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Biomedical subjects

E C Jong

Publications and source records attributed to E C Jong.

At least 19 recordsLinked to original sources
PubMed1999

Travel immunizations.

An updated approach to selecting and prioritizing immunizations for the international traveler is presented. This article addresses vaccines against yellow fever, typhoid fever, cholera, meningococcal meningitis, rabies, tetanus, diphtheria, measles, mumps, rubella, polio, varicella, and influenza. Vaccine preparations, dosing regimens, efficacy, adverse effects, indications, and contraindications are discussed in the context of pre-travel preparation.

Humans↗
PubMed1998

Immunizations for international travel.

Immunization recommendations for international travelers is a complex subject that takes into consideration the geographic destination, planned activities during travel, health conditions at destination, length of trip, and underlying health status of the traveler. The final immunization program is also determined by how much time is available before departure and the worldwide availability of vaccines and their cost. In some cases, preventive behaviors and chemoprophylaxis may protect against the risk of infection when immunizations are unavailable or unobtainable.

Bacterial Vaccines↗
PubMed1997

Travel medicine problems encountered in emergency departments.

This article reviews some common illnesses and conditions that prompt traveling patients to seek medical care in the emergency department in the United States. It also presents an emergency department approach to the initial diagnosis and treatment of travelers who are experiencing adverse side effects from pretravel immunizations and returned travelers who fear unusual, serious or exotic conditions and want immediate medical attention.

Communicable Diseases↗
PubMed1992

Immunizations for international travelers.

Immunizations for international travel are an important component of pretravel medical care. Travelers should receive protection against vaccine-preventable exotic diseases, and their immunity against common infectious diseases should be reviewed and updated. There are no immunizations for some important infectious hazards of travel. In the course of considering a traveler's risk for exposure to infectious disease on the basis of geographic destination, style of travel, and anticipated activities, the health care provider should discuss preventive measures and personal behavior with regard to food and water, avoidance of insect bites, personal safety, and sexual activity.

Humans↗
PubMed1992

General advice for the international traveler.

Medical concerns of the traveling patient may be organized into pre-travel medical advice and preparation, maintenance of health and behavioral modification during travel, and post-travel diagnosis and treatment for travelers returning with illness or a significant change in their general health. Pre-travel medical advice and preparation may be done in large part by well-informed primary-care providers, although patients with special health conditions or unusually complicated or high-risk itineraries may be best referred to a travel medicine specialist. Although diagnosis and treatment of exotic and tropical diseases usually falls within the area of expertise of the infectious diseases specialist, primary physicians should be familiar with the geographic distribution and presentation of the more common of these diseases, so that appropriate referrals will be made.

Altitude Sickness↗
PubMed1989

Travel-related infections: prevention and treatment.

Some 15 million Americans travel abroad each year, half of them to developing countries. Not only are they venturing farther afield than ever before but they are more inclined to be adventurous. A high percentage of these hardy souls acquire some form of infection. Physicians should know the risks, their geographic distribution, and both prophylactic and therapeutic strategies.

Adult↗
PubMed1988

Diagnosis of paragonimiasis by immunoblot.

A sensitive and specific immunoblot assay was used to rapidly and accurately diagnose paragonimiasis. The immunoreactivity of a complex Paragonimus westermani Chaffee antigen was evaluated by SDS-PAGE and Western blot analysis. Initial probing with pooled human serum from proven Paragonimus infections revealed many bands, including a significant antibody response to an approximately 8,000 molecular weight (8 kDa) protein. Forty-three of 45 proven paragonimiasis serum specimens had antibodies to this diagnostic band. Of 29 normal serum specimens and 210 serum specimens from patients with other parasitic and nonparasitic infections, only 1 serum, from a schistosomiasis haematobium patient, reacted positively. These results indicate that our immunoblot for paragonimiasis, which uses a comparatively crude antigen, is highly sensitive (96%) and specific (99%).

Animals↗
PubMed1986

Mast cell-mediated toxicity to schistosomula of Schistosoma mansoni: potentiation by exogenous peroxidase.

Mast cells, when incubated in vitro with hydrogen peroxide (H2O2) and iodide, are cytotoxic to schistosomula of Schistosoma mansoni, as determined morphologically by dye exclusion, motility, and refractility and by transmission and scanning electron microscopy. When intact mast cells were incubated with schistosomula, mast cell degranulation with extracellular release of mast cell granules (MCG) was only observed in the presence of added H2O2 (10(-4) M). The secreted MCG, which contain small amounts of endogenous peroxidase activity, adhered to the surface of schistosomula. By 15 to 30 min, the mast cell-H2O2 system in the presence of iodide (10(-4) M) produced marked disruption of the tegumental and internal structures of the schistosomula. No helminthic damage was noted if any component of the incubation mixture (mast cells, H2O2 or iodide) was omitted. MCG could substitute for intact mast cells in the H2O2 and iodide-dependent cytotoxic system; MCG-mediated killing of schistosomula was inhibited by the hemeprotein inhibitor azide, suggesting that the cytotoxic reaction required endogenous peroxidase. The cytotoxicity was increased by eosinophil peroxidase bound to the MCG surface. These findings suggest a mechanism by which mast cells may contribute to the host cytotoxic response to helminths. H2O2 formed by nearby inflammatory cells may induce mast cell secretion, and the released MCG, through their endogenous peroxidase content (or bound eosinophil or neutrophil peroxidase), may react with H2O2 and a halide to form a system toxic to the adjacent helminth.

Animals↗
PubMed1984

Human neutrophil-mediated killing of schistosomula of Schistosoma mansoni: augmentation by schistosomal binding of eosinophil peroxidase.

Eosinophil peroxidase (EPO) is a major component of the large cytoplasmic granules of eosinophils, and is released onto the surface of schistosomula when eosinophils adhere to antibody and complement coated organisms. EPO is a strongly cationic protein, which can bind to the surface of schistosomula with retention of peroxidatic activity. The binding per se was not toxic to the organisms under our conditions, but EPO-coated schistosomula were rapidly killed when H2O2 and halide were added, under conditions in which uncoated schistosomula were unaffected. The toxicity of the surface-bound EPO system was not significantly inhibited by albumin (20 mg/ml), in contrast to the complete inhibition by this concentration of protein when the EPO was free in solution. Purified polymorphonuclear leukocytes (PMNs) from normal donors were toxic to uncoated schistosomula in medium containing antischistosomal antibody and complement, and this toxicity was significantly increased when EPO was bound to the surface of the organisms. The toxicity of PMNs to EPO-coated schistosomula was inhibited but not abolished by the hemeprotein inhibitor azide. This is compatible with the involvement of surface-bound EPO in an enzymatic attack on the organism, utilizing H2O2 generated by PMNs stimulated by adherence to antibody and complement-coated schistosomula. PMN adherence to schistosomula is increased by surface-bound EPO, and this also may contribute to the enhancement of neutrophil-mediated toxicity by EPO. These findings indicate a mechanism by which two inflammatory cells, the eosinophil and neutrophil, may interact to enhance the destruction of a target organism.

Animals↗
PubMed1983

Oxidative response of phagocytes to parasite invasion.

Phagocytes destroy intracellular pathogens and extracellular targets in part by the production of toxic oxygen metabolites--namely, superoxide, hydrogen peroxide, hydroxyl radicals and possibly singlet molecular oxygen. The toxicity of hydrogen peroxide is increased greatly by peroxidase and a halide. A peroxidase that can be used for this purpose is present in neutrophils and monocytes (myeloperoxidase), but is lost when the monocyte matures into a macrophage; a different peroxidase is present in eosinophils. The latter enzyme, because of its strong positive charge, binds to the surface of parasites; any phagocyte in the region, when appropriately stimulated, may provide the hydrogen peroxide required for completion of the peroxidase system. Further, peroxidase-coated organisms are more readily killed when ingested by macrophages than are uncoated organisms. Oxygen-dependent toxicity requires the production of toxic oxygen products by phagocytes in amounts sufficient to overcome the protective capacity of endogenous scavengers in the parasite. The latter include catalase and glutathione peroxidase, which degrade hydrogen peroxide, and superoxide dismutase which dissipates superoxide. The host defence against parasites appears to depend in part on this balance between toxic oxygen metabolites and scavengers.

Animals↗
PubMed1983

Successful praziquantel treatment of paragonimiasis following bithionol failure. A case report.

A patient from Southeast Asia with cough and hemoptysis was documented to have pulmonary paragonimiasis. Initial treatment with bithionol failed. The patient was then treated with praziquantel 75 mg/kg body weight a day for 2 days under an investigational protocol. Subsequent follow-up studies showed clinical improvement and indicated parasitologic cure. A concurrent asymptomatic Clonorchis infection was also cured following praziquantel treatment. Side effects were minor.

Adult↗