Summary Of Exposure |
A) BACKGROUND: Venezuelan equine encephalitis (VEE) is caused by an RNA arbovirus (name from "arthropod borne viruses") of the alphavirus genus which is a member of the Togaviridae family. The causative agent of VEE is a 40- to 45-nm, single-stranded RNA virus.
B) TRANSMISSION: Alphaviruses are transmitted by the bite of a mosquito. Equidae or other mammals serve as amplifying hosts and source of mosquito infection. During epizootic epidemics, a large variety of mosquito vectors transmit subtypes IAB and IC of the VEE.
C) VECTOR: Vectors for transmission of the virus include a large variety of mosquito vectors, including species of the general Aedes, Psorophora, and Mansonia, which transmit subtypes IAB and IC during epizootic epidemics.
D) EPIDEMIOLOGY: Historically, large equine epizootics have occurred at 5 to 10 year intervals in Venezuela, Columbia, Ecuador, and Peru prior to 1973, with mortality rates as high as 40%.
1) DISTRIBUTION: Major epidemics can occur periodically and somewhat sporadically when various strains can occur in equids. In tropical areas, VEE cases can often overlap with dengue fever and malaria because the signs and symptoms of acute febrile illness are similar; therefore, cases may be underreported in some areas where clinical awareness and laboratory studies are lacking.
2) CASE FATALITY RATE: Overall case fatality rate is less than 1%, with most of the fatalities reported in children. Cases presenting with encephalitis may have a mortality rate approaching 20%.
E) WITH POISONING/EXPOSURE
1) INCUBATION PERIOD: 2 to 5 days.
2) ADVERSE EFFECTS: FLU-LIKE ILLNESS: Following the incubation period, a sudden onset of a flu-like illness occurs, with chills and spiking fever, malaise, photophobia and severe headache. This is followed by myalgias, sore throat, coughing, nausea, vomiting, and sometimes diarrhea. Tachycardia, conjunctival infection, and sometimes nonexudative pharyngitis may be seen on physical examination. During the flu-like illness stage, some patients may exhibit evidence of CNS involvement, which may progress to severe encephalitis. In severe cases, residual neurologic damage may also occur. Children are more likely to develop VEE-associated encephalitis. CNS effects including disorientation, ataxia, mental depression, and seizures can be develop in up to 14% of infected individuals, especially in children. COMMON: Lymphadenopathy. INFREQUENT: Less common effects include photophobia, seizures, confusion, coma, tremors, and diplopia. DURATION: The acute phase lasts up to 4 to 6 days.
3) CONVALESCENT PERIOD: After 4 to 6 days the acute illness subsides, and convalescent signs/symptoms, including asthenia and lethargy, may continue for up to 3 weeks. In more severe cases, symptoms may last up to 8 days. Full recovery usually takes 1 to 2 weeks. Excellent short-term and long-term immunity results on recovery from infection.
4) BIPHASIC PERIOD: Occasionally a biphasic course is noted, with acute symptoms reappearing following a brief remission, within a week after initial onset.
5) BIOLOGIC TERRORISM: A biological terrorist attack with aerosolized virus may cause infections of the olfactory nerve and spread directly to the CNS, resulting in an associated high morbidity and mortality.
6) PREGNANCY: Severe congenital neuroanatomical anomalies or fetal demise may occur if VEE infection occurs during pregnancy.
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Vital Signs |
3.3.1) SUMMARY
A) Chills and fever and increased pulse are common.
3.3.3) TEMPERATURE
A) Sudden onset of chills and fever occurs following a 2 to 5 day incubation period after exposure (Mangiafico et al, 2002; Douglas, 1996).
B) CASE SERIES: In a study of 42 cases of endemic VEE detected in Panama from 1961 to 2004 most clinical signs and symptoms were characterized by nausea, vomiting, diarrhea, fever, headache and tremors. Of the 33 cases that exhibited clinical adverse events, fever (94%) was the most common event reported (Quiroz et al, 2009).
3.3.5) PULSE
A) Pulse rate may be elevated during acute illness (Douglas, 1996).
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Heent |
3.4.3) EYES
A) Conjunctival injection is commonly seen on physical examination during the initial phase of illness (Douglas, 1996). Photophobia and diplopia may occur during the initial onset of illness.
B) CASE SERIES: In a study of 42 cases of endemic VEE detected in Panama from 1961 to 2004 most clinical signs and symptoms were characterized by nausea, vomiting, diarrhea, fever, headache and tremors. Of the 33 cases that exhibited clinical adverse events, retroorbital pain (27%) occurred frequently (Quiroz et al, 2009).
3.4.6) THROAT
A) Nonexudative pharyngitis and cough may occur during the acute phase of illness (Douglas, 1996; Sanford, 1994).
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Cardiovascular |
3.5.2) CLINICAL EFFECTS
A) TACHYARRHYTHMIA 1) WITH POISONING/EXPOSURE a) Physical examination during the initial phase of illness commonly reveals tachycardia (Douglas, 1996).
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Respiratory |
3.6.2) CLINICAL EFFECTS
A) ACUTE RESPIRATORY INSUFFICIENCY 1) WITH POISONING/EXPOSURE a) Patients who progress to CNS involvement with encephalitis may experience a central respiratory failure (Douglas, 1996).
B) COUGH 1) WITH POISONING/EXPOSURE a) CASE SERIES: In a study of 42 cases of endemic VEE detected in Panama from 1961 to 2004 most clinical signs and symptoms were characterized by nausea, vomiting, diarrhea, fever, headache and tremors. Of the 33 cases that exhibited clinical adverse events, cough (3%) occurred rarely (Quiroz et al, 2009).
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Neurologic |
3.7.2) CLINICAL EFFECTS
A) CENTRAL NERVOUS SYSTEM FINDING 1) WITH POISONING/EXPOSURE a) Clinical signs of mild CNS involvement may occur during the early flu-like illness phase and may include headache, somnolence, photophobia, diplopia, and confusion (Mangiafico et al, 2002; Douglas, 1996; Sanford, 1994; Casamassima et al, 1987).
B) HEADACHE 1) WITH POISONING/EXPOSURE a) CASE SERIES: In a study of 42 cases of endemic VEE detected in Panama from 1961 to 2004 most clinical signs and symptoms were characterized by fever, headache, nausea, vomiting, diarrhea, and tremors. Of the 33 cases that exhibited clinical adverse events, headache (55%) was frequently reported (Quiroz et al, 2009).
C) TREMOR 1) WITH POISONING/EXPOSURE a) CASE SERIES: In a study of 42 cases of endemic VEE detected in Panama from 1961 to 2004 most clinical signs and symptoms were characterized by nausea, vomiting, diarrhea, fever, headache and tremors. Of the 33 cases that exhibited clinical adverse events, tremors (27%) occurred frequently (Quiroz et al, 2009).
D) SEIZURE 1) WITH POISONING/EXPOSURE a) CASE SERIES: In a study of 42 cases of endemic VEE detected in Panama from 1961 to 2004 most clinical signs and symptoms were characterized by nausea, vomiting, diarrhea, fever, headache and tremors. Of the 33 cases that exhibited clinical adverse events, seizures (3%) occurred rarely (Quiroz et al, 2009).
E) ENCEPHALOMYELITIS 1) WITH POISONING/EXPOSURE a) Severe cases may progress to encephalitis, which has been characterized by seizures, meningeal signs or meningitis, tremor, delirium, stupor, coma, spastic paralysis, abnormal reflexes, cranial nerve palsies, nystagmus, nuchal rigidity and central respiratory failure. Most severe cases will result in residual neurologic damage (Douglas, 1996; Sanford, 1994). Children are more likely to develop VEE-associated encephalitis (Paessler & Weaver, 2009).
b) CNS pathologic findings in severe encephalitis cases have included edema, meningeal and perivascular inflammation, intracerebral hemorrhages, neuronal degeneration, and vasculitis (Douglas, 1996).
c) CASE SERIES: In a study of 42 cases of endemic VEE detected in Panama from 1961 to 2004 most clinical signs and symptoms were characterized by nausea, vomiting, diarrhea, fever, headache and tremors. Of the 33 cases that exhibited clinical adverse events, encephalitis (9%) occurred infrequently (Quiroz et al, 2009).
F) CSF CELL CONTENT: RAISED 1) WITH POISONING/EXPOSURE a) The cerebrospinal fluid contains up to 500 cells per cubic millimeter (predominantly lymphocytes) in the most severe cases of encephalitis (Douglas, 1996). Pleocytosis with modest increases in protein and normal glucose concentrations have been reported (Sanford, 1994).
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Gastrointestinal |
3.8.2) CLINICAL EFFECTS
A) NAUSEA, VOMITING AND DIARRHEA 1) WITH POISONING/EXPOSURE a) Onset of nausea and vomiting generally occurs following an initial period of a flu-like illness. Occasionally diarrhea occurs during the same time frame (Douglas, 1996; Sanford, 1994).
B) NAUSEA AND VOMITING 1) WITH POISONING/EXPOSURE a) CASE SERIES: In a study of 42 cases of endemic VEE detected in Panama from 1961 to 2004 most clinical signs and symptoms were characterized by nausea, vomiting, diarrhea, fever, headache and tremors. Of the 33 cases that exhibited clinical adverse events, nausea (21%) and vomiting (21%) were common (Quiroz et al, 2009).
C) DIARRHEA 1) WITH POISONING/EXPOSURE a) CASE SERIES: In a study of 42 cases of endemic VEE detected in Panama from 1961 to 2004 most clinical signs and symptoms were characterized by nausea, vomiting, diarrhea, fever, headache and tremors. Of the 33 cases that exhibited clinical adverse events, diarrhea (9%) occurred infrequently (Quiroz et al, 2009).
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Hepatic |
3.9.2) CLINICAL EFFECTS
A) LIVER ENZYMES ABNORMAL 1) WITH POISONING/EXPOSURE a) In severe cases, hepatic enzymes (serum LDH and glutamic-oxaloacetic transaminase) may be elevated. Pathologic liver changes have included hepatocellular degeneration and necrosis (Douglas, 1996).
B) HEPATIC FAILURE 1) WITH POISONING/EXPOSURE a) CASE SERIES: In a study of 42 cases of endemic VEE detected in Panama from 1961 to 2004 most clinical signs and symptoms were characterized by nausea, vomiting, diarrhea, fever, headache and tremors. Of the 33 cases that exhibited clinical adverse events, hepatic failure (3%) occurred rarely (Quiroz et al, 2009).
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Genitourinary |
3.10.2) CLINICAL EFFECTS
A) ACUTE RENAL FAILURE SYNDROME 1) WITH POISONING/EXPOSURE a) CASE SERIES: In a study of 42 cases of endemic VEE detected in Panama from 1961 to 2004 most clinical signs and symptoms were characterized by nausea, vomiting, diarrhea, fever, headache and tremors. Of the 33 cases that exhibited clinical adverse events, renal failure (3%) occurred rarely (Quiroz et al, 2009).
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Hematologic |
3.13.1) SUMMARY
A) Low peripheral leukocyte count has been reported in severe cases.
3.13.2) CLINICAL EFFECTS
A) LEUKOPENIA 1) WITH POISONING/EXPOSURE a) Often the peripheral leukocyte count is decreased, with decreases in both lymphocytes and neutrophils. The peripheral leukocyte count is less often normal, with a relative lymphopenia (Douglas, 1996). In some cases a striking leukopenia and lymphopenia may be present. Leukopenia has been reported in two-thirds of patients by the third day of illness (Sanford, 1994). In one case, leukopenia was noted 2 weeks after the onset of illness (Mangiafico et al, 2002).
B) HEMORRHAGE 1) WITH POISONING/EXPOSURE a) CASE SERIES: In a study of 42 cases of endemic VEE detected in Panama from 1961 to 2004 most clinical signs and symptoms were characterized by nausea, vomiting, diarrhea, fever, headache and tremors. Of the 33 cases that exhibited clinical adverse events, hemorrhage (3%) occurred rarely (Quiroz et al, 2009).
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Dermatologic |
3.14.2) CLINICAL EFFECTS
A) PURPURA 1) WITH POISONING/EXPOSURE a) Petechiae over the distal forearms and hands was reported in the early stages of VEE in one case (Mangiafico et al, 2002).
B) ERUPTION 1) WITH POISONING/EXPOSURE a) CASE SERIES: In a study of 42 cases of endemic VEE detected in Panama from 1961 to 2004 most clinical signs and symptoms were characterized by nausea, vomiting, diarrhea, fever, headache and tremors. Of the 33 cases that exhibited clinical adverse events, rash (3%) occurred rarely (Quiroz et al, 2009).
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Musculoskeletal |
3.15.2) CLINICAL EFFECTS
A) JOINT PAIN 1) WITH POISONING/EXPOSURE a) CASE SERIES: In a study of 42 cases of endemic VEE detected in Panama from 1961 to 2004 most clinical signs and symptoms were characterized by nausea, vomiting, diarrhea, fever, headache and tremors. Of the 33 cases that exhibited clinical adverse events, renal failure (3%) occurred rarely (Quiroz et al, 2009).
B) MUSCLE PAIN 1) WITH POISONING/EXPOSURE a) CASE SERIES: In a study of 42 cases of endemic VEE detected in Panama from 1961 to 2004 most clinical signs and symptoms were characterized by nausea, vomiting, diarrhea, fever, headache and tremors. Of the 33 cases that exhibited clinical adverse events, myalgia (21%) occurred frequently (Quiroz et al, 2009).
C) BACKACHE 1) WITH POISONING/EXPOSURE a) CASE SERIES: In a study of 42 cases of endemic VEE detected in Panama from 1961 to 2004 most clinical signs and symptoms were characterized by nausea, vomiting, diarrhea, fever, headache and tremors. Of the 33 cases that exhibited clinical adverse events, back pain (6%) occurred infrequently (Quiroz et al, 2009).
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Immunologic |
3.19.2) CLINICAL EFFECTS
A) LYMPHADENOPATHY 1) WITH POISONING/EXPOSURE a) Lymphadenopathy is common, and may be seen in up to one-third of patients during the acute phase of illness (Sanford, 1994).
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Reproductive |
3.20.1) SUMMARY
A) Fetal encephalitis and hydranencephaly has been reported. VEE virus may be embryotoxic, fetotoxic, and teratogenic to humans.
3.20.2) TERATOGENICITY
A) MICROCEPHALY 1) Fetal encephalitis, which may occur during the first and second trimesters, may progress to massive and widespread necrosis of brain tissue, hemorrhages, and resorption of brain material, resulting in hydranencephaly. In one infant the absence of a cerebellum was reported (Douglas, 1996; Sever, 1985). In 3 cases of human maternal exposure, postmortem examinations of the fetuses showed massive necrosis and hemorrhage of the cerebrum and cerebellum, with signs of brain resorption. A stillborn 33-week-old fetus was reported with microcephaly, microphthalmia, hypoplasia of the medulla, small remnant rests of neural tissue in the cranial cavity, and subluxed hips (Casamassima et al, 1987).
2) CASE REPORT - Immunization with TC-83, a live attenuated Venezuelan equine encephalitis virus vaccine, during the first trimester of pregnancy resulted in hydrops fetalis and fetal demise. Postmortem examination showed marked autolysis of the brain. Hydrops was shown by generalized subcutaneous edema, hydrothorax, ascites, and a large multi-lobulated cystic hygroma (Casamassima et al, 1987).
B) ABORTION 1) Increased rates of abortions and stillbirths have been reported in studies of epidemics of Venezuelan equine encephalitis in Latin America. A high frequency of abortions was reported in women with encephalitis (Sever, 1985).
C) CNS EFFECTS 1) Children whose mothers had encephalitis between week 13 and 36 of pregnancy tended to have severe damage of the central nervous system (Sever, 1985a). Some of these children had microphthalmia, no cerebellum, and only small nests of nervous tissue in the cranial cavities. Massive brain necrosis was evident in some cases.
D) ANIMAL STUDIES 1) Studies of female monkeys given VEE virus vaccine has shown that fetal infections have resulted in brain damage and cataracts in the offspring (Sever, 1985).
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