2013 multistate outbreaks of Cyclospora cayetanensis infections associated with fresh produce: focus on the Texas investigations.

The 2013 multistate outbreaks contributed to the largest annual number of reported US cases of cyclosporiasis since 1997. In this paper we focus on investigations in Texas. We defined an outbreak-associated case as laboratory-confirmed cyclosporiasis in a person with illness onset between 1 June and 31 August 2013, with no history of international travel in the previous 14 days. Epidemiological, environmental, and traceback investigations were conducted. Of the 631 cases reported in the multistate outbreaks, Texas reported the greatest number of cases, 270 (43%). More than 70 clusters were identified in Texas, four of which were further investigated. One restaurant-associated cluster of 25 case-patients was selected for a case-control study. Consumption of cilantro was most strongly associated with illness on meal date-matched analysis (matched odds ratio 19·8, 95% confidence interval 4·0-∞). All case-patients in the other three clusters investigated also ate cilantro. Traceback investigations converged on three suppliers in Puebla, Mexico. Cilantro was the vehicle of infection in the four clusters investigated; the temporal association of these clusters with the large overall increase in cyclosporiasis cases in Texas suggests cilantro was the vehicle of infection for many other cases. However, the paucity of epidemiological and traceback information does not allow for a conclusive determination; moreover, molecular epidemiological tools for cyclosporiasis that could provide more definitive linkage between case clusters are needed.

Donor-derived Trypanosoma cruzi infection in solid organ recipients in the United States, 2001-2011.

Although Trypanosoma cruzi, the parasite that causes Chagas disease, can be transmitted via organ transplantation, liver and kidney transplantation from infected donors may be feasible. We describe the outcomes of 32 transplant recipients who received organs from 14 T. cruzi seropositive donors in the United States from 2001 to 2011. Transmission was confirmed in 9 recipients from 6 donors, including 3 of 4 (75%) heart transplant recipients, 2 of 10 (20%) liver recipients and 2 of 15 (13%) kidney recipients. Recommended monitoring posttransplant consisted of regular testing by PCR, hemoculture, and serology. Thirteen recipients had no or incomplete monitoring; transmission was confirmed in five of these recipients. Four of the five recipients had symptomatic disease and all four died although death was directly related to Chagas disease in only one. Nineteen recipients had partial or complete monitoring for T. cruzi infection with weekly testing by PCR, hemoculture and serology; transmission was confirmed in 4 of 19 recipients with no cases of symptomatic disease. Our results suggest that liver and kidney transplantation from T. cruzi seropositive donors may be feasible when the recommended monitoring schedule for T. cruzi infection is followed and prompt therapy with benznidazole can be administered.

Transmission of Babesia microti by blood transfusion in Texas.

In the USA, seasonal tickborne transmission of Babesia microti occurs in the Northeast and upper Midwest. A resident of Texas became infected through a red blood cell transfusion from an asymptomatic local donor who had summered in Massachusetts. The patient's infection was diagnosed by blood smear examination in January, 7 weeks post-transfusion. He died 1 week later from variceal haemorrhage complicated by haemolysis. Premortem patient specimens and archived blood from the donor unit tested positive for B. microti antibodies and DNA. Babesiosis should be included in the differential diagnosis of post-transfusion haemolytic anaemia or thrombocytopenia, regardless of the geographical region or season.

Accumulation of chloroquine by membrane preparations from Plasmodium falciparum.

Chloroquine susceptibility and resistance have been associated respectively with the uptake and efflux of chloroquine by Plasmodium falciparum. We made membrane preparations from parasitized and unparasitized red cells in order to study chloroquine accumulation in a cell-free system. The accumulation of [3H]chloroquine by these preparations is inhibited by unlabeled chloroquine and thus is specific. Only membranes from parasitized red cells demonstrate time-dependent chloroquine accumulation; membranes from unparasitized red cells do not. Chloroquine accumulation is eliminated by detergent (0.05% Triton X-100) and reduced by a hypertonic medium, consistent with accumulation inside membrane vesicles rather than binding to membranes. Accumulation is energy dependent; it has a specific requirement for ATP, which cannot be replaced with GTP, CTP, UTP, TTP or ADP, an apparent Km of 21 microM and an apparent Vmax of 4.6 pmol (mg protein)-1 h-1. Vesicle acidification is MgATP dependent, and is reversed by NH4Cl. Chloroquine accumulation is inhibited by reduced medium pH, N-ethylmaleimide or oligomycin, but not by vanadate or ouabain. These studies demonstrate that membrane vesicles prepared from parasitized red cells provide a model system for the study of chloroquine accumulation by P. falciparum.

Energy dependence of chloroquine accumulation and chloroquine efflux in Plasmodium falciparum.

Chloroquine inhibits the growth of susceptible malaria parasites at low (nanomolar) concentrations because of an energy-requiring drug-concentrating mechanism in the parasite secondary lysosome (food vacuole) which is dependent on the acidification of that vesicle. Chloroquine resistance results from another energy-requiring process: efflux of chloroquine from the resistant parasite with a half-time of 2 min. Chloroquine efflux is inhibited reversibly by the removal of metabolizable substrate (glucose); it is also reduced by the ATPase inhibitor vanadate. These results suggest that chloroquine efflux is an energy-requiring process dependent on the generation and hydrolysis of ATP. Chloroquine efflux cannot be explained by differences in drug accumulation between chloroquine-susceptible and -resistant parasites because the 40-50-fold difference in initial efflux rates between -susceptible and -resistant parasites is unchanged when both parasites contain the same amount of chloroquine. Although chloroquine efflux is phenotypically similar to the efflux of anticancer drugs from multidrug-resistant (mdr) mammalian cells, it is not linked to either of the mdr-like genes of the parasite.

Cyclospora.

Although Cyclospora infection has been documented in humans worldwide since at least 1977, it is only in the past 2 years that this organism has come into prominence as a result of major foodborne outbreaks in the United States and Canada. Cyclospora causes significant gastrointestinal disease in immunocompetent and immunocompromised hosts and can be successfully treated with trimethoprim-sulfamethoxazole. The infection is under-recognized because our methods for diagnosis are rudimentary and insensitive. The mechanisms by which the parasite causes disease, the range of animal hosts, and the natural reservoir are unknown. Cyclospora is a unique coccidian parasite that has just begun to emerge; as yet, we have no clue as to where it comes from or where it hides.

Laboratory-acquired malaria, leishmaniasis, trypanosomiasis, and toxoplasmosis.

Because of renewed interest in parasitic diseases, increasing numbers of persons in clinical and research laboratories have the potential for exposure to parasites and therefore are at risk for acquiring parasitic infections. In this review of laboratory-acquired parasitic infections, we concentrate on protozoan diseases that frequently have been reported to be laboratory acquired: malaria, leishmaniasis, trypanosomiasis (American and African), and toxoplasmosis. These diseases can be severe, even fatal, and may be difficult to diagnose. Many laboratorians who have acquired these diseases did not recall having had an accident. Of those with recognized accidents, needlestick injuries were the most common. Laboratories should have established protocols for handling specimens that may contain viable organisms and for responding to laboratory accidents.

Recommendations for treating leishmaniasis with sodium stibogluconate (Pentostam) and review of pertinent clinical studies.

Pentavalent antimonial compounds have been the mainstay of the treatment of visceral, cutaneous, and mucosal leishmaniasis for approximately half a century. Pentostam (sodium stibogluconate) is the pentavalent antimonial compound available in the United States (through the Centers for Disease Control). As dosage regimens for treating leishmaniasis have evolved, the daily dose of antimony and the duration of therapy have been progressively increased to combat unresponsiveness to therapy. In the 1980s, the use of 20 mg/kg/day (instead of 10 mg/kg/day) of antimony was recommended, but only to a maximum daily dose of 850 mg. The authors have concluded on the basis of recent efficacy and toxicity data that this 850-mg restriction should be removed; the evidence to date, which is summarized here, suggests that a regimen of 20 mg/kg/day of pentavalent antimony, without an upper limit on the daily dose, is more efficacious and is not substantially more toxic than regimens with lower daily doses. We recommend treating all forms of leishmaniasis with a full 20 mg/kg/day of pentavalent antimony. We treat cutaneous leishmaniasis for 20 days and visceral and mucosal leishmaniasis for 28 days. Our judgment of cure is based on clinical criteria.

Babesiosis in Wisconsin: a potentially fatal disease.

Babesiosis is emerging as an important tick-borne zoonosis in the United States. Most reported cases of this parasitic disease have been acquired in the Northeast. To date, only two clinical cases of Babesia microti infection acquired in the upper Midwest have been described. We report eight more cases. Most if not all of the 10 total cases probably were acquired in northwestern Wisconsin. Three cases (30% of 10) we now report were fatal and occurred in elderly patients (65-75 years old) who died after complicated hospital courses. One patient probably had had a latent Babesia infection that activated because of immunosuppression attributable to high-dose corticosteroid therapy and to splenic infarctions caused by cholesterol emboli. All three fatal cases were diagnosed incidentally and highlight the importance of considering the diagnosis of babesiosis in febrile patients who have been in babesiosis-endemic areas; examining their blood smears carefully; and treating promptly with clindamycin and quinine, and, if indicated, exchange transfusion. Medical personnel should be knowledgeable about this zoonosis, which is not limited to the northeastern United States, and is potentially serious, sometimes fatal.

An outbreak of cyclosporiasis in Florida in 1995: a harbinger of multistate outbreaks in 1996 and 1997.

Before 1995, only one outbreak of cyclosporiasis had been reported in the United States. To identify risk factors for Cyclospora infection acquired in Florida in 1995, we conducted a matched case-control study (24 sporadic cases and 69 controls) and retrospective cohort studies of clusters of cases associated with two May social events (attack rates = 15.4% [8 of 52] and 54.5% [6 of 11]). In univariate analysis of data from the case-control study, consumption of fresh raspberries (odds ratio [OR] = 6.0, 95% confidence interval [CI] = 1.1-31.7) and bare-handed contact with soil (OR = 5.4, 95% CI = 1.4-20.7) were associated with infection; soil contact was also implicated in multivariate analysis. For the events, mixed-fruit items that had only fresh raspberries and strawberries in common had elevated relative risks (3.7 and 4.2), but the confidence intervals overlapped 1.0. The raspberries eaten at the events and by sporadic case-patients were imported. Given the cumulative evidence of the three studies and the occurrence in 1996 and 1997 of outbreaks in North America associated with consumption of Guatemalan raspberries, food-borne transmission of Cyclospora was likely in 1995 in Florida as well.

An outbreak of cyclosporiasis in 1996 associated with consumption of fresh berries- Ontario.

BACKGROUND: A large foodborne outbreak of cyclosporiasis occurred in North America in 1996. An index cluster of cases associated with a catered event on May 11, 1996, in Ontario sparked the recognition of this outbreak in Canada. OBJECTIVES: To describe the Ontario experience with the North American outbreak of cyclosporiasis in 1996. PATIENTS AND METHODS: Public health units investigated the index and subsequent event-associated clusters. Investigations included retrospective cohort studies of clusters, traceback of suspect foods and a case-control study of sporadic cases. These activities, coordinated with those in the United States, were part of an international investigation. RESULTS: In Ontario, 232 cases of cyclosporiasis (20 laboratory-confirmed and 72 clinically defined cases associated with seven events plus 140 additional laboratory-confirmed sporadic cases) were identified between May 1 and July 30, 1996. For the index cluster, a strawberry flan with raspberries and blueberries was the only significant exposure (relative risk 2.16, P=0.02). Fresh berries were served at all seven events associated with clusters of cases. Raspberries were definitely served at three events, possibly served at three events, and not served at one event. Only imported berries were available in Ontario in May 1996, when initial clusters and sporadic cases were identified. The raspberries served at the two events with well documented traceback data came from Guatemala. Univariate analyses of the matched case-control study demonstrated that illness was associated with consumption of raspberries (matched odds ratio 21.0, 95% CI 3.48 to 448) and strawberries (matched odds ratio 28.5, 95% CI 4.02 to 478). Further evidence amassed by the international investigation compellingly implicated Guatemalan raspberries as the vehicle of the outbreak. CONCLUSION: Cyclosporiasis may be acquired domestically from the consumption of contaminated produce. The scope and vehicle of this international foodborne outbreak were recognized through a coordinated public health response.

A foodborne outbreak of cyclosporiasis caused by imported raspberries.

BACKGROUND: Cyclospora cayetanensis is a recently recognized parasite that causes prolonged diarrheal illness. Its modes of transmission have not been fully determined, although some investigations before 1996 implicated water. Outbreaks of cyclosporiasis in the United States in 1996 and 1997 are evidence of the increasing incidence of this disease. This report describes an outbreak of cyclosporiasis in persons who attended a luncheon on May 23, 1996, near Charleston, South Carolina. METHODS: In this retrospective cohort study, we interviewed all 64 luncheon attendees and the chef regarding food and beverage exposures. A case of cyclosporiasis was defined as diarrhea (> or = 3 loose stools per day or > or = 2 loose stools per day if using antimotility drugs) after attending the luncheon. We identified sporadic cases of cyclosporiasis and traced the implicated food. RESULTS: Of 64 luncheon attendees, 38 (59%) met the case definition. Persons who ate raspberries (relative risk [RR] = 5.4; 95% confidence interval [CI], 2.2-13.2) or potato salad (RR = 1.8; 95% CI, 1.2-2.6) were at significantly increased risk for illness. The population attributable risk percentages were 73% for raspberries and 20% for potato salad. Cyclospora oocysts were found in stools from 11 (85%) of the 13 case patients submitting specimens for testing. Implicated raspberries originated in Guatemala. CONCLUSIONS: Our investigation is one of the first studies to implicate a specific food (raspberries) as a vehicle for transmission of Cyclospora. Because of the apparent increasing incidence of cyclosporiasis in the United States, family physicians should consider testing for Cyclospora in any patient with prolonged, unexplained diarrhea.

Cyclospora cayetanensis: a review, focusing on the outbreaks of cyclosporiasis in the 1990s.

Cyclospora cayetanensis, a coccidian parasite that causes protracted, relapsing gastroenteritis, has a short recorded history. In retrospect, the first 3 documented human cases of Cyclospora infection were diagnosed in 1977 and 1978. However, not much was published about the organism until the 1990s. One of the surprises has been the fact that a parasite that likely requires days to weeks outside the host to become infectious has repeatedly caused foodborne outbreaks, including large multistate outbreaks in the United States and Canada. In this review, I discuss what has been learned about this enigmatic parasite since its discovery and what some of the remaining questions are. My focus is the foodborne and waterborne outbreaks of cyclosporiasis that were documented from 1990 through 1999. The occurrence of the outbreaks highlights the need for health care personnel to consider that seemingly isolated cases of infection could be part of widespread outbreaks and should be reported to public health officials. Health care personnel should also be aware that stool specimens examined for ova and parasites usually are not examined for Cyclospora unless such testing is specifically requested and that Cyclospora infection is treatable with trimethoprim-sulfamethoxazole.

Leishmaniasis.

In 1903, Leishman and Donovan separately described the protozoan now called Leishmania donovani in splenic tissue from patients in India with the life-threatening disease now called visceral leishmaniasis. Almost a century later, many features of leishmaniasis and its major syndromes (ie, visceral, cutaneous, and mucosal) have remained the same; but also much has changed. As before, epidemics of this sandfly-borne disease occur periodically in India and elsewhere; but leishmaniasis has also emerged in new regions and settings, for example, as an AIDS-associated opportunistic infection. Diagnosis still typically relies on classic microbiological methods, but molecular-based approaches are being tested. Pentavalent antimony compounds have been the mainstay of antileishmanial therapy for half a century, but lipid formulations of amphotericin B (though expensive and administered parenterally) represent a major advance for treating visceral leishmaniasis. A pressing need is for the technological advances in the understanding of the immune response to leishmania and the pathogenesis of leishmaniasis to be translated into field-applicable and affordable methods for diagnosis, treatment, and prevention of this disease.

PIP: This paper discusses the pathogenesis and clinical management of leishmaniasis. Leishmaniasis is a vector-borne disease caused by obligate intramacrophage protozoa, characterized by diversity and complexity. It is endemic in areas of the tropics, subtropics, and southern Europe, in settings ranging from rain forests in Americas to deserts in western Asia, and from rural to periurban areas. Several clinical syndromes are categorized under the term leishmaniasis: most notably visceral, cutaneous, and mucosal leishmaniasis, which result from replication of the parasite in macrophages of the mononuclear phagocyte system, dermis, and naso-oro-pharyngeal mucosa, respectively. These syndromes are caused by a total of about 21 leishmanial species, which are transmitted by about 30 species of phlebotomine sandflies. Clinical manifestation of the disease depends on the type of leishmaniasis, which could be life-threatening systemic infection (visceral), chronic skin sores (cutaneous), or dreaded metastatic complications, which causes facial disfigurement (mucosal). Clinical management is directed to prevent death from visceral leishmaniasis and morbidity from cutaneous and mucosal leishmaniasis. Also included in its management is the ongoing research on immunoregulation of leishmaniasis in the understanding of the immune response to intracellular pathogens and rationalizing vaccine development. General principles on the disease diagnosis and treatment are outlined in this paper.

Laboratory-acquired parasitic infections from accidental exposures.

Parasitic diseases are receiving increasing attention in developed countries in part because of their importance in travelers, immigrants, and immunocompromised persons. The main purpose of this review is to educate laboratorians, the primary readership, and health care workers, the secondary readership, about the potential hazards of handling specimens that contain viable parasites and about the diseases that can result. This is accomplished partly through discussion of the occupationally acquired cases of parasitic infections that have been reported, focusing for each case on the type of accident that resulted in infection, the length of the incubation period, the clinical manifestations that developed, and the means by which infection was detected. The article focuses on the cases of infection with the protozoa that cause leishmaniasis, malaria, toxoplasmosis, Chagas' disease (American trypanosomiasis), and African trypanosomiasis. Data about 164 such cases are discussed, as are data about cases caused by intestinal protozoa and by helminths. Of the 105 case-patients infected with blood and tissue protozoa who either recalled an accident or for whom the likely route of transmission could be presumed, 47 (44.8%) had percutaneous exposure via a contaminated needle or other sharp object. Some accidents were directly linked to poor laboratory practices (e.g., recapping a needle or working barehanded). To decrease the likelihood of accidental exposures, persons who could be exposed to pathogenic parasites must be thoroughly instructed in safety precautions before they begin to work and through ongoing training programs. Protocols should be provided for handling specimens that could contain viable organisms, using protective clothing and equipment, dealing with spills of infectious organisms, and responding to accidents. Special care should be exercised when using needles and other sharp objects.

An outbreak in 1996 of cyclosporiasis associated with imported raspberries. The Cyclospora Working Group.

BACKGROUND: Cyclospora cayetanensis is a parasite that causes gastroenteritis. Until last year most of the documented cases of cyclosporiasis in North America were in overseas travelers. In 1996, a large outbreak of cyclosporiasis occurred in North America. We investigated this outbreak. METHODS: Health departments solicited information from clinicians and laboratories on cases of cyclosporiasis, which were then reported to the Centers for Disease Control and Prevention and to Health Canada. We conducted retrospective cohort studies for the cases associated with events (e.g., luncheons) and attempted to identify the sources of the implicated food. RESULTS: A total of 1465 cases of cyclosporiasis were reported by 20 states, the District of Columbia, and 2 provinces. Of these cases, 978 (66.8 percent) were laboratory confirmed and 725 (49.5 percent) were associated with 55 events that were held from May 3 through June 14. Raspberries were definitely served at 50 events and may have been served at 4 events. For 27 of the 41 events for which adequate data were available (65.8 percent), the associations between the consumption of berries (raspberries with or without other berries) and cyclosporiasis were statistically significant (P<0.05). For all 29 events for which there were good data, the raspberries definitely came from Guatemala (21 events, 72.4 percent) or may have come from Guatemala (8 events, 27.6 percent). As few as five Guatemalan farms could have accounted for the 25 events for which the raspberries could be traced to a single exporter per event. The mode of contamination of the raspberries remains unclear. CONCLUSIONS: This large outbreak of cyclosporiasis in North America in 1996 was associated with the consumption of Guatemalan raspberries. The outbreak illustrates the need to consider that a local cluster of foodborne illness may be part of a widespread outbreak and to pursue investigations to the source of the implicated vehicle.

Reevaluating the molecular taxonomy: is human-associated Cyclospora a mammalian Eimeria species?

Human-associated Cyclospora is a coccidian parasite that causes diarrheal disease. A reevaluation of the parasite's molecular taxonomy that takes into account newly published data for seven Eimeria species shows that Cyclospora belongs to the Eimeria clade (Eimeriidae family). The Cyclospora branch on the phylogenetic tree is between the branches of the eight avian and two mammalian Eimeria species that have been evaluated to date. Furthermore, preliminary results indicate that Cyclospora and Isospora belli, another coccidian parasite that causes diarrheal disease in humans, belong to different families. To improve our understanding of the taxonomy of human-associated Cyclospora, molecular evaluation of isolates of additional Cyclospora and Eimeria species is needed.

The return of Cyclospora in 1997: another outbreak of cyclosporiasis in North America associated with imported raspberries. Cyclospora Working Group.

BACKGROUND: In the spring of 1996, an outbreak of cyclosporiasis associated with fresh Guatemalan raspberries occurred in the United States and Canada. Another multistate outbreak of cyclosporiasis occurred in North America in the spring of 1997. OBJECTIVE: To identify the vehicle of the outbreak that occurred in the spring of 1997. DESIGN: Retrospective cohort studies of clusters of cases associated with events (such as banquets) and traceback investigations of sources of implicated produce. SETTING: United States and Canada. PATIENTS: Persons who attended events associated with clusters of cases of cyclosporiasis. MEASUREMENTS: Identification of clinically defined or laboratory-confirmed cases of cyclosporiasis and risk factors for infection. RESULTS: 41 clusters of cases were reported in association with events held from 1 April through 26 May in 13 U.S. states, the District of Columbia, and 1 Canadian province. The clusters comprised 762 cases of cyclosporiasis, 192 (25.2%) of which were laboratory confirmed. In addition, 250 laboratory-confirmed sporadic cases were reported in persons who developed gastrointestinal symptoms from April through 15 June, for a total of 1012 cases. Fresh raspberries were the only food common to all 41 events and were the only type of berry served at 9 events (22.0%). Statistically significant associations between consumption of raspberry-containing items and cyclosporiasis were documented for 15 events (40.5% of 37). For 31 of the 33 events with well-documented traceback data, the raspberries either definitely came from Guatemala (8 events) or could have come from Guatemala (23 events). The mode of contamination of the raspberries remains unknown. The outbreak ended shortly after the exportation of fresh raspberries from Guatemala was voluntarily suspended at the end of May 1997. CONCLUSIONS: Similar multistate, multicluster outbreaks of cyclosporiasis associated with consumption of Guatemalan raspberries have occurred in consecutive years. These outbreaks highlight the need for better understanding of the biology and epidemiology of Cyclospora cayetanensis and for stronger prevention and control measures to ensure the safety of produce eaten raw.

The natural history of cutaneous leishmaniasis in Guatemala.

The natural history of American cutaneous leishmaniasis was studied in Guatemala by analyzing the characteristics of 355 untreated leishmanial lesions, observing the evolution of 57 lesions on persons who received a placebo in treatment trials, and analyzing data from a population-based survey concerning the duration of 82 untreated lesions. Of 25 lesions caused by Leishmania mexicana that were followed prospectively, 22 (88%) completely reepithelialized by a median lesion age of 14 weeks, and 17 (68%) were classified as cured (no residual wound inflammation or reactivation during at least 6 months of follow-up). In contrast, 7 (22%) of 32 lesions caused by Leishmania braziliensis reepithelialized by a median lesion age of 13 weeks, and only 2 (6%) cured. These data demonstrate that the species of Leishmania is the primary determinant of the clinical course and outcome of untreated lesions and underscore the need for field-applicable diagnostic techniques that provide rapid species identification.

American cutaneous leishmaniasis in U.S. travelers.

OBJECTIVE: To characterize the exposures and practices of U.S. travelers who acquired cutaneous leishmaniasis in the Americas and to highlight problems they encountered in seeking medical care from U.S. physicians. DESIGN: A retrospective review of Centers for Disease Control and Prevention Drug Service records and a telephone survey of patients. PATIENTS: Fifty-nine civilian U.S. travelers with American cutaneous leishmaniasis for whom the Drug Service released sodium stibogluconate between 1 January 1985 and 30 April 1990; 58 travelers (98%) were interviewed. MAIN MEASUREMENTS: Travel destination, exposure duration, knowledge about leishmaniasis, and time from noticing skin lesions to release of drug. RESULTS: Overall, travelers acquired leishmaniasis in as many as 14 countries; 33 of 59 travelers (56%) were infected in Mexico or Central America. Twenty-seven travelers (46%) were conducting field studies and 23 (39%) were tourists, visitors, or tour guides. At least 15 persons (26% of the 58 interviewed travelers) were in forested areas for 1 week or less; at least 6 of these persons had a maximum exposure of 2 days. Ten persons (17%) were home at least 1 month before they noticed skin lesions. Patients consulted from one to seven physicians (mean, 2.1 physicians) before leishmaniasis was diagnosed. Overall, the median time from noticing lesions to the release of drug was 112 days (range, 13 to 1022 days); however, the median was only 55 days for 13 patients (22%) unusually knowledgeable about leishmaniasis and was a maximum of 60 days for 16 patients (28%) (including 7 of the 13 unusually knowledgeable patients) who generally consulted physicians exceptionally knowledgeable about infectious and tropical diseases. CONCLUSIONS: Travelers to forested areas in Mexico and Central and South America and their physicians need to be educated about the risk for acquiring leishmaniasis even during short stays, as well as about effective preventive measures; and appropriate medical management [corrected].