American Society Of Tropical Medicine And Hygiene Research Articles

57-Year-Old Man With Headache, Vomiting, and Gait Instability

A 57-year-old man, originally from Burma, presented to the emergency department with headache, nausea, vomiting, and unsteadiness in December 2020. He had no significant medical history and was not taking any medication. He reported worsening headaches associated with nausea and vomiting for the preceding 2 to 3 months. His headache was characterized as bifrontal and unchanged with positioning, coughing, or sneezing. His gait worsened, and he had 1 fall. The patient also had intractable hiccups for the preceding 2 months. Additionally, his family noted he was more forgetful, although the patient remained independent with his activities of daily living. He was born in Burma and lived there until 2008, when he moved to Thailand where he worked as a farmer. He moved to Minnesota in 2013 and worked at a meat processing factory. He endorsed regular cooked beef, pork, and poultry ingestion. He denied sick contacts, fevers, chills, pain, cough, diarrhea, or constipation. He reported no changes in his strength, sensation, vision, or hearing. He did not endorse other significant infectious exposure history or social history. On presentation, temperature was 36.1°C, heart rate 54 beats/min, blood pressure 127/109 mm Hg, and oxygen saturation 97% on room air. On physical examination, he was not in acute distress and had intermittent hiccups. Eyes were anicteric, and mucous membranes were moist. Cardiac examination revealed no murmurs, rubs, or gallops; rate and rhythm were regular. His extremities exhibited no edema. Lung fields were clear to auscultation. Abdominal examination was benign with no palpable organomegaly, and skin examination was unremarkable. On neurological examination, he was alert and oriented. He was able to follow 1- and 2-step commands, but unable to follow crossbody commands. Assessment of strength, sensation, coordination, and reflexes was normal. His gait was abnormal with a forward lean, short stride length, and reduced ground clearance. The initial laboratory results revealed a white blood cell count of 10.0×109/L (normal range, [3.4-9.6]×109/L). Head computed tomography (CT) revealed marked ventriculomegaly with widespread multifocal calcifications and cysts.1.Which one of the following is the next best step in management?a.Discharge home with anti-nausea medications and outpatient follow-upb.Electroencephalogramc.Lumbar puncture (LP)d.Magnetic resonance imaging (MRI) of the brain and spinee.Brain biopsy Conservative management with anti-nausea medications and outpatient follow-up would not be appropriate for this patient, given his progressive neurological abnormalities and CT findings. Although brain lesions can increase the risk of seizures, the patient did not present with signs or symptoms of seizure activity. Thus, electroencephalogram is not indicated. The symptoms along with the CT findings of marked ventriculomegaly and innumerable cysts raise a concern for elevated intracranial pressure (ICP). Performing an LP in this setting puts the patient at high risk for cerebral herniation. Given the CT images that were highly suggestive of neurocysticercosis (NCC), MRI is indicated for the diagnosis and further characterization of brain lesions. Moreover, MRI of the spine is recommended for patients with basal subarachnoid involvement given the strong association with spinal subarachnoid cysticerci.1White Jr., A.C. Coyle C.M. Rajshekhar V. et al.Diagnosis and treatment of neurocysticercosis: 2017 Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).Clin Infect Dis. 2018; 66: e49-e75Crossref PubMed Scopus (68) Google Scholar In rare cases, if advanced imaging and extended laboratory tests are unrevealing, brain biopsy may be necessary for diagnostic purposes. Brain and spine MRI with fast imaging employing steady-state acquisition and 3-dimensional constructive interference in steady-state sequences revealed widely disseminated, racemose NCC in varying stages, with subarachnoid, intraventricular, and paraspinal involvement. There were also meningeal inflammation and obstructive hydrocephalus, partly secondary to cyst location in the cerebral aqueduct and fourth ventricle. Echinococcus and cysticercosis serum IgG antibodies were positive.2.Which one of the following is the most likely pathogen responsible for the imaging and serological findings in this patient?a.Naegleria fowlerib.Schistosoma spp.c.Giardia spp.d.Taenia soliume.Echinococcus granulosus Naegleria fowleri is the causative organism for primary amebic meningoencephalitis. Diagnosis is made by LP and cerebral spinal fluid analysis. Neuroimaging findings are nonspecific and may include hydrocephalus, lesions, and meningeal enhancements. Schistosoma spp. may cause neuroschistosomiasis with symptoms of seizures and neurological deficits. Serology, urine antigen detection, and microscopy of the stool or urine are used for diagnosis. Giardia spp. is a protozoan that causes diarrhea and diagnosed by serology, nucleic acid assays, and stool microscopy; giardiasis infection does not present with central nervous system lesions. Infection with T solium, or pork tapeworm, can present as taeniasis (digestive system infection by a tapeworm) or cysticercosis (cyst formation by larvae). Cysticercosis is diagnosed with a combination of clinical symptoms, neuroimaging findings, and epidemiological exposures. Cystic echinococcosis (CE) is caused by E granulosus and most commonly involves the liver and lungs. Less commonly, CE may involve the brain, muscle, kidneys, and spleen. Although the sensitivity of serological testing for E granulosus is high, the specificity (as observed in this patient’s laboratory testing) is low.2Eckert J. Deplazes P. Biological, epidemiological, and clinical aspects of echinococcosis, a zoonosis of increasing concern.Clin Microbiol Rev. 2004; 17: 107-135Crossref PubMed Scopus (1247) Google Scholar The larger cyst size, presence of daughter cysts, and radiological appearance can help to differentiate CE from NCC. In addition, although there is an elevated risk of secondary CE with a spillage of viable Echinococcus parasite during cyst resection, postoperative inflammation in response to NCC spillage has not been described.3Krupa K. Krupa K. Pisculli M.L. Athas D.M. Farrell C.J. Racemose neurocysticercosis.Surg Neurol Int. 2016; 7: 12Crossref PubMed Scopus (10) Google Scholar Given the diagnosis of widespread racemose NCC with viable cysts, immediate antiparasitic therapy was contraindicated because of the risk of severe inflammation until the patient’s hydrocephalus and elevated ICP were adequately managed. The patient was initiated on high-dose corticosteroids and subsequently underwent a ventriculoperitoneal shunt placement and endoscopic septostomy for NCC. Unfortunately, third ventriculostomy and cystectomy were deemed too high risk because of the patient’s anatomy and risk of cyst spillage.3.Which one of the following antiparasitic therapies would you most likely recommend for this patient?a.Albendazole and praziquantelb.Niclosamidec.Metronidazoled.Chloroquinee.Ivermectin Neurocysticercosis presenting with more than 2 cysts should be treated with albendazole and praziquantel.4Garcia H.H. Gonzales I. Lescano A.G. et al.Cysticercosis Working Group in Peru. Efficacy of combined antiparasitic therapy with praziquantel and albendazole for neurocysticercosis: a double-blind, randomised controlled trial.Lancet Infect Dis. 2014; 14: 687-695Abstract Full Text Full Text PDF PubMed Scopus (123) Google Scholar Niclosamide is an anthelmintic medication that has been used for taeniasis, but is not effective for cysticercosis. Metronidazole is a treatment of giardiasis, trichomoniasis, and amebiasis, not for infection with T solium. Chloroquine, an antimalarial agent, is not an effective therapy for this patient. Ivermectin is antiparasitic therapy for onchocerciasis and strongyloidiasis. Albendazole and praziquantel were initiated for the patient after surgery and resolution of elevated ICP. Levetiracetam was initiated for seizure prophylaxis. Because of prolonged treatment with corticosteroids, the patient was screened for latent tuberculosis (TB) infection (LTBI) and strongyloidiasis. Strongyloidiasis serum IgG antibody was negative. The QuantiFERON-Tb Gold Plus test result was positive. Chest radiography did not reveal any signs of active TB.4.Given this patient’s NCC medication regimen, concurrent treatment with which one of the following anti-TB medications should be best avoided?a.Isoniazidb.Ethambutolc.Moxifloxacind.Kanamycine.Cycloserine Because of the association of hepatotoxicity with albendazole, isoniazid should be avoided because of the high risk of liver injury with combined antiparasitic and anti-TB therapy. Peripheral neuropathy and agranulocytosis have also been reported with isoniazid. Ethambutol is more commonly associated with visual disturbances and retrobulbar neuritis. Rifampicin and pyrazinamide are also associated with hepatitis. Fluroquinolones, such as moxifloxacin, can cause gastrointestinal disturbances, tendinitis, and QT interval prolongation. Adverse effects associated with kanamycin include ototoxicity and nephrotoxicity. Cycloserine can cause neurological symptoms such as confusion, dizziness, and psychosis. Unfortunately, despite deferring LTBI therapy, the patient had transaminitis. Trimethoprim-sulfamethoxazole was transitioned to pentamidine and the dose of albendazole was reduced.5.Which one of the following is true regarding the transmission and prevention of NCC?a.Humans can get cysticercosis by consuming T solium cysts undercooked pork.b.Humans can get cysticercosis after ingesting T solium eggs.c.Pickling and salting meat are methods of eliminating viable cysticerci.d.Hand hygiene before food preparation does not adequately prevent cysticercosis.e.Vaccination for humans living in endemic areas can prevent cysticercosis. Eating cysterici in undercooked pork causes a tapeworm infection, also known as taeniasis, but will not directly cause cysticercosis. Instead, cysticercosis occurs after an individual ingests T solium eggs found in contaminated foods or more commonly autoinoculation of eggs excreted stool from self or a household tapeworm carrier.5Garcia H.H. Gonzalez A.E. Gilman R.H. Taenia solium cysticercosis and its impact in neurological disease.Clin Microbiol Rev. 2020; 33 (e00085-19)Crossref PubMed Scopus (32) Google Scholar Pickling and salting pork do not adequately eliminate viable cysticerci in meat. Instead, freezing or cooking the meat can destroy viable cysticerci. Good hygiene after toileting and before food preparation with soap and water can prevent transmission of T solium eggs from tapeworm carriers to other people. No vaccine for cysticercosis has been approved in humans. In some endemic countries, vaccination of pigs has been used to prevent porcine cysticercosis and subsequent transmission to humans.6Gabriël S. Mwape K.E. Hobbs E.C. et al.Evidence for potential elimination of active Taenia solium transmission in Africa?.N Engl J Med. 2020; 383: 396-397Crossref PubMed Scopus (11) Google Scholar Ultimately, his transaminitis resolved and was felt to be from trimethoprim-sulfamethoxazole. Albendazole was reinitiated at a lower dose, but adequate dose for NCC. The patient was discharged from the hospital with the plan to initiate LTBI treatment in the outpatient setting and screen household contacts for taeniasis. Cysticercosis is endemic to regions Latin America, sub-Saharan Africa, and South and Southeast Asia.1White Jr., A.C. Coyle C.M. Rajshekhar V. et al.Diagnosis and treatment of neurocysticercosis: 2017 Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).Clin Infect Dis. 2018; 66: e49-e75Crossref PubMed Scopus (68) Google Scholar Humans become the dead-end host after ingesting the embryonated eggs of T solium, which is found in the stool of tapeworm carriers such as pigs and human household members. The embryos hatch in the gastrointestinal tract, invade through the bowel wall, and disseminate hematogenously to present as cysticercosis. In contrast, humans are the definite host after ingesting the larval cysts of T solium found in undercooked pork. After consuming the cysts, humans have taeniasis with adult tapeworm infection of the intestinal tract. Tapeworm infestation, although not a direct cause of cysticercosis, does increase the risk of fecal-oral autoinfection of T solium eggs, leading to the future development of cysticercosis. Cysticercosis may be divided into NCC and extraneural cysticercosis. Neurocysticercosis may be further characterized as parenchymal and/or extraparenchymal. After ingestion of T solium, the phases of infection consists of an initial viable phase, early inflammatory phase, degenerating phase, and nonviable phase. The most common presenting symptom of intraparenchymal NCC is seizures.5Garcia H.H. Gonzalez A.E. Gilman R.H. Taenia solium cysticercosis and its impact in neurological disease.Clin Microbiol Rev. 2020; 33 (e00085-19)Crossref PubMed Scopus (32) Google Scholar Altered vision, focal neurological symptoms, meningitis, and encephalitis have also been reported.5Garcia H.H. Gonzalez A.E. Gilman R.H. Taenia solium cysticercosis and its impact in neurological disease.Clin Microbiol Rev. 2020; 33 (e00085-19)Crossref PubMed Scopus (32) Google Scholar Although symptom onset is usually within 3 to 5 years, patients may present more than 30 years after initial ingestion.7Serpa J.A. Graviss E.A. Kass J.S. White Jr., A.C. Neurocysticercosis in Houston, Texas: an update.Medicine (Baltimore). 2011; 90: 81-86Crossref PubMed Scopus (69) Google Scholar Extraparenchymal NCC can involve the ventricles, subarachnoid space, spine, and eye. Patients with extraparenchymal involvement often report symptoms of elevated ICP, including headache, nausea, vomiting, altered mental status, and decreased visual acuity. They may also present with seizures and focal neurological deficits. Spinal cysticerci can affect the spinal cord and peripheral nerve roots, causing radicular pain, paresthesia, and sphincter dysfunction. Racemose NCC is a severe form of extraparenchymal NCC characterized by multiple confluent cysts seen in the subarachnoid space.3Krupa K. Krupa K. Pisculli M.L. Athas D.M. Farrell C.J. Racemose neurocysticercosis.Surg Neurol Int. 2016; 7: 12Crossref PubMed Scopus (10) Google Scholar Routine laboratory evaluation is of lower diagnostic yield. Patients with cysticercosis often have normal liver function test results and eosinophil counts. Ova and parasite stool testing is often insensitive, because most patients do not have live intestinal tapeworms on presentation but may be useful in endemic regions. Instead, the diagnosis of cysticercosis is made on the basis of symptoms, neuroimaging, and epidemiological exposures.1White Jr., A.C. Coyle C.M. Rajshekhar V. et al.Diagnosis and treatment of neurocysticercosis: 2017 Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).Clin Infect Dis. 2018; 66: e49-e75Crossref PubMed Scopus (68) Google Scholar Computed tomography of the head and MRI of the brain should be performed on patients suspected of having NCC. Patients with basal subarachnoid involvement should undergo MRI of the spine.1White Jr., A.C. Coyle C.M. Rajshekhar V. et al.Diagnosis and treatment of neurocysticercosis: 2017 Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).Clin Infect Dis. 2018; 66: e49-e75Crossref PubMed Scopus (68) Google Scholar Imaging may reveal cystic, enhancing, and/or “cigar-shaped” calcified lesions. Leptomeningeal enhancement and hydrocephalus may also be seen. Serological testing may aid in diagnosis, but negative serological test results do not exclude NCC, especially in patients with characteristic clinical symptoms and imaging findings, nor do positive test results indicate an active infection, as patients from endemic areas may have developed antibodies because of a previous infection.8Garcia H.H. Gilman R.H. Catacora M. Verastegui M. Gonzalez A.E. Tsang V.C. Cysticercosis Working Group in Peru. Serologic evolution of neurocysticercosis patients after antiparasitic therapy.J Infect Dis. 1997; 175: 486-489Crossref PubMed Scopus (76) Google Scholar The sensitivity for NCC determined by enzyme-linked immunotransfer blot serology has been reported to be 86%.1White Jr., A.C. Coyle C.M. Rajshekhar V. et al.Diagnosis and treatment of neurocysticercosis: 2017 Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).Clin Infect Dis. 2018; 66: e49-e75Crossref PubMed Scopus (68) Google Scholar However, serological test results may be negative in disease with low cyst burden. Finally, the real-time polymerase chain reaction assay for T solium DNA is highly sensitive and specific for active subarachnoid and ventricular NCC and is even more sensitive when performed on cerebrospinal fluid.9O’Connell E.M. Harrison S. Dahlstrom E. Nash T. Nutman T.B. A novel, highly sensitive quantitative polymerase chain reaction assay for the diagnosis of subarachnoid and ventricular neurocysticercosis and for assessing responses to treatment.Clin Infect Dis. 2020; 70: 1875-1881Crossref PubMed Scopus (19) Google Scholar Quantitative polymerase chain reaction results are furthermore correlated with response to therapy. The treatment of NCC is individualized and dependent on symptoms. Patients with clinical manifestations of elevated ICP, such as headache, nausea, vomiting, papilledema, and somnolence, should first be treated with corticosteroids to lower inflammation and cerebral edema. This patient’s case was complicated by a diagnosis of LTBI. Previous research suggests that patients treated with corticosteroids have a 5-fold increased risk of developing a new diagnosis of TB.10Jick S.S. Lieberman E.S. Rahman M.U. Choi H.K. Glucocorticoid use, other associated factors, and the risk of tuberculosis.Arthritis Rheum. 2006; 55: 19-26Crossref PubMed Scopus (327) Google Scholar Less is known about the risk of reactivation of TB in patients with LTBI. Because of the progression of symptoms and concern for worsening ICP, our care team decided that the risk of TB reactivation was outweighed by the benefit of corticosteroid treatment. However, it remains clear that treating such complex cases should be individualized. Coinfection with T solium and M tuberculosis is not unexpected given their overlapping widespread distributions and has been previously reported.11Rani A. Pushker N. Kulkarni A. Balasubramanya R. Bajaj M.S. Simultaneous ocular and systemic cysticercosis and tuberculosis.Infection. 2006; 34: 169-172Crossref PubMed Scopus (3) Google Scholar The diagnostic differential for brain lesions includes NCC and cystic tuberculomas. Latent TB infection treatment is individualized and consists of a rifamycin-based regimen or isoniazid monotherapy regimen. Obstructive hydrocephalus secondary to NCC is managed with surgical removal of the offending cysticercus or placement of an external ventricular shunt.1White Jr., A.C. Coyle C.M. Rajshekhar V. et al.Diagnosis and treatment of neurocysticercosis: 2017 Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).Clin Infect Dis. 2018; 66: e49-e75Crossref PubMed Scopus (68) Google Scholar Communicating hydrocephalus is treated with ventriculoperitoneal shunt placement or third ventriculostomy.1White Jr., A.C. Coyle C.M. Rajshekhar V. et al.Diagnosis and treatment of neurocysticercosis: 2017 Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).Clin Infect Dis. 2018; 66: e49-e75Crossref PubMed Scopus (68) Google Scholar Once the elevated ICP has resolved, antiparasitic therapy may be initiated for patients with viable and/or degenerating cysts. The treatment for patients with low cystic burden (1 to 2 cysts) consists of albendazole. Patients with more than 2 cysts should be treated with a combination of albendazole and praziquantel, given evidence of the higher radiographic resolution as compared with albendazole alone.4Garcia H.H. Gonzales I. Lescano A.G. et al.Cysticercosis Working Group in Peru. Efficacy of combined antiparasitic therapy with praziquantel and albendazole for neurocysticercosis: a double-blind, randomised controlled trial.Lancet Infect Dis. 2014; 14: 687-695Abstract Full Text Full Text PDF PubMed Scopus (123) Google Scholar The duration of treatment is typically between 10 and 14 days but may be extended depending on the cyst burden. Because antiparasitic medications can cause life-threatening inflammation as viable cysts degenerate, adjunctive corticosteroids are recommended to decrease the seizure risk.1White Jr., A.C. Coyle C.M. Rajshekhar V. et al.Diagnosis and treatment of neurocysticercosis: 2017 Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).Clin Infect Dis. 2018; 66: e49-e75Crossref PubMed Scopus (68) Google Scholar A typical corticosteroid regimen begins 1 day before the initiation of antiparasitic medications, is continued for 1 to 2 weeks, and ends with a taper.12Garcia H.H. Nash T.E. Del Brutto O.H. Clinical symptoms, diagnosis, and treatment of neurocysticercosis.Lancet Neurol. 2014; 13: 1202-1215Abstract Full Text Full Text PDF PubMed Scopus (300) Google Scholar Repeat neuroimaging should be performed every 6 months to monitor cyst resolution.1White Jr., A.C. Coyle C.M. Rajshekhar V. et al.Diagnosis and treatment of neurocysticercosis: 2017 Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).Clin Infect Dis. 2018; 66: e49-e75Crossref PubMed Scopus (68) Google Scholar The authors report no competing interests.

American Society of Tropical Medicine and Hygiene (ASTMH) - 69th Annual Meeting. Virtual - November 15-19, 2020

American Society of Tropical Medicine and Hygiene (ASTMH) - 69th Annual Meeting. Virtual - November 15-19, 2020

Reducing the Carbon Footprint of Academic Conferences: The Example of the American Society of Tropical Medicine and Hygiene.

.We calculated carbon emissions associated with air travel of 4,834 participants at the 2019 annual conference of the American Society of Tropical Medicine and Hygiene (ASTMH). Together, participants traveled a total of 27.7 million miles or 44.6 million kilometers. This equates to 58 return trips to the moon. Estimated carbon dioxide equivalent (CO2e) emissions were 8,646 metric tons or the total weekly carbon footprint of approximately 9,366 average American households. These emissions contribute to climate change and thus may exacerbate many of the global diseases that conference attendees seek to combat. Options to reduce conference travel–associated emissions include 1) alternating in-person and online conferences, 2) offering a hybrid in-person/online conference, and 3) decentralizing the conference with multiple conference venues. Decentralized ASTMH conferences may allow for up to 64% reduction in travel distance and 58% reduction in CO2e emissions. Given the urgency of the climate crisis and the clear association between global warming and global health, ways to reduce carbon emissions should be considered.

Challenges and Strategies for Biomedical Researchers Returning to Low- and Middle-Income Countries after Training.

The brain drain of professionals from low- and middle-income countries (LMICs) to developed countries is well documented and partially due to the challenges faced by biomedical researchers to establish themselves back at home, after training abroad. These challenges may result in the loss of highly trained individuals from LMICs and reduce the availability of local expertise to develop/inform best practices in health care and to direct locally relevant research. The path of training of LMIC researchers in high-income countries is well documented. However, strategies for a successful reintegration of biomedical researchers back to their home research institutions in LMICs are less clear. We report observations of workshops addressing repatriation needs of researchers returning to their home countries after training abroad during the American Society of Tropical Medicine and Hygiene (ASTMH) 2017 and 2018 annual meetings. Strategies proposed include maintaining connections with the home research institution, ideally through collaborations, planning 18 months ahead before returning with grants applications submitted, and engaging in networking throughout the training period. In addition to presenting our observations, we hope to build a network to facilitate this process, compile resources, and identify expertise within the ASTMH to develop robust strategies to allow young biomedical researchers to flourish in LMICs.

Diagnosis and Treatment of Neurocysticercosis: 2017 Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).

In the first section, the panel summarizes background information relevant to the topic. In the second section, the panel poses questions regarding the diagnosis and treatment of NCC, evaluates applicable clinical trial and observational data, and makes recommendations using the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) framework.1 The following 27 clinical questions were answered: I. How should NCC be diagnosed? II. What imaging studies should be used to classify disease? III. What additional tests should be performed before initiation of therapy? IV. How should antiparasitic and anti-inflammatory therapy be monitored? V. What is the role of antiparasitic drugs in VPN? VI. What is the role of anti-inflammatory therapy in management of VPN? VII. What is the role of antiepileptic drugs in VPN? VIII. What follow-up is recommended after initial antiparasitic therapy for patients with VPN? IX. What should be the initial approach to the patient with multiple enhancing lesions from NCC? X. What is the role of antiepileptic medications in patients with SEL from cysticercosis with seizures? XI. What is the role of antiparasitic drugs in patients with SEL? XII. What is the role of anti-inflammatory therapy in SEL? XIII. How should patients with SEL be followed? XIV. What should the initial approach be to patients with calcified lesions suggestive of CPN? XV. What is the role of antiparasitic drugs, antiepileptic drugs, and anti-inflammatory medications in the management of patients with CPN? XVI. Is there a role for surgical therapy in refractory cases? XVII. How are extra parenchymal cysts best identified? XVIII. What is the optimal approach to management of IVN in the lateral and third ventricles? XIX. What is the optimal surgical approach to management of IVN in the fourth ventricles? XX. What is the optimal approach to adherent IVN? XXI. Does medical therapy as an adjunct to procedures or as primary therapy have an impact on outcome in treating patients with IVN? XXII. What is the role of medical therapy in SAN in the basilar cisterns or Sylvian fissures? XXIII. What is the role of neurosurgery in SAN? XXIV. How is SN best treated? XXV. What is the optimal management of OC? XXVI. Should children be managed differently from adults? XXVII. Should management be different in pregnant women?

Diagnosis and Treatment of Neurocysticercosis: 2017 Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).

In the first section, the panel summarizes background information relevant to the topic. In the second section, the panel poses questions regarding the diagnosis and treatment of neurocysticercosis (NCC), evaluates applicable clinical trial and observational data, and makes recommendations using the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) framework [1]. The following 27 clinical questions were answered: How should neurocysticercosis be diagnosed? What imaging studies should be used to classify disease? What additional tests should be performed prior to initiation of therapy? How should antiparasitic and anti-inflammatory therapy be monitored? What is the role of antiparasitic drugs in viable parenchymal neurocysticercosis? What is the role of anti-inflammatory therapy in management of viable parenchymal neurocysticercosis? What is the role of antiepileptic drugs in viable parenchymal neurocysticercosis? What follow-up is recommended after initial antiparasitic therapy for patients with viable parenchymal neurocysticercosis? What should be the initial approach to the patient with multiple enhancing lesions from neurocysticercosis? What is the role of antiepileptic medications in patients with single enhancing lesions from cysticercosis with seizures? What is the role of antiparasitic drugs in patients with single enhancing lesions? What is the role of anti-inflammatory therapy in single enhancing lesions? How should patients with single enhancing lesions be followed? What should the initial approach be to patients with calcified lesions suggestive of calcified parenchymal neurocysticercosis? What is the role of antiparasitic drugs, antiepileptic drugs, and anti-inflammatory medications in the management of patients with calcified parenchymal neurocysticercosis? Is there a role for surgical therapy in refractory cases? How are extraparenchymal cysts best identified? What is the optimal approach to management of ventricular neurocysticercosis in the lateral and third ventricles? What is the optimal surgical approach to management of ventricular neurocysticercosis in the fourth ventricles? What is the optimal approach to adherent ventricular neurocysticercosis? Does medical therapy as an adjunct to procedures or as primary therapy have an impact on outcome in treating patients with ventricular neurocysticercosis? What is the role of medical therapy in subarachnoid neurocysticercosis in the basilar cisterns or Sylvian fissures? What is the role of neurosurgery in subarachnoid neurocysticercosis? How is spinal neurocysticercosis best treated? What is the optimal management of ocular cysticercosis? Should children be managed differently than adults? Should management be different in pregnant women? BACKGROUND Neurocysticercosis, caused by the larval form of the cestode parasite Taenia solium, is a major cause of seizure and neurologic disease worldwide and is common among immigrant populations in the United States. Highly endemic regions include Latin America, sub-Saharan Africa, and parts of Asia [2, 3]. In endemic areas, it is linked to approximately 29% of cases of seizures [4]. Estimates suggest that there are >2000 cases per year in the United States, with hospital charges of nearly $100 million per year [5, 6]. Humans can be hosts to both the tapeworm form and larval forms of the parasite. Taeniasis (also termed taeniosis) refers to infestation of the human intestines with the tapeworm form. The tapeworm is acquired by ingestion of undercooked pork. The scolex evaginates and attaches to the intestinal wall, and segments termed proglottids form a long ribbon-like chain referred to as the strobili. The gravid proglottids and eggs are passed in stool. Humans can also develop cysticercosis after ingestion of ova. Cysticercosis refers to infection of the tissues with the larval cyst (or metacestode). Normally, pigs host the cysts, which are acquired by ingestion of ova or proglottids from human feces. However, humans can be infected by ingestion of ova and develop cysticercosis. Neurocysticercosis refers to cysticercosis involving the central nervous system, including the brain parenchyma, ventricles, basilar cisterns, sulci, gyri, spine, and retina. The pathogenesis, natural history, clinical manifestations, and management vary with the location of the cysticerci [3]. For example, the main clinical manifestations vary between different forms of disease (Table 1). Parenchymal NCC typically presents with seizures or headache. Ventricular NCC most often presents with obstructive hydrocephalus. Subarachnoid NCC can present with communicating hydrocephalus, meningitis, stroke, or focal neurologic findings. Mixed forms are also common. Due to the complexity of diagnosis and management, the American Society for Tropical Medicine and Hygiene (ASTMH) and the Infectious Diseases Society of America (IDSA) agreed to jointly develop guidelines for the diagnosis and management of NCC.

Diagnosis and Treatment of Neurocysticercosis: 2017 Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).

Diagnosis and Treatment of Neurocysticercosis: 2017 Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).

Diagnosis and Treatment of Leishmaniasis: Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).

It is important to realize that leishmaniasis guidelines cannot always account for individual variation among patients. They are not intended to supplant physician judgment with respect to particular patients or special clinical situations. The IDSA and ASTMH consider adherence to these guidelines to be voluntary, with the ultimate determinations regarding their application to be made by the physician in the light of each patient's individual circumstances.

Diagnosis and Treatment of Leishmaniasis: Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).

"Diagnosis and Treatment of Leishmaniasis: Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH)" published on 11 Jan 2017 by The American Society of Tropical Medicine and Hygiene.

Diagnosis and Treatment of Leishmaniasis: Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH).

It is important to realize that leishmaniasis guidelines cannot always account for individual variation among patients. They are not intended to supplant physician judgment with respect to particular patients or special clinical situations. The IDSA and ASTMH consider adherence to these guidelines to be voluntary, with the ultimate determinations regarding their application to be made by the physician in the light of each patient's individual circumstances.

Partnerships that Facilitate a Refugee's Journey to Wellbeing.

The current global refugee crisis involves 65.3 million persons who have been displaced from their homes or countries of origin. While escaping immediate harm may be their first priority, displaced people go on to face numerous health risks, including trauma and injuries, malnutrition, infectious diseases, exacerbation of existing chronic diseases, and mental health conditions. This crisis highlights the importance of building capacity among health-care providers, scientists, and laboratorians to understand and respond to the health needs of refugees. The November 2016 American Society of Tropical Medicine and Hygiene (ASTMH) conference in Atlanta will feature an interactive exhibit entitled "The Refugee Journey to Wellbeing" and three symposia about refugee health. The symposia will focus on tropical disease challenges in refugee populations, careers in refugee health, and recent experiences of governmental agencies and nongovernmental organizations in responding to the global refugee crisis. We invite ASTMH attendees to attend the exhibit and symposia and consider contributions they could make to improve refugee health through tropical disease research or clinical endeavors.

Alan Magill, ASTMH Immediate Past President, 1953-2015.

The sudden and untimely death of Alan Jon Magill at age 61 on September 19, 2015 has led to a growing list of remembrances from a grieving community of friends and colleagues seeking to support his family and has been accompanied by a growing recognition of his extraordinary and unique contributions to the field of tropical diseases. At his death, Alan was the director of the Malaria Program at the Bill & Melinda Gates Foundation (BMGF) since 2012, and was also the immediate past president of the American Society of Tropical Medicine and Hygiene (ASTMH). Both positions underscored his enormous commitment and contributions to tropical medicine over the past decades. Alan's education was at Lamar University (BS 1976), University of Rhode Island (MS 1978), and Baylor College of Medicine (MD 1984). His post graduate training in the U.S. Army (at Tripler Army Medical Center in Hawaii and at Walter Reed Army Medical Center) was serendipitous, as it allowed him to join his partner and later wife Janiine as she trained as a pediatrician. Thus began the bulk of his career as a physician scientist within the Walter Reed system, combining clinical parasitology and research on product development of new interventions, including drugs and diagnostics. During his fellowship, Alan first focused on leishmaniasis, as troops from Desert Storm brought home challenging clinical presentations of cutaneous disease. He worked on rapid diagnostic tests and polymerase chain reaction-based assays for cutaneous leishmaniasis; the latter cleared Food and Drug Administration approval. This work established him as a lifelong leishmaniac, and his expertise was firmly grounded in clinical management and his strategic thinking about the need for new interventions. He was subsequently an advisor to leishmania vaccine development programs at the Infectious Diseases Research Institute and the BMGF. Alan then took on several broad roles; first, on detail to the parasitology program at the U.S. Naval Medical Research Unit No. 6 Peru; second, Chair of the U.S. Army Malaria Board for the Office of the Surgeon General; third, Director of the Division of Experimental Therapeutics at the Walter Reed Army Institute of Research; and finally research coordinator of both the Malaria Drug and Anti-Parasitic Research Programs at the U.S. Army Medical Research and Materiel Command. The breadth of these activities solidified Alan's knowledge of the clinical and product development challenges facing the malaria field. Alan's achievements in malaria within the Walter Reed Army Institute of Research program included the development of the first American malaria rapid diagnostic test and driving the development of two key treatments, intravenous artesunate and tafenoquine. He identified new malaria drug scaffolds that advanced into lead optimization. He led challenge trials of vaccine candidates in the United States and vaccine field trials in Africa. In addition, while in Peru, he helped to characterize malaria drug resistance patterns at a time when older therapies were losing efficacy, leading to engagement on methods of detection, monitoring of drug resistance, implementation of changes in national policy, and training on the use of new drug regimens. Subsequently, Alan joined the Defense Advanced Research Projects Agency in 2009, where he directed programs of innovative plant-protein therapeutics and biologics, as well as advancing influenza vaccine candidates into early clinical trials. Alan's diverse experiences served the malaria field well in 2010, when he participated in the Malaria Eradication Research Agenda (malERA) project. His contributions were critical to the establishment of Single Encounter Radical Cure and Prophylaxis (SERCAP) as a research priority for malaria drug development, enabling progress toward malaria eradication. His contributions as a member of this highly consultative process demonstrated leadership skills, which were to serve him well in his subsequent position at the BMGF. A listing of Alan's many management and leadership positions almost gets in the way of recognizing his enormous commitment to graduate medical education. His generosity with his time and energy placed him in a vortex of activities to advance graduate medical education of parasitology writ large, and malaria specifically. He was first recognized as an outstanding teaching resident during his internal medicine residency. This was the harbinger for what would become a life-long commitment to education, working through ASTMH, its subgroup, the American Committee on Clinical Tropical Medicine and Travelers' Health (Clinical Group) and the annual Update Course in Clinical and Tropical Medicine, as well as numerous other organizations that represent infectious diseases (Infectious Disease Society of America, American Society of Microbiology) and global health (CDC Traveler's Health and courses sponsored by the Gorgas Course in Tropical Medicine, Universidad Peruana Cayetano Heredia, and Johns Hopkins Bloomberg School of Public Health, to name a few). Alan's contributions to ASTMH began with his membership in 1991. He served as Councilor, Corporate Liaison, and on the Legislative Affairs Committee. He was a member of the American Committee on Clinical Tropical Medicine and Travelers' Health for 8 years, culminating in his service as President in 2007. He was president of ASTMH in 2014, bringing to this position his remarkable optimism, enthusiasm, and focus. He was seriously engaged in malaria elimination at this time, but during his presidential year a large Ebola outbreak in Africa became a primary focus of the tropical medicine community. He led efforts by the Society to address this epidemic, including careful attention to political challenges, scientific advances and human rights concerns. More broadly, he was greatly interested in the future of the Society, and he left a profound impact on the blueprint for future Society activities. 63rd ASTMH Annual Meeting, New Orleans, Louisiana, November 2, 2014 Alan's decision to join BMGF as Director of the Malaria Program was not made lightly. He considered the opportunity to drive the Foundation's malaria eradication strategy and its implementation as the culmination of his career. His engaging presentations at the Harvard/Barcelona/Basel Science of Eradication course over the past three years reflected his evolving framework for malaria eradication. Upon arrival at the BMGF, he worked to advance the malaria eradication strategy, applying his strong base as a malaria clinician to rethink the role of drugs as prevention, appropriate strategies to eliminate parasite reservoirs, and reshaping the vaccine development agenda to maximize impact on the eradication of malaria. His strategy was strongly endorsed by Foundation leadership and offered an enormous step forward for the field. Malaria elimination and eventual global eradication are far more achievable goals than we dreamed until very recently, in no small part because of his energy, talent, wisdom, compassion, and commitment. Through his career, Alan was a master at relating to his team and colleagues. He maintained independence of thought, but was engaged both internally and externally with those that would challenge his thinking. His passion for the history of malaria, understanding of the biological basis of disease, and unique experiences in product development of drugs and vaccines grounded his approach and cemented his credibility with the malaria research and policy communities. The integration of his program into a proactive, forward looking agenda, has resulted in a framework from which it is possible to believe, as he did, that “Malaria Delenda Est”—malaria must be destroyed. This was the inscription on the medal that he awarded, in the military tradition, to the members of his team at the BMGF. The medal given by Dr. Magill to his team at the BMGF. What is extraordinary is that since Alan's death many people have individually noted how he connected with them personally, giving whatever time was needed. This includes his staff, colleagues, and grantees. Moreover, he managed to do this while also being extraordinarily well-read, a voracious learner, a generous teacher, a malaria expert, a leishmaniac, an historian, a leader, and above all a family man. He certainly came across as smart and hardworking, but he didn't seem extraordinary. As David Brandling-Bennett noted, “After last week, I had to conclude that he was truly extraordinary, but he disguised it so well that individually we didn't realize it.” An avid outdoorsman, Alan's favorite activities included climbing mountains and hiking, activities which he enjoyed with family and friends, in the Seattle area and beyond. He is survived by his wife Janiine Babcock, daughter Lara Magill and her spouse Jonathan Krynitsky, daughter Sarah Magill, and brother Donald Magill. We thank his family for sharing him with us.

Out of (west) Africa-who lost in the end?

On October 29, 2014, 4 days before the annual meeting of the American Society of Tropical Medicine and Hygiene (ASTMH) to be held in New Orleans, LA, meeting registrants received an e-mail letter from the Louisiana Department of Health and Hospitals stating “we have requested that any individuals that will be traveling to Louisiana following a trip to the West African countries of Guinea, Liberia, and Sierra Leone or have had contact with an Ebola-infected individual remain in a self-quarantine for the 21 days following their relevant travel history…we see no use in you traveling to New Orleans to simply be confined to your room.” This communication made it clear that those recently in countries experiencing the 2014 Ebola epidemic would not be able to participate in the meeting. The ASTMH sent their own communication stating that the Society did not agree with the State's policy, but had no choice but to abide. However inconvenient and upsetting this decision might have been, what really matters transcends the mere disturbance of long-planned schedules. More broadly, we lost on five levels. First, there was a loss for evidence-based public health. Applying a blanket ban on travel for anyone within 3 weeks of arriving from Guinea, Liberia, or Sierra Leone, independent of the category of risk, was certainly expedient, but profoundly unjust, and also an inefficient public health measure. Those of us working in research and public health are tasked with producing evidence to be passed onto policy makers to help them make informed decisions. In these decisions they will have to weigh the evidence against a range of practical considerations—no easy chore. In this case, the decision was made “out of an abundance of caution.” Are our fellow citizens reassured? Do they feel better cared for? The majority most probably do, but this response appears proportional to the fear instilled by these very decisions—a dangerous vicious circle. Alarmism and misinformation call for drastic measures, and the process feeds itself. Enacting measures such as quarantine or a travel ban on everyone, when evidence says otherwise, sends contradictory messages to an already scared population. Disparate policies in different states and countries increase confusion. Second, there was a loss considering the human factor. Think about physically and emotionally worn-out volunteers returning from a demanding experience in harsh conditions—where en-passant their own lives are at stake, and where they see so many people die. Imposing disproportionate restrictions (all the way to quarantine) will most certainly not help. These volunteers should feel welcome and cared for rather than ostracized. Beyond financial means, human resources are absolutely critical to help contain the Ebola epidemic and to provide care for the ill. Many would volunteer twice or more to serve in endemic countries, but will not feel encouraged if they have to go through 3-week restrictions each time they return home. Some would opt for hibernating in less hostile countries, but many lives will be disrupted. A related concern is how long these measures will be kept in place, and whether they will be updated as risks decrease. Third, there was a practical loss, as we increased isolation of the affected countries, when what they actually needed was being supported and being heard. There is much that Ebola-afflicted countries can contribute. There are local doctors and nurses who have seen more Ebola patients than anyone else in the world. There are social workers who have been in direct touch with communities. There are those who have been applying control measures and have learned what works and what does not work. There are the potential trialists for the studies to come. And there are those who constitute the backbone of response and research. All of these residents of afflicted countries have been de-facto excluded from the international debate, where the decisions that affect their countries are made. Fourth, there was a loss for all disease control in Ebola-afflicted countries. A blanket travel ban excluded all local experts, regardless of their area of expertise, from attending the ASTMH meeting. These countries desperately need a coordinated response to help them deal with all aspects of health, as Ebola has been the final blow for already shaky health systems. Yet, with the ban on attendance at the ASTMH meeting, experts on human immunodeficiency virus (HIV) infection, tuberculosis, malaria, and many other locally endemic diseases were unable to learn from their international counterparts. Finally, there was a loss for international science. Scientific debate is stifled if those who have the “fingers on the pulse” are excluded. A gathering such as that provided by the ASTMH meeting is ideal for the exchange of experiences and information, and for discussions and debate to establish a research agenda toward finding solutions. We need all those with first-hand experience to contribute, but the travel ban prevented this. Of course, meetings are not the full solution to international health problems, but they offer an important step in that direction. A silver lining, perhaps, is that increased light has been shone on the importance of evidence-based public health policy, with rational decisions replacing those based on fear.

Knowledge, Attitudes, and Practices of US Practitioners Who Provide Pre‐Travel Advice

As international travel increases, many health care professionals are being asked to provide pre-travel advice. We designed an anonymous web-based survey to assess the extent to which primary care providers (PCPs) provide travel medicine advice and how their understanding and delivery of itinerary-specific advice and management compare with that of travel medicine specialists. We surveyed randomly selected US PCPs registered in the Pri-Med Institute (now pmiCME) database and US travel medicine specialists from the International Society of Travel Medicine (ISTM), American Society of Tropical Medicine and Hygiene (ASTMH), and Centers for Disease Control and Prevention (CDC) yellow fever (YF) vaccine provider mailing lists. SAS software (SAS Institute, Cary, NC, USA) was used for all analyses. Of 14,932 e-mails sent to valid e-mail addresses, 902 yielded complete or partially completed surveys (6.0% response rate). Eighty percent of respondents personally provided pre-travel advice (95% of travel medicine specialists versus 73% of PCPs). About two thirds of PCPs (68%) providing pre-travel consultations saw <50 travelers per year whereas 30% of travel medicine specialists saw <50 travelers per year. More travel medicine specialists (59%) than PCPs (18%) saw >500 travelers per year. Familiarity with travel-specific vaccines (YF, Japanese encephalitis) and provision of written educational materials increased as volume of travelers increased. Familiarity with antimalarial side effects and malaria resistance patterns, and knowledge scores based on brief pre-travel scenarios were higher in travel medicine specialists, ASTMH or ISTM certificate holders, and respondents who saw more pre-travel patients. Many PCP survey participants provided pre-travel advice, but most saw few travelers. Volume of travelers and holding an ASTMH or ISTM certificate had the greatest influence on knowledge of travel medicine and provision of appropriate advice and recommendations. Creating easily accessible travel medicine education programs for US providers from a wide range of disciplines is needed to improve the management of travelers.

Changes at Our Journal

I am honored and thrilled to serve as the new Editor-in-Chief of the American Journal of Tropical Medicine and Hygiene (AJTMH). I am also humbled because this will be a challenging task, and Jim Kazura left big shoes to fill. Jim's skillful leadership of the Journal for the last 15 years has been an enormous service to the membership of the American Society of Tropical Medicine and Hygiene (ASTMH) and the larger scientific community. Memories are fading, but many of us well remember some difficult days for the journal at about the turn of the century. Jim turned things around quickly after he took the helm, and under his tenure the Journal has been a leading voice in tropical medicine research. Indeed, most will agree that the AJTMH is the leading journal in the world addressing the full range of topics in tropical medicine.

62nd Annual Meeting of the American Society of Tropical Medicine and Hygiene (ASTMH). Washington, D.C., USA - November 13-17, 2013.

62nd Annual Meeting of the American Society of Tropical Medicine and Hygiene (ASTMH). Washington, D.C., USA - November 13-17, 2013.

62nd Annual Meeting of the American Society of Tropical Medicine and Hygiene (ASTMH). Washington, D.C., USA - November 13-17, 2013.

62nd Annual Meeting of the American Society of Tropical Medicine and Hygiene (ASTMH). Washington, D.C., USA - November 13-17, 2013.

Ethiopian Love Song

In 1972, as a “defrocked” debutante, I worked at a mission hospital in Haiti. It was a summer like no other: full of life, death, and love in unexpected guises. In short, the trip was transformative, drawing me to new worlds like a moth to a flame. Before long, I decided to study tropical medicine. A decade later—as an infectious diseases trainee—my Chief took me aside. “Can you speak with an applicant?,” he asked. And so I met Abraham Verghese, an Indian-American MD raised in Ethiopia. Soon, we were deep in conversation. What sparked our rapport, I later wondered. Was it spiritual provenance? (In 52 AD, Saint Thomas visited southern India and planted the ancient church of Verghese's forbears; in 301 AD, Saint Gregory led my Armenian ancestors to embrace a similar Christian faith.) Or perhaps it was a common love of tropical medicine, history, or literature. Because our Boston fellowships did not overlap, I never found out. Now, fast forward another dozen years. In 1994, when I was back in Los Angeles, Verghese published My Own Country, his breakout non-fiction book about acquired immunodeficiency syndrome (AIDS) sufferers in Tennessee. In 1998, his reputation grew with The Tennis Partner, a second powerful memoir set in Texas. Soon, I invited Verghese to speak at an American Society of Tropical Medicine and Hygiene (ASTMH) conference (for the record, he declined, albeit graciously). Finally, at a 2011 University of California at Los Angeles lecture, we reconnected in person. “What happened to your long hair?” were his first words. What the heck?, I thought. Then, I smiled. Writers' memories run deep. Anyway, this piece is not about chance encounters or reunions but Cutting for Stone, Verghese's latest medical blockbuster largely set at an Ethiopian mission hospital. Released in 2009, the novel remains on many bestseller lists even today. Before long (assuming it does not languish in Hollywood development hell), the story will bloom anew on the silver screen. Should I write about it for the Tropical Bookshelf? I waffled earlier this year, still unsure if the sprawling work was suited to AJTMH. Then, I reread the 540-page folio, savoring its story and themes. I also sampled a handful of reviews. There is so much more to say, I gasped. How could the critics have missed so much? Here is another tasting menu of a global saga of love, loss, and redemption, an author's passion for medicine, and a modern literary classic.

Cholera Elimination in Hispaniola

A catastrophic confluence of factors contributed to the rapid spread of cholera in Haiti following its introduction in late 2010. The outbreak is now the largest in modern history to affect a single country1; cases from Haiti comprised nearly half of the cholera cases reported worldwide in 2012.2 Although cases of cholera related to this outbreak have occurred in the Dominican Republic, the United States,3 and possibly in Cuba and other countries,4,5 spread in these other countries has been nil or limited. The factors responsible for rapid spread in Haiti include: long-standing water and sanitary inadequacies in Haiti; the further disruptions to water and sanitary systems imposed by the earthquake; above average rainfall; high water and ambient temperatures; and insufficient capacity of the government infrastructure to respond to the crisis. In 2008, before the earthquake, 63% of Haitians had access to improved sources of drinking water, and only 17% of the population had access to improved sanitation.6 To address these inadequacies, in January 2012 the Pan American Health Organization (PAHO), the United States Centers for Disease Control and Prevention (CDC), and the United Nations Children's Fund (UNICEF) put forward a call to action for international partners to support the governments of Haiti and the Dominican Republic with their long-term vision to strengthen water, sanitation, and hygiene (WASH) conditions in their respective countries.7 The same group supported the development of national plans for the elimination of cholera transmission on the Island of Hispaniola. In Haiti, the National Plan outlined a 10-year strategy to strengthen and sustain broad efforts for prevention and control of cholera infection, including water and sanitation infrastructure, surveillance, health promotion, and treatment measures.8 Plans in the Dominican Republic focused on bridging gaps in WASH access, and improving surveillance, health communication, and treatment. Partners were asked to assist the National governments to finance and implement these plans. In follow-up to the call for action, the initial partnership was expanded to involve a much broader coalition of partners; more than 20 partners have signed a Declaration of Support.9 One key partner, the American Society of Tropical Medicine and Hygiene (ASTMH), committed the use of its journal (through this issue) to document and explore important issues related to cholera transmission and the public health response in Haiti. Despite the challenges faced by Haiti after the earthquake, investments in laboratory, surveillance, and response capacity made possible the rapid detection of the cholera outbreak10; a national surveillance system was established with remarkable speed and has provided essential information on cases and mortality ratios.1 Critical augmentations of these systems are documented in this special issue. To facilitate urgent response to focal increases in case rates, an “alert and response” system was developed.11 To complement reporting based on clinical syndromes, a laboratory-enhanced surveillance system was established and is providing information on the proportion of diarrhea attributable to cholera and other causes.12 The outbreak strain in Hispaniola exhibits characteristics of both the El Tor and classical biotypes,13 and it was difficult to anticipate overall attack rates or the overall proportion of Vibrio cholerae infections that might lead to severe disease in the immunologically naive population of Haiti. A seroepidemiologic survey confirmed very high rates of infection—often subclinical.14 This survey and evaluations of case series helped identify risk factors for disease. Although symptomatic cholera presented uniformly across all age groups in one large urban treatment setting with high human immunodeficiency virus (HIV) prevalence, disease severity was associated with older age, but not with HIV infection.15 Access to and use of safe drinking water, sanitation, and hygiene remain the cornerstone of the effort to prevent cholera and many other enteric diseases, which remain leading causes of childhood illness and death. Evaluation of access to water and sanitation services has identified the continuing and large unmet needs, and helped to inform efforts to improve these services.16 Sustained efforts will be necessary to achieve long-term improvements.9 Early in the epidemic, oral cholera vaccine (OCV) was recognized as a potential additional intervention that could save lives rapidly in the short-run.17 However, in the face of substantial global vaccine supply shortages and the realities of post-earthquake Haiti, more data were needed to make an informed policy decision about who to target for, and the feasibility of, vaccination.18 To that end, two cholera vaccination projects documented the feasibility of such interventions in rural and urban conditions of Haiti.19,20 This experience, and evidence from models,21 suggests that in Haiti, combined WASH and OCV vaccination strategies are likely to be complementary and potentially synergistic. An impressive package of technical cooperation, including the special studies and experiences documented in this issue of the American Journal of Tropical Medicine and Hygiene, has greatly contributed to the response to cholera in Haiti. Much more has to be done to ensure access to potable water and sanitation, and there is a need to use all available cost-effective tools to prevent, detect, and control cholera, to save lives more rapidly, and ultimately to end cholera transmission.

61st Annual Meeting of the American Society of Tropical Medicine and Hygiene (ASTMH), Atlanta, Georgia, USA - November 12-15, 2012

61st Annual Meeting of the American Society of Tropical Medicine and Hygiene (ASTMH), Atlanta, Georgia, USA - November 12-15, 2012