പുകയില ഒരു മാരക രോഗകാരിയാണെന്നും അത്‌ പുകവലിക്കുന്നവനെ മാത്രമല്ല അവനോട്‌ സഹവസിക്കുന്നവരുടേയുംആരോഗ്യത്തെബാധിക്കുന്നു.പുകയിലയുടെ പുക ശ്വസിക്കുന്നവര്‍ക്കും ഇത് രോഗം വരുത്തിവയ്ക്കുന്നു എന്ന് സാരം.

യുവാക്കളില്‍ പുകവലി കുറഞ്ഞിട്ടുണ്ടെങ്കിലും മറ്റുതരത്തിലുള്ള പുകയില ഉല്‍പന്നങ്ങള്‍ കൂടുതലായി ഉപയോഗിച്ചു വരുന്നതായും ഇതുമൂലം പുകയില കാരണമാകുന്ന അര്‍ബുദ രോഗികളുടെ എണ്ണം ക്രമാതീതമായി വര്‍ധിക്കുന്നതായും ഈ രംഗത്ത് ഗവേഷണം നടത്തുന്നവര്‍ അഭിപ്രായപ്പെടുന്നു.

 നൂറുപേര്‍ അര്‍ബുദംമൂലം മരിക്കുമ്പോള്‍ അതില്‍ 30പേര്‍ പുകവലി കാരണം രോഗം വന്നു മരിക്കുന്നവരാണ്. പുകയില ഉപയോഗം ശ്വാസകോശാര്‍ബുദം, സ്‌തനാര്‍ബുദം, രക്താര്‍ബുദം, ശ്വസനനാളി, ആമാശയം, മൂത്രസഞ്ചി, സെര്‍പിക്‌സ്‌, അന്നനാളി തുടങ്ങിയ ഭാഗങ്ങളിലെ കാന്‍സര്‍ എന്നിവയ്‌ക്കും മസ്‌തിഷ്‌കാഘാതം, അന്ധത, തിമിരം, ഹൃദയരോഗങ്ങള്‍, ആസ്‌തമ, ന്യുമോണിയ, വന്ധ്യത, കുട്ടികളില്‍ ഭാരക്കുറവ്‌ എന്നീ രോഗങ്ങള്‍ക്കും കാരണമാകുന്നു. നിഷ്‌ക്രിയ ധൂമപാനം തലച്ചോറിലെ കാന്‍സര്‍, മസ്‌തിഷ്‌കാഘാതം, വന്ധ്യത, സഡന്‍ ഇന്‍ഫാന്റൈല്‍ ഡെത്ത്‌ സിന്‍ഡ്രം എന്നീ രോഗങ്ങള്‍ക്കും കാരണമാകുന്നു.

ഒരു സിഗരറ്റില്‍ നാലായിരത്തില്‍പരം രാസപദാര്‍ഥങ്ങള്‍ അടങ്ങിയിരിക്കുന്നു. അതില്‍, 600ഓളം രാസവസ്തുക്കള്‍ നേരിട്ട് കാന്‍സര്‍ ഉണ്ടാക്കാന്‍ കഴിയുന്നവയാണ്. ശ്വാസകോശാര്‍ബുദത്തിലെ പ്രധാന വില്ലനാണ് പുകയില. സിഗരറ്റ്പുകയിലെ അമ്പതില്‍പ്പരം രാസവസ്തുക്കള്‍ അര്‍ബുദകാരികളാണ്. വായ, തൊണ്ട, അന്നനാളം എന്നിവിടങ്ങളിലെ അര്‍ബുദത്തിനുള്ള പ്രധാന കാരണം പുകയിലയാണ്. മൂത്രസഞ്ചി, വൃക്ക, പാന്‍ക്രിയാസ് എന്നിവയില്‍ ക്യാന്‍സറിനുള്ള പരോക്ഷ കാരണവും പുകയിലതന്നെ. പുകയിലയില്‍ അടങ്ങിയ നിക്കോട്ടിന്‍ എന്ന രാസവസ്തു പുകയെടുത്ത് പത്തുസെക്കന്‍ഡിനുള്ളില്‍ തലച്ചോറില്‍ ലഹരിയായി പ്രവര്‍ത്തിക്കുന്നു. ഇത് ഹൃദ്രോഗത്തിനും രക്തസമ്മര്‍ദം ഉയര്‍ത്തുക വഴിപക്ഷാഘാതത്തിനുംകാരണമാകുന്നു.സിഗരറ്റില്‍അടങ്ങിയിട്ടുള്ളതില്‍കാര്‍ബണ്‍മോണോക്സൈഡ്ശ്വാസകോശാര്‍ബുദത്തിനിടയാക്കും. സിഗരറ്റിലെ ഏറ്റവും കൊടിയ രാസവസ്തുവായ ബെന്‍സ് പയറിന്‍ രക്തത്തില്‍ കലര്‍ന്ന് ശരീര കോശങ്ങളെ നശിപ്പിക്കുകയും എല്ലാ അവയവങ്ങളെയും ക്ഷയിപ്പിക്കുകയും ചെയ്യും.

 ഇന്ത്യയില്‍ കാന്‍സര്‍ രോഗികളില്‍ 90 ശതമാനത്തിനും ശ്വാസകോശത്തിലും തൊണ്ടയിലും വായയിലുമാണ് രോഗം ബാധിക്കുന്നത്. പുകവലിയില്‍നിന്ന് പിന്മാറി പുകയില അടങ്ങിയ പാന്‍മസാലകള്‍ പോലുള്ളവയുടെ വര്‍ധിച്ചുവരുന്ന ഉപഭോഗമാണിതിനുകാരണം.ഈ ദുരന്തം ഒഴിവാക്കാന്‍ പുകയിലയോടുള്ള അഭിനിവേശം ഇല്ലാതാക്കുകയും   പുകയിലയുടെ ദോഷവശങ്ങളെക്കുറിച്ച് പൗരന്മാരെ ബോധവാന്മാരാക്കുകയും ചെയ്യേണ്ടതുണ്ട്.സ്കൂള്‍ തലത്തില്‍ത്തന്നെ  ബോധവല്‍ക്കരണ പ്രവര്‍ത്തനങ്ങള്‍ ആരംഭിച്ചുകഴിഞ്ഞു.കൂടാതെ COTPA 2003ഉം കേരളത്തില്‍ നടപ്പിലാക്കിവരുന്ന  പാന്‍മസാല നിരോധനവും ഈ രംഗത്തുള്ള നല്ല ചുവടുവെപ്പായിമാറിയിട്ടുണ്ട്.

                                  JAPANESE ENCEPHALITIS

 AGENT

Japanese encephalitis (JE) virus is a single-stranded RNA virus that belongs to the genusFlavivirus and is closely related to West Nile and Saint Louis encephalitis viruses.

TRANSMISSION

JE virus is transmitted to humans through the bite of an infected mosquito, primarily Culexspecies. The virus is maintained in an enzootic cycle between mosquitoes and amplifying vertebrate hosts, primarily pigs and wading birds. Humans are incidental or dead-end hosts, because they usually do not develop a level or duration of viremia sufficient to infect mosquitoes.

Japanese encephalitis (JE) virus, a flavivirus, is closely related to West Nile and St. Louis encephalitis viruses. JE virus is transmitted to humans through the bite of infected Culex species mosquitoes, particularly Culex tritaeniorhynchus.

The virus is maintained in a cycle between mosquitoes and vertebrate hosts, primarily pigs and wading birds. Humans are incidental or dead-end hosts, because they usually do not develop high enough concentrations of JE virus in their bloodstreams to infect feeding mosquitoes.

JE virus transmission occurs primarily in rural agricultural areas, often associated with rice production and flooding irrigation. In some areas of Asia, these conditions can occur near urban centers.

EPIDEMIOLOGY

JE virus is the most common vaccine-preventable cause of encephalitis in Asia, occurring throughout most of Asia and parts of the western Pacific (Map 3-08). Local transmission of JE virus has not been detected in Africa, Europe, or the Americas. Transmission principally occurs in rural agricultural areas, often associated with rice cultivation and flood irrigation. In some areas of Asia, these ecologic conditions may occur near, or occasionally within, urban centers. In temperate areas of Asia, transmission is seasonal, and human disease usually peaks in summer and fall. In the subtropics and tropics, seasonal transmission varies with monsoon rains and irrigation practices and may be prolonged or even occur year-round.

In endemic countries, where adults have acquired immunity through natural infection, JE is primarily a disease of children. However, travel-associated JE can occur among people of any age. For most travelers to Asia, the risk for JE is extremely low but varies based on destination, duration, season, and activities.

From 1973 through 2011, there were 58 published reports of travel-associated JE among travelers from nonendemic countries. From the time of licensure of a JE vaccine in the United States in 1992 through 2011, only 7 JE cases among US travelers have been reported to CDC.

The overall incidence of JE among people from nonendemic countries traveling to Asia is estimated to be <1 case per 1 million travelers. However, expatriates and travelers who stay for prolonged periods in rural areas with active JE virus transmission are likely at similar risk as the susceptible resident population (5–50 cases per 100,000 children per year). Travelers on even brief trips might be at increased risk if they have extensive outdoor or nighttime exposure in rural areas during periods of active transmission. Short-term (<1 month) travelers whose visits are restricted to major urban areas are at minimal risk for JE. In some endemic areas there are few human cases among residents because of natural immunity among older people or vaccination; however, JE virus is usually still maintained in these areas in an enzootic cycle between animals and mosquitoes. Therefore, susceptible visitors may be at risk for infection.

CLINICAL PRESENTATION

Most human infections with JE virus are asymptomatic; <1% of people infected with JE virus develop clinical disease. Acute encephalitis is the most commonly recognized clinical manifestation of JE virus infection. Milder forms of disease, such as aseptic meningitis or undifferentiated febrile illness, can also occur. The incubation period is 5–15 days. Illness usually begins with sudden onset of fever, headache, and vomiting. Mental status changes, focal neurologic deficits, generalized weakness, and movement disorders may develop over the next few days.

• The classical description of JE includes a parkinsonian syndrome with masklike facies, tremor, cogwheel rigidity, and choreoathetoid movements.
• Acute flaccid paralysis, with clinical and pathological features similar to those of poliomyelitis, has also been associated with JE virus infection.
• Seizures are common, especially among children.
• Common clinical laboratory findings include moderate leukocytosis, mild anemia, and hyponatremia. Cerebrospinal fluid (CSF) typically has a mild to moderate pleocytosis with a lymphocytic predominance, slightly elevated protein, and normal ratio of CSF to plasma glucose.

The case-fatality ratio is approximately 20%–30%. Among survivors, 30%–50% have serious neurologic, cognitive, or psychiatric sequelae.

DIAGNOSIS

JE should be suspected in a patient with evidence of a neurologic infection (such as encephalitis, meningitis, or acute flaccid paralysis) who has recently traveled to or resided in an endemic country in Asia or the western Pacific. Laboratory diagnosis of JE virus infection should be performed by using a JE virus–specific IgM-capture ELISA on CSF or serum. JE virus–specific IgM can be measured in the CSF of most patients by 4 days after onset of symptoms and in serum by 7 days after onset. A ≥4-fold rise in JE virus–specific neutralizing antibodies between acute- and convalescent-phase serum specimens may be used to confirm the diagnosis. Vaccination history, date of onset of symptoms, and information regarding other flaviviruses known to circulate in the geographic area that may cross-react in serologic assays need to be considered when interpreting results.

Humans have low levels of transient viremia and usually have neutralizing antibodies by the time distinctive clinical symptoms are recognized. Virus isolation and nucleic-acid amplification tests are insensitive in detecting JE virus or viral RNA in blood or CSF and should not be used for ruling out a diagnosis of JE.

TREATMENT----There is no specific antiviral treatment forJE; therapy consists of supportive care and management of complications.

PREVENTION------The best way to prevent mosquito borne diseases, including JE, is to avoid mosquito bites.The natural transmission cycle involves Culex tritaeniorhynchus and other Culex mosquitoes, such as Cx. gelidus and Cx. Vishnui, which breed primarily in ricefields and feed on humans in the early evenings.The infected mosquito transmits the virus to humans and animals during biting. The mosquitoes breed where there is abundant water such as rice paddies and become infected by feeding on pigs and wild birds infected with the Japanese encephalitis virus. The disease is not directly transmitted from person to person.Fogging operations with malathion technical is advised to be conducted in these areas where suspected JE cases were occurred to interrupt any further transmission. Technical malathion thermal fogging itself becomes an unavoidable part of vector control in JE outbreak.

Vaccine---There is a vaccine for Japanese encephalitis but it is usually not recommended for members of the general public. The vaccine is only recommended for endemic areas in Asia and Western Pacific Region, particularly in rural areas.

                                                                     HANTAVIRUSE

Hantaviruses are single-stranded, enveloped, negative sense RNA viruses in the Bunyaviridae family. Humans may become infected with hantaviruses through contact with rodent urine, saliva, or feces. Some strains of hantaviruses cause potentially fatal diseases in humans, such asHantavirus hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS), while others have not been associated with known human disease.Human infections of hantaviruses have almost entirely been linked to human contact with rodent excrement, but recent human-to-human transmission has been reported with the Andes virus in South America.The name hantavirus is derived from the Hantan River area in South Korea, for which Hantaan virus is named. It was isolated in the late 1970s by Karl M. Johnson and Ho-Wang Lee.The hantaviruses are a relatively newly discovered genus of viruses. An outbreak of Korean Hemorrhagic Fever among American and Korean soldiers during the Korean War (1951–1953) was later found to be caused by a hantavirus infection. More than 3000 troops became ill with symptoms that included renal failure, generalized hemorrhage, and shock. It had a 10% mortality rate. This outbreak sparked a 25-year search for the etiologic agent. Ho-Wang Lee, a South Korean virologist, Karl M. Johnson, an American tropical virologist, and his colleagues isolated Hantaan virus in 1976 from the lungs of striped field mice.

Two major clinical syndromes

Hemorrhagic fever with renal syndrome

Main article: Hantavirus hemorrhagic fever with renal syndrome (HFRS)

Hemorrhagic fever with renal syndrome (HFRS) is a group of clinically similar illnesses caused by species of hantaviruses from the family Bunyaviridae. It is also known as Korean hemorrhagic fever, epidemic hemorrhagic fever, and nephropathis epidemica. The species that cause HFRS include Hantaan River, Dobrava-Belgrade, Saaremaa, Seoul, and Puumala. It is found in Europe, Asia, and Africa.

In hantavirus induced hemorrhagic fever, incubation time is between two to four weeks in humans before symptoms of infection present. Severity of symptoms depends on the viral load.

Hantavirus pulmonary syndrome

Hantavirus pulmonary syndrome (HPS) is found in North, Central and South America.It is an often fatal pulmonary disease. In the United States, the causative agent is Sin Nombre virus carried by deer mice. Prodromal symptoms include flu-like symptoms such as fever, cough, myalgia, headache, and lethargy. It is characterized by a sudden onset of shortness of breath with rapidly evolving pulmonary edema that is often fatal despite mechanical ventilation and intervention with potent diuretics. It has a fatality rate of 38%.

Entry into host cells is thought to occur by attachment of virions to cellular receptors and subsequent endocytosis. Nucleocapsids are introduced into the cytoplasm by pH-dependent fusion of the virion with the endosomal membrane. Subsequent to release of the nucleocapsids into cytoplasm, the complexes are targeted to the ER-Golgi Intermediate compartments (ERGIC) through microtubular associated movement resulting in the formation of viral factories at ERGIC.The species that cause hantavirus hemorrhagic fever have not been shown to transfer from person to person. Transmission by aerosolized rodent excreta still remains the only known way the virus is transmitted to humans. Similar negative-stranded RNA viruses, such as Marburg and Ebola hemorrhagic fevers, can be transmitted by contact with infected blood and body fluids, and are known to spread to patient-care workers in African hospitals. But those viruses do not transfer readily in the modern hospital setting with universal precautions. In general, drop-let and/or fomite transfer has not been shown in the hantaviruses in either the hemorrhagic or pulmonary forms