. The mortality rate was 5%. The main cause of death was asphyxiation due to massive hemoptysis from pulmonary hemorrhage and acute respiratory failure.
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PMID:Leptospirosis in Chonbuk Province of Korea in 1987. 227 9

Leptospirosis is a zoonosis with protean clinical manifestation. Diagnosis requires a high index of suspicion and is confirmed by isolation of the organism or, more commonly, by serologic studies. In the fall of 1987, after severe flooding, we saw 93 patients with leptospirosis, confirmed by a microagglutination test. Thirteen percent of the patients had no clinical or laboratory findings except fever and headache, but the rest had mild to severe manifestations. Jaundice, renal failure, and aseptic meningitis were not common, but pulmonary symptoms, when present, were striking. The mortality rate was 5%. The main cause of death was asphyxiation due to massive hemoptysis from pulmonary hemorrhage and acute respiratory failure.
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PMID:Leptospirosis in Chonbuk Province of Korea in 1987: a study of 93 patients. 280 20

Leptospirosis was first recognized as an occupational disease of sugar plantation workers in Hawaii in 1907. Since then, shifts have been noted in the animal transmission cycles, the occupational groups at risk, and an increasing recognition of cases associated with avocational exposure. Surveys of the small mammal populations indicate rats, mice, and mongooses are the most important vectors in Hawaii. Serologic surveys of workers in high-risk occupations show antibody prevalence rates ranging from 12 to 82 percent. The epidemiology of leptospirosis in Hawaii is described, based on 182 cases reported to the Hawaii Department of Health from 1970-1984. The most common infecting serovar was mankarso in the Icterohaemorrhagiae serogroup; other serovars in the Icterohaemorrhagiae group were also frequently implicated as causing disease. The manifestations of disease noted by physicians in Hawaii are similar to those observed in the continental U.S. Fever, myalgia, and headache were the most common symptoms reported in the majority of cases in Hawaii; jaundice was noted in the records of 24 percent. Recommendations made to interrupt the cycle of transmission and reduce the chances of exposure in occupational settings include the control of rodent populations and vaccination of domestic animals. Personal hygiene among workers is to be encouraged, and the development of prophylactic measures is suggested either by immunization or by chemoprophylaxis.
Int J Zoonoses 1986 Jun
PMID:Leptospirosis in Hawaii: shifting trends in exposure, 1907-1984. 353 49

Some cases of human cerebro-spinal meningitis associated with swine streptococcal infections were reported. Five piggery workers were involved. A 23 year old nursing mother and four male attendants suffered persistent headaches followed by stiffneck and what a physician diagnosed as meningitis and was treated in a hospital. Typical clinical signs of cold, mucopurulent catarrh with diarrhea and other symptoms were seen. Precautionary measures to be taken when swine encephalitis is suspected were also discussed.
Int J Zoonoses 1986 Dec
PMID:Emerging zoonoses in Africa. 1: Swine encephalitis in man. 355 38

Two epidemics of a new virus disease, tanapox, occurred in 1957 and 1962 among the Wapakomo tribe along the Tana River in Kenya. Several hundred people were affected by a short febrile illness with headache and prostration and the disease was characterized by a single pock-like lesion on the upper part of the body. A pox virus, unrelated to the vaccinia-variola group, has been incriminated as the causative agent. The virus has a limited host range and has been grown only in human and monkey tissue cultures, and so far the only animals that have proved susceptible in the laboratory have been monkeys. The characteristic lesions have been reproduced in a human volunteer. Histopathological and electron microscopic studies indicate that the virus belongs to the pox group, but serological tests show that it differs from other animal pox viruses, including yabapox virus of monkeys. A similar if not identical pox virus has caused epidemics in primate colonies in the U.S.A. It is suggested that tanapox is a zoonosis and that the disease is transmitted from monkeys to man in Kenya.
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PMID:Tanapox: a new disease caused by a pox virus. 554 25

A case of paranasal sinusitis due to Pasteurella multocida (P. multocida) is reported. A 39-year-old woman presented with chief complaints of rhinorrhea and headache. The patient kept a cat in her house and kept such close contact with it as to wake up by being licked every morning. Bacteriological examination revealed P. multocida isolated from her nasal discharge and also from the saliva of the cat kept by the patient. The two isolates were compatible with respect to biochemical properties, serotype and drug susceptibility. Therefore, P. multocida infection in this case was considered to have originated from the pet cat. P. multocida infection has been increasing recently. One of the reasons is a pet boom. In order to prevent acquiring the infection from a pet animal, we should have knowledge about this infection, advise the patient to avoid close contact with pets, and provide valuable information concerning these problems to society from the viewpoint of zoonosis.
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PMID:[Paranasal sinusitis due to Pasteurella multocida]. 846 82

Human ehrlichiosis is a recently described zoonosis caused by a rickettsia that infects leukocytes. Most patients have fever, headache, chills, and myalgias and develop leukopenia, thrombocytopenia, anemia, and elevations in serum hepatic aminotransferases. The cause of the peripheral leukopenia and thrombocytopenia is not known. We studied peripheral blood smears, bone marrow aspirates, and bone marrow biopsy specimens from patients with serologically proven ehrlichiosis to characterize the pathologic changes associated with leukopenia or thrombocytopenia, to detect the presence of immunohistologically demonstrable ehrlichiae, and to establish the infected host target cell(s). Specimens were obtained from 12 patients, and immunohistology for Ehrlichia chaffeensis was performed on tissue sections, aspirated bone marrow, and peripheral blood smears. Mean leukocyte and platelet counts available for nine patients were white blood cell count 3,300/microL (range, 1,100 to 10,300/microL) and platelets 61,000/microL (range, 40,000 to 82,000/microL). Findings included myeloid hyperplasia (eight cases), megakaryocytosis (seven cases), granulomas (eight cases), marrow histiocytosis (one case), myeloid hypoplasia (one case), pancellular hypoplasia (one case), and normocellular marrow (two cases). Morulae of E chaffeensis were detected in four of 10 cases examined by immunohistology. Most ehrlichiae were detected within histiocytes, although morulae were rarely present within lymphocytes. Leukopenia, thrombocytopenia, or pancytopenia apparently most often results from peripheral sequestration or destruction; however, hypoplasia of marrow elements is present occasionally. Immunohistologic demonstration of E chaffeensis offers a direct means for establishing the etiologic diagnosis. These observations show the relatively frequent occurrence of bone marrow granulomas and suggest that infection of cells of the reticuloendothelial system may participate in the pathogenesis of human ehrlichiosis.
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PMID:Human ehrlichiosis: hematopathology and immunohistologic detection of Ehrlichia chaffeensis. 849 79

Pneumonia is one manifestation of acute Q fever following infection with Coxiella burnetii. Fever, headache, and myalgia dominate the clinical picture of Q fever pneumonia. Cough is nonproductive and may be absent despite the presence of pneumonia. While in most instances pneumonia results in an illness of mild-to-moderate severity, on occasion it is rapidly progressive and results in respiratory failure. Infection occurs as a result of inhalation of contaminated aerosols. Infected cattle, sheep, and goats are the usual reservoirs for this zoonosis. In some areas, infected parturient cats serve as the reservoir, and in such instances, rounded opacities are seen on the chest radiograph. The diagnosis of C. burnetii pneumonia is usually confirmed by demonstration of a fourfold or greater rise in antibody titer. Treatment is usually with a tetracycline or rifampin for 7 to 10 days.
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PMID:Coxiella burnetii (Q fever) pneumonia. 874 74

Murine typhus, caused by Rickettsia typhi, is an important zoonosis in all parts of the world. The disease is transmitted from rodents to humans by fleas. In this article we describe the first three cases of serologically proven murine typhus imported into Norway during the 1990s. The patients were Norwegian tourists who had visited respectively Guinea-Bissau, Crete and Thailand. They all became acutely ill with fever, chills and severe headache 1-10 days after return to Norway. None of them had a rash. Two patients were admitted to hospital, and one was treated with ciprofloxacin for suspected typhoid fever. All the patients recovered without sequelae. The diagnosis of murine typhus was based on detection of IgM-anti-bodies against R typhi in serum samples during reconvalescence.
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PMID:[Endemic typhus imported to Norway]. 926 2


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