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Friday, March 29, 2019

An overview: Chikungunya fever

An overview Chikungunya feverIntroductionThe derivation of chikungunya came from Tanzania, when in that respect were reports of a dengue-like symptom bam in 1952-1953, in the Newala and Masasi Districts of the Southern Province. However, dengue was later on excluded on the basis that this pestilential involved patients suffering from debilitating core perturbs and shorter pensiveness period which are not clinical features of dengue. Consequently, the affection was called chikungunya (Robinson 1955) a word from the Makonde dialect describing patients contorted posture (Lumsden 1955). Chikungunya is an arthropod borne computer virus (arbovirus) of the genus Alphavirus from Togaviridae family. It is convey to valets mainly by day biting mosquito species genus genus genus Aedes aegypti and Aedes albopictus (Townson and Nathan 2008). Chikungunya virus (CHIKV) contains a positive-sense single stranded RNA genome, enclosed in an icosahedral nucleocapsid (combination of nucle ic acid and capsid) all enclosed in a phospholipid bilayer envelope. imbed in the envelope are multiple copies of twain encoded glycoproteins E1 and E2, a handsome glycoprotein E3, and a hydrophobic peptide 6K (Strauss and Strauss 1994). HistoryThere were no previous account cases of chikungunya or dengue in Tanzania before the chikungunya epidemic in 1952 1953 thus, the inhabitants were highly susceptible in acquiring CHIKV contagions (Robinson 1955). Prescott et al, 2002 stated that herd underground that is, the immunity that is acquired by a large proportion of the population either finished vaccination, or from previous holdtals, thereby rendering the population resistant to the banquet of the diseases. Further much, opposite operators could deal contributed to the epidemic including records of unusually high rainwater during February to whitethorn 1952. Consequently, this condition was thought to provide suitable breeding environment for the mosquitoes to diffu se their population, suggesting that the main transmitter of infections were mosquitoes (Lumsden 1955). However, not single when high rainfall was implicate in enhancing mosquitoes breeding environment, but also water filled trunk jars dug in the inhabitants huts floor in preparation for the drought season. Consequently, these jars are rarely nailly emptied, which further enhanced mosquitoes populations. Another modify factor to the epidemic could be the living conditions and lifestyles of the indigenous populations. Animals such as fowl, pigeons and on occasion goats were reared in the inhabitants huts. Consequently, these vertebrates could also serve as CHIKV hosts, and thus, this has provided opportunities for transmittances between animals and humans. During early January 1953, the incidence of the epidemic has reached its peak (Lumsden 1955). However, once a person has acquired the infection, that person lead become repellent to further infections with the same vir us (Robinson 1955). Subsequently, this means that as herd immunity increases, the number of viraemic inhabitants decreases.AimConsequently, it has inspired this literature surveil on chikungunya in assessing its outbreaks incidence and prevalence, its associations with dengue and the vectors. Furthermore, from this to determine if it poses a take chances that Western medicine should be planning for.clinical FeaturesChikungunya has a viraemic pensiveness period of 3-12 days (Robinson 1955). Rezza et al. (2007) described chikungunya as a mild and self limited disease in most of the patients. with patients presenting with clinical features such as fever ranging from 39-39.8oC, fatigue, skin rash (some epochs itches), headache, common offend (arthalgia), muscle suffering (myalgia), diarrhoea, vomiting, photophobia, and conjunctivitis. Furthermore, Kannan et al. (2009) observed most of the above symptoms with inclusion of oedema, oral ulcers, nausea, and haemorrhage. Arthalgia and myalgia involves extremities such as wrists, ankles, hands, feet and phalanges. However, arthalgia, myalgia, oedema, lethargy, and weakness persisted even subsequently fever had subsided (Kannan et al. 2009). However, the La reunification outbreak observed vertical transmissions from mother to child, with newborns presenting with chikungunya infection without prior meshing of mosquitoes. These infants presented with fever, pain, poor feeding, disseminated intravascular coagulation (DIC), petechiae, distal joint oedema, and thrombocytopenia. Also involved were frightening neonatal infections including encephalitis and haemorrhagic fever. Furthermore, there were cases whereby transient brain haemorrhages were manifold by the presence of DIC (Grardin et al. 2008). Table 1 represents divers(prenominal) clinical features that were associated with chikungunya infection during several outbreaks.Clinical Features associated with ChikungunyaMost commonJoint pain (96.6%) febrilityFeverF everFever (96.3%)Joint painJoint painArthalgiaHeadache (71.2%)ArthritisFatigueMyalgiaMuscle pain (62.6%)Myalgia uncase rashHeadacheCutaneous eruptions (32.5%)ArthralgiaHeadacheAnorexiaHeadacheMuscle painNauseaRashDiarrhoeaItch/ RashSore pharynxItch/ RashOedemaVomitingOral ulcerphotalgiaEye painConjunctivitisVomitingEye congestionleast commonHaemorrhageReferenceRenault et al. 2007Yosulf et al. 2008Kannan et al. 2009Distribution of ChikungunyaThe World Health musical arrangement (WHO) alerted the Global Alert and Response Network in attest 2005, of an imminent outbreak of chikungunya fever in the Comoro Islands. It was the first Southwestern Indian marine islands to be concerned in the epidemic, subsequently other countries were later implicated in this epidemic. The emergence of the epidemic in Mayotte was imported from Grande-Comore by mid-April and by the end of April Mauritius was also implicated. Overall, the Southwestern Indian nautical character was believed to be afflict ed by the first emergence of CHIKV (Renault et al. 2007). In April 2005, a chikungunya infection which started in Grande-Comorre was imported into La reunion (French Overseas Territory), became its first dire account case, in March 2004 to April 2005. It resulted in the establishment of a good operational epidemiologic surveillance musical arrangement by the islands local bureau with the following objectives monitor epidemic trends, characterise cases and detect new transmission clusters to provide orientations for prevention and vector control. Unfortunately, the collection of data was not conducted scientifically, as the figures of reported cases were not scientifically correlated (Renault et al. 2007). Moreover, there were also flaws in the correlation of the epidemic curve as the capacity of the surveillance system was not sufficient to evaluate the number of cases. Consequently, this resulted in an underestimated number of reported cases. (Renault et al. 2007). Approximat ely 3% cases did not correspond with the criteria defining pretend cases as an abrupt onset of fever 38.5oC accompanied by debilitating joint pain. However, Renault et al. (2007) argued that these were mainly collectable to some atypical cases that were sustain by research laboratory testing and also due to errors in reporting cases. Moreover, there could have been misdiagnosis of chikungunya infection as not all of the atypical cases were laboratory confirmed and also the previous year there were outbreak of dengue. By April 2006, 203 deaths which were either instantlyly or indirectly attributed to chikungunya infection with the mortality rate of 0.3/ cat valium people with a median age of 79. Consequently, the number of deaths was minimal. Moreover, the low immune status of the individual as indicated by the age could have been a contributing factor to the death, as some of these individuals were presented with other underlying conditions. However, direct association between d eath and infection was not confirmed due to the absence of autopsies, consequently this made it difficult to assess the extent chikungunya virus had on death.Mayotte, an island of the Comoros archipelago was involved in the first CHIKV outbreak in April 2005 to July 2006 alter approximately 6346 residents. The outbreak involved two waves, with peak occurring in the plunk for wave aroIn the Maldives, an outbreak occurred during declination 2006 to April 2007 with 11879 confirmed and suspected cases. Out of the 197 populate Maldives islands 121 islands reported CHIKV. The epidemic was thought to be associated with unusually high rainfall from October 2006 to March 2007 and post tsunami construction activities which provided breeding sites for mosquitoes. (Yoosuf et al. 2008). On the east seashore of Madagascar, in Toamasina, Chikungunya virus and Dengue type 1 virus outbreak were reported during January to March 2006. The study involved interrogating 4,242 residents in 27 neighbou rhoods, of which 2,863 were suspected cases and of these 44 were hospitalised cases. 55 patients serum were sampled after passing the criteria which included having less(prenominal) than five days of fever as well as one- one-third of these symptoms headache, myalgia, arthralgia, retroorbital pain or rash. The results included 24 dengue patients, 4 chikungunya and 10 co-infections. As the study was only based on clinical investigations, and only a few samples were analysed, there were insufficient investigation to measure the Chikungunyas and Dengues contributions in the 2 peaks of the epidemic curve. Furthermore, 2 of the 24 Dengue patients had IgM Chikungunya virus. This could be caused by false positive or false negative results, resulting in misdiagnosis or they were in fact co-infections (Ratsitorahina et al. 2008).The cases represented on the map are either confirmed cases or suspected cases. Reference 1 Krastinova et al. 2006, 2 Rezza et al. 2007, 3 Pastorino et al. 2004, 4 Sissoko et al. 2008, 5 Lumsden 1955, 6 Tamburro and Depertat 2009, 7 CDC 2009, 8 WHO 2008, 9 Yoosuf et al. 2009.Transmission of CHIKVCHIKV requires an invertebrate and vertebrate host in order to complete its replication cycle (Pardigon 2009). Invertebrate hosts also known as explicit hosts are mainly the Aedes mosquito species. The Aedes mosquito becomes give subsequent to ingesting viraemic kin meal from infected vertebrate hosts. The blood meal containing CHIKV actuate to the gut, there CHIKV undergo replication within the gut wall. Subsequently, CHIKV contain mechanisms permitting its penetration into the mosquitoes tissues. From there, it passes through either the bloodstream or by other methods (not well known) to different sites of the body such as the salivary glands where it undergoes further replication. Extrinsic incubation period (EIP) is defined as the time taken for the vector to transmit CHIKV after ingesting a viraemic blood meal. Subsequently, there are factors that could influence the duration of the EIP including temperature which increases when the EIP decreases. This is thought to be an inverse proportional relationship. Moreover, the quantity of viraemic blood ingested is other factor (Cook and Zumla 2009). Furthermore, Ross (1956) research demonstrated that a mosquito could harbour viral particles for up to 30 days. Gould and Higgs (2009) suggested that vertical transmission of CHIKV from infected mosquitoes result in infected mosquitoes eggs. These eggs, due to their dessicated nature, are able to survive for long period of time in the environment where it hatches during the rainy season. Sylvatic transmission cycle involves vertebrate hosts such as primates, birds, and rodents which serve as natural hosts (Pardigon 2009). However, humans were considered accidental hosts, resulting in urban transmission cycles producing epidemics. After taking a viraemic bloodmeal from an infected human the domestic mosquitoes can also become infec ted thereby contributing to the outbreaks (Gould and Higgs 2009). Distributions of Aedes albopictus and Aedes aegyptiThe main vectors of chikungunya are Aedes aegypti and Aedes albopictus. The vector involved in the 2005/2006 Mayotte outbreak was Aedes albopictus which resided locally on the island (Sissoko et al. 2008). Aedes albopictus was involved in the 2006 Dengue fever and Chikungunya outbreak in Madagascar. The mosquito was anchor in drums, buckets, coconut shells, discarded cans, pots wet containers and tyres (Ratsitorahina et al. 2008). In the 2007 Italian outbreak, the only vector present was Aedes albopictus (Rezza et al. 2007). The main vector associated with recent outbreaks was Aedes albopictus. Effect of climate changeMost of the cases occurred after reports of high rainfall. tie-in with Dengue Fever and MalariaIn the 1999-2000 Democratric Republic of Congo outbreak, patients had acquired simultaneous CHIKV and plasmodium falciparum infection. However, there were no t sufficient evidence to prove co-infection between the two but it was assumed by the authors that it was probable (Pastorino et al. 2004). Compared to CHIKV, dengue virus is of the genus Flavirivirus from Flaviridae family and contains 4 serotypes (Dayal-Drager 2004 cited by Seyler et al. 2009). The 2006 Madagascar outbreak showed that the mosquito can harbour both Chikungunya and dengue virus (Ratsitorahina et al. 2008). CHIKV is often masked by dengue fever due to convertible clinical features. Consequently, a study by Vazeille et al. (2008) demonstrated that Aedes aegypti has a higher susceptibility in Dengue 2 virus and a lower susceptibility to CHIKV. Moreover, studies by Vazeille et al. (2008) and Moutailler et al. (2009) demonstrated that Aedes albopictus are more effiecient at harbouring CHIKV than dengue 2 virus. Importation into EuropeFranceBetween March 2005 to August 2006, 80 visitors from Chikungunya infected countries in the Southwest Indian Ocean region (La Reunion, Mauritius, Mayotte, Comoros and India) confirmed chikungunya infection at Piti-Salptrine Hospital in Paris, France (Hochedez et al. 2007).ItalyIn 2007, a massive CHIKV outbreak occurred in the Emilia Romagna region in northeastern Italy. There were 205 identified cases with frebile illness reported in Castiglione di Cervia and Castiglione di Ravenna villages (171) separated by the river in Revana province, and Cervia (13) and other villages (21), between July 4 to family 27. The epidemic was believed to be imported from Kerala, India (CHIKV epidemic infested area) by a man, who after two days of his arrival in Castiglione di Cervia developed frebile illness. The majority of the cases were the immemorial (median age 60) representing increased incidence with age. Aedes albopictus which causes Chikungunya was also found in the area of the epidemic which further propagated the virus. Positive CHIKV sequences were detected in 90 captured Aedes albopictus mosquitoes from Castiglione di Cervia and 125 from Castiglione di Ravenna. Most cases occurred in Castiglione di Cervia and Castiglione di Ravenna Villages with peak incidence during third week of August. The 13 Cervia cases were local transmission introduced from Castiglione through migration (Rezza et al. 2007).Other European CountriesDue to travelling, several European countries have encountered CHIKV from viraemic travellers from epidemic countries (Panning et al. 2008). The study was conducted at the Bernhard-Nocht Institute for tropic medicate in Hamburg, Germany involved 680 patients.ReferencesBeran, G. W. (1994) Handbook of zoonoses. segmentation B Viral. 2nd Edition. CRC Press LLC Florida. CDC. (2009) bam notice. 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