The Kuduudshe/Kuduudiye fever (chikungunya fever)
A fever that was never witnessed in this region is doing rounds in parts of Mandera County, Bula Hawo and surrounding areas. The fever is also said to prevalent in Southern Somalia. Residents call it Kaduudiye or Kuduudshe.
Dr. Mohamoud Abdi Yonis, a Medical Doctor & Emergency Obstetric Surgeon at the International Medical Corps, Somalia Mission shares more information on this arbovirus.
Day after day as you proceed to your clinical experience, different disease entities will challenge you due to different reasons including appearance of new diseases, reappearance of eradicated disease, rare diseases and encountering diseases which are not common to your geographical area and for me this is the case of KADUUDSHE FEVER (an arthropod-borne virus (arbovirus) that causes acute febrile polyarthralgia and arthritis. The name chikungunya is derived from a local language of Tanzania meaning “that which bends up” or “stooped walk” because of the incapacitating arthralgia caused by the disease.)
In Southern Somalia, over the past few years several outbreaks of the virus had been noticed (Mogadishu) and it was last year when I heard about it which puzzled me a lot and to make the matter even worse, it was last month after two of my co-workers acquired the infection with typical clinical features. After my intense readings, the KADUUDSHE was chikungunya fever (Thanks to my Medical director at work, Mohamed Hussein who shared us valuable information) and consequently I thought it is worthwhile to publish & share it with my fellow physicians working across South Somalia & even Somaliland (particularly Berbera).
Chikungunya virus is endemic in parts of West Africa where it appears to be maintained in a cycle involving humans, Aedes mosquitoes, primates and perhaps other animals. Serosurveys of humans in parts of West Africa have identified antibodies to chikungunya virus in 35 to 50 percent of the population in the absence of recognized outbreaks.
Spread and resurgence
Chikungunya virus spreads by means of travel of infected individuals between regions where competent mosquitoes exist for perpetuation of local transmission. After chikungunya virus was identified during an outbreak in East Africa in Tanzania in the early 1950s, the virus was noted to be the cause of multiple outbreaks in many countries of central, southern, and western Africa. Outside Africa, the first documented chikungunya fever outbreak was in Thailand in 1958. This was followed by outbreaks in multiple other Asian countries, including India, Sri Lanka, Malaysia, Indonesia, Cambodia, Vietnam, Myanmar, the Philippines, and Pakistan.
Chikungunya virus transmission occurs in a cycle involving humans, several species of Aedes mosquitoes that inhabit forests and villages, and animals (non-human primates and perhaps other animals). In Asia and elsewhere, however, major outbreaks are sustained by mosquito transmission among susceptible humans.
Mosquito vectors- The major chikungunya virus mosquito vectors are Aedes aegypti and Aedes albopictus. These vectors are also capable of transmitting dengue virus, which, like chikungunya virus, is increasing in geographic range and intensity of transmission.
Aedes Eegypti & A. Albopictus In Somalia?
The only information obtainable about Somalia was provided verbally by Dr. K. Hocking, who in 1942 had observed Aedes aegypti in the coastal villages of the south and at Berbera in the north. At that time an epidemic of dengue had broken out at Mogadishu, making it necessary to carry out control operations against the vector. This mosquito has only been found in the ports of Merca, Mogadishu, Warsheikh and Berbera. Its distribution is therefore mainly coastal.
(Extracted from SURVEY OF AEDES AEGYPTI AND OTHER YELLOW-FEVER VECTORS IN SOMALIA AND THE FRENCH TERRITORY OF THE AFARS AND ISSAS by WHO)
Seasonal synchrony- In order for a viremic traveler to initiate a local outbreak in a non-endemic area, there must be seasonal synchrony between the geographic source of ongoing viral transmission and the geographic destination vulnerable to introduction of infection. For example, transmission of chikungunya virus in Italy during the summer of 2007 was successful because of presence of virus in an individual traveling within the northern hemisphere between India and Italy and typical example in Somalia settings occurs the same way whereby the virus outbreak occurs in Mogadishu and other coastal towns like Warsheikh in March-April 2016 and immediately the virus spread to the neighboring towns of Jowhar and surrounding villages.
The extrinsic incubation period is the period between a mosquito blood meal from a viremic host and the transmission of virus to a new host. The extrinsic incubation period varies depending on the virus, the mosquito vector, and environmental conditions including temperature and humidity. In general, the warmer the temperature, the shorter the extrinsic incubation period and the sooner the mosquito can transmit virus to a new host. In cool temperatures and in many temperate areas, a mosquito may die before the extrinsic incubation period is complete.
Chikungunya is a single-stranded RNA virus of the genus Alphavirus (Togaviridae family). It was first isolated from mosquitoes and humans during an outbreak in Tanganyika (Tanzania) in 1952-53. Thus far, three lineages distinguishable by genotypic and antigenic characteristics have been identified: the clusters of central/east Africa, West Africa, and Asia.
The pathogenesis of the severe and persistent joint symptoms that characterize chikungunya virus infections is uncertain. Some data suggest that macrophage-derived products such as tumor necrosis factor-alpha, interferon-gamma, and macrophage chemoattractant protein-1 may play important roles in the joint tissue damage.
Clinical signs and symptoms begin abruptly with fever and malaise following an incubation period of two to four days (range 1 to 14).Fever may be high grade (40ºC); the usual duration of fever is three to five days (range 1 to 10 days). Polyarthralgia begins two to five days after onset of fever and commonly involves multiple joints (often 10 or more joint groups. Joints affected include hands (50 to 76 percent), wrists (29 to 81 percent), and ankles (41 to 68 percent). Arthralgia is symmetrical in 64 to 73 percent and involves distal joints more than proximal joints. Involvement of the axial skeleton was noted in 34 to 52 percent of cases. Pain may be intense and disabling, leading to immobilization.
Skin manifestations have been reported in 40 to 75 percent of patients. The most common skin manifestation is macular or maculopapular rash (usually appearing three days or later after onset of illness and lasting three to seven days). The rash often starts on on the limbs and trunk, can involve the face, and may be patchy or diffuse. Additional manifestations may include headache, myalgia, and gastrointestinal symptoms.
On physical examination periarticular edema or swelling has been observed in 32 to 95 percent of cases. In one series large joint effusions were noted in 15 percent of cases. Peripheral lymphadenopathy (most often cervical) may be present (9 to 41 percent of cases). Conjunctivitis may be observed.
The most common laboratory abnormalities are lymphopenia and thrombocytopenia. Liver enzymes may be elevated.
Persistent symptoms — Following acute illness (usually lasting 7 to 10 days), some patients may experience persistent rheumatologic signs and symptoms including arthritis/arthralgia, edematous polyarthritis of fingers and toes, morning pain and stiffness and severe tenosynovitis (especially of wrists, hands and ankles). Carpal tunnel syndromes may result from hypertrophic tenosynovitis.
Severe complications — In older reports chikungunya fever has been described as a self-limited illness, although severe complications and death have been reported in the more recent outbreaks. It is unclear whether these differences reflect a modulation in virus virulence, improved epidemiologic observation, or both. Severe complications and death occur more often among patients older than 65 years and in those with underlying chronic medical problems.
Severe complications include respiratory failure, cardiovascular decompensation, myocarditis, acute hepatitis, renal failure and neurologic involvement. Meningoencephalitis is the most common neurologic complication; other manifestations include acute flaccid paralysis and Guillain Barré syndrome.
Diagnostic techniques for identification of chikungunya virus include serology, viral culture and molecular techniques . Serology is the primary tool for diagnosis in the clinical setting. IgM anti-chikungunya virus antibodies (detected by direct enzyme-linked immunosorbent assay [ELISA]) are present starting about five days (range 1 to 12 days) following onset of symptoms and persist for several weeks to three months. IgG antibodies begin to appear about two weeks following onset of symptoms and persist for years.
TREATMENT AND PREVENTION
Treatment of chikungunya infection consists of supportive care including anti-inflammatory agents that relieve symptoms in many patients and analgesic agents . No antiviral agents have been shown to be effective in human infection, although ribavirin and interferon-alpha appear to have in vitro activity against virus replication.
Chloroquine sulfate has been suggested as a possible treatment because of its anti-inflammatory properties, but has not been demonstrated to be effective. For seriously ill patients, there are insufficient data for use of corticosteroids or antiviral therapy. The documentation of long-term viral persistence in non-human primates raises questions about the roles immune dysregulation and persistent virus in chronic symptoms.
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