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 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new viral disease (Maridi haemorrhagic fever) occurred in the South Sudan in 1976. It was obviously identical with an epidemic which occurred at the same time in Zaire. The virus is morpologically closely similar to the Marburg virus. During the Maridi epemic 124 of 238 patients died (52%). Characteristic symptoms were fever and headache (100%), diarrhoea (83%), retrosternal pain (82%), vomiting (68%), haemorrhages (62%), morbilliform or vesicular rash (52%). At post-mortem there were changes in liver, kidney, myocardium and lungs, similar to those in the Marburg virus disease, as were those observed in bone marrow and peripheral blood. Despite these analagous findings, the clinical course and results of immunofluorescence indicate that it is a new disease. The epidemic ended after suitable isolation measures had been taken. There was no specific treatment but in some cases convalescent plasma and interferon were tried. The disease is transmitted among humans by direct contact or by contact with blood or excreta of patients. No animal reservoir has been found. It is possible for this disease to be imported also into countries with a modorate climate.
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PMID:[Maridi haemorrhgic fever: a new viral disease (author's transl)]. 2 83

A large outbreak of haemorrhagic fever (subsequently named Ebola haemorrhagic fever) occurred in southern Sudan between June and November 1976. There was a total of 284 cases; 67 in the source town of Nzara, 213 in Maridi, 3 in Tembura, and 1 in Juba. The outbreak in Nzara appears to have originated in the workers of a cotton factory. The disease in Maridi was amplified by transmission in a large, active hospital. Transmission of the disease required close contact with an acute case and was usually associated with the act of nursing a patient. The incubation period was between 7 and 14 days. Although the link was not well established, it appears that Nzara could have been the source of infection for a similar outbreak in the Bumba Zone of Zaire.In this outbreak Ebola haemorrhagic fever was a unique clinical disease with a high mortality rate (53% overall) and a prolonged recovery period in those who survived. Beginning with an influenza-like syndrome, including fever, headache, and joint and muscle pains, the disease soon caused diarrhoea (81%), vomiting (59%), chest pain (83%), pain and dryness of the throat (63%), and rash (52%). Haemorrhagic manifestations were common (71%), being present in half of the recovered cases and in almost all the fatal cases.Two post mortems were carried out on patients in November 1976. The histopathological findings resembled those of an acute viral infection and although the features were characteristic they were not exclusively diagnostic. They closely resembled the features described in Marburg virus infection, with focal eosinophilic necrosis in the liver and destruction of lymphocytes and their replacement by plasma cells. One case had evidence of renal tubular necrosis.Two strains of Ebola virus were isolated from acute phase sera collected from acutely ill patients in Maridi hospital during the investigation in November 1976. Antibodies to Ebola virus were detected by immunofluorescence in 42 of 48 patients in Maridi who had been diagnosed clinically, but in only 6 of 31 patients in Nzara. The possibility of the indirect immunofluorescent test not being sufficiently sensitive is discussed.Of Maridi case contacts, in hospital and in the local community, 19% had antibodies. Very few of them gave any history of illness, indicating that Ebola virus can cause mild or even subclinical infections. Of the cloth room workers in the Nzara cotton factory, 37% appeared to have been infected, suggesting that the factory may have been the prime source of infection.
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PMID:Ebola haemorrhagic fever in Sudan, 1976. Report of a WHO/International Study Team. 30 55

Fourteen patients with radiculomyelitis following acute haemorrhagic conjunctivitis (AHC) were seen in Bangkok during October to December 1974. Most patients developed weakness of extremities 2 weeks after AHC. Prodromal symptoms consisted of fever and malaise for a few days, followed by the acute onset of root pain in the legs and flaccid paralysis. Knee and ankle reflexes were absent or diminished. Cerebrospinal fluid examination revealed lymphocytosis and an increase in protein. Electromyographic findings were consistent with anterior horn cell or motor root lesions. Ten of the 12 cases in which virological studies were performed showed definite serological evidence of AHC virus infection. Six patients received corticosteroid treatment but apart from relief of pain no significant improvement was seen. Motor weakness in 10 patients was less at the end of 2 months, but in 4 it remained unchanged. The occurrence of disabling neurological sequelae calls for effective public health control of AHC outbreak.
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PMID:Radiculomyelitis complicating acute haemorrhagic conjunctivitis. A clinical study. 124 77

Otitis media primarily affects children, but can also lead to lifelong sequelae. Middle ear histopathologic changes and clinical manifestations can represent any part of a disease continuum, from acute to recurrent to chronic otitis media. Acute otitis media is most often caused by an acute respiratory viral infection and secondary replication of bacteria in the middle ear space and tissues, leading to symptoms and signs of infection (ie, fever, pain, tympanic membrane erythema). Antimicrobial therapy is the mainstay of management, and clinical response to different antimicrobial drugs appears to be similar. The bacteriologic efficacy of these drugs, however, is quite variable. Clearly, antimicrobial treatment of acute otitis media, which currently is largely empiric, must be fine-tuned on the basis of patient and disease variation.
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PMID:Otitis media update: pathogenesis and treatment. 172 95

Fatigue, pain, and emotional upset remain the most common problems affecting humanity and for which we still know so very little. Chronic fatigue syndrome is most likely a number of as yet unproven various undifferentiated illnesses that are exceedingly difficult to distinguish from depression. There probably is a subset of patients with CFS who do have true immune dysfunction and persistent viral infection, and this particular group of patients should be further investigated. This group is the minority of patients who present with chronic fatigue. Although chronic fatigue syndrome may be the result of an organic illness in psychologically susceptible individuals, it remains most important to assess underlying psychologic factors that then need to be addressed. These factors may very likely have a profound effect on immune function, but more research is needed in this area. The diagnostic evaluation of patients with chronic fatigue syndrome should initially focus on causes for fatigue other than Epstein-Barr viral infection. Significant underlying medical conditions should be ruled out, and extensive inquiry into symptoms suggestive of depression and anxiety should be aggressively pursued. Treatment should include psychiatric support and counseling, good nutrition, adequate rest, and a gradual increase in activity. Anti-inflammatory agents and serotonin-replenishing antidepressants are helpful when muscle pain and tenderness are a major part of the patient's symptoms. Psychoactive drugs are useful when indicated. Low doses of antidepressants such as doxepin (10-25 mg at night) are generally well tolerated and have shown efficacy in numerous patients, although there are no reports of controlled trials.
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PMID:Chronic fatigue and depression in the ambulatory patient. 187 21

In many cases of chronic intractable pain without any discernible causes, when both Western medical treatment and acupuncture treatment failed to eliminate the pain, this pain is often due to the unrecognized presence of viral or bacterial infection. Even effective anti-viral or bacterial agents often fail to eliminate or inhibit the infection, as these drugs may also fail to reach the most painful area where often unrecognizable circulatory disturbances co-exist. Using the Bi-Digital O-Ring Test Molecular Identification Method, we were able to localize substance P and thromboxane B2 (a good indicator of the presence and degree of circulatory disturbances) in the painful area along with virus or bacteria. Based on the Bi-Digital O-Ring Test localization method for specific substances or microbes, the author has successfully treated cases of chronic intractable pain by the combination of anti-viral or bacterial agents with either manual acupuncture, electro-acupuncture or transcutaneous electrical stimulation through a pair of surface electrodes. Among a variety of infections, the most common cause of severe intractable pain was herpes simplex virus, and the most common bacterial cause of intractable pain of moderate degree was campylobacter. In addition, chlamydia was a very common cause of mild intractable pain. When peripheral nerve fibers are hypersensitive from nerve injury due to viral infection, in addition to the drug therapy for infection, use of Vitamin B1 25 mg., 2 times a day for an average adult often accelerates recovery time. As an anti-viral agent for the herpes virus family, the author found that EPA (Omega 3 fish oil, Eicosa Pentaenoic Acid, C20:5 omega 3), at doses between 180 mg. and 350 mg (depending upon body weight) 4 times a day for 2 to 6 weeks, without prescribing the common anti-viral agent Acyclovir, often eliminated the symptoms due to viral infection including all well-known types of the herpes virus, such as herpes simplex virus, Epstein-Barr virus, and cytomegalovirus. Epstein-Barr virus and cytomegalovirus are usually not associated with intractable severe pain, but they are often associated with a recurrent burning or itching sensation and they can cause intractable frequent muscle twitching. Viruses belonging to the herpes family almost always exist between the midline of one side of the spinal cord and the midline of the front of the body where these nerves from the spinal cord end and the same virus is localized only on one side of the body at the same spinal level.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Treatment of acute or chronic severe, intractable pain and other intractable medical problems associated with unrecognized viral or bacterial infection: Part I. 197 80

The human retrovirus HTLV-1 (Human T-cell Lymphotrophic Virus) is responsible for malignant proliferations of mature T lymphocytes. It is also now implicated in neurological disorders dominated by spastic paraplegia. A study of 140 cases of lumbar and root pain enabled us to identify 8 of apparently idiopathic atypical lumbar and root pain which led to the discovery of a positive HTLV-1 serology performed routinely. These cases were remarkable in terms of the rarity and minimal extent of spinal cord signs and of Lasegue's sign, their duration of more than a year and the existence of neurological signs indicative of central involvement. In 2 patients there was secondary progression to a spastic paraparesis. It would appear that the neurotropism of HTLV-1 virus is not limited to the central nervous system but that it can also involve the peripheral nervous system as indicated by certain cases in the literature as well as those collected in Martinique, an endemic area for the virus. Rheumatologists should be aware of this possibility when confronted with such cases of atypical lumbar and root pain and should seek the existence of an HTLV-1 virus infection among other viral etiologies, in particular when the patient concerned comes from an endemic area.
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PMID:[Atypical lumbar and nerve-root pain associated with the HTLV-1 virus]. 215 Apr 50

The clinical profile of cluster headache, in Italy better known as "Horton's histaminic headache" is described. The Author makes an inventory of all pathogenetic theories about this excruciating pain syndrome that strikes men more than women. On the basis of findings of the Author and his School over a ten-year period, there is a "periodic lack of immunitary oversee". The salient points of various stages of this study are: low frequency of HLA-B14 antigen with, in contrast, high frequency of the HLA-DR5 antigen of the major histocompatibility system. The HLA B18 antigen of the same major histocompatibility system has been found in patients who respond to lithium therapy. A lack of the HLA-B18 antigen has been found in cluster headache patients who are "non-responders" to lithium therapy. Low titers of antibody response in the pain free periods of these subjects, and high titers in the painful periods has also been found in the serum of cluster headache patients; the lack of alpha 1-antitrypsin in basal conditions; increase of IgE (PRIST) values in painful periods; high titers of C1qSp and KgBt circulating immuno-complexes. The cellular immunity studies of the patients showed an increase of the leukocyte subpopulations Leu7+ and Leu M3+. Besides, the natural killer function that contributes to the defense-mechanism against viral disease, was very low. High titers of anti-herpes simplex 1 and 2 viruses and anti-Epstein-Barr virus have been found in cluster headache patients and in a few observations of Burkitt's lymphoma with associated cluster headache, studied in Sahel area too.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New findings in cluster headache. 215 Apr 89

Herpes zoster (shingles) is a viral infection that results from a reactivation of a dormant varicella zoster virus. It has been estimated that more than 300,000 new cases are seen in the United States each year. Several factors influence the incidence of infection, with increasing age being the most consistent. Postherpetic neuralgia is the No. 1 cause of intractable, debilitating pain in the elderly and is the leading cause of suicide in chronic pain patients over the age of 70.
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PMID:Treatment of acute herpetic neuralgia. A case report and review of the literature. 229 95

Oral complications of cancer therapy often have systemic consequences. Pain and discomfort are common and can lower intake of fluid and nutrients, which in severe cases can lead to dehydration and malnutrition, requiring hospitalization. Oral infections are frequent accompaniments of cancer treatment. Herpes simplex virus is the most common symptomatic oral viral infection, and, in latently infected patients the virus is frequently reactivated after cytoreductive therapy. Viral (infectious) oral mucositis is often indistinguishable from noninfectious mucositis. Bacterial infections are less commonly observed today, perhaps because of the routine use of empiric broad-spectrum antibiotics; however, many episodes of septicemia in neutropenic patients apparently originate from oral microorganisms. Fungal infections are frequent and are usually due to Candida species. Spread to the esophagus or systemic dissemination can occur. Noninfectious oral mucositis can be used as a marker of toxic effects in other organs, especially hepatic veno-occlusive disease. In bone marrow transplant patients with mucositis, hepatic veno-occlusive disease is six times more frequent than in such patients without mucositis.
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PMID:Oral complications of cancer therapies. Infectious and noninfectious systemic consequences. 218 56


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