What is Chikungunya Fever?
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Chikungunya fever is an acute infectious disease caused by the chikungunya virus (CHIKV), transmitted through Aedes mosquitoes. It is characterized primarily by fever, rash, and joint pain. The first outbreak of chikungunya was confirmed in Tanzania in 1952, and the virus was isolated in 1956. The disease mainly prevails in Africa and Southeast Asia, with large-scale outbreaks occurring recently in the Indian Ocean region.
### Diagnosis
- **Diagnostic Criteria**
- **Differential Diagnosis**
- **Treatment**
### General Treatment
- Symptomatic treatment
- Preventive measures
- Pathological changes
- Control measures
### Overview
Chikungunya fever (chikungunya fever) is caused by the chikungunya virus (CHIKV) and is transmitted via Aedes mosquitoes. The disease is characterized primarily by fever, rash, and joint pain. The first chikungunya outbreak was confirmed in Tanzania in 1952, and the virus was isolated in 1956. The disease mainly prevails in Africa and Southeast Asia, with large-scale outbreaks occurring recently in the Indian Ocean region. Clinical symptoms resemble those of dengue fever, making misdiagnosis common. Although the mortality rate is low, large-scale outbreaks can occur in areas with high mosquito density.
In China, cases of chikungunya infection were reported in Yunnan during the 1980s, and recently, imported cases have been detected among workers returning from Sri Lanka. This technical guideline aims to assist clinicians and infectious disease prevention professionals in monitoring imported chikungunya cases, conducting mosquito density surveillance, and effectively preventing local transmission and outbreaks.
### Virology
CHIKV belongs to the Semliki Forest antigenic complex within the Togaviridae family's Alphavirus genus. The virus is approximately 70nm in diameter, has an envelope, and contains three structural proteins (capsid protein C, envelope proteins E1 and E2) and four non-structural proteins (nsP1, nsP2, nsP3, and nsP4). CHIKV's genome is a single-stranded positive-sense RNA, about 11-12 kb long. The viral genome encodes in the order 5'-NS1-NS2-NS3-NS4-C-E3-E2-E1-3'. Phylogenetic analysis of the partial E1 gene divides CHIKV into three groups: Group 1 includes all West African isolates, Group 2 includes Asian isolates, and Group 3 includes East, Central, and Southern African isolates.
CHIKV reproduces in cells such as Vero, C6/36, BHK-21, and HeLa, causing cytopathic effects. It does not affect blood cells like primary lymphocytes, T-lymphocytes, B-lymphocytes, or monocytes. CHIKV can infect non-human primates and suckling mice.
CHIKV is sensitive to physical and chemical factors, including acid, heat, lipid solvents, detergents, bleach, phenol, 70% alcohol, and formaldehyde.
### Source of Infection
Humans and non-human primates are the main hosts of CHIKV. Acute-phase patients, asymptomatic carriers, and infected non-human primates are the primary sources of infection.
1. Patients: Acute-phase chikungunya patients are the main source of infection. During the first 2-5 days after onset, patients develop high viremia, making them highly contagious.
2. Asymptomatic carriers: They are important sources of CHIKV.
3. Non-human primates: In jungle-type endemic areas, they are also a major source of infection. African green monkeys, baboons, red-tailed monkeys, chimpanzees, gibbons, macaques, and bats can naturally or experimentally be infected with CHIKV, producing viremia.
### Transmission Route
Aedes aegypti and Aedes albopictus are the primary vectors for this disease. Transmission occurs mainly through bites from infected Aedes mosquitoes. Laboratory transmission may occur via aerosols, but there are no reports of direct human-to-human transmission.
### Population Susceptibility
Humans are universally susceptible to CHIKV, with infections manifesting as either symptomatic or asymptomatic.
### Epidemiological Features
#### Geographic Distribution
Chikungunya fever is primarily transmitted by mosquitoes and mainly distributed in Africa, South Asia, and Southeast Asia. Major countries affected in Africa include Tanzania, South Africa, Zimbabwe, Zaire, Senegal, Angola, Nigeria, Uganda, Rhodesia, Comoros, Mauritius, Madagascar, Mayotte, Seychelles, and Réunion Island. In Asia, it affects India, Sri Lanka, Myanmar, Vietnam, Thailand, Laos, Cambodia, Philippines, and Malaysia. Between 2005-2007, large-scale outbreaks occurred in the Indian Ocean islands, India, and Southeast Asia, affecting millions of people.
#### Population Distribution
People of any age can be infected, but differences exist between old and new epidemic areas. In newly affected or imported areas, all age groups can be affected. In long-term endemic areas in Africa and Southeast Asia, children are more frequently affected. There is no difference based on gender, occupation, or race.
#### Seasonal Distribution
The main epidemic season is summer and autumn, though in tropical regions, outbreaks can occur year-round. Seasonal distribution is related to mosquito activity. Analysis of African outbreaks shows that chikungunya peaks cyclically, often recurring after intervals of 3-4 years or longer, possibly due to virus transmission and immunity among natural primate hosts.
#### Imported Cases
In areas where Aedes mosquitoes exist, if the mosquito population reaches a certain density and natural conditions are suitable, an outbreak can occur upon introduction of CHIKV.
### Pathogenesis
The pathogenesis of chikungunya fever is not fully understood, but recent research suggests the following:
#### Viral Invasion
After being bitten by an infected mosquito, humans typically develop symptoms within two days. High viremia occurs on days 1-2 after onset, decreasing on days 3-4 and usually disappearing by day 5. The virus binds to receptors on macrophages, skin cells, endothelial cells, fibroblasts, choroid plexus cells, and cerebellar meningeal cells through its envelope proteins E1 and E2. It enters the cell via clathrin-mediated endocytosis, replicates, and causes cell necrosis and apoptosis. The virus can also cross the placenta and infect the fetus, leading to miscarriage or fetal death. Animal experiments show that the virus easily invades the central nervous system, liver, spleen, and connective tissue of newborn mice.
#### Immunological Mechanisms
Studies have found that some cytokines increase in patient serum 2-6 days after infection, including interferon-gamma-induced protein-10 (CXCL-10), interleukin-8 (IL-8), monocyte chemotactic protein-1 (MCP-1), and interferon-gamma-induced monokine (MIG/CXCL9), with CXCL-10 showing the highest increase. Interferon-gamma, tumor necrosis factor-alpha, and Th2 cytokines such as IL-1b, IL-6, IL-10, and IL-12 remain within normal ranges. During recovery, CXCL-10 and MCP-1 levels decrease. Since CXCL-10 plays a chemotactic role in cellular immune responses, the severity and progression of the disease may be related to its sustained high concentration. Animal experiments show that interferon-alpha plays a key antiviral role.
### Clinical Manifestations
The incubation period is 2-12 days, usually 3-7 days.
#### Acute Phase
1. Fever: Sudden onset, chills, fever up to 39°C, accompanied by headache, nausea, vomiting, loss of appetite, and lymphadenopathy. Fever lasts 1-7 days before subsiding; some patients experience a mild secondary fever (biphasic fever) around day 3, lasting 3-5 days before normalizing. Some patients exhibit conjunctival injection and mild photophobia.
2. Rash: About 80% of patients develop a rash on the trunk, limbs, palms, and soles 2-5 days after onset. The rash presents as macules, papules, or purpura, with normal skin between lesions, and may cause itching. The rash fades after several days, often with mild desquamation.
3. Joint Pain: Concurrent with fever, multiple joints and vertebrae experience pain and swelling, often accompanied by generalized myalgia. Joint pain is migratory, worsening with movement, and more severe in the morning. The condition progresses rapidly, often resulting in functional impairment within minutes or hours. Small joints such as hands, wrists, ankles, and toes are commonly affected, as well as larger joints like knees and shoulders. Wrist compression causing severe pain is characteristic of the disease. Synovial fluid accumulation is rare, and X-rays appear normal.
4. Other Symptoms: Rarely, patients may develop meningitis, hepatitis, myocarditis, or mucosal bleeding.
#### Recovery Phase
After the acute phase, most patients' joint pain and stiffness resolve completely. Some patients experience persistent joint pain and stiffness lasting weeks to months, or even over three years. A few patients may have residual joint dysfunction.
### Testing
#### Routine Tests
1. Blood tests: White blood cell counts are usually normal; occasionally, leukopenia and lymphopenia occur, along with mild thrombocytopenia.
2. Biochemical tests: Some patients show elevated ALT, AST, and creatine kinase (CK).
3. Cerebrospinal fluid tests: Meningoencephalitis patients show changes consistent with viral damage.
#### Serological Tests
1. Specific IgM antibodies: Detected using ELISA or immunochromatography methods. Capture method results for IgM antibodies are reliable. Generally, IgM antibodies appear on day 1 after onset, becoming positive in most patients by day 5.
2. Specific IgG antibodies: Detected using ELISA, immunofluorescence antibody testing (IFA), or immunochromatography methods. Generally, IgG antibodies appear on day 2 after onset, becoming positive in most patients by day 5.
#### Pathogen Detection
1. Nucleic Acid Testing: RT-PCR and Real-time PCR methods detect viral nucleic acids in most patients' sera within 4 days of onset.
2. Virus Isolation: Serum samples collected within 2 days of onset are used to isolate the virus using Vero, C6/36, BHK-21, and HeLa sensitive cells.
### Diagnosis
#### Diagnostic Criteria
1. Epidemiological Data: Living in chikungunya-endemic areas or traveling to these areas within 12 days, with a history of mosquito bites within 12 days prior to illness.
2. Clinical Manifestations: Acute onset with fever as the initial symptom, followed by rash and severe joint pain within 2-5 days.
3. Laboratory Tests:
- Positive serum-specific IgM antibodies.
- Fourfold increase in serum-specific IgG antibody titer in convalescent phase compared to acute phase.
- Detection of chikungunya virus RNA in patient samples.
- Isolation of chikungunya virus from patient samples.
#### Differential Diagnosis
1. Dengue Fever: Both diseases share the same vector and similar clinical manifestations. Chikungunya fever has a shorter fever duration, more pronounced and prolonged joint pain, and milder bleeding tendency. Differentiation relies on specific laboratory testing.
2. O’nyong-nyong and other alphavirus infections: Similar clinical presentations require specific testing for differentiation.
3. Fifth Disease: Caused by parvovirus B19, it starts with facial erythema and subsequent maculopapular rash. Joint involvement manifests as polyarthropathy, often affecting proximal finger/toe joints and wrist, knee, and ankle joints. Parvovirus B19-specific antibodies and nucleic acid tests are positive.
4. Other: Requires differentiation from influenza, measles, rubella, infectious mononucleosis, rheumatic fever, bacterial arthritis, etc.
### Treatment
There is no specific drug treatment; management focuses on symptomatic relief.
#### General Treatment
Rest during the febrile phase and take precautions against mosquito bites.
#### Symptomatic Treatment
1. Cooling: Physical cooling methods are recommended for high fever. Avoid alcohol rubs in patients with obvious bleeding symptoms. NSAIDs can be used, avoiding aspirin-like drugs.
2. Pain Relief: Analgesics can be used for severe joint pain.
3. Meningoencephalitis Treatment: Focus on preventing cerebral edema. Mannitol and furosemide can be used to reduce intracranial pressure.
4. Rehabilitation Therapy: For joint pain or mobility issues.
### Prevention Measures
Prevention involves:
1. Controlling the source of infection: Treat patients locally to reduce transmission opportunities. Implement mosquito isolation measures during viremia (within 5 days of onset). Report suspected and confirmed cases promptly.
2. Interrupting transmission routes: Use mosquito nets, screens, and doors in patient rooms. Eliminate mosquitoes and their breeding sites.
3. Protecting susceptible populations: Currently, no vaccine exists; focus on personal mosquito protection.
### Pathological Changes
1. Skeletal Muscle: Fibroblast infection, with significant viral presence in the epimysium, minimal presence in the perimysium and endomysium, and macrophage infiltration in the epimysium. In CHIKV-infected neonatal mice, severe necrotizing myositis occurs, characterized by muscle fiber necrosis and lymphocyte/macrophage infiltration.
2. Joints: Viral antigens are present in fibroblasts of the joint capsule.
3. Skin: Viral antigens are present in fibroblasts of the deep dermis.
4. Central Nervous System: Mouse experiments show severe vacuolar degeneration of choroid plexus epithelial cells, with significant viral presence in choroid plexus epithelial cells, ependymal cells, and cerebellar meningeal cells, without obvious changes in brain parenchyma or blood-brain barrier microvascular endothelial cells.
5. Liver: Immunohistochemistry and transmission electron microscopy show viral antigens and budding in liver sinusoidal endothelial cells, macrophages, and Kupffer cells of infected mice.
6. Spleen: Viral antigens are observed in the red pulp.
### Control Measures
Case Management and Case Finding
Healthcare facilities should promptly report suspected chikungunya cases to enable early intervention. Patients in the viremic phase (within 4 days of onset) should be protected from mosquito bites. After receiving case reports, epidemiological investigations should be conducted, including activity history, contact tracing, and identifying infection sources and locations. Unreported or undiagnosed cases within two weeks before and five days after onset should be identified to guide subsequent control measures such as emergency spraying and elimination of breeding sites.
Media Emergency Monitoring and Control
(1) Mosquito Emergency Monitoring
Following an outbreak, county-level disease prevention and control centers conduct emergency mosquito monitoring in affected areas, focusing on points of origin and surrounding regions. Surveys inspect indoor and outdoor water containers and mosquito larval breeding sites among 50-100 households, calculating Breteau and Container indices every three days. Adult Aedes mosquitoes are captured for virus isolation and typing. Assessments of epidemic diffusion risks are made based on media monitoring and control situations.
(2) Media Control
During outbreaks, rapid measures are taken to eliminate adult mosquitoes and breeding sites based on mosquito species and local breeding characteristics. Special attention is given to mosquito control in hospitals, schools, government offices, and construction sites within affected areas.
- Emergency spraying to kill adult mosquitoes at locations where transmission may occur. Spraying is repeated weekly for three cycles.
- Clearing mosquito breeding sites within a 100-meter radius of the point of origin. Larger-scale emergency mosquito control may be conducted based on risk assessments and media monitoring results.
Evaluate the effectiveness of mosquito control measures. When the epidemic is effectively controlled, with no new cases in one month and Breteau and Ovitrap indices below 5, emergency response can be concluded.
Community Mobilization and Health Education
When local outbreaks occur, extensive public campaigns and community mobilization efforts are initiated to engage communities and the general public in environmental sanitation and mosquito breeding site elimination through patriotic health campaigns.
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