Algorithms in the diagnosis and management of exotic diseases. XIX. Major tropical viral infections: smallpox, yellow fever, and Lassa fever.
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Diagnosis, Differential↗
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A neutralization test survey for Lassa Fever activity in Lassa, Nigeria.
5-8% of 434 sera collected in Lassa village, Nigeria, in August 1970 were positive by neutralization test for Lassa fever (LF) virus. A second survey in March 1971 found 15 of 47 complete compounds tested in Lassa, Dille and Yuba villages had at least one peron with serologically demonstrable experience with LF virus. 67% of positive compounds had more than one infected member. Four of 17 hospital staff sero-converted between August 1970 and March 1971 without symptoms, evidence that subclinical infections of LF occr.
Adolescent↗
Nosocomial Outbreak of Lassa Fever in Conakry, Guinea, 2022.
BACKGROUND: Lassa fever is endemic in Guinea, with high seroprevalence in the forest region. However, clinical cases have been only anecdotally reported. In August 2022, a nosocomial outbreak occurred at a private clinic in the capital, Conakry, an area previously considered low risk. METHODS: Suspected cases were confirmed by real-time reverse-transcription polymerase chain reaction within 24 hours. Viremia was monitored during hospitalization, and whole-genome sequencing was performed in-country within 13 days of outbreak detection. Outbreak investigation involved rodent testing in the home village of the suspected primary case. RESULTS: Six cases were laboratory-confirmed, 5 of which were healthcare workers of the clinic. The case fatality rate was 16.7%. Viral RNA remained detectable in blood of survivors for a median of 26 days (interquartile range, 24-41 days) post-disease onset. Epidemiological investigations identified a suspected primary case, who had died of a febrile disease compatible with Lassa fever, had contact with all secondary cases, and had a travel history from Kissidougou area. Three near-complete and 1 partial Lassa virus genomes were recovered from the secondary cases, which phylogenetically clustered with genomes from central Guinea. Consistent with a common transmission source, the 4 genomes were almost identical. Rodent testing revealed a new reservoir area in eastern-central Guinea. CONCLUSIONS: This outbreak highlights the vulnerability of healthcare settings in low-prevalence areas of West Africa to nosocomial Lassa virus transmission due to human mobility. Facilitated by capacity-building programs for viral hemorrhagic fevers, rapid diagnosis, genomic analysis, and ecological assessment enabled an efficient outbreak response and control.
Lassa Fever↗
Diagnosis of Lassa fever and the isolation and management of patients.
The clinical spectrum of Lassa fever is described and discussed in terms of the possible pathophysiological events involved. Early diagnosis is essential to permit prompt isolation of the potentially infectious patient. Lassa fever may be suspected on clinical grounds, but specific early diagnosis depends upon isolation of the virus. Virus isolation is best accomplished from serum obtained during the first 2 weeks of illness. The patterns of viraemia and virus excretion described in this paper are useful guidelines for determining the duration of patient isolation. Problems encountered in the isolation, management, and transport of the patient with Lassa fever are discussed.
Diagnosis, Differential↗
Audiometric comparison of Lassa fever hearing loss and idiopathic sudden hearing loss: evidence for viral cause.
A recently published prospective study on acute sensorineural deafness in Lassa fever among a West African population showed the audiometric pattern of a known virally induced hearing loss. Using the audiometric data from the patients with Lassa fever in that study, we analyzed and classified the initial hearing loss and final recovery into three groups by pure-tone average values and then did the same for 222 patients with idiopathic sudden hearing loss (SHL) in our study. Statistical analyses of the severity of initial hearing loss and the hearing recovery pattern indicate that the clinical course of our 222 patients with idiopathic SHL showed no statistically significant differences from the clinical course of the patients with Lassa fever. We found a marked difference in age, however, and a clinically significant difference in the incidence of bilateral hearing loss. In reviewing the literature on sudden sensorineural hearing loss, we found no apparent relation between severity of viral illness and initial hearing loss or subsequent recovery. Cummins et al. suggest that virally induced hearing loss in Lassa fever is linked to the host's immune response and not to the viremia. We thus propose a virally induced immune response mechanism for idiopathic sensorineural SHL. Further prospective studies are needed for verification.
Acute Disease↗
Lassa fever (arenaviruses) as a public health problem.
Two "new" virus infections, Marburg and Lassa fever, now constitute diseases of public health importance in several countries of Africa, especially West Africa. Lassa fever has an insidious onset, is initially difficult to diagnose, has "nonspecific" clinical symptoms which have been confused with yellow fever and typhoid, shows evidence of persistent infection, is tremendously contagious, has a high mortality rate, and in particular exhibits unusual nosocomial propensity. It has also been shown to be the cause of premature births and spontaneous abortions in pregnant women. The virus is transmitted by the respiratory route and by direct contact with contaminated materials. Persistent complement-fixing antibodies have been demonstrated in patients recovered from the disease. The causative agent, a member of the arenavirus group, is known to be enzootic in rodents, especially Mastomys natalensis.
Animals↗
Lassa fever: review of epidemiology and epizootiology.
The basic ecology of Lassa fever appears to involve enzootic transmission of virus in commensal populations of a single murine species, Mastomys natalensis. Virus may spill over from the rodent cycle to man by various routes. Secondary spread between humans may occur within domiciliary groups, and persons infected within the community who develop clinical disease may introduce the virus into hospital and begin a cycle of nosocomial infection.Between 1969, when Lassa fever was first described, and June 1975, the disease was recognized on 9 discrete occasions, affecting 114 persons. Over one-third of these infections were acquired by person-to-person spread within hospitals. In only one outbreak (in Sierra Leone) were the majority of cases acquired in the community. Recent observations have indicated hyperendemic disease in eastern Sierra Leone. Cases have occurred in Nigeria, Sierra Leone, and Liberia, and serological evidence exists for activity of the virus elsewhere in West and Central Africa. Seasonal factors appear to play a role in the appearance of human cases. Attack rates have been higher in adults than in children. The source of infection and potential routes of virus transmission in the various epidemics are discussed, and perspectives for future epidemiological research are presented.
Adolescent↗
Lassa fever--an autopsy report from the eastern part of Nigeria.
Autopsy findings of a case of Lassa fever from the Eastern part of Nigeria are presented. The authors suggest that in Lassa fever there is an involvement of the brain in the nature of encephalitis.
Adult↗
Use of the complement fixation (CF) test in Lassa fever surveillance. Evidence for persistent CF antibodies.
A survey to detect individuals with antibodies to Lassa virus was undertaken among hospital personnel in the eastern and southern provinces of Sierra Leone late in 1974. Sera were evaluated by the complement fixation test. The data obtained showed that some contacts of Lassa fever patients in the 1972 epidemic had developed antibodies to the virus; individuals who had never reported being sick also showed evidence of infection, with significant CF antibody titres in their sera. Surviving Lassa fever patients from the 1972 epidemic still had easily measurable levels of persisting CF antibodies. The significance of these data is discussed; in addition it is recommended that the CF test should continue to be the method of choice in mass surveys for this virus disease until other tests can be developed.
Adolescent↗
Lassa fever, Marburg and Ebola virus diseases and other exotic diseases: is there a risk to Canada?
There are seven exotic diseases of concern; three of these, the most unpredictable and least understood, are Lassa fever, Marburg virus disease and Ebola virus disease. In this article the epidemiologic aspects of these diseases are discussed, with particular emphasis on exportation from their indigenous areas in Africa and on the occurrence of secondary cases. Any of these conditions could be brought into Canada either by aeromedical evacuation or inadvertently. Between 1972 and 1978 there were seven occasions when Canada could have been involved with handling cases of Lassa fever. The Government of Canada has purchased several containment bed and transit isolators. These units, with filtered air under negative pressure, accommodate infectious patients being transported and cared for without contaminating medical attendants or the environment.
Adult↗
Lassa fever: review of virology, immunopathogenesis, and algorithms for control and therapy.
Lassa fever is an acute viral illness which causes consideration morbidity and mortality in the West African subregion. Recent studies have revealed that platelet and endothelial dysfunction might play a central role in the pathophysiology of this disease. Guidelines for the management of cases of the disease have recently been revised by the Centres for Disease Control, recommending care in local hospitals with use of meticulous barrier nursing techniques. This article reviews the epidemiology, immunology, pathogenesis and pathology, and current algorithms for prevention and therapy.
Algorithms↗
Lassa fever encephalopathy: clinical and laboratory findings.
Clinical and laboratory findings are reported in nine patients who developed acute encephalopathy during the course of Lassa fever. The encephalopathy manifested 3-17 days after disease onset with confusion, followed rapidly by tremor (seven patients), grand mal convulsions (seven), abnormal posturing (three) and coma (eight); focal neurological signs and evidence of raised intracranial pressure were not seen. Eight patients died, most commonly from respiratory arrest following a protracted fit. Development of encephalopathy did not correlate with the presence of virus in cerebrospinal fluid (CSF), nor with virus antibodies in CSF and/or serum; thus, neither direct cytopathic nor immune-mediated mechanisms seem to be involved in its pathogenesis.
Adolescent↗
Handling patients with suspected Lassa fever entering Great Britain.
A special isolation unit has been created at the Hospital for Tropical Diseases, London, for the reception of patients arriving in Great Britain from West Africa with suspected Lassa fever. The management of such patients and the operation of the unit are described. Experience during the first eighteen months of operation has been very satisfactory and valuable lessons have been learned concerning the diagnosis and treatment of Lassa fever and the nursing of patients.
Africa, Western↗
Lassa fever: response to an imported case.
In February, 1976, a Peace Corps worker returned to the United States from Sierra Leone with an undiagnosed illness later recognized as Lassa fever. To assess the risk of transmission and to contain a potential outbreak, we identified 552 contacts as having had exposure to the patient before the start of strict isolation procedures, and maintained intensive surveillance on these contacts for 21 days. At the end of the surveillance period, no illness had developed in contacts. One month later, a serologic survey among 29 of the contacts judged to be at high risk gave no evidence of infection. In response to the importation of this communicable and highly fatal disease, procedures for the isolation of the patient, the identification, surveillance and management of contacts and the handling of laboratory specimens were developed and implemented. These procedures could be adapted to future introductions of highly contagious diseases.
Adult↗
A serological survey of Lassa fever in Liberia.
A serological survey was undertaken at four Liberian hospitals in 1974 in which serum samples were taken from 104 health workers and 61 patients. Six persons had Lassa fever antibodies: four midwives and two students of midwifery. Of those persons who had lived in Loffa County, 4 of 22 midwives were seropositive whereas none of the other 39 residents were positive (P = 0.014).
Adult↗
Lassa fever in Onitsha, East Central State, Nigeria in 1974.
Three cases of Lassa fever occurred in Onitsha, East Central State, Nigeria, in January and February 1974. The first case was a 19-year-old Nigerian; the other 2 cases were German missionary physicians at St Charles Borromeo Hospital, Onitsha, one of whom cared for the patient who was the first case. Thus, 2 of the 3 cases were hospital acquired. Investigations failed to discover a village outbreak or the source of virus for the first case. A serosurvey of 258 hospital staff members and contacts of the 3 cases showed no other persons with antibody to Lassa virus. The absence of Lassa virus antibody in a high-risk group indicates a low or nonexistent level of past Lassa virus activity in southeastern Nigeria.
Adult↗
The pathology of human Lassa fever.
Pathological findings have been described in only a small number of cases of Lassa fever since the virus was first isolated in 1969. Morphologically, eosinophilic necrosis of hepatocytes was the most frequent finding and focal necroses, often extensive, were present in most cases. These findings are similar to the lesions previously described in Argentinian and Bolivian haemorrhagic fever. Focal interstitial pneumonitis, focal tubular necrosis in the kidney, lymphocytic infiltration of the splenic veins, and partial replacement of the splenic follicles by amorphous eosinophilic material have been described, but the significance of these findings is unclear. More detailed and sophisticated investigations are required in the future if pathogenetic mechanisms are to be unravelled.
Humans↗