Italiano Farmacia on line: comprare cialis senza ricetta, acquistare viagra internet.


Infectious Disease and the ExtremeSport Athlete Craig C. Young, , Mark W. Niedfeldt, ,Laura M. Gottschlich, Charles S. Peterson, Matthew R. Gammons, MDaDepartment of Orthopaedic Surgery, Medical College of Wisconsin, 9200 W.
Wisconsin Ave., Milwaukee, WI 53226, USAbDepartment of Family and Community Medicine, Medical College of Wisconsin, 9200 W. Wisconsin Ave., Milwaukee, WI 53226, USA cDepartment of Cell Biology, Neurobiology, and Anatomy, Medical College of Wisconsin, 9200 W. Wisconsin Ave., Milwaukee, WI 53226, USA dMayo Clinic College of Medicine, Arizona Sports Medicine Center, 5111 N. Scottsdale Road,Suite 101, Scottsdale, Arizona 85250, USAeKillington Medical Clinic, Vermont Orthopedic Clinic, PO Box 205, Killington, VT, USA Today’sathletesareoftenunsatisfiedwiththetraditionalsportsofthepast.
Even sports that were considered ‘‘extreme’’ in previous generations, suchas the marathon, have been made harder by adding length (eg, ultramar- athons), by adding events (eg, triathlons), or by placing them in extreme loca-tions (eg, jungles, mountains, or deserts). Other extreme sports are based onactivities such as climbing and skateboarding. Physicians taking care of athleteswho participate in these sports face a variety of challenges including the expo-sure of these athletes to unusual infectious diseases This article discusses infections that may be more likely to occur in the ex- treme sport athlete, such as selected parasitic infections, marine infections,freshwater-borne diseases, tick-borne disease, and zoonoses. Epidemiology,presentation, treatment, complications, and return-to-sport issues are discussedfor each of these diseases.
PARASITESParasitic infection can plague athletes traveling to and competing in the devel-oping world. Extreme sport athletes may be at increased risk because they of-ten travel through poorer, rural areas of tropical and subtropical regions toreach their destinations. Risk from a specific parasite depends on the region *Corresponding author. Department of Orthopaedic Surgery, Medical College of Wiscon-sin, 9200 W. Wisconsin Ave., Milwaukee, WI 53226. E-mail address: (C.C. Young).
ª 2007 Elsevier Inc. All rights reserved.
of the world traveled, contact with food or water, and whether traveling inrural or urban areas.
Approximately 8% of travelers returning from the developing world re- quire medical treatment during or after travel. Travelers to sub-SaharanAfrica, south central Asia, the Caribbean, and Central or South Americawho have diarrhea are more likely to have a parasitic cause than a bacterialone. Only in Southeast Asia is traveler’s diarrhea more likely to be causedbe bacteria Parasitic infection can occur from ingestion of contaminatedfood and water, from environmental exposure, or from person-to-person orperson-to-soil contact. Parasitic illness can be manifest in a variety of ways,depending on the causative organism. A returning traveler who has eosino-philia and fever has a high likelihood of having a parasitic infection. Othercommon findings include fever, diarrhea, weight loss, neurologic symptoms,dermatologic findings, eosinophilia or other laboratory abnormalities, andova on stool studies.
Amoebiasis, caused by Entamoeba histolytica, is the most common urban gas- trointestinal parasite and the second most common parasitic disease worldwideUp to 90% of people in endemic countries are asymptomatic carriers of am-oebiasis. Although typically thought of as a tropical infection, travelers tosouthern Italy have contracted the illness Entamoeba histolytica uses proteases to invade intestinal mucosa or to enter the portal circulation, creating hepatic abscess and killing host cells on contact. Thediagnosis of amoebiasis is made by finding cysts or trophozoites in stool. Treat-ment must eliminate the amoebas in tissue and the luminal amoebas to preventrecurrence. Amoebic colitis and liver abscess, if left untreated, can be fatal, andis the second leading cause of death from parasitic infection worldwide . Thetreatment is with metronidazole or tinidazole followed by iodoquinol or paro-momycin . Asymptomatic carriers can be treated with iodoquinol or paro-momycin alone.
Fever following travel can indicate malaria infection, the most common cause of undifferentiated fever in travelers to areas endemic for malaria. TheAnopheles mosquito serves as the vector for malaria transmission, and travelersto endemic areas should use preventive measures such as screens, nets, repel-lent containing deet (N,N-diethyltoluamide; 30%–35%), and permethrin sprayon clothing. Chloroquine, atovaquone proguanil, or mefloquine can be usedprophylactically, which decreases the risk of malaria but does not completelypreclude infection.
Most patients who have malaria exhibit a regular pattern of fever every 48 to 72 hours. Ninety percent of Plasmodium falciparum infections are acquired in sub-Saharan Africa, whereas 70% of Plasmodium vivax infections are acquired inLatin America and Asia When malaria is suspected, blood smears and other appropriate diagnostic laboratory testing should be performed serially as necessary. Those whohave severe complications or who have Plasmodium falciparum infection often re-quire inpatient treatment for intensive therapy and to address potential anemia, INFECTIOUS DISEASE AND THE EXTREME SPORT ATHLETE seizure, renal failure, or respiratory distress. Specific treatment depends on thePlasmodium species and on antimalarial resistance.
Intestinal nematode, or roundworm, infections such as Ascaris lumbricoides (roundworm), Trichuris trichiura (whipworm), Strongyloides stercoralis, and hook-worm can cause serious health problems, most notably malnutrition and di-minished capacity for work. Hookworm requires a soil phase as a part of itsdevelopment, and infection is from soil transmission. The cause of a soil-transmitted helminth disease is variable, with prevalences as high as69.9% to 100% from a mixture of Ascaris lumbricoides, Trichuris trichiura, andhookworm in natives of endemic regions Hookworm infection can oc-cur easily, as illustrated by a case when a traveler merely visited a beach inThailand .
Most individuals remain asymptomatic but can exhibit iron deficiency ane- mia, hypoalbuminemia, and eosinophilia. Delays in appearance of stool ovacan make diagnosis of acute hookworm infection difficult, and resistance to em-piric treatment with ivermectin can make initial treatment a challenge Di-agnosis is made by detection of eggs or larvae in stool. Treatment is withalbendazole or mebendazole.
Strongyloidiasis is caused by the nematode parasite Strongyloides stercoralis.
Transmission may be from person to person or from contact with soil. Auto-infection can also be a prominent feature of the Strongyloides lifecycle . Stron-gyloidiasis among East African and Cambodian immigrants to Australia is 11%and 42%, respectively . In children living in Papua New Guinea, Strongy-loides infects 40% in the youngest age group Infection with Strongyloides may be asymptomatic but can progress to dissem- inated infection or fatal hyperinfection. Symptoms can involve the gastrointes-tinal system and pulmonary system, or can disseminate to other organ systems.
Pulmonary Strongyloides infection can lead to a refractory bronchial asthma,cause an acute eosinophilic pneumonia, or can be fulminant and fatal. Arthritismay be associated with Strongyloides infection, causing painful, swollen joints.
Treatment with nonsteroidal anti-inflammatory drugs can be effective for thesymptoms, but corticosteroids can induce a life-threatening Strongyloides hyper-infection syndrome, and antihelminth therapy should be given first Strongyloidiasis can affect athletes traveling to tropical and subtropical re- gions. Eosinophilia raises suspicion, and diagnosis can be made by detectingeggs or larvae in stool, sputum, pleural fluid, or tissue and confirmed with se-rologic testing . Even with laboratory testing, diagnosis can be elusive withStrongyloides. In a study of people who have microscopically proven Strongyloidesinfection, only 73% of travelers had a positive serology compared with 98% ofimmigrants from endemic countries. There was no difference with eosinophilia,with 81% in both groups When established, strongyloidiasis should betreated with ivermectin or albendazole. Local deworming projects in less devel-oped countries have had mixed results, with developing resistance and diffi-culty with sustainability of the projects making it likely that helminth risk totraveling athletes will remain Travelers to the tropics can develop cutaneous manifestations that can easily be misdiagnosed. Hookworm can manifest as cutaneous larva migrans (CLM),acquired by skin contact with the soil. Case reports show CLM after a beachvacation to Thailand . Itchy, sleep-disrupting papules typically affect thefeet and buttocks and develop into linear or serpiginous red streaks. Larva cur-rens from Strongyloides stercoralis can present as an intensely itching wheal in a ser-piginous line that progresses 5 to 15 cm/h Myiasis, whereby larvaeinvasively feed on living tissue, is traditionally considered a low risk in trav-elers to tropical areas. Adventure athletes and travelers to the tropics, however,have a higher risk of screwworm infestation with increased exposureand the physical duress of competition.
Other parasitic infections to consider in the returning traveling athlete in- clude infections with other protozoa such as Leishmania, extraintestinal nema-todes such as Filaria, cestodes (flat worms), trematodes (flukes) such asSchistosoma, and ectoparasites such as lice and scabies. Athletes who travel totropical and subtropical regions of the world must use preventive measures,and practitioners who care for these athletes at home should be aware of thepossibility of parasitic infection and use appropriate diagnostics and treatments.
MARINE INFECTIONSAlthough folklore commonly considers seawater an antiseptic, in reality, sea-water contains many potential pathogens including Escherichia coli, Pseudomonasaeruginosa, Mycobacterium marinum, Staphylococcus aureus, Streptococcus species, Clos-tridium species, and Vibrio species Thus, even small lacerations and abra-sions are at risk for atypical skin infections that have a tendency to berefractory to standard antimicrobial treatment Marine infections are also common after marine envenomation or fish bites.
Many marine fish spines, including those of surgeonfish and stingrays, havespines that break off during the defensive ‘‘attack’’ and result in contaminationof the wound with not only a neurotoxic venom but also fragments of thespine, mucus coating, and pieces of the sheath Coral reef scrapes arealso often contaminated with foreign material, various microbes, and toxinsfrom multiple sources . These contaminates lead to a high rate of sec-ondary bacterial infection and delayed healing.
All marine-related wounds should be vigorously irrigated and debrided, if necessary. Antibiotics are not usually needed for new and minor wounds un-less the victim has an impaired immune system Because of the relativelyhigh prevalence of atypical pathogens, any significant wound or any nonheal-ing wound should be cultured before starting antibiotics. In general, ciproflox-acin and trimethoprim-sulfamethoxazole are the best antibiotics for empiriccoverage of marine bacteria . Alternative antibiotics include tetracyclineand doxycycline. Athletes should be warned about the potential photosensitiz-ing effect of these antibiotics and instructed to take appropriate precautions tolimit ultraviolet radiation exposure. Because of the limited access to treatment,athletes participating in multiday adventure races often present for treatment INFECTIOUS DISEASE AND THE EXTREME SPORT ATHLETE a considerable time after suffering the injury. For these athletes, delayed woundclosure should be considered. Although delayed wound closure often leads toa poorer cosmetic result; it is associated with improved wound healing and de-creased risk of infection Another situation in which delayed wound clo-sure should be considered is in the case of a large wound that has beenimmersed in seawater. In these wounds, early suturing often leads to delayedhealing; thus, strong consideration should be given to delayed wound closureunless suturing is needed to protect vital underlying structures . All athleteswho have marine wounds need to have an up-to-date tetanus booster becauseof the high risk of associated Clostridium infection.
Many marine wounds (eg, stingray, jellyfish, coral) are accompanied by en- venomation. Mild envenomation results predominantly in skin irritation. Se-vere envenomation may lead to neurologic, respiratory, cardiovascular,musculoskeletal, renal, and gastrointestinal complications or even failure Some of the more severe poisons such as the box-jellyfish and stonefishhave commercially available antivenom. In general, avoid using freshwater torinse off any hydroid (eg, jellyfish) fragments to prevent further nematocyst dis-charge. Instead, most wilderness medicine authors recommend using a solutioncomposed of 50% acetic acid (5% concentration) and 50% isopropyl alcohol(40%–70% concentration) or seawater . Some toxins (eg, stingray) areheat labile, and soaking the wound in nonscalding hot water (up to 45C/113F) for 30 to 90 minutes may provide some relief. Because systemic symp-toms may have a delayed onset of several hours, all athletes who have marineenvenomation should be carefully observed for an extended period FRESHWATER-BORNE DISEASESFreshwater can also harbor sources of infectious disease for athletes. Athletesoften come in contact with water during training and competition, but manydo not realize that the development of the host country, the season, and theduration of exposure put them at significant risk for water-borne diseases .
Some of the more common water-borne disease threats come from Giardia,Cryptosporidium, and Schistosoma species.
Giardia lamblia (also known as Giardia intestinalis and Giardia duodenalis) is a common protozoan parasite that can be found throughout the worldbut has a higher incidence in the summer and autumn and in develop-ing countries located in temperate climates . It is one of the most com-mon causes of chronic diarrhea Usually spread by way of the fecal-oralroute, the pathogenic mechanism of Giardia is believed to be by adherence tothe small intestine mucosa through ingestion of cysts in drinking water,food, or recreational surface water or by close person-to-person contact Giardia infection can be caused by exposure to as few as 10 to 25 cystsand has an incubation period ranging from 3 to 40 days, with transmission pos-sible for up to 6 months . While 25% to 30% of infected persons are asymp-tomatic, symptoms commonly include abdominal cramps, foul-smelling andgreasy stools, flatulence, bloating, nausea, excessive tiredness, anorexia, and weight loss. Unlike many waterborne diseases, eosinophilia and urticaria arenot common findings Definitive diagnosis is traditionally made by exam-ination of stool for ova and parasite by trichrome iodine staining or by directimmunofluorescence; however, enzyme-linked immunosorbent assay (ELISA)testing is becoming the preferred method . Metronidazole is the treatmentof choice, with albendazole as a second line for resistant cases Symptomsof mild to moderate diarrhea can also be improved with the use of loperamideor bismuth preparations The cornerstone of prevention, as with any fecal-oral infection, is diligent hand washing and not ingesting anything that has notbeen fully cooked or peeled.
Cryptosporidium parvum is another protozoan parasite that is a cause of water- borne disease worldwide Like Giardia, it is more common in developingcountries, but because of its resistance to eradication by chlorine and other pu-rification techniques, there continue to be many outbreaks even in industrial-ized countries Spread by the fecal-oral route, Cryptosporidium infectionis often a cause of persistent diarrhea . Although the pathogenic mechanismis unknown, Cryptosporidium is thought to infect the small bowel preferentially. There are two genotypes of Cryptosporidium: genotype 1, which causesinfection in humans; and genotype 2, which causes infection in animals Different phenotypes have also recently been demonstrated that affect the se-verity of symptoms and, therefore, it may take as little as 10 oocysts or asmany as 1000 to cause symptomatic disease . Infection is through inges-tion of cysts in drinking water, food, or recreational surface water or by closeperson-to-person contact. Symptoms of disease include persistent (>14 days) orchronic (>30 days) watery diarrhea, cramping, abdominal pain, fatigue, nau-sea, vomiting, occasional low-grade fever, dyspepsia, and asthenia . Inthe past, the diagnosis has been confirmed by acid-fast stain of fecal samples,looking for oocysts or monoclonal-direct immunoassay, but due to the low sen-sitivity of these traditional techniques, ELISA testing has become the mainstayof laboratory testing . Treatment for Cryptosporidium infection remains symp-tomatic control with loperamide or bismuth preparations . Some studieshave shown paromomycin and azithromycin to decrease symptoms and para-sitic load, but these medications are not the mainstay of treatment for immuno-competent persons at this time .
Schistosomiasis, caused by a helminth parasite, affects more than 200 million people worldwide and is endemic to sub-Saharan Africa, South America, andSoutheast Asia Three main species cause most of the infections:Schistosoma mansoni and Schistosoma japonicum are responsible for disease affectingthe pulmonary system, gastrointestinal tract, or hepatosplenic tract, whereasSchistosoma haematobium usually affects the urinary tract . Humanscontract the disease by swimming in freshwater infected with Schistosoma cer-caria, which are larvae secreted by the host snail species Biomphalaria glabrataand Biomphalaria straminea The infection course follows three stages.
Stage 1 consists of an itchy maculopapular rash that is caused by the cercariapenetrating the skin after swimming in infested water and resolves in 48 to INFECTIOUS DISEASE AND THE EXTREME SPORT ATHLETE 72 hours Stage 2, acute schistosomiasis, occurs 4 to 6 weeks afterexposure and is characterized by Katayama fever, a manifestation of the im-mune-mediated response to the release of the first set of eggs from the matureschistosomes . Signs and symptoms of Katayama fever are similar toa serum sickness reaction and include fever, malaise, eosinophilia, hepatosple-nomegaly, diarrhea, urticaria, edema, cough, wheezing, arthralgias, headache,abdominal pain, lymphadenopathy, and micro- or macrohematuria .
Stage 3, chronic schistosomiasis, results from granulomatous or fibrotic re-sponses (or both) to further egg deposition. Depending on the infecting speciesand the extent of infection, different manifestations can occur. Chronic infec-tion by Schistosoma mansoni and Schistosoma japonicum can cause pulmonary fibrosisthat can lead to pulmonary hypertension and cor pulmonale, periportal fibro-sis, portal hypertension, and portosystemic anastamoses In rarecases, central nervous system involvement occurs, with infection of the spinalcord and brain with passage of eggs through the paravertebral venous plexusChronic Schistosoma haematobium infection can cause urinary granulomas,obstructive uropathy, hydronephrosis, and calcified fibrotic bladder or ureter(or both) .
Diagnosis of acute schistosomiasis is usually made by correlating the typical signs, symptoms, and exposure history to water in an endemic area and con-firmed by eosinophilia and schistosome eggs found in stool or urine. Diagnosis of chronic schistosomiasis is usually made by antibodydetection by ELISA, indirect hemagglutination, and the circuoval precipitintest Often, exposed travelers will remain asymptomatic, and diagnosis ismade years later by CT of the head, chest, or abdomen or by cystoscopy. The mainstay of treatment for schistosomiasis is praziquantel; however, praziquantel is only effective against the adult schisto-some. Therefore, repetitive treatment courses may be necessary to prevent re-occurrance . Recently, there have been reported cases of resistance topraziquantel. Therefore, close monitoring and documentation of clearance ofdisease is necessary . Recent research has shown that application of deet be-fore swimming in endemic areas can reduce the risk of contraction of disease TICK-BORNE DISEASESTick-borne diseases potentially pose a threat to athletes who participate in out-door activities. Ticks can be found throughout the United States, and the diag-nosis of tick-borne diseases should be based on the history, clinicalpresentation, and known epidemiology of the disease. Coinfections are rela-tively common, with babesiosis occurring in 23% and ehrlichiosis occurringin up to 30% of patients who have Lyme disease Prophylaxis aftera tick bite is generally not recommended, but treatment of suspected diseaseshould not be delayed for laboratory diagnosis in all cases.
Ticks generally require 24 to 48 hours of attachment to transmit disease; they should therefore be removed from the skin as soon as possible. The best way to remove a tick is by grasping the tick as close to the skin as possiblewith tweezers or a hand and gently pulling with straight traction. Avoid squeez-ing the body during tick removal because this theoretically may cause the tickto regurgitate its stomach contents, thereby increasing the risk of disease. Avoidtwisting the tick because this may result in the breaking off of mouthparts. Donot apply anything such as petroleum jelly, gasoline, or heat to the tick becausenone of these methods have proved effective in detaching the tick and may in-crease the risk of disease transmission. After tick removal, monitor the attach-ment sites for any signs of infection .
Prevention is best accomplished by applying a deet-containing repellent be- fore outdoor activities. Other helpful measures include wearing long-sleevedand long-legged clothing and body examination after being in the outdoors.
Although there have been no specific reports of outbreaks of tick-borne dis- ease during athletic events, athletes have similar risks to others participating inoutdoor activities in endemic areas. Return-to-play decisions should be basedon the same factors one would use for other illnesses. Because many tick-bornediseases present with an influenza-like syndrome, absence of fever and resolu-tion of malaise and fatigue are the main criteria for return to activity.
Lyme disease is the most common vector-borne infectious disease in the United States . It can be found throughout the United States, but ismost commonly reported in endemic areas: the coastal Northeast and partsof the upper Midwest. Borrelia burgdorferi is the spirochete that causes the infec-tion. There are typically three stages of Lyme disease. Stage 1, early localized,occurs 7 to 10 days after a tick bite. Three fourths of patients develop the char-acteristic rash, erythema migrans, at the site of the tick bite. The rash is an an-nular macule or papule with central clearing. Infected persons commonlyexperience influenza-like symptoms with low-grade fevers, fatigue, arthralgias,headaches, cough, and lymphadenopathy. Symptoms of stage 2, early dissem-inated, include secondary skin lesions, adenopathy, and central nervous systemsymptoms. These symptoms typically occur within a few weeks of the initialinfection. Stage 3, late chronic disease, may present with arthritis, dermatitis,keratitis, Bell’s palsy, meningoencephalitis, and myocardial abnormalities.
It is important to recognize endemic versus nonendemic areas when diagnos- ing Lyme disease. Patients from endemic areas who present with erythema mi-grans should be treated, and no laboratory testing is required. For patients innonendemic areas who have unclear symptoms, ELISA testing can be usedwith reasonable sensitivity (89%) but relatively poor specificity (72%). PositiveELISA test should be confirmed with Western blot testing. Routine testing isnot recommended after a tick bite The overall risk of infection after a tick bite is very low and almost never occurs unless the tick has been attached at least 36 hours. This is true evenfor endemic areas. Prophylaxis with one 200-mg dose of doxycycline is effec-tive but not routinely recommended. Patients who sustain a tick bite should INFECTIOUS DISEASE AND THE EXTREME SPORT ATHLETE be monitored for up to 30 days post bite For those who develop symp-toms, antibiotic treatment is curative in most cases. Two to 3 weeks of treat-ment with doxycycline (100 mg twice per day) or amoxicillin (500 mg threetimes per day) is generally effective for adults. Patients who have severe orlate disease may require hospitalization and intravenous antibiotics .
Return to play for uncomplicated Lyme disease should be based on resolu- tion of clinical symptoms. Late disease, especially with cardiac complications orarthritis, should be guided by consultation with a specialist and may requireseveral months out of competition.
Rocky Mountain spotted fever (RMSF) is caused by Rickettsia rickettsii and is the most common rickettsial disease in the United States . RMSF is a mis-nomer because this disease is found most commonly in the Atlantic easternstates. RMSF has been reported in all states except Maine, Alaska, and Hawaii.
The highest infection rates are in young children. Most people infected remem-ber having a tick bite, and symptoms generally start 5 to 7 days after inocula-tion. Classic presentation includes an acute onset of fever, chills, and headache,with the onset of a rash in the first few days. Lesions first appear on the palms,soles, wrists, ankles, and forearms and then extend over the trunk, buttock, andface. The rash is initially maculopapular but becomes more petechial as thedisease progresses .
Diagnosis is based primarily on clinical signs and symptoms. Laboratory testing has limited use. Skin biopsy of the rash using immunofluorescent stain-ing is relatively specific but has low sensitivity. Complete blood count is gener-ally normal. Mild elevations in liver enzyme levels and thrombocytopenia aresometimes found Human monocytic ehrlichiosis (HME), caused by Ehrlichia chaffeensis, and hu- man granulocytotropic anaplasmosis (HGA), formerly human granulocyticehrlichiosis, caused by Anaplasma phagocytophilum, are epidemiologically separatebut clinically indistinguishable . HME is generally found in the south-central and southeastern United States, whereas HGA occurs in the upper Mid-west and northeastern United States.
It can be difficult to distinguish between the clinical presentation of ehrlichio- sis and RMSF Signs and symptoms of Ehrlichia infection include an in-fluenza-like syndrome and generally begin 7 days after the tick bite. In additionto fever, chills, malaise, cough, headache, and myalgias, an infected person maydevelop a maculopapular, macular, or petechial rash. This rash differs from therash of RMSF because it rarely (<5%) affects the palms and soles. Laboratoryfindings may include leukopenia, thrombocytopenia, and elevated liverenzymes. Confirmation of the diagnosis of ehrlichiosis may be detected byseroconversion .
Treatment and return to activity after infection with Rickettsia, Ehrlichia, or Anaplasma are similar. Antibiotics should be started as soon as a clinical suspi-cion is raised and should not be delayed for laboratory testing. Doxycycline,100 mg twice a day for adults or 2.2 mg/kg for children, is the first-linedrug. No clear guidelines exist for duration of treatment, but antibiotics should be continue for at least 3 days after fever resolves, usually 5 to 7 days minimum. Chloramphenicol is an alternative treatment, but its use is limited by po-tential toxicity. Return to play after treatment should not be considered untilclinical symptoms resolve.
Babesiosis most often occurs in the northeastern United States and is the only tick-borne disease caused by a protozoan in this country Symptomsinclude fever, sweating, myalgias, and headache. Laboratory findings includehemolytic anemia, hemoglobinuria, and in severe cases, jaundice and renal fail-ure. Peripheral smear will sometimes demonstrate organisms within erythro-cytes. The diagnosis is generally made by blood smears, although serologicand polymerase chain reaction testing is available .
Symptomatic treatment is recommended for mild disease. For patients who have severe symptoms such as persistent high fever and progressive anemia,quinine (650 mg) and clindamycin (600 mg) three times a day for 7 days is rec-ommended. Alternative treatments include atovaquone and azythromycin For mild disease, return to activity may start as symptoms and anemia im-prove. Athletes who have severe cases should be monitored closely and notstart activity until anemia, fevers, and any renal complications have resolved.
ZOONOSESZoonoses are animal diseases that are transmissible to humans. Humans gen-erally acquire the disease through close contact with an infected animal. Routesof transmission include infectious saliva from bite wounds; aerosol from bodyfluids (especially respiratory); scratches; hand-to-mouth transmission of micro-organisms, cysts, or oocysts from infected animal feces; insect bites when theinsect is acting as a reservoir between the animal and humans; and contamina-tion of water or the environment with disease-containing animal urine.
Leptospirosis is a zoonosis with protean manifestations caused by the spiro- chete Leptospira interrogans. Synonyms for the disease include Weil’s disease,swineherd’s disease, rice-field fever, cane-cutter fever, swamp fever, mud fever,hemorrhagic jaundice, Stuttgart disease, and canicola fever. The organism in-fects a variety of mammals, especially rodents, cattle, swine, dogs, horses,sheep, and goats. When infected, animals may shed the organism in their urineintermittently or continuously throughout life . Organisms may remain vi-able for days to months in soil and water, and humans most often become in-fected after exposure to freshwater contaminated by rodent urine . Portalsof entry include cuts or abraded skin, mucous membranes, or conjunctiva. Inthe United States, most cases are reported from the southern and Pacific coastalstates, with Hawaii consistently reporting the most cases. Most clinical cases oc-cur in the tropics , and the incidence of leptospirosis in some endemiccountries appears to be increasing, with Thailand reporting a 30-fold increasebetween 1995 and 2000, possibly due to an increase in the rat population Outbreaks may occur from common-source exposures. Participation in a tri- athlon where the swimming portion was in contaminated freshwater has beenfound to be responsible for outbreaks of leptospirosis. An outbreak occurred in INFECTIOUS DISEASE AND THE EXTREME SPORT ATHLETE 98 of 834 athletes (12%) participating in an Illinois triathlon Another re-cent outbreak among athletes participating in the ‘‘Eco-Challenge Sabah2000’’ competition occurred in Borneo, Malaysia. The athletes presentedwith fever, jaundice, headache, and myalgias after returning home, and 44%of 158 athletes contacted met the case definition Leptospirosis is associated with a variable clinical course. The disease may manifest as a subclinical illness followed by seroconversion, a self-limited sys-temic infection, or a severe, potentially fatal illness accompanied by multiorganfailure. Leptospirosis presents with the abrupt onset of fever, rigors, myalgias,and headache in 75% to 100% of patients. Although leptospirosis has oftenbeen described as a biphasic illness, less than 50% of cases exhibit a biphasiccourse Most cases of leptospirosis are mild to moderate; however, thecourse may be complicated by renal failure, uveitis, hemorrhage, acute respira-tory distress syndrome, myocarditis, and rhabdomyolysis . The clinical fea-tures and routine laboratory findings of leptospirosis are not specific. Theorganism can be cultured, but the diagnosis is more frequently made by sero-logic testing .
Although most Leptospira infections are self-limiting, antimicrobial treatment results in a shorter duration of illness. Doxycycline and penicillin have beenshown to be effective in placebo-controlled trials Parenteral penicillin,doxycycline, and third-generation cephalosporins are acceptable options in hos-pitalized patients, although in areas endemic for leptospirosis and rickettsial in-fection, a regimen other than penicillin should be considered Mortalityrates in hospitalized patients who have leptospirosis have ranged from 4% to52%, with higher mortality rates occurring in patients requiring ICU admissionon presentation . No vaccine is available in the United States for humanimmunization. The major preventive measure is to avoid potential sources ofinfection. Consider prophylaxis with doxycycline (200 mg/wk) for individualssuch as river rafters and swimmers who will be exposed to leptospires in highlyendemic environments Hantaviruses compose a genus of enveloped viruses within the family Bu- nyaviridae. These pathogens are associated with two severe, acute febrile ill-nesses: hemorrhagic fever with renal syndrome (HFRS) in Europe and Asiaand hantavirus cardiopulmonary syndrome, also known as hantavirus pulmo-nary syndrome (HPS), in the Americas.
Each hantavirus is specifically associated with a single species of wild rodent, which serves as its primary natural reservoir. The deer mouse is the primaryvector in the United States The incidence of hantavirus infections in hu-mans fluctuates with rodent densities Hantaviruses are shed in the urine,feces, or saliva of acutely infected reservoir rodents, and transmission to hu-mans generally occurs by way of the aerosol route Athletes who competein outdoor activities in wilderness areas or who camp are at higher risk ofexposure.
HFRS first came to the attention of Western medicine during the Korean War, when febrile illness accompanied by hemorrhage and renal failure developed in 3000 United Nations soldiers . HFRS has a variable incuba-tion period and is characterized by five phases. The initial febrile phase lasts3 to 7 days and is characterized by fever, malaise, headache, abdominalpain, nausea, vomiting, facial flushing, petechiae, and conjunctival hemorrhage.
A hypotensive phase follows, which can lead to shock, blurred vision, andhemorrhagic signs. An oliguric phase lasting 3 to 7 days is followed by a diureticphase lasting days to weeks. The complete convalescence may take weeks tomonths. Mortality resulting from shock, uremia, or multiorgan hypoperfusionoccurs in 1% to 10% . Early treatment with ribavirin may reduce hemor-rhage, renal failure, and mortality in HFRS HPS was discovered in 1993, when a series of cases of unexplained fever and acute respiratory distress syndrome was recognized among members of the Na-vajo tribe at the northern border between New Mexico and Arizona Themortality rate was approximately 80% in the initial patients.
The clinical progression of HPS advances through four sequential stages.
Typically, a period of 3 weeks elapses between exposure to a hantavirus andthe first symptoms . The febrile stage typically lasts 3 to 5 days and ischaracterized by fever, myalgias, and malaise. This stage is difficult to distin-guish from a number of nonspecific viral syndromes. The disease rapidly in-creases in severity, often leading to nausea, vomiting, abdominal pain,weakness, and sometimes diarrhea and headache. Classic features of upper re-spiratory tract infection such as rhinorrhea, pharyngitis, coryza, and ear painare absent in most patients who have hantavirus diseases. The simultaneousappearance of thrombocytopenia, a left-shifted granulocytic series, and an im-munoblast count that exceeds 10% of the total lymphoid series is referred to asthe diagnostic triad . A dry cough often heralds the sudden transition to thecardiopulmonary phase which is characterized by shock and pulmonaryedema . Hypoxia and circulatory compromise often lead to death.
The pulmonary edema clears during the diuretic phase, and fever resolves. Complete recovery generally occurs but can take months . Serologictests are the main method for diagnosis of acute or remote infection byhantaviruses.
Treatment of HPS is supportive. Early recognition, hospitalization, and ade- quate pulmonary and hemodynamic support in an intensive care setting are im-portant. No specific antiviral therapy for HPS is available Given the limitedtreatment options and high mortality rates, emphasis needs to be on avoidanceof exposure to potentially infectious rodents, particularly in indoor spaces.
PREVENTION AND MEDICAL EVENT COVERAGEBecause of the nature of their sports, the use of protective clothing and sleepingareas by extreme athletes is usually limited. Thus, the use of insect repellent isparticularly important. Athletes should be encouraged to avoid untreated waterfor hydration and told to carry water purification tablets in their required firstaid supplies. Because many of the extreme sport events take place in relativelyisolated locations, it is essential that medical coverage planning include INFECTIOUS DISEASE AND THE EXTREME SPORT ATHLETE transportation and evacuation routes. For events in overseas locations, it is rec-ommended that all competitors have insurance that covers evacuation by heli-copter or fixed-wing aircraft because often, operators of medical evacuationservices will refuse to fly until they have proof of payment .
SUMMARYExtreme sport competition often takes place in locations that may harbor atyp-ical diseases. The lack of immediate medical care can complicate and worsenthe severity of these diseases. Physicians caring for extreme sport competitorsmust take a careful travel and exposure history and have a high index of sus-picion for unusual diseases.
[1] Young C. Extreme sports: injuries and medical coverage. Curr Sports Med Rep 2002;1(5): [2] Freedman D, Weld L, Kozarsky P. Spectrum of disease and relation to place of exposure among ill returned travelers. N Engl J Med 2006;354(2):119–30.
[3] Abd El Bagi M, Sammak B, Mohamed A, et al. Gastrointestinal parasite infestation. Eur [4] Edeling W, Verweij J, Ponsioen C, et al. Outbreak of amoebiasis in a Dutch family; tropics unexpectedly nearby. Ned Tijdschr Geneeskd 2004;148(37):1830–4.
[5] Stanley SJ. Amoebiasis. Lancet 2003;361(9362):1025–34.
[6] Kitchen L. Case studies in international travelers. Am Fam Physician 1999;60(2):471–4.
[7] Ryan E, Wilson M, Kain K. Illness after international travel. N Engl J Med 2002;347: [8] Al-Mekhlafi M, Azlin M, Nor Aini U, et al. Prevalence and distribution of soil-transmitted hel- minthiases among Orang Asli children living in peripheral Selangor, Malaysia, SoutheastAsia. J Trop Med Public Health 2006;37(1):40–7.
[9] Malvy D, Ezzedine K, Pistone T, et al. Extensive cutaneous larva migrans with folliculitis mim- icking multimetameric Herpes Zoster presentation in an adult traveler returning from Thai-land. J Travel Med 2006;13(4):244–7.
[10] Lawn S, Grant A, Wright S. Case reports: acute hookworm infection: an unusual cause of profuse watery diarrhoea in returned travelers. Trans R Soc Trop Med Hyg 2003;97(4):414–5.
[11] Vadlamudi R, Chi D, Krishnaswamy G. Intestinal strongyloidiasis and hyperinfection syn- [12] Caruana S, Kelly H, Ngeow J, et al. Undiagnosed and potentially lethal parasite infections among immigrants and refugees in Australia. J Travel Med 2006;13(4):233–4.
[13] Barnish G, Ashford R. Strongyloides cf. Fuelleborni and hookworm in Papua New Guinea: patterns of infection within the community. Trans R Soc Trop Med Hyg 1989;83(5):684–8.
[14] Richter J, Muller-Stover I, Strothmeyer H, et al. Arthritis associated with Strongyloides stercor- alis infection in a HLA B-27-positive African. Parasitol Res 2006;99(6):706–7.
[15] Kuzucu A. Parasitic diseases of the respiratory tract. Curr Opin Pulm Med 2006;12(3): [16] Sudarshi S, Stumpfle R, Armstrong M, et al. Clinical presentation and diagnostic sensitivity of laboratory tests for Strongyloides stercoralis in travelers compared with immigrants ina non-endemic country. Trop Med Int Health 2003;8(8):728–32.
[17] Bethony J, Brooker S, Albonico M. Soil-transmitted helminth infections: ascariasis, trichuria- sis, and hookworm. Lancet 2006;367(9521):1521–32.
[18] Wolf R, Marcos B, Orion E, et al. Widespread pruritic papulopustules after returning from Thailand. Am Fam Physician 2005;72(11):2313–4.
[19] Seppanen M, Virolainen-Julkunen A, Kakko I, et al. Myiasis during adventure sports race.
Emerg Infect Dis 2004;10(1):137–9.
[20] Siraj D, Luczkovich J. Nodular skin lesion in a returning traveler. J Travel Med 2005;12(4): [21] Zoltan T, Taylor K. Health issues for surfers. Am Fam Physician 2005;71(12):2313–7.
[22] Auerbach P, Halstead B. Injuries from nonvenomous aquatic animals. In: Auerbach P, editor.
Wilderness medicine. 4th edition. St. Louis (MO): Mosby; 2001. p. 1418–49.
[23] Auerbach P. Envenomation by aquatic vertebrates. In: Auerbach P, editor. Wilderness med- icine. 4th edition. St. Louis (MO): Mosby; 2001. p. 1488–506.
[24] Auerbach P. Envenomation by aquatic invertebrates. In: Auerbach P, editor. Wilderness medicine. 4th edition. St. Louis (MO): Mosby; 2001. p. 1450–87.
[25] Auerbach P. A medical guide to hazardous marine life. 3rd edition. Flagstaff (AZ): Dive Alert [26] Ekdahl K, Anderson Y. Imported giardiasis: impact of international travel, immigration, and adoption. Am J Tropical Med 2005;72(6):825–30.
[27] Okhuysen P. Traveler’s diarrhea due to intestinal protoza. Clin Infect Dis 2001;33:110–4.
[28] Gascon J. Epidemiology, etiology and pathophysiology of traveler’s diarrhea. Digestion [29] Mathieu E, Levy D, Veverka F, et al. Epidemiologic and environmental investigation of a rec- reational water outbreak caused by two genotypes of Cryptosporidium parvum in Ohio in2000. Am J Tropical Med 2004;71(5):582–9.
[30] Aldo A. Tropical diarrhoea: new developments in traveller’s diarrhoea. Curr Opin Infect Dis [31] Corachan M. Schistosomiasis and international travel. Clin Infect Dis 2001;35:446–50.
[32] Moore E, Doherty J. Schistosomiasis among travellers returning from Malawi: a common [33] Nguyen L, Estrella J, Jett E, et al. Acute schistosomiasis in nonimmune travelers: chest CT find- ings in 10 patients. AJR Am J Roentgenol 2006;186:1300–3.
[34] Salanitri J, Stanley P, Hennessy O. Acute pulmonary schistosomiasis. Australas Radiol [35] Enk M, Caldeira R, Carvalho O, et al. Rural tourism as risk factors for the transmission of schistosomiasis in Minas Gerais, Brazil. Scielo Brazil 2004;99(1):105–8.
[36] Silva IM, Thiengo R, Conceicao MJ, et al. Cystoscopy in the diagnosis and follow-up of urinary schistosomiasis in Brazilian soldiers returning from Mozambique. Africa Rev InstMed Trop S Paulo 2006;48(1):39–42.
[37] Jackson F, Doherty J, Beherns R. Schistosomiasis prophylaxis in vivo using N,N-diethyl-m- toluamide (DEET). Trans R Soc Trop Med 2003;97(4):449–50.
[38] Chapman A, Bakken J, Folk S, et al. Diagnosis and management of tick-borne rickettsial dis- eases: Rocky Mountain spotted fever, ehrlichiosis, and anaplasmosis—United States: a prac-tical guide for physicians and other health-care and public health professionals. MMWRRecomm Rep 2006;55(RR-4):1–27.
[39] Gammons M, Salam G. Tick removal. Am Fam Physician 2002;66:643–5.
[40] Wilson M. Prevention of tick-borne diseases. Med Clin North Am 2002;86:219–38.
[41] Wormser G. Early Lyme disease. N Engl J Med 2006;354:2794–801.
[42] Wormser G, Nadelman R, Dattwyler R, et al. Practice guidelines for the treatment of Lyme disease. Clin Infect Dis 2000;31(Suppl 1):S1–14.
[43] Bratton R, Corey G. Tick-borne disease. Am Fam Physician 2005;71:2323–30.
[44] Homer M, Aguilar-Delfin I, Telford S, et al. Babesiosis. Clin Microbial Rev 2000;13: [45] Acha P, Szyfres B. Leptospirosis. Zoonoses and communicable disease common to man and animals. Washington, DC: 3rd Pan American Health Organization; 2001. p. 157.
[46] Kaufmann A, Weyant R. Leptospiraceae. Manual of clinical microbiology. 6th edition.
Washington, DC: ASM Press; 1995. p. 621.
INFECTIOUS DISEASE AND THE EXTREME SPORT ATHLETE [47] Bertherat E, Renaut A, Nabias R, et al. Leptospirosis and Ebola virus infection in five gold- panning villages in northeastern Gabon. Am J Trop Med Hyg 1999;60:610–5.
[48] Bovet P, Yersin C, Merien F, et al. Factors associated with clinical leptospirosis: a population- based case-control study in the Seychelles (Indian Ocean). Int J Epidemiol 1999;28:583–90.
[49] Sejvar J, Tangkanakul W, Ratanasang P, et al. An outbreak of leptospirosis, Thailand—the importance of the laboratory. Southeast Asian J Trop Med Public Health 2005;36:289–95.
[50] Morgan J, Bornstein S, Karpati A, et al. Outbreak of leptospirosis among triathlon partici- pants and community residents in Springfield, Illinois, 1998. Clin Infect Dis 2002;34(12):1593–9.
[51] Centers for Disease Control and Prevention. Update: outbreak of acute febrile illness among athletes participating in Eco-Challenge-Sabah 2000—Borneo, Malaysia, 2000. MMWR2000;49(36):816–7.
[52] Katz A, Ansdell V, Effler P, et al. Assessment of the clinical presentation and treatment of 353 cases of laboratory-confirmed leptospirosis in Hawaii, 1974–1998. Clin Infect Dis2001;33(11):1834–41.
[53] Levett P. Usefulness of serologic analysis as a predictor of the infecting serovar in patients with severe leptospirosis. Clin Infect Dis 2003;35(4):447–52.
[54] McClain J, Ballou W, Harrison S, et al. Doxycycline therapy for leptospirosis. Ann Intern [55] Suputtamongkol Y, Niwattayakul K, Suttinont C, et al. An open, randomized, controlled trial of penicillin, doxycycline, and cefotaxime for patients with severe leptospirosis. Clin InfectDis 2004;39(10):1417–24.
[56] Stefos A, Georgiadou S, Gioti C, et al. Leptospirosis and pancytopenia: two case reports and review of the literature. J Infect 2005;51(5):e277–80.
[57] Takafuji E, Kirkpatrick J, Miller R, et al. An efficacy trial of doxycycline chemoprophylaxis against leptospirosis. N Engl J Med 1984;310(8):497–500.
[58] Glass G. Hantaviruses. Curr Opin Infect Dis 1997;10:362.
[59] Hjelle B, Glass G. Outbreak of hantavirus infection in the Four Corners region of the United States in the wake of the 1997-1998 El Nino-southern oscillation. J Infect Dis 2000;181(5):1569–73.
[60] Schmaljohn C, Hjelle B. Hantaviruses: a global disease problem. Emerg Infect Dis [61] Sheedy J, Froeb H, Batson H, et al. The clinical course of epidemic hemorrhagic fever. Am J [62] Peters C, Khan A. Hantavirus pulmonary syndrome: the new American hemorrhagic fever.
Clin Infect Dis 2002;34(9):1224–31.
[63] Centers for Disease Control and Prevention. Infectious diseases update: outbreak, hantavi- rus infection—southwestern United States, 1993. JAMA 1993;270(3):306.
[64] Leduc J, Smith G, Johnson K. Hantaan-like viruses from domestic rats captured in the United States. Am J Trop Med Hyg 1984;33(5):992–8.
[65] Lee P, Goldgaber D, Gibbs CJ, et al. Other serotypes of hemorrhagic fever with renal syndrome viruses in Europe. Lancet 1982;2(8312):1405–6.
[66] Jenison S, Hjelle B, Simpson S, et al. Hantavirus pulmonary syndrome: clinical, diagnostic and virologic aspects. Semin Respir Infect 1995;10(4):259–69.
[67] Nichol S, Spirpoulou C, Morzunov S, et al. Genetic identification of a hantavirus associated with an outbreak of acute respiratory illness. Science 1993;262(5135):914–7.
[68] Duchin J, Koster F, Peters C, et al. Hantavirus pulmonary syndrome: a clinical description of 17 patients with a newly recognized disease. The Hantavirus Study Group. N Engl J Med1994;330(14):949–55.
[69] Mark B. Off the beaten path: rollover in the Namib desert. J Wilderness Med 2006;23(3):


Tecflow lithium grease + ptfe

Veiligheidsinformatieblad volgens 1907/2006/EEG Artikel 31 1 Identificatie van de stof of het preparaat en van de onderneming · Informatie over het produkt · Handelsnaam: Tecflow Lithiumgrease 400ml · Artikelnummer: 788849 · Toepassing van de stof / van de bereiding Smeermiddel · Fabrikant/leverancier: Tel:+31(0)251-225005 Fax:+31(0)251-272644· Inlichtingengevende s

SURGERY HOURS GRANGETOWN OUT OF HOURS SERVICE Our surgery is closed between 6pm and 9am, but you can still receive advice or information. Please telephone NHS Direct on 0845 4647. For urgent medical care please telephone 0845 603 3131. Middlesbrough Primary Care Trust is commissioning our out of hours service and can also be contacted on www.nhsdirect.nhs.ukDetails of all pri

Copyright © 2010-2014 Drugstore Pdf Search