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Clinical features and patient management of Lujo hemorrhagic fever.

Sewlall NH, Richards G, Duse A, Swanepoel R, Paweska J, Blumberg L, Dinh TH, Bausch D - PLoS Negl Trop Dis (2014)

Bottom Line: No major hemorrhage was noted.Shock and multi-organ system failure, often with evidence of disseminated intravascular coagulopathy, ensued in the second week, with death in four of the five cases.Distinctive treatment components of the one surviving patient included rapid commencement of the antiviral drug ribavirin and administration of HMG-CoA reductase inhibitors (statins), N-acetylcysteine, and recombinant factor VIIa.

View Article: PubMed Central - PubMed

Affiliation: Internal Medicine, Morningside MediClinic, Johannesburg, South Africa; Department of Medicine, University of the Witwatersrand, Johannesburg, South Africa.

ABSTRACT

Background: In 2008 a nosocomial outbreak of five cases of viral hemorrhagic fever due to a novel arenavirus, Lujo virus, occurred in Johannesburg, South Africa. Lujo virus is only the second pathogenic arenavirus, after Lassa virus, to be recognized in Africa and the first in over 40 years. Because of the remote, resource-poor, and often politically unstable regions where Lassa fever and other viral hemorrhagic fevers typically occur, there have been few opportunities to undertake in-depth study of their clinical manifestations, transmission dynamics, pathogenesis, or response to treatment options typically available in industrialized countries.

Methods and findings: We describe the clinical features of five cases of Lujo hemorrhagic fever and summarize their clinical management, as well as providing additional epidemiologic detail regarding the 2008 outbreak. Illness typically began with the abrupt onset of fever, malaise, headache, and myalgias followed successively by sore throat, chest pain, gastrointestinal symptoms, rash, minor hemorrhage, subconjunctival injection, and neck and facial swelling over the first week of illness. No major hemorrhage was noted. Neurological signs were sometimes seen in the late stages. Shock and multi-organ system failure, often with evidence of disseminated intravascular coagulopathy, ensued in the second week, with death in four of the five cases. Distinctive treatment components of the one surviving patient included rapid commencement of the antiviral drug ribavirin and administration of HMG-CoA reductase inhibitors (statins), N-acetylcysteine, and recombinant factor VIIa.

Conclusions: Lujo virus causes a clinical syndrome remarkably similar to Lassa fever. Considering the high case-fatality and significant logistical impediments to controlled treatment efficacy trials for viral hemorrhagic fever, it is both logical and ethical to explore the use of the various compounds used in the treatment of the surviving case reported here in future outbreaks. Clinical observations should be systematically recorded to facilitate objective evaluation of treatment efficacy. Due to the risk of secondary transmission, viral hemorrhagic fever precautions should be implemented for all cases of Lujo virus infection, with specialized precautions to protect against aerosols when performing enhanced-risk procedures such as endotracheal intubation.

No MeSH data available.


Related in: MedlinePlus

Clinical manifestations of Lujo haemorrhagic fever in Patient 5, including facial and neck swelling (A), subconjunctival haemorrhage (B), and maculopapular rash(C).
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Related In: Results  -  Collection


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pntd-0003233-g003: Clinical manifestations of Lujo haemorrhagic fever in Patient 5, including facial and neck swelling (A), subconjunctival haemorrhage (B), and maculopapular rash(C).

Mentions: On ID-2 myalgias became prominent and thrombocytopenia worsened (61,000/µL). On ID-3 the temperature was 38.6°C and non-bloody diarrhea and vaginal bleeding began, despite the patient being midcycle. Laboratory tests on ID-4 show a leukocyte count of 7,100/µL, elevated transaminases (AST 192 IU/L, ALT 81 IU/L), and a prolonged PTT of 60 seconds (control 31 seconds). Drowsiness and exudative pharyngitis, including a peri-tonsillar pseudo-membrane, were present. On ID-5 the patient complained of odynophagia and facial edema and a resting tremor were noted (Figure 3A). Despite being clinically hypovolemic, relative bradycardia (HR 68/minute) was present. Thrombocytopenia (48,000/µL) and transaminitis (AST 209 IU/L, ALT 82 IU/L) worsened. Intravenous recombinant factor VIIa (1.2 mg q6 hrs) was begun and the N-acetylcysteine was switched to IV administration (1 g q8 hrs). On ID-6, the facial edema was slightly improved but palatal ecchymoses were noted along with conjunctival injection. To cover possible bacterial or fungal super-infection, IV cefepime (2 g q12 hrs) and fluconazole (400 mg q12 hrs) were started.


Clinical features and patient management of Lujo hemorrhagic fever.

Sewlall NH, Richards G, Duse A, Swanepoel R, Paweska J, Blumberg L, Dinh TH, Bausch D - PLoS Negl Trop Dis (2014)

Clinical manifestations of Lujo haemorrhagic fever in Patient 5, including facial and neck swelling (A), subconjunctival haemorrhage (B), and maculopapular rash(C).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4230886&req=5

pntd-0003233-g003: Clinical manifestations of Lujo haemorrhagic fever in Patient 5, including facial and neck swelling (A), subconjunctival haemorrhage (B), and maculopapular rash(C).
Mentions: On ID-2 myalgias became prominent and thrombocytopenia worsened (61,000/µL). On ID-3 the temperature was 38.6°C and non-bloody diarrhea and vaginal bleeding began, despite the patient being midcycle. Laboratory tests on ID-4 show a leukocyte count of 7,100/µL, elevated transaminases (AST 192 IU/L, ALT 81 IU/L), and a prolonged PTT of 60 seconds (control 31 seconds). Drowsiness and exudative pharyngitis, including a peri-tonsillar pseudo-membrane, were present. On ID-5 the patient complained of odynophagia and facial edema and a resting tremor were noted (Figure 3A). Despite being clinically hypovolemic, relative bradycardia (HR 68/minute) was present. Thrombocytopenia (48,000/µL) and transaminitis (AST 209 IU/L, ALT 82 IU/L) worsened. Intravenous recombinant factor VIIa (1.2 mg q6 hrs) was begun and the N-acetylcysteine was switched to IV administration (1 g q8 hrs). On ID-6, the facial edema was slightly improved but palatal ecchymoses were noted along with conjunctival injection. To cover possible bacterial or fungal super-infection, IV cefepime (2 g q12 hrs) and fluconazole (400 mg q12 hrs) were started.

Bottom Line: No major hemorrhage was noted.Shock and multi-organ system failure, often with evidence of disseminated intravascular coagulopathy, ensued in the second week, with death in four of the five cases.Distinctive treatment components of the one surviving patient included rapid commencement of the antiviral drug ribavirin and administration of HMG-CoA reductase inhibitors (statins), N-acetylcysteine, and recombinant factor VIIa.

View Article: PubMed Central - PubMed

Affiliation: Internal Medicine, Morningside MediClinic, Johannesburg, South Africa; Department of Medicine, University of the Witwatersrand, Johannesburg, South Africa.

ABSTRACT

Background: In 2008 a nosocomial outbreak of five cases of viral hemorrhagic fever due to a novel arenavirus, Lujo virus, occurred in Johannesburg, South Africa. Lujo virus is only the second pathogenic arenavirus, after Lassa virus, to be recognized in Africa and the first in over 40 years. Because of the remote, resource-poor, and often politically unstable regions where Lassa fever and other viral hemorrhagic fevers typically occur, there have been few opportunities to undertake in-depth study of their clinical manifestations, transmission dynamics, pathogenesis, or response to treatment options typically available in industrialized countries.

Methods and findings: We describe the clinical features of five cases of Lujo hemorrhagic fever and summarize their clinical management, as well as providing additional epidemiologic detail regarding the 2008 outbreak. Illness typically began with the abrupt onset of fever, malaise, headache, and myalgias followed successively by sore throat, chest pain, gastrointestinal symptoms, rash, minor hemorrhage, subconjunctival injection, and neck and facial swelling over the first week of illness. No major hemorrhage was noted. Neurological signs were sometimes seen in the late stages. Shock and multi-organ system failure, often with evidence of disseminated intravascular coagulopathy, ensued in the second week, with death in four of the five cases. Distinctive treatment components of the one surviving patient included rapid commencement of the antiviral drug ribavirin and administration of HMG-CoA reductase inhibitors (statins), N-acetylcysteine, and recombinant factor VIIa.

Conclusions: Lujo virus causes a clinical syndrome remarkably similar to Lassa fever. Considering the high case-fatality and significant logistical impediments to controlled treatment efficacy trials for viral hemorrhagic fever, it is both logical and ethical to explore the use of the various compounds used in the treatment of the surviving case reported here in future outbreaks. Clinical observations should be systematically recorded to facilitate objective evaluation of treatment efficacy. Due to the risk of secondary transmission, viral hemorrhagic fever precautions should be implemented for all cases of Lujo virus infection, with specialized precautions to protect against aerosols when performing enhanced-risk procedures such as endotracheal intubation.

No MeSH data available.


Related in: MedlinePlus