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During epidemiologic studies of Rocky Mountain Spotted Fever in Mississippi in 1973, dogs were surveyed for antibodies tp spotted fever group antigens and for tick parasites infected with rickettsiae of the spotted fever group. Fifty-three (46%) of 116 serum samples had complement-fixing antibody titers greater than or equal to 1:8 as compared to only one (5%) of 21 samples from a group of dogs obtained from metropolitan Chicage. Fifty-two per cent of the dogs tested from Mississippi had microagglutinating antibodies titers greater than or equal to 1:8; 9% of dogs from Chicago had similar titers. Rickettsia rickettsii was demonstrated in only one (0.8%) of 129 Dermacentor variabilis removed from Mississippi dogs. Quite unexpectedly, 167 (18.9%) of 884 Rhipicephalus sanguineus taken from these dogs contained spotted fever group rickettsiae.
Feeding of 20 to 30 million units of vitamin D for 3 to 8 days prepartum previously prevented about 80% of expected milk fever cases in mature Jersey cows with histories of milk fever. In this experiment vitamin D was fed continuously through the year via 32,000 units of vitamin D added to each .455 kg of concentrate fed (approximately 100,000 to 580,000 units/day). Milk fever incidence was measured after 5 yr of age (third calf) at 43 parturitions in mature Jersey cows with histories of milk fever and at 139 parturitions in mature Jersey cows with no previous milk fever. Continuous feeding of vitamin D reduced incidence of milk fever in cows with previous milk fever from 60% in the controls to 26.1% in the group fed vitamin D. In the cows with no milk fever previously, feeding vitamin D did not reduce incidence of milk fever (controls 23.7%, vitamin-D-fed 28.3%).
In 1987 there was an unexplained increase in severe streptococcal diseases in Norway and other western countries. In Norway this increase was not accompanied by a corresponding increase in acute rheumatic fever. This study investigated the occurrence of scarlet fever and acute rheumatic fever in a rural district (approximately 15,000 inhabitants) of western Norway during the years 1862-1884. Four epidemics of severe scarlet fever occurred during this period. The local doctor treated 1,155 patients (96% children), of whom 154 (13.3%) died. Acute glomerulonephritis with subsequent kidney failure seems to have been a major cause of death. During the same period 76 patients (96% adults) were treated for acute rheumatic fever. These cases were not related to the severe epidemics of scarlet fever. It is probable that different, co-circulating strains of streptococci caused the infections, which were followed by glomerulonephritis and rheumatic fever. It is possible that rheumatic fever was caused by the strain that induced the more benign "Angina tonsillaris".
We studied the hospital records of 124 patients with a discharge diagnosis of acute rheumatic fever who were hospitalized in 21 Minneapolis-St. Paul hospitals during 1975 and 1976. After careful review of the hospital records, we found that 83 (67 per cent) of these patients did not have an acute illness. Seventeen (41 per cent) of the 41 cases with an acute illness were thought to adequately fulfill the Jones' Criteria for acute rheumatic fever. Upon review of the rheumatic fever registry of the Minnesota State Health Department, we found that less than one-half of the hospitalized patients had been reported to the registry. Cases that fulfilled and did not fulfill the Jones' Criteria were reported with equal frequency, indicating significant underreporting and overreporting of rheumatic fever. Evaluation of secondary rheumatic fever prophylaxis, both in those patients with acute rheumatic fever as well as in those with rheumatic heart disease, indicated that many patients who, in theory, should be receiving prophylaxis were not receiving it. These studies indicate a need for more thorough evaluation of the current epidemiology of rheumatic fever and the role of a rheumatic fever registry, and imply a need for reevaluation of these programs. (Am J Public Health 69:767-771, 1979).
A sample of 80 direct and 36 telephone encounters for fever was established in 1988 as part of a Norwegian study on fever as a clinical problem in general practice. Reasons for encounter (ICPC) and clinical examinations were recorded along with clinical laboratory tests, treatment, management and follow up (IC-Process-PC). The doctors assessed the diagnostic process by means of visual analogue scale. Duration of the fever conditions was estimated through a postal questionnaire. Patients with direct encounters presented a wide range of reasons for the encounters. Fever was the most frequent single presenting complaint (31%). The general practitioners put major emphasis on the clinical examinations. They prescribed drugs in 68% of the direct encounters. Seventy per cent of the prescriptions were general systemic anti-infectives. Penicillin accounted for 58% of antibiotics. Six (8%) patients were hospitalized, and three (4%) were referred to a specialist. The mean time until complete recovery was 15 days for direct and 19 days for telephone encounters. Fever may be a sign even when it is not a presenting complaint. Major emphasis is probably put on the clinical examination of febrile patients because of the complexity of symptoms and the wide range of diagnoses associated with fever.
The historical, clinical, ecological, and epidemiological features of Rocky Mountain spotted fever and Colorado tick fever, the two important tick-borne diseases in the United States, are reviewed. Rocky Mountain spotted fever, once considered a disease of the past, has again become a measurable public health problem. Its nationwide incidence has steadily increased since 1960 and has reached record proportions in 1976. The various factors responsible for this trend as well as for the mortality rates, which in spite of availability of effective antibiotics ranges from 5 to 10%, are discussed. Education of the public about ticks and their potential role as vectors of Rickettsia rickettsii and/or Colorado tick fever virus, and about the clinical manifestations of Rocky Mountain spotted fever, is considered the best means for preventing high incidence and mortality from these diseases.
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A patient who had been exposed to ticks and who had also been bitten by a laboratory rat developed fever, headache, and a rash. He was treated with chloramphenicol for Rocky Mountain spotted fever, and recovered. Blood cultures, however, grew Streptobacillus moniliformis, a causative agent of rat bite fever. The case report illustrates the clinical similarities between rat bite fever and Rocky Mountain spotted fever.
The Jones Criteria for guidance in the diagnosis of acute rheumatic fever were first published by T. Duckett Jones, MD, in 1944 and have been revised over the years by the American Heart Association. The current guidelines are an update of these criteria. For the first time, the guidelines are designed to establish the initial attack of acute rheumatic fever. Major manifestations, minor manifestations, and supporting evidence of antecedent group A streptococcal infection are discussed. These updated guidelines expand on the available tools to diagnose streptococcal pharyngitis and clarify the available antibody tests for detecting antecedent group A streptococcal infection. At the present time echocardiography without accompanying auscultatory findings is insufficient to be the sole criterion for valvulitis in acute rheumatic fever. Finally, this article addresses overdiagnosis of rheumatic fever and lists exceptions to the Jones Criteria, including recurrent attacks in individuals with a history of rheumatic fever.
The first case of epidemic hemorrhagic fever in Japan was seen in Osaka in 1960. The etiologic agent of this disease has not yet been isolated, but a close etiologic relation between Korean hemorrhagic fever and epidemic hemorrhagic fever in Japan has been suspected because of similarities in the clinical and pathological pictures of the two diseases. This relation has now been confirmed serologically by demonstrating specific immunofluorescent antibodies to Korean hemorrhagic fever virus in 19 of 20 sera obtained from subjects 7 to 17 years after an acute attack of epidemic hemorrhagic fever.
Case histories recorded by Hippocrates around 400 B.C. describe the clinical manifestations of scarlet fever and rheumatic fever, although the entities are not identified by name. Although the descriptions are not as detailed or complete as they would be today, they strongly suggest the existence of scarlet fever and rheumatic fever at that time. Hippocrates' references to these illnesses were presumably the first to be documented and/or discovered, as a thorough search of the worldwide medical literature revealed no prior descriptions.
Three parameters were used in 1976 and 1977 to assess the status of Rocky Mountain spotted fever (RMSF) in Connecticut--compilation and review of clinical data on suspected human cases for the 13-year period 1965--1977, examination of tick tissues for spotted fever-group rickettsiae by the hemolymph test and direct immunofluorescence, and analyses of mammalian sera for antibodies against Rickettsia rickettsii. There were six presumptive RMSF cases which probably originated in Connecticut. Four of these cases occurred in areas where the American dog tick, Dermacentor variabilis, abounds. A total of 2994 ticks were examined by the hemolymph test. Rickettsia-like organisms were observed in 67 (2.9%) of 2330 D. variabilis and two (0.6%) of 351 Ixodes sp. near scapularis. Fewer than one-half of these organisms stained positively with spotted fever-group conjugate. Microagglutination tests on 1093 mammalian sera indicated that eight (16%) of 49 raccoons, 14 (2.6%) of 549 white-tailed deer, eight (1.7%) of 470 white-footed mice, and one of two gray squirrels had agglutinins in titers greater than or equal to 1:8 against R. rickettsii. Spotted fever-group rickettsiae are present at low frequency in inland as well as coastal regions of Connecticut.
A 55-year-old male presented with a recurrent fever of over 38 degrees C, occurring at irregular intervals 1-6 times a month with chest, back or abdominal pain. After admission to our hospital, we found the following characteristics: 1) the febrile attacks were accompanied by obvious inflammatory findings and pleuritis or peritonitis; 2) the patient's elder sister had a similar periodic fever; and 3) there were no apparent causative factors responsible for his symptoms. Therefore, we diagnosed this as a case compatible with familial Mediterranean fever. The febrile attacks have been completely suppressed by daily colchicine. This is the seventh case of familial Mediterranean fever reported in Japan.
The antigenic relationships of 21 known or presumed Phlebotomus fever group serotypes and of 2 ungrouped, solvent sensitive, sandfly-associated arboviruses (Pacui and Charleville) were studied by complement fixation, plaque neutralization, and hemagglutination-inhibition methods. Results of complement fixation and neutralization tests were specific, allowing clear separation of the various serotypes, while those of the hemagglutination-inhibition test showed broader crossing and lack of specificity. Pacui virus was shown to be a member of the Phlebotomus fever serogroup. Six new Phlebotomus fever group serotypes are also described, increasing the known members of the group to 22. The implications of these and other recent data about the epidemiology of sandfly fever are discussed.
1790 patients from 11 countries were enrolled in a prospective international study to determine the incidence of allergic reactions to monthly intramuscular benzathine penicillin (penicillin G benzathine) injections to prevent recurrences of rheumatic fever. After 32,430 injections during 2736 patient years of observation, 57 of the 1790 patients (3.2%) had an allergic reaction. 4 had anaphylaxis, an incidence of 0.2% (1.2/10,000 injections), all in patients over 12 years of age, and 1 patient died, a fatality incidence of 0.05% (0.31/10,000 injections). These rates are similar to those described for patients without rheumatic fever who receive short-term treatment with parenteral penicillin. Rheumatic fever recurred in 8 of 1790 patients (0.45%) who received benzathine penicillin prophylaxis compared with 11 of 96 (11.5%) who did not comply with treatment. Life-threatening allergic reactions are rare in patients on long-term parenteral benzathine penicillin to prevent recurrences of rheumatic fever; the long-term benefits of such prophylaxis by far outweigh the risk of a serious allergic reaction.
The immunologic basis for protection against Brazilian purpuric fever, a septicemic infection associated with Haemophilus influenzae biogroup aegyptius bacteremia, is unknown. Passive immunization of infant rats with antiserum to whole bacterial cells of the homologous strain protects them from experimental bacteremia following bacterial challenge. In immunoblotting, antibody to a 145-kDa protein (P145) was present in protective antisera but not in nonprotective antisera. As judged by analysis of the antibodies eluted from whole bacterial cells and the agglutination of bacteria by antisera to P145, this protein is surface exposed. We prepared monospecific rat antisera to this protein by three methods: (i) immunization with whole bacterial cells and absorption with a Brazilian purpuric fever strain not expressing P145, (ii) immunization with gel-purified P145, and (iii) immunization with a P145-expressing transformant of a laboratory H. influenzae strain expressing this protein and absorption of the antiserum with the laboratory H. influenzae strain. These antisera had low antilipooligosaccharide antibody titers, were reactive only with P145, and had bactericidal activity in vitro. Following passive immunization, these antisera partially protected infant rats from bacteremia resulting from intraperitoneal challenge with bacteria. As assessed by immunoblotting, pooled adult human sera contained antibodies reactive with P145. Antibody to P145 may contribute to protection against Brazilian purpuric fever.
Human and animal sera from an endemic area of sandfly fever in Iran were tested by plaque reduction neutralization method against five different Phlebotomus fever virus serotypes (Naples, Sicilian, Karimabad, Salehabad, and I-47). The overall prevalence of Naples, Sicilian, and Karimabad virus antibodies among the human population was 17%, 25%, and 66%, respectively. All sera were negative against Salehabad and I-47 viruses. Age-specific antibody rates suggested that Sicilian and Karimabad viruses were endemic in the study area but that Naples virus activity was sporadic. These observations were confirmed by isolations of Sicilian and Karimabad viruses from sandflies collected in the study area. Among the animal sera tested, evidence of Phlebotomus fever virus infection was detected only in gerbils. Of 38 Rhombomys opimus tested, 34% had neutralizing antibodies against Sicilian virus and 32% against Karimabad. These results indicate that gerbils are infected with these two viruses and possibly might serve as reservoirs or amplifying hosts. The serologic studies also suggest that the ecology of Sicilian and Karimabad viruses involves chiefly sandflies, gerbils, and man, an epidemiologic pattern previously demonstrated for cutaneous leishmaniasis in the same region of Iran.