Imported Lassa fever, Pennsylvania, USA, 2010.
Because the incubation period ranges from a few days to >2 weeks (1,5) and many symptoms are nonspecific, the potential exists for human carriage of Lassa virus to areas outside those to which it is endemic, putting travel companions, close contacts, and healthcare providers at risk for secondary infection. Before 2010, five instances of imported Lassa virus were recorded in persons from West Africa to the United States. Although early instances involved sick persons who were airlifted to the United States for diagnosis and treatment (7-9), the 2 most recent occurrences (1989 and 2004) involved persons who were not identified as potentially infectious until healthcare was sought in the United States (10,11). Here we report a case in a person who became infected and sick during a trip to Liberia and sought care upon return to the United States.
A Liberian man 47 years of age living in the United States traveled to Liberia in January 2010. He arrived in Monrovia, then spent 5 days traveling throughout Nimba County in north-central Liberia, bordering Guinea and Cote d'Ivoire. He reported sleeping nightly in his rural native village in a dwelling infested with rats and recalled several rat carcasses on the bedroom floor. On the day of his departure from Liberia, he developed fever, chills, joint pain of the knees and ankles, anorexia, sore throat, diffuse skin tenderness, and mild shortness of breath; he began taking amoxicillin and chloroquine before departing Liberia.
The patient's symptoms persisted upon arrival in the United States, prompting him to seek medical attention on day 5 of his illness. When he sought treatment, he had fever of 103[degrees]F, pulse of 99 beats/min, respiratory rate of 15 breaths/min, and blood pressure of 120/80 mm Hg (online Appendix Table, www.cdc.gov/EID/content/16/10/1598appT.htm). His physical examination was notable for posterior cervical adenopathy and a palpable spleen tip (Table). He had no evidence of conjunctival, nasal, or oral petechiae; no skin rashes; and no signs of hemorrhage or other lesions. Initial laboratory data showed leukopenia and thrombocytopenia and minimal transaminase elevations (online Appendix Table). Empiric malaria treatment was initiated upon admission and was subsequently discontinued when Plasmodium spp. antigen testing was negative and thick and thin blood smears showed no evident parasitemia. By the next day, mild pharyngitis with slight tonsillar exudates had developed. On the third hospital day, substernal chest pain and profuse watery diarrhea developed. Increasing transaminases and a slight coagulopathy were noted. Lassa fever was considered in the differential diagnosis; contact precautions and, subsequently, airborne precautions were taken. Because of noted clinical improvement, he was not given empiric intravenous ribavirin.
On day 5 of hospitalization, Lassa virus was identified by real-time PCR by using samples collected 2 days earlier, and sequencing of the amplified fragment yielded a unique sequence similar to sequences from previous Lassa virus isolates from Liberia. Subsequent samples confirmed Lassa fever diagnosis on the basis of real-time PCR, viral culture, and serology (Table).
The patient's fever resolved by day 16 of his illness. After 2 successive negative blood real-time PCR results, he was discharged from the hospital on day 21 of his illness with instructions to avoid unprotected sexual intercourse for 2 months. No hearing abnormalities were noted at the time of discharge or during telephone conversations 2 weeks and 2 months later.
A contact investigation was undertaken by the hospital and local, state, federal, and international health agencies. Exposed persons were identified as any persons who potentially came into contact with the patient or his body fluids during his illness. Because no contacts had direct exposure to body fluids (other than the patient's wife in Africa with whom he had sexual intercourse before becoming ill and who remained well, according to telephone follow-up with the patient), no patient contacts were considered high risk for secondary transmission (10). In total, 140 persons, including the patient's family in the United States, co-workers, and hospital workers who had contact with him (but did not have direct contact with bodily fluids) were identified as low-risk contacts. Health communication materials were developed on the basis of previous Lassa fever contact tracing activities (10). All hospital and community contacts were provided a Lassa fever fact sheet and asked to seek medical consultation if fever or other signs and symptoms of Lassa fever appeared. Upon completion of 21 days of follow-up, no secondary cases were identified.
The spectrum of Lassa fever can run from asymptomatic seroconversion to severe hemorrhagic fever with multiple organ failure and death (1,2,6). Factors supporting the diagnosis of Lassa fever in returning travelers include relevant epidemiologic exposure (travel to rural West Africa), signs and symptoms consistent with Lassa fever, and the absence of other infectious agents that can account for the illness. Although this patient did not seek treatment for hemorrhagic signs, his fever, pharyngitis, chest pain, and diarrhea (1 ,6), as well as thrombocytopenia and elevated transaminases, were consistent with Lassa fever (6,12). Early institution of ribavirin can dramatically decrease death rates among patients with severe Lassa fever if given within the first 6 days of illness (12); therefore, empiric ribavirin should be considered for an ill patient suspected of having Lassa fever.
As in this case, early suspicion of Lassa fever should prompt isolation measures to avoid secondary transmission; laboratory testing should be limited to essential tests, and all laboratory specimens should be handled with appropriate biosafety precautions to avoid aerosolizing the virus (13). Experience in regions where Lassa virus is endemic suggests human-to-human transmission occurs through direct contact with blood and body fluids or large-particle inhalation; transmission through viral aerosolization is not seen; and generally, when universal precautions are undertaken, transmission is unlikely (14). Nonetheless, aerosol in addition to contact precautions were undertaken once Lassa fever was suspected, given the theoretical potential for acquiring infection through inhalation of airborne virus from respiratory secretions or, in this case, copious diarrhea.
The patient described in this report represents the sixth known occurrence of Lassa fever imported to the United States. Clinicians treating recent travelers to West Africa who are febrile should obtain detailed histories from patients to determine whether they have traveled into rural areas in which the potential for exposure to rodents exists. The symptoms, signs, and laboratory abnormalities of Lassa fever are nonspecific and can overlap with other tropical infections. Therefore, efforts should be made to promptly diagnose or rule out other infectious agents in a patient who has the appropriate travel and exposure history so that further diagnostic studies and empiric therapy with ribavirin can be undertaken rapidly. Moreover, as soon as Lassa fever is suspected, patients and their specimens should be handled with adequate precautions, the local health department and Centers for Disease Control and Prevention should be notified, and specimens should be sent for specific diagnostic testing.
We thank medical staff, local and state public health personnel, and the staff of the Centers for Disease Control and Prevention who assisted with this investigation.
(1.) McCormick JB, King IJ, Webb PA, Johnson KM, O'Sullivan R, Smith ES, et al. A case-control study of the clinical diagnosis and course of Lassa fever. J Infect Dis. 1987;155:445-55.
(2.) McCormick JB, Webb PA, Krebs JW, Johnson KM, Smith ES. A prospective study of the epidemiology and ecology of Lassa fever. J Infect Dis. 1987;155:437-44.
(3.) Monath TP, Newhouse VF, Kemp GE, Setzer HW, Cacciapuoti A. Lassa virus isolation from Mastomys natalensis rodents during an epidemic in Sierra Leone. Science. 1974;185:263-5. DOI: 10.1126/ science.185.4147.263
(4.) Carey DE, Kemp GE, White HA, Pinneo L, Addy RF, Fom AL, et al. Lassa fever. Epidemiological aspects of the 1970 epidemic, Jos, Nigeria. Trans R Soc Trop Med Hyg. 1972;66:402-8. DOI: 10.1016/0035-9203(72)90271-4
(5.) Monath TP, Mertens PE, Patton R, Moser CR, Baum JJ, Pinneo L, et al. A hospital epidemic of Lassa fever in Zorzor, Liberia, March-April 1972. Am J Trop Med Hyg. 1973;22:773-9.
(6.) Frame JD. Clinical features of Lassa fever in Liberia. Rev Infect Dis. 1989;11(Suppl 4):S783-9.
(7.) Frame JD, Baldwin JM Jr, Gocke DJ, Troup JM. Lassa fever, a new virus disease of man from West Africa. I. Clinical description and pathological findings. Am J Trop Med Hyg. 1970;19:670-6.
(8.) Zweighaft RM, Fraser DW, Hattwick MA, Winkler WG, Jordan WC, Alter M, et al. Lassa fever: response to an imported case. N Engl J Med. 1977;297:803-7. DOI: 10.1056/NEJM197710132971504
(9.) Macher AM, Wolfe MS. Historical Lassa fever reports and 30-year clinical update. Emerg Infect Dis. 2006;12:835-7.
(10.) Holmes GP, McCormick JB, Trock SC, Chase RA, Lewis SM, Mason CA, et al. Lassa fever in the United States: investigation of a case and new guidelines for management. N Engl J Med. 1990;323:1120-3. DOI: 10.1056/NEJM199010183231607
(11.) Centers for Disease Control and Prevention. Imported Lassa fever--New Jersey, 2004. MMWR Morb Mortal Wkly Rep. 2004;53:894-7.
(12.) McCormick JB, King IJ, Webb PA, Scribner CL, Craven RB, Johnson KM, et al. Lassa fever: effective therapy with ribavirin. N Engl J Med. 1986;314:20-6. DOI: 10.1056/NEJM198601023140104
(13.) Centers for Disease Control and Prevention. Update: management of patients with suspected viral hemorrhagic fever--United States. MMWR Morb Mortal Wkly Rep. 1995;44:475-9.
(14.) Helmick CG, Webb PA, Scribner CL, Krebs JW, McCormick JB. No evidence for increased risk of Lassa fever infection in hospital staff. Lancet. 1986;328:1202-5. DOI: 10.1016/S0140-6736(86)92206-3
Author affiliations: University of Pennsylvania, Philadelphia, Pennsylvania, USA (V. Amorosa, R. McConnell, K.E. Dillon, K. Hamilton); Philadelphia Veterans Affairs Medical Center, Philadelphia (V. Amorosa); Centers for Disease Control and Prevention, Atlanta, Georgia, USA (A. MacNeil, A. Patel, B.R. Erickson, S. Campbell, B. Knust, D. Cannon, D. Miller, C. Manning, P.E. Rollin, S.T. Nichol); and Philadelphia Department of Health, Philadelphia (A. Patel)
Address for correspondence: Valerianna Amorosa, Philadelphia VAMCMedicine, University and Woodlawn, Philadelphia, PA 19104, USA; email: email@example.com
Dr Amorosa is assistant professor of clinical medicine at the University of Pennsylvania and chief of infectious diseases at the Philadelphia Veterans Affairs Medical Center. Her research interests include HIV/hepatitis C co-infection.
Table. Day by day symptoms and clinical information for a man 47 years of age with Lassa fever, Pennsylvania, USA, 2010* Examination Date Symptoms findings Jan 13-17 Fevers and chills, sore throat, NA arthralgias, diffuse abdominal pain Jan 18 Fevers and chills, sore throat, Prominent parotids, watery diarrhea, diffuse posterior cervical abdominal pain. lymphadenopathy, slight spleen tip Jan 19 Fevers and chills, sore throat, Slight tonsillar substernal chest pain with exudates, slight inspiration and when lying spleen tip supine, diarrhea, diffuse abdominal pain. Arthralgias resolve. Jan 20 Fevers and chills; sore throat; Slight tonsillar substernal chest pain, worse exudates, slight when lying down; diarrhea. spleen tip Abdominal pain improving. Jan 21 Fevers and chills, sore throat, Slight spleen tip diarrhea. Chest pain resolves. Abdominal pain improving. Jan 22 Fevers and chills, sore throat. Prominent Diarrhea resolves. Abdominal sternocleidomastoid pain resolves. muscles Jan 23 Fevers and chills, sore throat Prominent sternocleidomastoid muscles Jan 24 Fevers and chills, sore throat Prominent sternocleidomastoid muscles Jan 25 Fevers and chills. Sore throat Prominent improves. sternocleidomastoid muscles Jan 26 Fevers and chills. Sore throat Neck less prominent improves. Fevers and chills. Sore throat Jan 27 resolves. Decreased parotid enlargement and lymphadenopathy Fevers and chills Jan 28-29 Fever resolves Jan 30-Feb 3 Dowel Date movements Clinical information Jan 13-17 NA NA Jan 18 12 Jan 19 [approximately Tests for Clostridium equal to] 18 difficile, cryptosporidium, Giardia spp., thick and thin blood smears for malaria, Epstein-Barr virus, and respiratory virus panel; all negative Jan 20 3 HIV negative Jan 21 5 Stool culture negative Jan 22 NA Stopped IV fluids. Jan 23 3, formed PCR positive for Lassa virus Jan 24 NA Jan 25 3, formed Jan 26 NA Jan 27 NA Jan 28-29 NA Jan 30-Feb 3 NA Date Clinical action Jan 13-17 NA Jan 18 Contact isolation ordered. Jan 19 Contact precautions. Blood samples to test for Lassa virus drawn. Jan 20 EKG done, ribavirin requested, airborne precautions Jan 21 Held off on ribavirin. CDC received specimen. Jan 22 Jan 23 Jan 24 Jan 25 Jan 26 Jan 27 Jan 28-29 Jan 30-Feb 3 * NA, not available; EKG, electrocardiogram; IV, intravenous; CDC, Centers for Disease Control and Prevention.
|Printer friendly Cite/link Email Feedback|
|Author:||Amorosa, Valerianna; MacNeil, Adam; McConnell, Ryan; Patel, Ami; Dillon, Katherine E.; Hamilton, Kei|
|Publication:||Emerging Infectious Diseases|
|Article Type:||Disease/Disorder overview|
|Date:||Oct 1, 2010|
|Previous Article:||Predicting need for hospitalization of patients with pandemic (H1N1) 2009, Chicago, Illinois, USA.|
|Next Article:||Type 2 diabetes mellitus and increased risk for malaria infection.|