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Gram-negative osteomyelitis frequently responds poorly to conventional therapy. Ciprofloxacin displays excellent in vitro activity against gram-negative bacilli and offers the potential for outpatient therapy. In this ongoing study, ciprofloxacin therapy is being evaluated for the treatment of gram-negative osteomyelitis. Twenty-three patients (16 men and seven women) have been treated under the protocol (750 mg orally twice daily for 1.5 to six months), and 14 patients have completed therapy. All patients had either growth on bone cultures from an open or percutaneous biopsy, or an arthrocentesis to confirm the diagnosis. Involved sites included ankle or tibia (seven patients), vertebra (four patients), hip (five patients), metatarsal (four patients), phalanx (two patients), and metacarpal (one patient); 16 patients had chronic disease, and seven patients had acute disease. Patients had a total of 28 gram-negative bacilli, 12 gram-positive cocci, and one anaerobic gram-negative rod, for an average of 1.8 pathogens per patient. Eighteen of the 28 gram-negative bacilli were Pseudomonas species. The geometric mean minimal inhibitory concentration for all the gram-negative bacilli was 0.15 microgram/ml. The geometric mean minimal inhibitory concentration for the gram-positive isolates was 0.41 microgram/ml. All patients who completed therapy experienced a cure, with a mean follow-up of 6.1 months. Infections in all patients, except for two who are still taking ciprofloxacin, are resolving, both clinically and radiologically. One patient who was not eligible for the protocol experienced a superinfection with methicillin-resistant Staphylococcus aureus. Side effects have included urticaria, lethargy, nausea, and transient elevations of liver and renal function test results. Overall, ciprofloxacin therapy was well tolerated. This study suggests that ciprofloxacin holds promise for the outpatient treatment of gram-negative osteomyelitis.
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PMID:Oral ciprofloxacin therapy for gram-negative bacillary osteomyelitis. 355 43

The essence of the problem, as previously reported, indicated that few complications of acute appendicitis occur as long as the infection is contained within the appendix, but once the invading bacteria have penetrated the peritoneal appendicular surface or have invaded the regional circulation, any one or more of a series of serious complications can develop. Thus, rightfully, emphasis has been placed upon early removal of the inflamed appendix before penetration has occurred as the best method of preventing complications. We have shown that early appendectomy is predicated on early diagnosis and that diagnostic delay is not limited to extremes of age. The diagnosis may be obscured by an accurate, although misleading, history of prior acute attacks, by precident acute disease, such as viral gastroenteritis and by unimpressive symptoms blunted by intercurrent chronic illness, such as diabetes mellitus. If the elements of periumbilical pain, anorexia, nausea or vomiting and the migration of pain to the right lower abdominal quadrant are contained within the clinical history, one must suspect transmural progression of acute appendicitis; frequent inpatient examinations will allow earliest diagnosis and, thereby, fewest perforations and their attendant serious complications. Misdiagnosis is common. Any patient observed for an ostensibly nonsurgical acute condition of the abdomen who fails to improve markedly during a brief course of appropriate specific or supportive therapy must be thoroughly re-evaluated as a potential surgical candidate. Despite the proliferation of accessible laboratory tests and imaging procedures, the early diagnosis of appendicitis rests upon the clinical skills of the physician. A high index of suspicion is crucial. As Doctor Warfield M. Firor, former senior surgeon commented: "Pain and tenderness at any point where the appendix can lie must raise the diagnostic possibility of appendicitis."
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PMID:Reasons for delay of the diagnosis of acute appendicitis. 670 39

Dengue is a mosquito-transmitted acute disease caused by any of four virus serotypes (DEN-1, DEN-2, DEN-3, and DEN-4) and characterized by the sudden onset of fever, headache, myalgia, rash, nausea, and vomiting. The disease is endemic in most tropical areas of the world and has occurred in U.S. residents returning from travel to such areas. This report summarizes information about cases of imported dengue among U.S. residents during 1993 and 1994.
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PMID:Imported dengue--United States, 1993-1994. 773 51

Although serologic studies have identified hantaviral infection in the United States, acute disease has not been recognized. This study describes 3 cases of domestically acquired hemorrhagic fever with renal syndrome (HFRS) in the United States. Infection was due to a local strain of Seoul virus (Baltimore rat virus). A review of the clinical features indicated a mild illness characterized by nausea, vomiting, renal and liver failure similar to HFRS described elsewhere for rat-borne viruses. Follow-up of 2 patients identified persistent hypertension and renal disease providing further evidence of an association between past hantaviral infection and hypertensive renal disease.
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PMID:Domestic cases of hemorrhagic fever with renal syndrome in the United States. 799 Oct 40

Dengue is a mosquito-transmitted acute disease caused by any of four virus serotypes (DEN-1, DEN-2, DEN-3, and DEN-4) and characterized by the sudden onset of fever, headache, myalgia, rash, nausea, and vomiting. The disease is endemic in most tropical areas of the world and can occur in U.S. residents returning from international travel. Serum samples from 68 persons with suspected imported dengue with onset in 1992 (1) were submitted to CDC from 23 states (Table 1). Of these, 17 (25%) cases (from 10 states) were serologically or virologically diagnosed as dengue. This report summarizes information about these 17 cases.
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PMID:Imported dengue--United States, 1992. 830 65

Anorexia is associated with disorders of all systems. Anorexia represents a consistent clinical manifestation during acute and chronic pathophysiological processes (infection, inflammation, injury, toxins, immunological reactions, malignancy and necrosis). Anorexia during disease can be beneficial or deleterious depending on the timing and duration. Temporary anorexia during acute disease may be beneficial to an organism since a restriction in the intake of micro- and macro-nutrients will inhibit bacterial growth. Long-term anorexia during chronic disease, however, is deleterious to an organism and may be associated with cachexia, which can ultimately result in death. Various mechanisms participate in the anorexia observed during disease, including cytokine action. Anorexia induced by cytokines is proposed to involve modulation of hypothalamic-feeding associated sites, prostaglandin-dependent mechanisms, modifications of neurotransmitter systems, gastrointestinal, metabolic, and endocrine factors. In addition, the anorexia-cachexia syndrome is multifactorial and may involve chronic pain, depression or anxiety, hypogeusia and hyposmia, chronic nausea, early satiety, malfunction of the gastrointestinal system, metabolic alterations, cytokine action, production of other anorexigenic substances and/or iatrogenic causes (chemotherapy, radiotherapy). Cachexia may result not only from anorexia and a decreased caloric intake, but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions), or a change in body metabolism. Research has focused on potential interventions to modify anorexia during disease and the anorexia-cachexia syndrome. Nutritional modifications and the use of specific steroids (such as megestrol acetate) are being tested in the clinical setting. Understanding the specific mechanisms responsible for anorexia during disease as well as their interactions is essential to develop interventions for the control of anorexia (during a critical time in a specific disease), and to devise less toxic immunotherapeutic regimens using cytokines.
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PMID:Anorexia during acute and chronic disease. 905 54

Dengue is a mosquito-transmitted acute disease caused by any of four virus serotypes (DEN-1, DEN-2, DEN-3 and DEN-4) and is characterized by acute manifestations that can include fever, headache, myalgia, arthralgia, rash, nausea, and vomiting. On August 25, 1995, public health authorities in Mexico notified the Texas Department of Health (TDH) of an ongoing outbreak of dengue fever in the state of Tamaulipas, which borders south Texas. Because of the year-round presence of the Aedes aegypti mosquito (a major vector for dengue) in southernmost Texas and the frequent movement of persons across the U.S.-Mexico border, the outbreak in adjacent Tamaulipas suggested an increased potential for imported and autochthonous cases in Texas, as had occurred during 1980 and 1986. In response to the notification from Mexico, TDH intensified surveillance efforts for dengue, resulting in identification of 29 laboratory-diagnosed cases in Texas residents, including seven persons with no history of travel outside the state. This report summarizes results of dengue surveillance in the U.S.-Mexico border area during 1995-1996.
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PMID:Dengue fever at the U.S.-Mexico border, 1995-1996. 892 3

Dengue is an acute disease caused by any of four mosquito-transmitted virus serotypes (DEN-1, DEN-2, DEN-3 and DEN-4) and characterized by the sudden onset of fever, headache, myalgias, rash, nausea, and vomiting. The disease is endemic in most tropical areas of the world and can occur in U.S. residents returning from travel to such areas. This report summarizes information about imported dengue among U.S. residents during 1995 and documents a substantially increased incidence of dengue in the Caribbean, Central America, and Mexico.
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PMID:Imported dengue--United States, 1995. 900 6

Dengue is a mosquito-transmitted acute disease caused by any of four dengue virus serotypes (DEN-1, DEN-2, DEN-3, and DEN-4) and characterized by the sudden onset of fever, headache, myalgia, arthralgia, rash, nausea, and vomiting. This disease is endemic in most tropical areas of the world and has occurred in U.S. residents returning from travel to such areas. CDC maintains a laboratory-based passive surveillance system for imported dengue among U.S. residents. This report summarizes information about cases of imported dengue among U.S. residents for 1996, which indicated that most persons for whom travel history was known probably acquired infection in the Caribbean islands or Asia.
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PMID:Imported dengue--United States, 1996. 967 16

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has caused a pandemic coronavirus disease-19 (COVID-19) that began in Wuhan city, China, in December 2019. Till 14th April, 19,39,801 people have been affected by this virus, of whom 1,20,897 died. Though respiratory symptoms are the typical manifestation of this disease, gastrointestinal (GI) symptoms such as anorexia, nausea, vomiting, loss of taste sensation, diarrhea, abdominal pain, and discomfort have been reported. The pooled prevalence of GI symptom is 17.6% (95% confidence interval, 12.3%-24.5%), as indicated in a meta-analysis. A few studies suggested that the presence of GI symptoms is associated with poorer prognosis. The virus is excreted in feces during the acute disease, and even after, the nasopharyngeal swab has become negative for viral ribonucleic acid. Fecal viral excretion may have clinical significance because of possible feco-oral transmission of the infection. Nearly, 10.5%-53% of patients with COVID-19, particularly those with severe disease, have been shown to have an elevation of hepatic enzymes though biochemical and clinical jaundice are uncommon. Knowledge about this disease in general and GI involvement, in particular, is currently evolving.
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PMID:Gastrointestinal and Hepatic Involvement in Severe Acute Respiratory Syndrome Coronavirus 2 Infection: A Review. 3283 95


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