EMERGING THREATS FROM VECTOR BORNE VIRAL ZONOOTIC DISEASES IN INDIA
The important vectors transmitting zoonotic diseases are mosquitos, flies, fleas, lice, biting flies, bugs, ticks, mites, snails, helminthes etc. which actively transmit pathogens from an infected reservoir host animal to another individual. Many of these are blood sucker , which ingest disease-producing microorganisms during a blood meal from an infected host (human or animal) and later inject it into a new host during their subsequent blood meal. Mosquitoes are the best known vector for transmission of a number of diseases (Samad, 2011). Vector-borne diseases are transmitted in two ways; mechanical and biological. In mechanical transmission, the disease causing agents are transported by flying insects (without any development in the vector) through contaminated legs, wings, mouthparts or through excretory materials (e.g. Anthrax, typhoid, Q fever). In the biological transmission the disease causing agents complete a development cycle in the vectors before transmission in to the vertibrate hosts. Vector-borne diseases are the major illnesses of man and animals now a day and caused by pathogens and parasites. Every year more than 1 billion vector-borne diseases develop globally with a case fatality of 1 million lives (Gubler, 2009).
Key facts
- Vector-borne diseases account for more than 17% of all infectious diseases, causing more than 700 000 deaths annually. They can be caused by either parasites, bacteria or viruses.
- Malaria is a parasitic infection transmitted by Anopheline mosquitoes. It causes an estimated 219 million cases globally, and results in more than 400,000 deaths every year. Most of the deaths occur in children under the age of 5 years.
- Dengue is the most prevalent viral infection transmitted by Aedes mosquitoes. More than 3.9 billion people in over 129 countries are at risk of contracting dengue, with an estimated 96 million symptomatic cases and an estimated 40,000 deaths every year.
- Other viral diseases transmitted by vectors include chikungunya fever, Zika virus fever, yellow fever, West Nile fever, Japanese encephalitis (all transmitted by mosquitoes), tick-borne encephalitis (transmitted by ticks).
- Many of vector-borne diseases are preventable, through protective measures, and community mobilisation.
Vectors
Vectors are living organisms that can transmit infectious pathogens between humans, or from animals to humans. Many of these vectors are bloodsucking insects, which ingest disease-producing microorganisms during a blood meal from an infected host (human or animal) and later transmit it into a new host, after the pathogen has replicated. Often, once a vector becomes infectious, they are capable of transmitting the pathogen for the rest of their life during each subsequent bite/blood meal.
Vector-borne diseases
Vector-borne diseases are human illnesses caused by parasites, viruses and bacteria that are transmitted by vectors. Every year there are more than 700,000 deaths from diseases such as malaria, dengue, schistosomiasis, human African trypanosomiasis, leishmaniasis, Chagas disease, yellow fever, Japanese encephalitis and onchocerciasis.
The burden of these diseases is highest in tropical and subtropical areas, and they disproportionately affect the poorest populations. Since 2014, major outbreaks of dengue, malaria, chikungunya, yellow fever and Zika have afflicted populations, claimed lives, and overwhelmed health systems in many countries. Other diseases such as Chikungunya, leishmaniasis and lymphatic filariasis cause chronic suffering, life-long morbidity, disability and occasional stigmatisation.
Distribution of vector-borne diseases is determined by a complex set of demographic, environmental and social factors. Global travel and trade, unplanned urbanization.
Zoonosis:
The diseases and infections, which are naturally transmissible between vertebrate animals and human are zoonotic and this phenomenon is refered to as zoonosis. Major impacts of zoonoses include illness, monetary loss, adverse effect on morale of personnel, unfavorable publicity and medico-legal implications. The common routes of transmission of zoonotic diseases are bites of insects and through faeces, urine, saliva, blood, semicooked food, milk, aerosole, oral and contact of infected individuals. There are thousands of diseases transmissible between animals and human and bears tremendous social reparcation and impose restriction on national and international trade. Zoonoses may be bacterial, viral, or parasitic, or may involve un-conventional agents. The important classes of zoonotic diseases are meta-zoonosis, transmitted biologically by the invertebrate’s vectors. The impact of zoonoses mostly depends upon the nature of aetiologic agent (very virulent, virulent, moderately virulent), ranges of reservoir hosts and life cycles in the vectors and hosts as well.
The diseases transmitted by arthropod vectors are one of the most dangerous and difficult to control, with an unpredictable spread of the disease. These diseases can be have larger range and high disease transmissibility. Vectors are living organisms that can transmit infectious diseases, most of which are zonootic in nature, between humans or from animals to humans. They ingest disease-producing microorganisms during a blood meal from an infected host (human or animal) and later inject it into a new host during their subsequent blood meal. Mosquitoes, followed by ticks, flies, sandflies, fleas, and triatomine bugs are some of the important disease vectors. Of the 1,407 recognized species of human pathogens, 816 (58%) are known to be zoonotic. Of the total, 177 are regarded as emerging or reemerging, most of which are viral zonootic diseases (Woolhouse and Gowtage-Sequeria 2005). Following are some of the important vector borne viral zonootic diseases in Indian context.
Risk factors associated with vector-borne zoonosis:
- Globalization of trade and travel, unplanned urbanization and environmental devastation due to climate change poses significant impact on VBDs transmission in recent years
- 2. Due to lack of awareness of some VBDs like dengue, chikungunya, Nipah and West Nile virus etc. have emerged in countries where they were previously unknown
- 3. Changes in agricultural practices, changes in the breeding places of vectors due to deforestation, draughts, variation in temperature and rainfall affect increase transmission or wipe out few of the VBDs
- 4. Lack of proper education, improve awareness and monitoring about the distribution of vectors, vector-borne diseases and other climate-sensitive diseases
- 5. A crucial element in catching vector-borne diseases is the behavioural change of curious people during travel and tourism and searching for feed and living places in wild environment
- 6. Poor national economy and lack of mobilizing fund for developing technical expertise
- 7. Lack of draconian measures often emerge or reemerge VBDs in developing worlds
JAPANESE ENCEPHALITIS
Japanese encephalitis (JE) is an inapparent to acute arthropod-borne viral infection and one of leading cause of viral encephalitis and neurological infection in Asia (Halstead et al 2008). It is due to infection with the JE virus (JEV), a mosquito-borne Flavivirus belonging to the family Togaviridae The main JEV transmission cycle involves Culex tritaeniorhynchus mosquitoes and similar species that lay eggs in rice paddies and other open water sources, with pigs and aquatic birds as principal vertebrate amplifying hosts (Burke et al 1988). Humans are generally thought to be dead-end JEV hosts, i.e. they seldom develop enough viremia to infect feeding mosquitoes i.e. less than 1% of human JEV infections result in JE. Approximately 20–30% of JE cases are fatal, with neurologic sequelae in 30–50% of survivors (Fischer et al 2008). JE is primarily a disease of children and most adults in endemic countries have natural immunity after childhood infection, but all age groups are affected. In most temperate areas of Asia, JEV is transmitted mainly during the warm season, when large epidemics can occur. In the tropics and subtropics, transmission can occur year-round but often intensifies during the rainy season (Fischer et al 2010). A large scale outbreak of JE was reported in 1973 from Bankura and Burdwan districts of West Bengal. Since 1972, JE has spread to newer areas epidemics/outbreaks were also reported from Assam, Andhra Pradesh, Bihar, Uttar Pradesh, Madhya Pradesh, Karnataka, Kerala, Tamil Nadu, Goa, Pondicherry and Maharashtra.
Clinical signs and symptoms:
Humans Beings:
JE has an incubation period of 5 to 15 days and the vast majority of infections are asymptomatic as only 1 in 250-300 infections develop into encephalitis. Fever, headache and malaise are other non-specific symptoms of this disease which may last for a period of between 1 and 6 days. Signs which develop during the acute encephalitic stage include neck rigidity, cachexia, hemiparesis, convulsions and a raised body temperature between 38 and 41 degrees celsius. Mental retardation developed from this disease usually leads to coma. Mortality of this disease varies but is generally much higher in children. Life-long neurological defects such as deafness, emotional liability and hemiparesis may occur in those who have had central nervous system involvement.
Animals:
Pigs: JE virus is maintained between pig-mosquito-pig cycle in nature. Pig acts as an amplifying host of JE virus. The infection is inapparent in pigs. Pregnant sows may give birth prematurely to infected and often dead pigs. Horses: JE virus infection is prevalent in horses usually in an inapparant form. However, sometimes it could be acute with fatal encephalitis. Birds: The black crowned night heron, little egret and plumed egrets are important in transmission cycle showing high level of viraemia as well as seroconversion. Antibodies to JE virus have also been demonstrated in cattle, sheep and goat but these animals do not seem to play a significant role in the maintenance and transmission of JE virus in nature. Laboratory Diagnosis: The important diagnostic methods include (a) Isolation of virus from autopsy specimens of brain tissues, which can be achieved by inoculation of suckling mice, vertebrate cell culture or insect cell culture (C636 Aedes albopictus cell line). (b) Demonstration of viral antigen in the autopsy specimens of brain by fluorescent antibody technique. (c) Serological diagnosis by demonstration of virus specific IgM antibody by IgM antibody capture ELISA (MAC ELISA) in the acute serum sample of patients or demonstration of 4 fold or higher rise in antibody titre on testing paired sera by HI, CF or mouse neutralization test. Treatment: In the absence of a reliable antiviral drug, symptomatic treatment using antipyretic and anticonvulescent drugs with proper management is indicated. Maintenance of electrolytes balance and reducing of intracranial pressure is also advisable. Prevention and control: In India- JEEV is the purified inactivated vaccine available. However, for want of specific antiviral drugs and several limitations on the use of vaccine, vector control seems to be the only possible way to break the transmission cycle to control the disease. Prevention of mosquito bites and vector control by larvicides and insecticide house spraying are the best ways, besides water management in irrigation practices for paddy fields.
CRIMEAN CONGO HEMORRHAGIC FEVER
Crimean Congo hemorrhagic fever (CCHF) is one of the severe forms of hemorrhagic fever endemic in Africa, Asia, Eastern Europe and the Middle East with a near fatal mortality rate. India was always under the potential threat of CCHF viral infection until an outbreak hit parts of Gujarat. In India, the first laboratory confirmed case of CCHF was reported in January, 2011 from Ahmedabad, in Gujarat (Patel el al 20011). CCHF is a zoonotic viral disease caused by tick-borne virus Nairovirus (Family Bunyaviridae). Hyalomma tick is the vector responsible for viral transmission. Other ixodid ticks including members of the genera Rhipicephalus, Boophilus, Dermacentor, and Ixodes may also transmit the virus. These vectors have both trans-ovarial and transstadial transmission of virus, thus contributing to circulation of the virus in nature by remaining infected throughout their developmental stages and also by passing to the next generation. The CCHF virus circulates in an enzootic tick–vertebrate–tick cycle. The disease is generally asymptomatic in infected animals but highly fatal in humans. Human beings may acquire infection by direct contact with blood or other tissues of infected livestock or may become infected through a tick bite or crushing of infected tick. Further secondary cases are frequently seen due to human to human transmission via percutaneous or per mucosal exposure to blood and body fluids containing the virus. History of tick bite, high-risk occupations, contact with livestock and older age are risk factors. A variety of vertebrates like cattle, goats, donkeys, horses, etc., along with smaller wild life species like hares and hedgehogs act as a reservoir for the virus. A related species of the genus Nairovirus – Ganjam virus – that belongs to the Nairobi Sheep group is transmitted by Hemaphysalis ticks. This virus has veterinary importance in India and has been demonstrated in mosquitoes, man, and sheep. Clinical signs and symptoms: Human beings are the only host in whom the disease manifestations are visible. The typical course of CCHF infection has four distinct phases-incubation period, prehemorrhagic phase, haemorrhagic phase, and convalescent phase. The incubation period is in the range of 3-7 days. The disease begins by nonspecific prodromal accompanied by hypotension, relative bradycardia, tachypnea, conjunctivitis, pharyngitis, and cutaneous flushing or rash. The prehemorrhagic phase lasts for 4-5 days and in a majority of the patients it progresses to hemorrhagic phase. The hemorrhagic phase is generally short and has a rapid course with signs of progressive hemorrhage and diathesis. The disease is fatal in 40-60% of the cases. In severe cases, death occurs as a result of multiorgan failure, disseminated intravascular coagulation, and circulatory shock. Laboratory diagnosis: As CCHF virus is classified as risk group 4 virus and hence the clinical samples are handled in specially-equipped, high biosafety level laboratories (BSL 3 plus or 4). The antemortem samples comprise of blood samples and the post-mortem samples include tissue samples (liver, spleen, bone marrow, kidney, lung and brain). (a) Virus Isolation: It is carried out in maximum bio-containment laboratory i.e. BSL – 4. The virus may be isolated from blood or tissue specimens in the first five days of illness. (b) Molecular Technique: The Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) is test of choice for laboratory diagnosis of CCHF virus infection. (c) Serology: IgG and IgM antibodies may be detected in serum by ELISA from about day six of illness. IgM remains detectable for up to four months, and IgG levels decline but remain detectable for up to five years. Treatment: According to World Health Organization (WHO), ribavirin is the anti-viral medication of choice for CCHF and the recommended dose is an initial dose of 30 mg/kg followed by 15 mg/kg for four days and then 7.5 mg/kg for six days for a total of 10 days. A new specific immunoglobulin CCHF-Venin that contains antibodies to CCHF virus has been prepared, but limited studies are available, which show the beneficial effects of immunotherapy in CCHF. Prevention and control measures: These include use of tick repellents, avoidance of tick prone areas, and regular examination of clothing and skin for ticks. While handling livestock or domesticated animals, appropriate acaricidal agents should be used to control tick population. Protective clothing and gloves should be used whenever there is chance of contact with skin or mucous membranes of viremic animals, particularly when blood and tissues are handled. Consumption of unpasteurized milk and uncooked meat should be avoided. CCHF V irus can be inactivated by disinfectants including 1% hypochlorite and 2% glutaraldehyde; and can be destroyed by heating at 56°C (133°F) for 30 min.
WEST NILE FEVER
West Nile virus (WNV) is an arthropod borne virus of the genus Flavivirus under family Flaviviridae and is found in both tropical and temperate regions. It mainly infects birds, but is known to infect humans, horses, dogs, cats, bats, chipmunks, skunks, squirrels and domestic rabbits. The main route of human infection is through the bite of an infected mosquito, mainly Culex spp. The disease causes mortality in horses, domestic and wild birds. In India, this virus is known to be active in mosquitoes, birds and pigs. It has also been associated with human encephalitis cases. In India, presence of West Nile antibodies in humans was first reported from Bombay by Banker in 1952 and confirmed by Smithburn in 1954 by detecting the WNV neutralizing antibodies. WNV neutralizing antibodies (about 20-30%) have been detected in human sera collected from Tamil Nadu, Karnataka, Andhra Pradesh, Maharashtra, Gujarat, Madhya Pradesh, Orissa and Rajasthan. The WNV strain P-4230 has been isolated from a laboratory worker who got lab infected while handling the Indian mosquito strain G-2266 and the Egyptian human strain E-101 on consecutive two days (Virus Research Centre, Annual Report-1956). Clinical signs and symptoms: Human beings: The incubation period of disease is usually 3 to 14 days. The symptoms of severe neuroinvasive disease include headache, high fever, neck stiffness, stupor, confusion, seizure, chorioretinitis, disorientation, coma, tremors, convulsions, muscle weakness, and paralysis. Animals: Most infections in animals are subclinical. WNV infection in horses typically cause listlessness, depression, somnolence, listlessness, apprehension, hyperexcitability and meningoencephalitis. Approximately 90% of symptomatic cases in horses result in neurological disease with case fatality rates of 30-40% (Venter et al., 2011). However, WNV infection in horses has not been documented in India. General signs of infection in birds include lethargy, recumbency, and in some cases, hemorrhage. Laboratory diagnosis: (a) The most efficient technique is detection of IgM antibody to WNV in serum or cerebral spinal fluid (CSF) collected within 8 days of illness onset using the IgM antibody capture enzyme-linked immunosorbent assay (MAC-ELISA). (b) Other methods to confirm WNV infection include IgG antibody sero-conversion (or significant increase in antibody titers) in two serial specimen, neutralization assay, RT-PCR technique, and virus isolation by cell culture (CDC, 2011). Treatment: Currently, there are no effective medicines available for the management of WNV infection. Treatment in patients with severe disease may require supportive therapy such as hospitalization, mechanical ventilation, intravenous fluids and prevention of secondary infections. Prevention and control: The integrated vector control strategies includes the use of personal protection measures like protective clothing, bed nets, both chemical and neem based repellants, insecticides, insecticide impregnated curtains, and biological control methods by larvivourus fish, introducing natural parasites and predators and bacterial agents.
KYASANUR FOREST DISEASE
Kyasanur Forest Disease (KFD) is a tick-borne viral disease characterised by sudden onset of fever and/or headache followed by hemorrhagic manifestations such as conjunctival congestion, bleeding gums, epistaxis, haemoptysis, haematemesis and malena. Heavy mortality in two species of monkeys viz. the black faced langur (Semnopithecus entellus) and the red faced bonnet monkey (Macaca radiata) in March 1955 in forests of Shimoga district, Karnataka led to the disease discovery. Investigations resulted in the isolation of the virus from monkeys, man and ticks. The disease is now localised in five districts (Shimoga, Chikamagalur, Uttar Kannada, Dakshina Kannada and Udupi) of Karnataka. Recently, in 2014, a new focus of KFD virus activity has been reported in a tribal area of Kerala (Babasaheb et al 2015). The causative agent is a Flavivirus, which is transmitted to man through the bite of a tick Haemaphysalis spinigera. KFD is mainly seasonal and most cases occur during the inter-monsoon period i.e., from December to June. Epidemics coincide with nymphal activity of ticks, which is high from December to May; hence nymphs are considered as the most important stage for human transmission. Adults are more susceptible than the children primarily because children in this age group rarely visit the forest and males more than the females. The number of human cases occurring each year varied from 40 to ~1000 with a mortality rate of 4-15%. KFD epizootics in monkeys are a regular feature in the area. However, in enzootic state, KFD virus circulates through small mammals such as rodents, shrews, ground birds and an array of tick species. Cattle are the important source of blood meal for these adult ticks but do not play a role in the virus transmission cycle. Clinical signs and symptoms: The onset is sudden with chills; frontal headache and high fever about 40oC. The clinical symptoms include continuous fever for 12 days or longer, usually associated with severe myalgia, cough, diarrhea, vomiting and photophobia. The incubation period is of 2- 7 days. The convalescent phase is prolonged. Often, there is a relapse after 1 to 2 weeks of a febrile period. The second phase lasts for 2- 12 days and is marked by the same symptoms. Neck stiffness, mental disturbance, giddiness and abnormality of reflexes are additional complications in the second phase of illness. The ratio of apparent:inapparant infection is 1:1. The attack rate is 5 per 100 in a given village. Recovered persons have a life-long immunity. Diagnosis: (a) Isolation of the virus from the acute serum by inoculation of suckling mice (b) Demonstration of a rise in titre of antibodies in paired serum samples (acute and convalescent) by haemagglutination inhibition and mouse neutralization tests. Prevention and control: This includes measures related to avoidance of tick bites and eradication of ticks. An inactivated vaccine for KFD virus is routinely being manufactured in the laboratory of Karnataka State Government for human immunization.
CHIKUNGUNYA FEVER
Chikungunya is a mosquito-borne viral disease of great public health concern in India. Chikungunya fever (CHIK fever) caused by chikungunya virus (CHIKV) is transmitted by the mosquito, Aedes aegypti. The virus is currently causing one of the largest reported outbreaks of CHIK fever in last 40 years. Chikungunya is believed to have originated in Africa where it has maintained in ‘sylvatic cycle’ involving wild primates and forest dwelling mosquitoes such as Aedes furcifer, Ae. luteocephalus, or Ae. taylori. The first recorded chikungunya outbreak in India was in Kolkata in 1963. This was followed by epidemics in Tamil Nadu, Andhra Pradesh and Maharashtra in 1964–65 and in Barsi in 1973. The virus re-emerged in 2006 after a gap of 32 years and caused an explosive outbreak affecting states like Andhra Pradesh, Karnataka, Maharashtra, Madhya Pradesh, Tamil Nadu, Gujarat and Kerala. During 2009–2010, cases were also reported from Maharashtra. In the subsequent years, CHIKV spread to other states: Goa, Orissa, Rajasthan, West Bengal, Andaman & Nicobar Islands and Puducherry. In the year 2011 cases were reported from all states except Punjab, Dadra and Nagar Haveli and Lakshadweep. The virus is transmitted by culicine mosquitoes, Aedes aegypti, Ae. albopictus and Ae. Polynesiensis, although Culex and Anopheles have also been reported for the transmission in some cases. The common reservoirs for Chikungunya virus are monkeys, lemurs and other vertebrates. The role of cattles and rodents has also been reported in the transmission of the virus. Chikungunya virus usually shows a periodicity with re-occurrence of disease in the community after interval of 3-4 years. A recently published study has reported some mutations in the virus at E1-226V portion of the genome, which possibly have made it possible for the virus to survive longer in humans and mosquitoes, explaining, to its rapid spread. Clinical signs and symptoms: The symptoms develop after an incubation period of 4 to 7 day. A clinical triad of ‘fever, rashes and arthralgia’ is suggestive of chikungunya fever. Movement at the joints causes excruciating pain to the person forcing to make bend up position giving it the name ‘Chikungunya’. The clinical features also include severe headache, chills and rigors, nausea and vomiting. The fever may disappear to return in one or two days giving it the name of ‘Saddle back fever’. Rashes occur mainly on trunks or extensor surfaces of the limbs and are itching in nature usually accompanied by secondary rise in the temperature. Laboratory Diagnosis: (a) Serological diagnosis against neutralising and HI. IgM capture ELISA is the most sensitive serologic assay, and is necessary to distinguish the disease from dengue. (b) RT-PCR is confirmatory for the identification of chikungunya virus. (c) The virus isolation procedures need to be done under BSL-3 precautions Prevention and control: The only mode of prevention is use of physical and biological means of protection from the vector. Center for Disease Control and Prevention (CDC) has advised a repellent containing 30 to 50% DEET (N, N-diethyl-m-tolumide).
Chandipura virus encephalitis:
Chandipura virus (CHPV) is a vesiculovirus of Family Rhabdoviridae. The virus, known to be carried in dormant stage by sandflies, which live near domestic animals like cows and buffaloes and is transferred from the fly to human beings specifically during monsoon. Cases clinically diagnosed as viral encephalitis from Raipur in central India in 1980 showed CHPV etiology, confirmed by isolation of CHPV virus from the acute sera Chandipura virus has been isolated in from a pool of 253 unidentified Phlebotomine sandflies (Phlebotomus spp.) in the Maharashtra State of India (Dhanda et al., 1970) and from unidentified Sergentomyia in the Karimnagar district in Andhra Pradesh, India (Geevarghese et al., 2005). CHPV was incriminated as the etiological agent of large-scale encephalitis outbreaks in children (9 months to 15 yr of age) in various districts of Andhra Pradesh in 2003 with high case fatality rate (CFR) of 55.6% (Rao et al., 2004).
Ganjam Virus Disease: Ganjam virus (GANV), a tick-borne arbovirus of veterinary importance causing high morbidity and mortality in exotic and crossbred sheeps and goats, is widely prevalent in India (Banerjee 1996). It causes an acute febrile illness in sheep and goat characterized by fever, anorexia, lumbar paralysis and high fatality. It was first isolated from Haemaphysalis intermedia ticks collected from sheep in Ganjam district of Orissa state in 1969. Subsequently, the virus was also isolated from ticks collected from sheep and goat from Shimoga district and also from Culex vishnui mosquito from Vellore and acute sera of sheep from Chittoor district of Andhra Pradesh. The virus was also isolated from Rhipicephalus haemaphysaloids ticks collected in Pune city in 2004-05 and from sheep of Chittoor district, Andhra Pradesh.
Bhanja virus:
The Bhanja virus of family Bunyaviridae, was first isolated from adult tick H. intermedia, collected from a goat with lumbar paralysis in Bhanjanagar, Orissa, in December, 1954 (Hubalek 1987). Later, the virus has been isolated from various countries such as Nigeria, Italy, Senegal, Southern USSR, Yugoslavia and Bulgaria. Generally in adults, the virus causes an unapparent infection but in young ruminants (lamb, kid, calf) it is pathogenic, causing fever and neurological symptoms. In spite of the presence of virus in small ruminant and ticks, the human cases of bhanja virus has not been reported from India. This might be due to underreporting system and poor diagnostic facilities. The wide geographical distribution and presence of antibody in domestic animals could probably make Bhanja virus as an emerging virus infection.
The increase incidence of VBDs is related to the availability of vectors, pathogens and transmission to the definitive hosts. Changes in environmental temperature directly affect emergence and transmission of VBPs through pathogen-host interaction, and indirectly through changes in ecosystem and species composition. As temperatures increases in some geographical areas, the vectors have been spreading to areas were previously was too cold. For example, two mosquito vectors that carry malaria in Asia are now available in the USA-Mexico border. Leishmanial vector are now available in USA and few of the European country. More frequent droughts in some areas can cause a decrease in vectors densities that require water for their life cycle. A decline in biodiversity alters predator-prey relationships; a decline in the predators of vectors can increase vector populations. Movement of human population and deforestation can also expand distribution of pathogens and increase exposure routes. Collectively, arthropods are responsible for millions of illness in man and animals each year. Over the past 30 years, there has been a global emergence and re-emergence of infectious disease in man and animals and vectorborne diseases in particularly showed an increased in frequency of epidemic transmission and crossing of geographic barrier. A major problem is that the most important vector-borne diseases occurred in the tropics, usually in the areas where resources are limited and surveillance is poor. However, the shrinking world, with highly increased human and animal mobility due to air travel and commerce (globalization) has made these diseases not just problems of the tropics; they present the global community with possibly its greatest health problem and threat to economic security today. This underscores the need for physicians, veterinarians and ecobiologist in endemic and non-endemic areas to be aware of vector-borne diseases and to be knowledgeable about where they occur and how to recognize and treat them. There is strong need to set rules that prevent emission of greenhouse gases that influence local/ regional ecology, alter the life cycles of certain diseases in vectors and animals. It is mandatory to preserve 20-25% forests areas and wetlands to maintain healthy ecology and keep vectors in forest; now a day this requirement is greatly ignored. Developing and implementing early warning systems to reduce exposure to environmental hazards and limit susceptibility in exposed populations is also lacking. It needs to develop expert manpower, deploy innovative disease prevention techniques and work to improve diagnostic testing for vector-borne diseases. Development of new pesticides is needed aimed at controlling disease vectors with species specificity (affecting only the target vectors), environmentally safe and low susceptibility to resistance. Routine monitoring in the genetics of vector-borne pathogens also needed to understand the changes in the genomes with their changing ecology and host tropism. The registered vet equipped to deal with a number of insect borne infectious and zoonotic diseases need to deploy in the cross border areas, hilly areas, low land, marshy land, airport and forest areas of a country to keep constant monitoring of the existing or emerging vectors and vector-borne diseases and design preventive and control strategies accordingly.
Compiled & Shared by- Team, LITD (Livestock Institute of Training & Development)
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Reference-On Request.
