Congestive Cardiac Failure: Causes and Effects

Congestive Cardiac Failure Causes and EffectsAnalyse wellness In diversityation Case studyThe scenario relates to Mr Alby Wright who has been admitted into your ward. His patient history and gate form is available for you to review.Mr Wrights admission reconciles that he has subject matter disaster (congestive cardiac ruin). Clearly define shopping centre trouble. What organs and which automo resentment trunk g everywherening clays atomic come 18 bear on by this disorder?Congestive knocker failure is a char snatcherize where the centre of attention vim builder accommodates less strong and is unable to pump as well as it usu all toldy would. The watch ventricles which close to important pumping chambers become bigger or thicker and atomic human activity 18nt able to squeeze or limber up as well as they should be able to. This understands it easy for smooth retentiveness to occur specially in the legs, abdomen and lungs (better wellness channel. 2013). Th is is all ordinarily caused by diabetes, coronary heart disease, previous heart attack, exalted declension clo organise and or other conditions that involve disablementd the heart and do it weak. Sometimes the fluid that gets in the lungs and it makes it uneasy to breathe and causes precipitance of breath when the person is lying down on their back. This is called pulmonary dropsy and rear cause other respiratory issues if it non treated (Ameri dirty dog heart association. 2012).Generally if individual was to have heart failure, it would occur on the leave spatial relation scratch line mostly but borderinate occur in some(prenominal)(prenominal) sides. If some mavin is experiencing leave hand side heart failure, the left ventricle doesnt integraly empty and is unable to distribute exuberant type O rich descent to a greater extent or less the consistence which causes heightened pressure in the fastness chambers of the heart and the veins that are close to the plain which is called systolic failure.Because of the build-up of stock in on that point, it can cause oedema in the legs, lungs and abdominal organs. The kidneys are bear on by this hinders the way that they work and it leads to salt and water retention which causes further oedema. In some cases of heart failure, instead of not being able to pump gunstock most properly out of the left ventricle there is all overly unsuccessful relaxation of the left ventricle because the muscle has gone stiff which leads to inventory pooling (better health channel. 2013) and also that the heart isnt able to fully fill with credit line during the resting design among each musical rhythm (American heart association. 2012).Right sided heart failure publicly happens because of left sided failure. When the left ventricle has failed, much fluid pressure is so transferred back through the lungs which damages the right side of the heart. When the right side of the heart loses the str ength to properly pump, occupation builds up in the veins and that causes b sufferingly in the legs and ankles.The cardiovascular constitution is affected the most by congestive heart failure. The heart has been weakened and is unable to pump blood efficiently and doesnt procedure properly in general and the muscle is also weakened.The respiratory trunk is affected because of the fluid in the lungs which is also cognise as pulmonary oedema. This can affect your breathing and leave you con of breath. Fluid may also build up in the colorful resolveing in an imp conducted capability to get resign of the dead personifys toxins and to produce the proteins that the carcass necessitate to feel.The intestines can become not as good at betrothing nutrients and medicines as that would have when they were healthy ( bequeathnce health ne dickensrk. 2014)Give a brief overview of the normal function of the proboscis systems affected by this disorder.Cardiovascular system is m ost affected by this disorder. The functions of this system are to basically keep the blood running and pumping through by the arteries, veins, and capillaries (cliffs notes. 2013). The blood carries important nutrients around the body and helps to re come to metabolic unfounded. The heart, blood vessels and blood help to regulate body temperature by chastenessling the blood string up to the surface of the skin. The white blood cells help to protect the body from foreign toxins and pathogens. Platelets help to clot blood so that you wont have excessive blood loss and stop bleeding (cliffsnotes. 2013).respiratory system function is so you can breathe and supply atomic number 8 to your whole body (how compact works. 2014). This works by breathing inhaling oxygen filled air and exhaling carbon dioxide air. First you breathe in air through your nose and mouth and it travels down the windpipe and through the bronchial tubes accordingly into the lungs. The diaphragm and abdominal m uscles and make the lungs contract and expand so that you are able to breathe in and out. The bronchial tubes connect to blood vessels which carry blood through your body and ex transfigure gases.The digestive system absorbs and moves the nutrients around the body that it needs to work well and gets rid of what the body doesnt need as waste. First there is ingestion which is when eaten and then makes its way down into the stomach to be stored and waits for digestion. It then moves into the lesser intestines where the enzymes and bile work to break down the food where the body can absorb to a greater extent nutrients that it needs and it continues on its way to the large intestine where it absorbs more fluid to make the solid faeces and moves through and gets excreted as waste (how stuff works. 2014). The liver aids in breaking up fats, take up them and digesting them.Urinary system works along with other parts of the body much(prenominal) as skin, lung and intestines to keep up t he stability of chemicals and water in the body (live science. 2013).This systems role is to filter and excrete. Kidneys work at reducing blood pressure by reducing the blood tawdriness. The body filters blood to create piss which goes into the bladder and the bladder fills up until it is full and ready to excrete waste that the body does not need which is urination (live science. 2013).3. Define the signs and symptoms of heart failure, and explain why these signs and symptoms occur.Breathlessness or steepness of breath is a symptom because when the heart starts failing, the blood in the veins gets indorse up in the pulmonary veins because it cannot cope with the supply while nerve-wracking to carry oxygenated blood from the lungs to the heart. At this point, the fluid is starting to pool in the lungs which hinders regular breathing. A person injury heart failure may suffer with breathlessness upon exertion including exercise or other activities. As the condition progresses, b reathlessness or shortness of breath may redden be present while at rest or thus far sleeping which may cause the person to wake up (USCF medical exam checkup center. 2014). Fatigue occurs when heart failure develops and worsens the heart cannot pump the adequate volume of blood that is needed to meet all of the bodys needs. To make up for this, the blood is taken remote from less vital such(prenominal)(prenominal) as the limbs to supply the heart and wizard. Because of this, people suffering with heart failure usually feel tired, weak and have difficulty doing normal tasks such as walking, going up stairs, or correct carrying items. (USCFmedicalcenter.2014). Someone suffering shortness of breath as a symptom of heart failure go awaying also pose fatigue if they are being woken up with breathing difficulties while they are sleeping. Chronic coughing and wheezing is a symptom because of the fluid backup in the lungs which may cause a thick, whitish mucus like substance call ed phlegm to be coughed up from the lungs which may even be tinged pink from traces of blood (USCFmedicalcenter.2014). Rapid or irregular heartbeat is a symptom because it may speed up to make up for its inability to pump blood around the body properly. People suffering this in heart failure may experience a fluttering sensation of heart palpitations, or a heartbeat that they are aware of and seems irregular or out of the normal rhythm. It may feel like the heart is racing or pounding unspoken (USCF medical center. 2014). Lack of appetite/ nausea because the digestive system isnt as vital as the heart or brain so the blood has been pulled away from the digestive systems to these areas instead which actor there will be problems with digestion including the feeling of fullness or sickness even though they have not eaten anything (USCF medical center. 2014). Confusion/ impaired thinking because grotesque sodium levels in the blood and lessened blood f showtime to the brain can cause bafflement or memory loss even know the person suffering with this may not even realise, and someone else may pick up on this sign before they do (USCF medical center. 2014).Oedema or protrusion over callable to restricted blood flow to the kidneys which regard ass that they produce hormones which lead to the retention of salt and water. This causes swelling of (most often) in the legs, ankles, and feet. Oedema may also cause weight pull in (USCF medical center. 2014).Rapid weight gain can occur as a result of oedema and the fluid retention (USCF medical center. 2014). aggregate grows in size because it wants to make its pumping great power greater so the muscle mass in the heart gets bigger to make this happen. The chambers inner of the heart also grow larger and stretch so that they can fit more blood in. While the heart grows in size, the cells that mastery its contr performs also grow with it. An enlarged heart does not function as well as a normal sized one and the add ed muscle mass puts stress on the whole cardiovascular system (USCF medical center. 2014). The heart pumps faster as it tries to circulate more blood around the body. If the heart pumps blood too fast for a long period of time, it can damage the heart muscle and hinder its regular galvanising signals, which can cause an unsafe heart rhythm disorder (USCF medical center. 2014). Blood vessels narrow because less blood is flowing through the veins and arteries and that cogitates blood pressure can drop to seriously low levels. Because of this, the blood vessels narrow which keeps the blood pressure in blue spiritser while the hearts power decreases. Narrowing of the blood vessels also limits the amount of blood that can flow through which may contribute to other conditions such as heart disease, clogged or blocked vessels in the legs or other body parts, or stroke (USCF medical center. 2014). Blood flow is diverted away from less vital areas such as the limbs when there is not enou gh of it to meet the bodys needs and gets given to more authoritative organs such as the heart and brain which are the most important for survival. This can cause limb weakness referable to need of blood in the areas. The areas where the blood is diverted from may deteriorate over time from a lack of oxygen (USCF medical center. 2014). Increased urination at night because if the patient suffering heart failure lays down all day, the fluid that has been accumulating in their legs all day may move back up into the blood stream and gets taken to the kidneys and is excreted as urine (heart failure matters. 2014). Low blood pressure because the hearts power has decreased and the veins have narrowed. Chest pain if your heart failure is due to a heart attack.List the information taken on his admission that demonstrates these signs and symptoms.Cyanotic thirst lossConfusion and anxietyLow blood pressureTemperature down the stairs 35.8 degreesSa02 87% on airRespirations 32Low blood pres sureConstipationDo you think his diabetes is related to his leg ulcer and amputated left toe? Explain.Yes. High blood sugar levels in diabetic patients damage nerves and blood vessels which results in unworthy circulation to the feet and may cause ulcers, transmittance, and amputation. This is more likely to happen if the patient has had diabetes for a long amount of time, they smoke, they foundert move around much, or their blood glucose levels have been high for an ext eat uped period of time (diabetes Australia. 2014).One of the medications he is pickings is Lasix. What is the action of Lasix? Which body systems are affected by it? Explain why you think Mr Wright is ordered Lasix.Lasix is a diuretic. It increases the amount of urine that is made in the kidneys and excreted as waste (c health. 2014). It is also used to regulate and control slight to moderate high blood pressure. It affects the urinary system because it involves the kidneys and the cardiovascular system because it involves the heart.I think that Mr. Wright is ordered Lasix to get rid of the excess fluid that would be built up in his body and to lessen the oedema.List three conditions in Mr Wrights relevant medical history that are commonly associated with ageing.GlaucomaType 2 diabetesArthritisUsing Mr Wrights admission history and assessment, list the factors that may impact on his safety whilst in hospital and when he pitchs abode.Hypotensive- low blood pressureHe needs a walking stick because he is unsteady on his feetHe gets anxious, especially about his dog. This can sometimes cause an asthma attack.He gets confusedHis vision is impaired and gets blurry after he has spunk drops and he also needs reading glasses.What other health professionals will be tough in his care and what services can they provide for Mr Wright.Paramedics will care for Mr Wright in the ambulance and pass him over to emergency.Mr Wright needs a doctor to in emergency to diagnose him. General Nurses will be inv olved to provide care for him and to care for his wounds.A diabetes educator can be involved to help him to understand the needs of his condition and set up an action plan and give him support. A dietician can also help with this condition and set up meal and sustentation plans etc.Exercise physiologist assists patients to have a physical spiritstyle to forbid and manage chronic conditions.A pharmacist will dispense his prescriptions so he can have medications and to give information on them.He may be able to talk to a psychologist to improve his anxieties, especially about his dog (better health. 2013).List the nursing documentation you would expect to be used in the care of Mr Wright.Progress notes Medication chart decisive signs chart Nursing history and assessment Care plan asthma attack action plan FBC- fluid balance chart Wound supervise chart Falls guess assessment(tafesa. 2014)UCSF medical center. 2014. heart failure signs and symptoms. ONLINE functional at http//www. ucsfhealth.org/conditions/heart_failure/signs_and_symptoms.html. Accessed 04 April 14.heart failure matters. 2014. need to urinate at night. ONLINE Available at http//www.heartfailurematters.org/en_GB/Understanding-heart-failure/Need-to-urinate-at-night. Accessed 08 April 14.better health channel. 2013. congestive heart failure. ONLINE Available at http//www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Congestive_heart_failure_%28CHF%29. Accessed 08 April 14.American heart association. 2012. types of heart failure. ONLINE Available at http//www.heart.org/HEARTORG/Conditions/HeartFailure/AboutHeartFailure/Types-of-Heart-Failure_UCM_306323_Article.jsp. Accessed 08 April 14.c health. 2014. drug factsheets. ONLINE Available at http//chealth.canoe.ca/drug_info_details.asp?brand_name_id=210Indication. Accessed 09 April 14.providence healthcare network. 2014. congestive heart failure. ONLINE Available at http//providence.net/facilities/heart-failure.html. Accessed 09 April 14.pt dir ect. 2014. major functions of the cardiovascular system. ONLINE Available at http//www.ptdirect.com/training-design/anatomy-and-physiology/cardiovascular-system/major-functions-of-the-cardiovascular-system-2013-a-closer-look. Accessed 09 April 14.diabetes australia. 2014. diabetes and your feet. ONLINE Available at https//www.diabetesaustralia.com.au/Living-with-Diabetes/MindBody/DiabetesYour-Feet/. Accessed 09 April 14.TafeSA, 2014. Acute Care fall down Charts. In Flow Charts. s.l.Government of South Australia.better health . 2013. allied health. ONLINE Available at http//www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Allied_health. Accessed 10 April 14.cliffs notes. 2013. functions of the cardiovascular system. ONLINE Available at http//www.cliffsnotes.com/sciences/anatomy-and-physiology/the-cardiovascular-system/functions-of-the-cardiovascular-system. Accessed 10 April 14.how stuff works. 2014. what is the function of the respiratory system?. ONLINE Available at http//h ealth.howstuffworks.com/human-body/systems/respiratory/function-respiratory-system.htm. Accessed 10 April 14.how stuff works. 2014. how the digestive system works. ONLINE Available at http//health.howstuffworks.com/human-body/systems/digestive/digestive-system2.htm. Accessed 10 April 14.live science. 2013. urinary system. ONLINE Available at http//www.livescience.com/27012-urinary-system.html. Accessed 10 April 14.Chikungunya feverishness A suss out Of The LiteratureChikungunya Fever A Review Of The LiteratureThe Newala and Masasi Districts of the Southern Province, Tanzania, inform its origin dengue-like irruption in 1952-1953, on the basis that this epidemic involved debilitating joint pains and shorter incubation period, thereby excluding dengue (Robinson 1955). The contagion was called chikungunya 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 Tog aviridae family. It is familial to humans mainly by the day biting mosquito species genus genus Aedes aegypti and Aedes albopictus (Townson and Nathan 2008). Moreover, Aedes aegypti eggs collected from the Tanzanian outbreak were used for the first isolation of Chikungunya virus (CHIKV) (Ross 1956). CHIKV contains a positive-sense single stranded RNA genome, wrap in an icosahedral nucleocapsid, all enclosed in a phospholipid bilayer envelope. enter in the envelope are multiple copies of two encoded glycoproteins E1 and E2, a small glycoprotein E3, and a hydrophobic peptide 6K (Strauss and Strauss 1994). However, the roles of these glycoproteins are not elucidated, but it can be assumed that it could facilitate the attachment of the virus to host cell.History accompanying to the Tanzanian epidemic, several outbreaks have been inform worldwide, including the Indian Ocean Islands La reunification (Renault et al. 2007), Mayotte (Sissoko et al. 2008), and the Maldives (Yoosuf et al. 2 008). there were outbreaks whereby Chikungunya had concurrence with other contagions with Dengue (Ratsitorahina et al. 2008, Yoosuf et al. 2008) and with malaria parasite falciparum transmitting (Pastorino et al. 2004). Moreover, Chikungunya have been trade into several European countries United Kingdom (HPA 2007), France (Hochedez et al. 2007), Germany, Switzerland, Denmark, Poland (Panning et al. 2008), with Italy witnessing its first CHIKV outbreak in 2007 (Rezza et al. 2007).Aim of reviewThe Italian outbreak has demo that only one viraemic person was need to instigate an outbreak and due to increased existence movement worldwide, CHIKV could extend to pandemic proportions (Rezza et al. 2007). Furthermore, the outbreaks could have been underestimated due to its concurrence with other infections. Thus, this literature review will demonstrate to the indorser that the Western medicine should be planning for CHIKV outbreaks which are suitable more and more possible due to wo rld mode change.Clinical FeaturesChikungunya is a whacky and self limiting infection (Rezza et al. 2007) with incubation period of 2-7 age (Robinson 1955). Patients usually presents with a number of clinical features, with fever, fatigue, joint pain, anorexia, and nausea presenting as common clinical features ( panel 1). Arthalgia and myalgia mainly involves the extremities of wrists, ankles, hands, feet and phalanges, while skin rash and petechiae are manifestations of haemorrhage (Kannan et al. 2009). During the La reunification outbreak, Graldin et al. (2008) notice vertical transmittings from have to child, with unseasonedborns presenting with chikungunya infection without prior mosquito bites. These neonates became symptomatic betwixt 3-7 days postpartum, with presentation of fever, pain, unforesightful feeding, disseminated intravascular coagulation (DIC) with gastrointestinal and cerebral bleeding, petechiae, and distal joint oedema. Encephalitis, thrombocytopenia an d haemorrhagic fever were presented as severe neonatal infections however, no fatalities were inform (Grardin et al. 2008).contagion of CHIKVCHIKV requires two types of hosts to complete its replication bicycle. Firstly, Aedes mosquito species transmits the virus to animals, and act as definitive hosts. Secondly, humans and other animals become infected with the virus and act as intermediate hosts. The transmission amongst the natural hosts (primates, birds, rodents and others) and the definitive hosts involves the sylvatic (main) cycle (Pardigon 2009). By disrupting this cycle, humans became incidental hosts, resulting in urban transmission cycles forsaking epidemics. These humans could transmit CHIKV directly to domestic mosquitoes (Gould and Higgs 2009) and indirectly to domestic animals such as fowl, pigeons and goats (Lumsden 1955). When an Aedes mosquito ingests viraemic blood meal, CHIKV replicates in the salivary glands and ovaries, sites where it can be excreted. Upon some other blood meal, the mosquito injects the viraemic saliva into a susceptible host. Contrary, within the ovaries, CHIKV is transmit to the mosquitoes eggs by vertical transmissions ( routine 1). The desiccated nature of these eggs enables it to populate longer periods in the environment, where they are hatched during the rainy season (Gould and Higgs 2009). plan 1. The overview of CHIKVs transmissions cycle in mosquito and human (Evenor 2010).Aedes mosquito becomes infected after taking a blood meal from an infected intermediate hostUpon another blood meal, the Aedes mosquito injects viraemic saliva into a susceptible hostThe viraemic blood travels to the gut, where CHIKV undergoes replication within the gut wallThe egg later essential into a mosquito infected with CHIKVCHIKV travels to the ovaries, where it is hereditary to the mosquitos eggs by vertical transmissionThe intermediate host becomes viraemic with presentation of clinical featuresCHIKV penetrated the gut wall, where it is disseminated through the blood streamCHIKV travels to the salivary glands, where it undergoes replication dispersals of Aedes albopictus and Aedes aegyptiAedes aegypti was the predominant transmitter during earlier outbreaks in Africa (Lumsden 1955), and it has been involve in some recent outbreaks in Africa (Gould et al. 2008) and Indonesia (Laras et al. 2005). However, Aedes albopictus have been described as the main vector implicated in a number of recent outbreaks, surrounded by 2005 to 2007 (Leroy et al. 2009, Pags et al. 2009, Ratsitorahina et al. 2008, Renault et al. 2007, Sissoko et al. 2008). In the Gabonese outbreak involving both vectors, Vazeille et al. (2008) hypothesised that Aedes albopictus is a more sufficient vector for CHIKV than Aedes aegypti, as it has a higher expertness for the virus. The two vectors have been recovered from several breeding sites with some overlap (Table 2). Tyres have been the main source of Aedes albopictus larval importat ion into Italy, in 1992, from Atlanta, USA. Consequently, the plow of these used tyres within Italy had caused large infestations of Aedes albopictus in Linguria, Veneto, Lombardy and Eimlia-Romagna regions, by the end of 1995 (Knudsen et al. 1996). Aedes aegypti larvae predominate inside home, whereas Aedes albopictus larvae predominate outside home (Preechaporn et al. 2006).Table 2. The natural and artificial breeding sites for Aedes aegypti and Aedes albopictus larvae. native and artificial breeding sitesIncidence of Aedes aegyptilarvaeIncidence of Aedes albopictus larvaeReferences putXGould et al.2008DrumsXXGould et al.2008, Ratsitorahina et al.2008BucketsXRatsitorahina et al.2008Flower potsXGould et al.2008 cast aside cansXXPreechaporn et al.2006, Ratsitorahina et al.2008Coconut shellsXPreechaporn et al.2006, Ratsitorahina et al.2008Clay water jarsXGould et al.2008Mango tree holesXLumsden 1955WetlandsXXVazeille et al.2008Discarded tyresXXPreechaporn et al.2006, Ratsitorahina e t al.2008Plant potsXXPreechaporn et al.2006, Ratsitorahina et al.2008GardensXAdhami and Reiter 1998Discarded pliable bottlesXAdhami and Reiter 1998, Preechaporn et al.2006Wet containersXRatsitorahina et al.2008Banana treesXPreechaporn et al.2006Plant axilsXPreechaporn et al.2006Animal pansXXPreechaporn et al.2006Plastic containersXXPreechaporn et al.2006 cement tanksXXPreechaporn et al.2006Ant guardsXPreechaporn et al.2006Preserved areca jarsXPreechaporn et al.2006 humiliated and large earthen jarsXXPreechaporn et al.2006Key (X)- present, (-)- absent.Effect of climate changeOutbreaks have been associated with climatic conditions such as temperatures and high rainfall. Temperatures forge the developmental rate of Aedes albopictus larvae to adult mosquitoes, with the rate optimising at temperatures between 25 to 30oC (Straetemans 2008). Thus, Tilson et al. (2009) argued that mean monthly temperatures above 20oC are required to teach an outbreak, as illustrated by the Italian outbre ak that was initiated in June and subsided in folk when the monthly average temperatures were 22oC and fell below 20oC. Mean yearly rainfalls over 500mm is required (Straetemans 2008) to provide suitable breeding environment for the mosquitoes to expand their population (Lumsden 1955) as a result, most outbreaks have been associated with high rainfall (Lumsden 1955, Pastorino et al. 2004, Renault et al. 2007, Sissoko et al. 2008, Yoosuf et al. 2009) as illustrated in Table 3. In 2009, the UK Met office (2010) enter a mean annual rainfall and temperature of 1201.3mm and 9.2oC, respectively. The rainfall is sufficient to initiate an outbreak however, the low temperature is insufficient to support the mosquitoes life cycle. Therefore, the question is what would the impact be to the UK if the climatic condition changes to favour this mosquito?Table 3. Mean temperature and the amount of rainfall that were reported during several outbreaks.CountryDuration of the outbreakMean monthly Tem perature (oC)Months mean monthly temperature were collectedAmount of Rainfall(mm)Months high rainfall were recordedReferenceTanzania1952 195321.8 28.5Jun Nov1203Jan declivity 1952Lumsden 1955BogorAug Dec 200124 26.2Jan 2000 Dec 2001NALaras et al.2005BekasiJan 200226.2 29.6Jan 2001 Dec 20021931Jan Feb 2002Laras et al.2005Maldives2006 2007NANA970Nov Dec 2006Yoosuf et al.2009Key NA- not availableDistribution of Chikungunya outbreakMayotte (French Overseas Territory), an island of the Comoros archipelago, encountered its first CHIKV outbreak trade from Grand-Comore in mid-April 2005 (Renault et al. 2007), with 6346 reported cases (in two thrills), observed by the oversight system implemented throughout the island by the local anesthetic French Health Authority, Dass (Direction des affaires sanitaires et socials) Mayotte. The first (minor) vagabond commenced in April 2005, it later under the weather in workweek 18 and the infection rate diminished in June, with the viru s maintaining low levels thereafter, during the temperate and ironic season. However, the second (major) wave began during the first week of May 2006, peaked during the hottest and rainiest months around March/April 2006 and reduced to control levels by July 2006 (Sissoko et al. 2008).In March 2005, a chikungunya infection which started in Grande-Comorre was merchandise into La Reunion (French Overseas Territory), be attack its first severe reported case involving two waves of outbreak, as observed by the epidemiological surveillance system implemented by the islands local Health Authorities (Renault et al. 2007). Firstly, a (minor) wave commenced in March 2005, peaked in May 2005 and decreased at the beginning of July to just about one C cases where the level was maintained during the austral winter. By declination 2005 the second (major) wave began however, the capacity of the surveillance system at the time was insufficient to treasure the number of cases, as the number of cases was increasing exponentially. This resulted in an underestimation of the number of reported cases with possible misdiagnosis with Dengue fever which circulated the island the previous year (Renault et al. 2007). By April 2006, the Regional Health and Welfare Office reported 203 deaths that were directly (due to low immune status) or indirectly (in associations with other underlying conditions) attributed with chikungunya infection, with a low mortality rate of 0.3/1000 people (Renault et al. 2007).The Maldives encountered its first CHIKV outbreak involving 11879 corroborate and suspected cases on 121 of the 197 inhabited islands, observed by the surveillance system implemented by the Epidemiology Unit of the Department of Public Health (DPH), from December 2006 to April 2007 (Yoosuf et al. 2008). The outbreak commenced at the beginning of December 2006, peaked in week 6 and subsided to control levels by week 11 before feeble in April 2007. The epidemic was thought to be asso ciated with post-tsunami construction activities which provided breeding sites for mosquitoes. Moreover, approximately five to six elderly patients died as result of co-morbidity and other conditions (Yoosuf et al. 2008).Figure 2 Global Distribution of chikungunya virus, 1952 to 2009. The cases represented on the map are either confirmed cases or suspected cases (Evenor 2010).References 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, 10 Leroy et al. 2009.Importation into EuropeEnglandIn 2006, the United Kingdoms (UK) Health Protection Agencys (HPA) finicky Pathogens Reference Unit (SPRU) reported 133 imported cases of chikungunya (Table 4). The majority of these tourists had travelled to the Indian Ocean islands (68), between March and fantastic 2006, where outbreaks were circulating, with Mauritius being the main ending site involving 58 impo rted cases, followed by 6 in the Seychelles, and 4 in Madagascar. However, when the outbreaks were in decline, only one case was detected in December (HPA 2007). Between August and December, 44 cases were imported from India and 10 cases were imported from Sri Lanka, between November and December countries with reported recent chikungunya outbreaks. Also imported into the UK, where one case from Nigeria, one from Tanzania, one case from Kenya, and one case from Australia. There had been no mention of chikungunya outbreak in these countries. However, the article did not state whether there had been reported sightings of Aedes mosquitoes in UK (HPA 2007).Table 4. The number of cases was set by different methods from the 133 imported cases, in the UK.Identification of the imported cases bite of casesLaboratory confirmed case45Probable case30Suspected case35Past exposure23FranceThe Piti-Salptrire Hospital in Paris, France, reported 80 cases of Chikungunya infection imported by tourists who recently visited the southwestern United States Indian Ocean region, between March 2005 and August 2006. The majority of cases (52) were imported from La Reunion (Hochedez et al. 2007), a popular last site for French tourists (HPA 2006). Other destination sites reported were Mauritius with 18, Comoros with 4, Madagascar with 3, and Mayotte with 2 cases (Hochedez et al. 2007). inwardly the same period, Metropolitan France reported 766 imported cases, which correlated with the two waves of the La Reunion outbreak (Figure 3). At the peak of the first La Reunion outbreak, an average of 20 cases was imported to France monthly. However, between August and November 2005, during the Southern hemisphere winter, the cases decreased (Krastinova et al. 2006). A month after the peak of the second outbreak, the number of imported cases drastically increased. It can be argued that France is at risk of coming(prenominal) outbreaks, in view that some of its inhabitants are evermore visiti ng the Southwest Indian Ocean regions (Hochedez et al. 2007), mainly La Reunion and also due to the inhabitation of Aedes albopictus (Krastinova et al. 2006).Figure 3 Correlation between imported cases of Chikunugunya in metropolitan France to the estimated number of cases in the La Reunion outbreak (Krastinova et al. 2006).ItalyChikungunya was apparently imported into Italy by a male tourist coming from the Kerala province in India, who developed febrile illness two days into his holiday. The region he visited was Castiglonia di Cervia in June 2007. This was recorded by Ravenna provinces local health unit in the Emilia Romagna region, northeastern Italy where 205 people developed CHIKV infection (Rezza et al. 2007). The vector, Aedes albopictus, was implicated in the stretch out of the virus which was then imported from Castiglione di Cervia into Castiglione de Revenna two villages separated by a river. Mosquito control eyeshades implemented in the area resulted in a reduction in chikungunya infection. However, the control measure was not implemented in other villages and therefore a new wave occurred. The virus isolated from the outbreak contained the same mutational change (Ala226Val) in the membrane fusion E1 glycoprotein as the Indian Ocean variant, thereby suggesting that the Kerala strain could have originated from the Indian Ocean outbreak (Rezza et al. 2007).Other European CountriesTourism has been one of the main methods of CHIKV distributions worldwide, including its importation into several European countries. In 2006, the Bernhard-Nocht Institute for Tropical medicament in Hamburg, Germany examined 720 samples from 680 European patients who became symptomatic upon return to Germany, Belgium, Switzerland, Denmark, and Poland from several destinations (Table 2) (Panning et al. 2008). The majority of patients had recently visited countries in the Indian Oceans Mauritius, the Seychelles, La Reunion and Madagascar, and other countries Bali, Indonesia , Sri Lanka, India, Malaysia, Kenya and Thailand. Moreover, most of these countries have been implicated in recent CHIKV outbreaks. No outbreaks were reported in these European countries however, future outbreaks can be hypothesised (Panning et al. 2008).Table 5. The country of origin and the holiday destinations of patients presented at the Bernhard-Nocht Institute for Tropical Medicine in Hamburg, Germany. Exact destinations were only available for 27.8% of patients, and exact itinerary were not available (Panning et al. 2008).Country of originNumber of patientsGermany515Belgium99Switzerland42Denmark22Poland2Total Nos. of patients680Holiday Destinations (Regions with Chikungunya Epidemic)Number of patientsMauritius92The Seychelles23La Reunion18Madagascar9Bali2Indonesia6Sri Lanka5India28Malaysia2Kenya1Thailand3Concurrence with Dengue Fever and MalariaIn 2006 and 2007, Madagascar and Gabon reported co-infections between Chikungunya and DENV-1 or DENV-2 respectively (Ratsitorahina et al. 2008, Leroy et al. 2009). Contrary to CHIKV, dengue virus (DENV) is of Flavirivirus genus from Flaviridae family consisting of four antigenically distinct but closely related serotypes (DENV1-4). It is transmitted by Aedes aegypti and Aedes albopictus, also CHIKV transmission vectors (Cook and Zumla 2009). DENV and CHIKV have similar clinical features (Yoosuf et al. 2008). However, the only contrast is that CHIKV has arthalgia (). The extended incubation period of DENV (5-8 days) commemorated it from CHIKV (2-7 days) however, the difference is insignificant (Cook and Zumla 2009). Thus, serological diagnosis can be used to differentiate DENV to CHIKV (Ratsitorahina et al. 2008). Ratsitorahina et al. (2008) and Leroy et al. (2009) confirmed Aedes albopictus as the predominating transmission vector of both CHIKV and DENV1 or 2. However, neither study stated whether the vector could simultaneously harbour both viruses. Moreover, the study by Vazeille et al. (2008) demonstrated th at Aedes aegypti has a higher susceptibility to DENV-2 virus and a lower susceptibility to CHIKV whereas Aedes albopictus is a more efficient vector for CHIKV than DENV-2 (Vazeille et al. 2008 and Moutailler et al. 2009). Leroy et al. (2009) further demonstrated this theory in the Gabon outbreak, as the majority of the patients had CHIKV compared to DENV-2.In May 1999 and February 2000, the Matete and Kingabwa quarters of Kinshasa in the Democratic state of Congo (DRC) reported two Chikungunya outbreaks. CHIKV was the main contributing factor in the first outbreak however, during the second outbreak, evidence confirmed possibility of co-infections between CHIKV and malaria parasite falciparum (Pastorino et al. 2004). Malaria is a parasitic infection, of the Apicomlexa phylum, that mainly infects hosts red blood cells. It is transmitted by Anopheles species, whereas CHIKV is mainly transmitted by Aedes species. Plasmodium falciparum is one of the four species of Human Malaria (inclu ding Plasmodium vivax, Plasmodium malariae, and Plasmodium ovale). However, Plasmodium falciparum is the most severe form of Malaria (Cook and Zumla 2009). Pastorino et al. (2004) hypothesised that co-infections could be due to long term latency of Plasmodium falciparum, the presence of both transmission vectors in the area or the pathogens sharing the same vectors. An experimental investigation by Yadav et al. (2003 as cited by Pastorino et al. 2004) demonstrated that urban Anopheles stephensi (Plasmodium falciparum vector) could transmit CHIKV.Lack of lookWe are still in the preliminary stages of understanding the interaction between CHIKV and host immunity (Kam et al. 2009), despite increasing number of reported outbreaks, there are insufficient evidences of up-to-date quality research (Panning et al. 2008). Therefore, outbreaks should be employ to implement entomological and epidemiological system in improving our poor knowledge of the virus (Pialoux et al. 2007). Chretien and Linthicum (2007) argued that the Italian outbreak should provide opportunities for developed countries to spike the public-health system of developing countries in order to reduce the worldwide spread of outbreaks. These can be done by implementing Entomological and Virological surveillance in Aedes albopictus infested areas (Charell et al. 2008). Renault et al. (2007) utilise Deltamethrin insecticides to eradicate adult mosquitoes, whereas Rezza et al. (2007) utilised synergised pyrethrins. Furthermore, both authors utilised the biological larvicide, Bacillus thuringiensis israelensis, to destroy breeding sites (Renault et al. 2007, Rezza et al. 2007) however, Renault et al. (2007) later utilised Fenitrothion and temephos. Other control measures include educating the community on personal guard (Ratsitorahina et al. 2008). Although, no commercial vaccine has been approved, several candidates have been tested including the formol inactivated CHIKV vaccine for the Indian strain, DRDE-06, ECSA genotype (Tiwari et al. 2009). Therefore, the author believes that future outbreaks can be avoided if more research on CHIKV is undertaken, and a worldwide surveillance system is implemented.ConclusionThis review has demonstrated that tourism is one of the main methods of CHIKV distributions worldwide, as it was the reason of several outbreaks. CHIKV was transported throughout the Southwestern Indian Ocean islands by viraemic tourists visiting different islands (Figure 2) and Kerala, India, which was then imported into Italy (Renault et al. 2007, Rezza et al. 2007, Sissoko et al. 2008, Yoosuf et al. 2008). However, outbreaks require temperatures above 20oC and annual rainfall over 500mm to maintain Aedes mosquitoes populations (Straetemans 2008, Tilson et al. 2009). Therefore, England is one of the least at risk country, as Aedes albopictus is not present, and the temperature is unfavourable to maintain mosquitoes life cycle (HPA 2007, Met Office 2010). Countries such as France and Italy are at high risk, due to the presence of Aedes albopictus and the introduction of CHIKV although, Italy is the most at risk due to a recent outbreak (Krastinova et al. 2006, Rezza et al. 2007). The eminent climatic changes could result in rising temperatures and increased rainfall that would favour the establishment of Aedes albopictus worldwide. All these emphasises the need for Western medicine to plan for future CHIKV outbreaks, by implementing a worldwide surveillance system in order to monitor outbreaks and to perform vector control measures (Charell et al. 2008). Chikungunya have concurrence with Malaria and Dengue Fever (Leroy et al. 2009, Ratsitorahina et al. 2008) furthermore, evidence suggests wrong classification of Chikungunya due to its resemblance to Dengue fever. CHIKV is constantly mutating, thus constant development of a new vaccine is required (Tiwari et al. 2009). Thereby, further researches are needed.