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Synonyms: Circling disease, Meningoencephalitis, silage disease

It is an infectious fatal disease of wide range of animals and man characterized by encephalitis. It also causes abortion, endometritis and repeat breeding in farm animals. Historically, Listeria was first isolated in 1926 from a natural disease of rabbits characterized by mononuclear leucocytosis and therefore named as Bacillus monocytogenes by Murray and coworker at Cambridge. Later, Pierie who isolated similar bacillus from liver of gerbils in 1927 named it Listerella hepatolytica in honour of surgeon Joseph Lister and finally renamed it Listeria in 1940 due to taxonomic reasons.

Etiology: The disease is caused by L. monocytogenes. The genus Listeria consists of a group of Gm + bacteria of low G+C content closely related to Bacillus, Clostridium, Enterococcus, Streptococcus and Staphylococcus. Out of 6 species reported, only L. monocytogenes and L. ivanovii are considered virulent. Human cases of L. ivanovii infection are rare whereas L. monocytogenes is an important food borne pathogen. L. monocytogenes has been isolated from a variety of food products. Meat, poultry, dairy and vegetable products have been implicated as vehicles of listeriosis. The organism can be isolated from faeces and silage. The organism can be easily destroyed by ordinary disinfectants but may survive in soil and silage for a considerable period of time.

L. monocytogenes is small, coccoid with a tendency to occur in chains. It is aerobic or microaerophilic. It grows on ordinary media within a temperature range of 4-42°C. Growth is improved by addition of glucose, blood or liver extract. Colonies are β haemolytic on blood agar. It ferments glucose and salicin producing acid without gas. Lactose, maltose and sucrose are fermented slowly or not at all and mannitol is not fermented. It is catalase +. It shows tumbling motility when grown at 25°C but at 37°C is non-motile. It is because peritrichous flagella are produced by the bacillus optimally at 20-30°C but scantily or not at all at 37°C.

Leptospirosis is a worldwide zoonosis. According to the occupational groups involved and the nature of the disease presentations, different names have been used, e.g. seven-day fever found commonly in Japan, Cane cutter's disease in Australia, Rice field Leptospirosis in Indonesia and Fort Bragg fever, which appeared as an outbreak in the US. Weil's disease, which is one of the severe forms of this disease, occurs in many countries, including India and other South-East Asian Countries, China, continental Europe and England. Leptospirosis exists in all the five inhabited continents and in a large number of countries. It occurs in tropical, subtropical and temperate zones. Leptospirosis is also an important cause of abortions, stillbirths and reproductive failures in cattle and pigs. Periodic ophthalmia in horse is commonly associated with leptospiral infections. Leptospirosis was first recognized in humans in 1886 by Weil and characterized by icterus. Leptospira have been isolated from a variety of animal species and humans manifesting various clinical syndromes such as mud fever and swine herd disease.

Etiology: The etiologic agent of leptospirosis is Leptospira interrogans. It is a thin spiral organism 0.1mm x 6 -20mm, with tightly set coils, and it is characterized by very active motility, by rotating ("spinning") and bending. Usually one or both ends of this single-cell organism are bent or hooked, but straight forms also occur that rotate and travel more slowly than hooked forms. The cells have pointed ends, either or both of which are usually bent into a distinctive hook. Two axial filaments (periplasmic flagella) with polar insertions are located in the periplasmic space. The structure of the flagellar proteins is complex. Leptospires exhibit two distinct forms of movement, translational and nontranslational. Morphologically, all leptospires are indistinguishable, but the morphology of individual isolates varies with subculture in vitro and can be restored by passage in hamsters. Leptospires have a typical double membrane structure in common with other spirochetes, in which the cytoplasmic membrane and peptidoglycan cell wall are closely associated and are overlain by an outer membrane. Leptospiral lipopolysaccharide has a composition similar to that of other Gram-negative bacteria, but has lower endotoxic activity. Leptospires may be stained using carbol fuchsin counterstain. Leptospires are obligate aerobes with an optimum growth temperature of 28 to 30°C. They produce both catalase and oxidase. They grow in simple media enriched with vitamins (vitamins B₂ and B₁₂ are growth factors), long-chain fatty acids, and ammonium salts. Long-chain fatty acids are utilized as the sole carbon source and are metabolized by b-oxidation. Because of their narrow diameter, the leptospires are best visualized by dark-field illumination or phase contrast microscopy and they do not stain readily with aniline dyes. The free living (L. biflexa) and parasitic leptospires (L. interrogans) are morphologically indistinguishable.

Glanders is a contagious, acute or chronic, usually fatal anthropo zoonotic disease of Equidae caused by Burkholderia mallei and characterized by serial development of ulcerating nodules that are most commonly found in the upper respiratory tract, lungs, and skin. The first recorded description of glanders is from the third century from Aristotle. In 1664, glanders was recognized as a contagious disease and in 1830, it's zoonotic potential was suspected. In the late 1800's, the Mallein test (1891) was developed for diagnosis of glanders. By 1910, the U.S., Canada and Great Britain all implemented glanders controlprograms. B. mallei was eradicated from the United States in 1929.

Etiology: It is caused by Burkholderia mallei. It is a straight or slightly bent Gm - non-spore forming, non-motile rod. The organisms in old culture appear as pleomorphic. The organisms can grow in ordinary media but addition of defribinated horse blood or glycerol accelerate the growth. Colonies have hop like odour and slime consistency. The organisms are readily destroyed by direct sunlight and most of the disinfectants. They can survive for 20 days in water and 6 weeks in contaminated stable. This organism is closely related to the agent of melioidosis, Burkholderia pseudomallei.

Susceptible hosts: The most susceptible hosts are horses, mules and donkeys. Infections can also occur in dogs, cats, goats and camels; cats may be particularly susceptible. Hamsters and guinea pigs can be infected in the laboratory. It is an occupational /professional hazard to human being. Laboratory samples are highly infectious to humans. Infection have been observed in sheep and goats. Guinea pigs, rabbits and field mice may be infected fatally. Cattle and pigs are absolutely resistant.

Geographic Distribution: Glanders is seen in some Middle Eastern countries, the Indian subcontinent, Southeast Asia, parts of China and Mongolia, and Africa. Sporadic cases are also seen in South America. Sporadic cases of glanders were identified between 1985-86 to 1990-91 from the states of Haryana, Himachal Pradesh and Punjab. Since reemergence of glanders in July - August 2006 in and around Pune and Panchgani area of Maharastra, several cases have been reported among equines of different states viz., Andhra Pradesh, Uttar Pradesh, Uttarakhand and Punjab. During the year 2006-07, National Research Centre on Equines, Hissar tested 4395 samples and 97 were detected positive and B. mallei was isolated from 8 of these cases.

Synonyms: Calf scour, white diarrhea, septicaemia of calves

Colibacillosis is one of the important diseases in new born calves, piglets, lambs and foals caused by E. coli and characterized by marked postration, profuse diarrhea and septicaemia.

Etiology: Colibacillosis is associated with pathogenic serotypes of E. coli. Certain serotypes cause diarrhea and others cause septicaemia.

(a)  Enterotoxigenic E. coli: is the most common enteropathogen that causes diarrhea in new born farm animals. It causes bacteria by adhering to, colonizing and producing enterotoxins in the small intestine. They are not invasive. The enterotoxins produced by E. coli are of two types: heat stable (ST) and heat labile (LT).

(b)  Enteropathogenic E. coli: they attach tightly to the epithelial cells of the villus of small intestine. They do not produce toxins and seldom invade the intestine.

(c)  Enterohaemorrhagic E. coli: They are Shiga toxin or verotoxin producing strains of E. coli. They are not an important cause of diarrhea in farm animals but some produce diarrhea in calves. E. coli O157:H7, one of the important enterohaemorrhagic E. coli strains cause a broad range of clinical disease in humans including diarrhea in humans and haemorrhagic colitis and highly fatal haemolytic-uremic syndrome in children. 195

Brucellosis, one of the most ancient diseases, continues to be a problem for humans and animals throughout the world causing enormous economic losses and significant human morbidity in endemic areas. The bacterial pathogen is classified by the CDC as a category B pathogen that has the potential for development as a bioweapon. It is one of the important zoonotic disease and considered as the most common laboratory acquired pathogen with >5 lakh human cases reported annually around the world. Brucellosis is a chronic infection which can result in infertility, delayed heat, interrupted lactation, loss of calves, wool, meat and milk production in animals and undulant fever in humans. Although in most of the counties, brucellosis is a nationally notifiable disease and reportable to the local health authority, it is underreported and official numbers constitute only a fraction of true incidence of the disease. Although the true incidence of human brucellosis is unknown, the estimated burden of the disease varies widely from <0.03 to >160 per 1 lakh population. Although only 17 countries in the world are free from the disease, it has been reported in many countries including India. Bovine brucellosis is endemic in all the states in India and appears to be on the increase in recent time, perhaps due to increased trade and rapid movement of livestock. The preponderance of natural bull service in rural India is perhaps yet another important factor in the maintenance and spread of infection. The Government of India has made it mandatory to regularly screen all the breeding bulls from artificial insemination centres, for brucellosis and to use brucellosis free bulls for semen production.

Etiology: Brucella sp. are facultative intracellular Gram - ve coccobacilli, nonspore forming and non-capsulated. It infects macrophages with principal involvement of liver, spleen and bone marrow. Nine Brucella species are currently recognized, seven of them that affect terrestrial animals are: B. abortus, B. melitensis, B. suis, B. ovis, B. canis, B. neotomae and B. microti and two that affect marine mammals are B. ceti and B. pinnipedialis. The first three species are called classical Brucella and within these species seven biovars are recognized for B. abortus, three for B. melitensis and five for B. suis. The remaining species have not been differentiated into biovars.

Synonyms: Pearl's disease, scrofula

It is a chronic insidious contagious disease of man and animals caused by tubercle bacilli characterized by development of tubercles in lung tissue, lymph nodes or other organs resulting in caseation and calcification. The tubercles are frequently located in lungs and lymph nodes. But they may be formed in the liver, spleen, intestine, peritoneum, meninges and long bones. It is a zoonotic disease. Bovine tuberculosis, caused by Mycobacterium bovis (M. bovis) is considered as the serious epizootics of animals and humans. Bovine species are natural hosts to the disease, but a wide spectrum of domestic and wild animals, as well as man, can be infected. Animals reported as having been infected with M. bovis include North American bison (Bison bison), buffaloes (Syncerus caffer), elk (Cervus elaphus), domestic and wild pigs domestic (Sus scrofa), goats (Capra hircus), camels (Camelus bactrianus), dogs (Canis familiaris), cats (Fells catus), sheep (Ovis aries), possums (Trichosurus vulpecula), badgers (Meles meles), mink (Lutreola vison), ferrets (Putorius furo) and non-human primates. All species are not equally susceptible, and are often grouped into spill-over (end) hosts and maintenance hosts. Cattle and other bovine species are considered the primary and most well-known reservoirs or maintenance hosts. In countries where maintenance hosts are present endemically in the wild, infection from these populations to domestic cattle or other farm animals is difficult to avoid. In Africa, bovine TB primarily affects cattle; however, infection in other farm and domestic animals, such as sheep, goats, pigs, dogs and cats, is not uncommon. Wild ruminants and carnivores are also affected and are the natural reservoirs of the infectious agent in the wild. Man is also susceptible to the disease, the highest risk groups being individuals with concomitant HIV/AIDS infection. In Africa, human TB is widely known to be caused by M. tuberculosis; however, an unknown proportion of cases are due to M. bovis. This infection in humans is underreported as a result of the diagnostic limitations of many laboratories in distinguishing M. bovis from M. tuberculosis. TB is a neglected public health problem and accounts for about 25% of all avoidable adult deaths in developing countries. It is of socio-economic significance, as it can affect international trade in animals and animal products. Many factors account for the failure of developing countries to control and eradicate bovine TB, many of them politico-economic. Added to the high costs of a sustainable testing programme are problems of social unrest due to political instability and ethnic wars, resulting in the displacement of large numbers of human and animal populations; lack of veterinary expertise and communication networks; insufficient collaboration with bordering countries and hence a lack of quarantine; and smuggling of live animals across state boundaries. Scarce human and financial resources are often absorbed by action against the high incidence of other acute and fatal diseases, such as contagious bovine pleuropneumonia, foot and mouth disease, African and classical swine fever and parasitic diseases. The primary sources of infection for humans are consumption of unpasteurised milk and close association between humans and animals. Rural inhabitants and some urban dwellers in Africa still consume unpasteurised and soured milk potentially infected with M. bovis. Milk borne infection is the main cause of non-pulmonary TB in areas where bovine TB is common and uncontrolled.

Synonyms: Splenic fever, wool sorter's disease, Tarka

It is an infectious disease of livestock and worldwide in distribution. This is a zoonotic disease. It is also known as splenic fever because of enlargement of the spleen (splenomegaly).

Etiology: It is caused by a rod shaped bacteria of 4-8 µm X 1-1.2 µm known as Bacillus anthracis. It is non-motile, capsulated, aerobic, spore bearing and Gm+ in nature. The organisms remain in chains. It was the first pathogenic bacterium to be observed under the microscope, the first communicable disease to be transmitted by inoculation of infected blood, the first bacillus to be isolated in pure culture and shown to possess spores and the first bacterium used for preparation of an attenuated vaccine.

The capsule is polypeptide in nature being composed of a polymer of d(-) glutamic acid. Capsules are not formed under ordinary conditions of culture but only if the media contain added bicarbonate or are incubated under 10-25% CO₂. Capsules are formed in the body of an infected animal.

Spores are formed in culture or in the soil, but never in the animal body during life. Spores are formed only in the presence of O₂. Spores are central, elliptical or oval in shape. The spores are very resistant to physical and chemical agents. They have been isolated from naturally infected soil for as long as 60 years. They resist dry heat at 140°C for 1-3 h and boiling for 10 min.

Anthrax bacilli is Gm + and non-acid fast. When blood films containing anthrax bacilli are stained with polychrome methylene blue for a few seconds and examined under the microscope, an amorphous purplish material (capsule) is noticed around the bacilli called M'Fadyean's reaction. On agar places, irregularly round colonies are formed 2-3 mm in diameter raised, dull opaque, grayish white with a frosted glass appearance. Under the low power microscope, the edge of the colony is composed of long, interlacing chain of bacilli, resembling locks of matted hair. This is called "Medusa head appearance." Virulent capsulated strains form rough colonies while avirulent or attenuated strains form smooth colonies. On gelatin stab culture, a characteristic 'inverted fir tree' appearance is seen with slow liquefaction commencing from the top.

Crimean Congo hemorrhagic fever (CCHF) was first reported in the 12^th century as a hemorrhagic syndrome in present day Tajikistan. However, in the modern era, the first outbreak of the CCHF was reported in 1944-1945 in the Crimea region with more than 200 cases and the disease was called Crimean Hemorrhagic Fever. Ten years later in 1956, the virus was isolated from a febrile patient in Belgian Congo and this isolate was noted to have the same antigenic structure with the Crimean strains. For this reason, the virus was called Crimean Congo Hemorrhagic Fever. Nowadays, outbreaks of CCHF have been documented in Africa, the Middle East, Eastern Europe, and Western Asia including India. CCHF is a severe hemorrhagic fever with a case fatality rate of up to 50%.

Etiology: It is a tick-borne viral disease belonging to the family Bunyaviridae, genus Nairovirus. Like other Nairoviruses, CCHF virus is an enveloped single stranded negative-sense RNA virus and its tripartite genome consists of a small (S), a medium (M) and large (L) segment which encode for the nucleocapsid protein (NP), the envelope glycoproteins G1 and G2 and an RNA-dependent polymerase, respectively. The virus is transmitted to humans through the bite of infected ticks or by direct contact with viremic animals or humans. Infected humans can spread the disease via close contacts which may result in community outbreaks and nosocomial infections. It is an important human pathogen and could be used as a bioterrorism agent.

Pathogenesis: The pathogenesis of CCHF is not well understood. A common pathogenic feature of hemorrhagic fever viruses is their ability to disable the host immune response by attacking and manipulating the cells that initiate the antiviral response. This damage is characterized by marked replication of the virus together with dysregulation of the vascular system and lymphoid organs. Endothelial damage contributes to hemostatic failure by stimulating platelet aggregation and degranulation, with consequent activation of the intrinsic coagulation cascade. DIC is noted as an early and prominent feature of the disease process. In another study, the levels of interleukin IL-1, IL-6, and TNF-alpha were higher among patients who subsequently died as compared to survivors. The DIC score was higher among fatal cases, correlating positively with IL-6 and TNF alpha levels, and negatively with IL-10 levels. These findings demonstrate that proinflammatory cytokines play a major role in pathogenesis and mortality of patients with CCHF.

Marburg virus (MV) disease was named after the West German town where the largest outbreaks of human infection was reported. It is also known as Vervet monkey or green monkey disease as monkey species introduced the disease in Europe. Marburg disease virus was reported in 1967 in Frankfurt-on-Main and Marburg, West Germany and Belgrade, Serbia in vaccine factory workers who came in contact with blood, organs or cell cultures of African green monkeys. Ebola and Marburg hemorrhagic fevers are severe zoonotic diseases seen not only in humans but also in non-human primates. Most species of Ebolavirus and the only known species of Marburg virus occur in Africa. Primates are infected sporadically from an unknown source probably bats. Humans seem to become infected directly from bats in caves, as well as when they, come in contact with tissues from infected apes and other species. Once the virus has entered the population, it can spread from person to person. Some epidemics affect hundreds of people. Although the mortality rate varies, 90% case fatalities have been reported in the most pathogenic viruses. No vaccine is available and the only treatment is supportive. Epizootics in gorillas and chimpanzees are equally serious, and appear to threaten the survival of these species in the wild. Other wild mammals including duikers also seem to be killed during outbreaks. One species of Ebolavirus, Reston Ebolavirus, occurs in the Philippines. Until 2008, this virus was known only as an infection of nonhuman primates. It does not appear to be a human pathogen; although some people in contact with this virus have seroconverted, they remained asymptomatic. In December 2008, Reston ebolavirus was discovered in pigs during an unusually severe outbreak of porcine reproductive and respiratory syndrome (PRRS) in the Philippines.

Etiology: Ebola and Marburg hemorrhagic fever are caused by members of the genera Ebolavirus and Marburgvirus, respectively. These viruses are the only members of the family Filoviridae. The genus Ebolavirus contains four recognized species: Zaire ebolavirus (formerly Zaire Ebola virus), Sudan ebolavirus (formerly Sudan Ebola virus), Ivory Coast ebolavirus (formerly Cote d'Ivoire Ebola virus) and Reston ebolavirus (formerly Reston Ebola virus). At least 13 strains of these viruses have been identified. A fifth species, tentatively named Bundibugyo ebolavirus, was isolated from a recent outbreak in Uganda. Marburg virus contains a single species, Lake Victoria Marburgvirus (formerly Marburg virus). Six strains of Lake Victoria Marburgvirus had been recognized as of 1990; at least nine genetically distinct strains were identified from a more recent outbreak in the Democratic Republic of the Congo. Marburg virus contains ssRNA as genome. The virion is highly pleomorphic and measures 80 nm in diameter and 700-1000 nm in length. Filoviruses can be destroyed by autoclaving. Treatment with sodium hypochlorite (1:100 dilution of household bleach) or standard hospital disinfectants can also be used. Ebolaviruses are reported to be susceptible to 2% sodium hypochlorite, 2% glutaraldehyde, 5% peracetic acid and 1% formalin. These viruses can also be inactivated by ultraviolet light, gamma irradiation, 0.3% betapropiolactone for 30 minutes at 37°C (98.6°F), or heating to 60°C (140°F) for 1 hour. Marburgvirus is susceptible to 1% sodium hypochlorite, 2% glutaraldehyde or formaldehyde, ultraviolet light and heat.

Hantaviruses have been responsible for a variety of human illnesses particularly haemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). There are currently 47 recognized sero/genotypes of hantaviruses with considerable geographic diversity. Each hantavirus type appears to be specific to a different rodent host. The different hantavirus types are associated with different types of disease both in terms of target organs and disease severity. HFRS is primarily a disease of the Old World while HPS is a disease of New World. Although the disease may have first been recognized as early as 1000 years ago in China, it affected >3000 United Nations Soldiers during Korean war (1950-1953). Now it is reported that hantavirus affect as many as 2 lakhs people each year in Asia and Europe. The agent of this virus remained unknown until 1978 when Lee and his associates isolated and named Hantaan virus, after a river in South Korea. Other viruses antigenically related to Hantaan virus were characterized and placed under the genus Hantavirus and family Bunyaviridae.

Over the past few decades, the sharp increase of incidences of hantavirus disease in humans throughout the world has been reported. There are 47 recognized hantaviruses with considerable geographic diversity. But the number of hantavirus virus types recognized continues to grow. Hantaviruses cause persistent infections in rodent reservoirs which directly impact transmission of these zoonotic agents between rodents and from rodents to humans. Environmental, 127 demographic and physiological factors likely interact to mediate responses to hantaviruses in natural rodent populations. Although not much work has been carried out, comparisons of human and rodent immune responses to hantaviruses may provide insights into why hantaviruses often are fatal for humans but cause only persistent infections in rodents.

Nipah virus infection is an emerging zoonotic disease first described in 1999 and the virus is under the genus Henipavirus and family Paramyxoviridae. The disease is similar to another emerging zoonotic disease caused by Hendra virus and can spread from its wildlife reservoir to pigs and humans where it causes an often fatal disease. It is a notifiable disease in most countries and to be handled under highest biological security level 4 (BSL-4). In Malayasia an outbreak of viral encephalitis occurred over a 35 week period from September 29, 1998 to 31^st May, 1999 among pig farmers creating considerable anxiety and fear. Of the 265 cases reported to the Ministry of Health in Malaysia, 105 were fatal and the case fatality rate was 39.6%. The outbreak also spread to neighbouring Singapore where 11 workers of an abattoir developed the disease with one fatality. 93% of the reported cases involved those directly in the pig farming industries namely pig farm workers, pig farm proprietors, housewives and family members assisting in the farms. The majority of the cases occurred in those aged 20 and above (92.4%) and actively engaged in pig industry followed by the age group 10-19 years (6.4%). About 82.6% of the cases are male.

Etiology: Henipavirus is a genus of the family Paramyxoviridae and order Mononegavirales containing two members, Hendravirus and Nipah virus. The henipaviruses are naturally harboured by Pteropid fruit bats (flying foxes) and are characterized by a large genome (18.2 Kb), wide host range and their recent emergence as zoonotic pathogens capable of causing illness and death in domestic animals and humans.

The viruses are pleomorphic ranging in size from 40-600 nm in diameter. They possess a lipid membrane overlying a shell of viral matrix protein. At the core is a single helical strand of genomic RNA tightly bound to N (nucleocapsid) protein and associated with the L (large) and P (phospoprotein) proteins which provides the RNA polymerase activity. F (fusion) protein trimers and G (attachment) protein tetramers are embedded within the lipid membrane. The genome of the Nipah virus consists of a non-segmented, single stranded negative sense RNA. In common with other members of the Paramyxovirinae subfamily, the number of nucleotides in the Henipavirus genome is a multiple of six, known as the 'rule of six'. The Nipah virus has been classified by the CDC as a Category C agent.

Hendra, a disease of horse has been recognized in Australia since 1994-95 with zoonotic importance. It is caused by a virus under the genus Megamyxovirus and subfamily Paramyxovirinae and family Paramyxoviridae. This virus is also endemic in certain species of bat. Another zoonotic bat virus called Nipah virus has been placed under the same genus and family. It is transmitted between the horses through contact. Infected horses can develop a severe and fatal respiratory disease characterized by dyspnoea, vascular endothelial damage, pulmonary oedema and neurological signs. Experimental infection of cats and guinea pigs showed fatal respiratory disease. The transmission of virus from horse to horse and horse to man is through close contact. One person died of the disease due to respiratory failure and another one due to delayed onset of encephalitis. A number of diagnostic methods are available to provide prompt, sensitive and accurate diagnosis of the disease.

History: In 1994-95, a new viral zoonotic disease was identified in Queensland, Australia resulting in death of 2 human and 15 horses in two separate incidents. Again, in 1999 another horse died at the same place. The term 'Hendra' has been derived from the name of a place, suburb of Brisbane where first outbreak took place. In September 1994, a total of 15 horses died due to hyperacute respiratory disease. The trainer of the horse also died. In 1995, a farmer died of meningoencephalitis after having contact with a Hendra positive horse. In the 1999, a mare died of Hendra virus infections.

Etiology: The Hendra virus is under the new genus Megamyxovirus and family Paramyxoviridae. The Hendra virus was isolated in Vero cells from lung specimens and produced CPE within 3 days. The virus can grow in MDCK, BHK, RK13, LLC-MK2 and MRC5 cells. It also grows in cells derived from birds, reptiles, amphibians, fish and in embryonated chicken eggs. The virus does not have haemagglutinin or neuraminidase activity. The virus is pleomorphic in shape, 38-600 nm in diameter and enveloped with two glycosylated transmembrane proteins of different lengths (15 and 18 nm). It differs from respirovirus and rubulavirus in not using sialic acid containing receptors. The virions are labile and infectivity is destroyed by heat, lipid solvents, non-ionic detergents, formaldehyde and oxidizing agents. Virions contain one molecule of negative sense ssRNA about 15 Kb long which codes 8 proteins. The Hendra virus is the largest of all known viruses under Paramyxoviridae. The genetic studies showed that Hendra virus is more similar to Morbillivirus or intermediate between Morbillivirus and Respirovirus. The amino acid homology between Hendravirus and Morbillivirus varies from 17-21% (P protein) to 40-42% (M protein) compared to 6-10% and 8% respectively for other members of Paramyxoviridae. A new Hendra like virus has been identified as a cause of respiratory and neurological disease in pigs and humans in Malaysia, called Nipah virus, after a village where the first human case occurred. (The amino acid homology of N protein between Hendra and Nipah is 92%, whereas in case of P&V it is 80-85%). Like, Hendra virus, the Nipah virus is thought to have emerged from a fruit bat (Pteropus hypomelanus).

This is an acute viral encephalitis having public health importance. It is under the genus Flavivirus and family Flaviviridae. The genus Flavivirus comprises of group of arbovirus though a few members of the genus have no known vector. The genus contains over 70 viruses of which 40 are mosquito borne, 16 are tick borne and 18 have no known vector. The type species of the genus is yellow fever virus. Although all flaviviruses are serologically relate, they can also be grouped serologically into distinct groups: dengue serological group, the JE serological group and a less serologically cohesive yellow fever virus group. The disease has been recognized in Japan since 1871 and was named Japanese B encephalitis to distinguish it from 'encephalitis A' (encephalitis lethargica, Von economo's disease) which was then prevalent. The virus was first isolated in Japan during an epidemic in 1935.

Etiology: JE virus is under the genus Flavivirus and family Flaviviridae. The genome is about 11 kb which encodes 3 structural proteins (C, capsid protein, PrM the membrane precursor protein that is cleaved proteolytically by a cellular protease to form the M protein in mature virions, and E, envelope protein) and 7 non-structural (NS) protein (NS1, NS2a, NS2b, NS3, NS4a, NS4b, NS5). The Eglycoprotein is the most immunologically important protein. The Japanese encephalitis serological group of flaviviruses comprises eight virus species and two subtype viruses with a geographic range encompassing all continents except Antarctica. The major virus species and their geographic range are as follows: the Japanese encephalitis virus ( JEV) in eastern, southern and southeastern Asia, Papua New Guinea and the Torres Strait of northern Australia; the West Nile virus (WNV) in Africa, southern and central Europe, India, the Middle East and North America and as Kunjin virus ( a subtype of WNV) in Australia and Papua New Guinea; the Murray Valley encephalitis virus (MVEV) in Australia, Papua New Guinea and the western Indonesian archipelago and the St. Louis encephalitis virus (SLEV) in North and South America. The other minor members of the group are Usutu (USUV), Koutango and Yaounde viruses in Africa; Cacipacore virus in South America and Alfuy, a subtype of MVEV, in Australia.

Chikungunya has been emerged as an important public health problem in the Indian Ocean Islands and India recently. Epidemiological, geographical and demographic data suggested that 1.38 million people were affected by the disease in India in 2006. The actual incidence of the disease may have been higher but underreporting did not reveal the actual picture. A large proportion of those who became ill consulted private health care professional or sought alternative medical care such as Ayurveda or homeopathy not included in the data collected by Govt. officials.

During the epidemic, rural hospitals, private and public clinics flooded with victims of Chikungunya. The virus did not kill its victims but inflicted considerable pain and misery besides local, regional and national financial burden towards health care. Only National Institute of Virology (NIV) and National Institute of Communicable Disease (NICD) provided accurate diagnosis of the disease. The Chikungunya assumed epidemic proportions because viral agent mutated, the vectors discovered the new ways to spread and the host lacked immunity to fight the disease. Modern transport systems - cars, buses, trains and aircraft particularly the movement of humans played a key role in spreading the disease that helped to maintain man-mosquito man cycle.

Etiology: First isolated in Tanzania in 1953, Chikungunya is under genus Alphavirus and family Togaviridae. It contains a single stranded positive sense RNA with a length of 12 Kb coding 4 non-structural (nspl - nsp 4) and 3 structural proteins (E1-E3). Among the structural protein, El protein correlates with serological response in human hosts and also modulates penetration of the virus in the mosquito species. Genetic analyses and historical accounts suggest that the Chikungunya virus originated in tropical Africa and subsequently evolved into 3 distinct genotypes - the East African, the West African and the Asian genotypes. The Asian genotypes have a high degree of nucleic acid sequence homology among themselves but the African strains exhibit wider sequence diversity and have been shown to undergo genetic micro-evolutions even during the course of an epidemic. Prior to the 2006 epidemic in India, the 3 genotypes were restricted to the geographical areas only. Previous outbreaks in India (1963 and 1973) were caused by the Asian genotypes, but the 2005 epidemic in the Indian Ocean Islands and the 2006 epidemic in India have been attributed to the East African genotype which arrived in India 5 years ago.

Dengue is a mosquito-borne viral disease and considered to be a major health problem globally. It is also called break-bone fever, dandy fever, denguero bouquet fever, giraffe fever, Polka fever and 5 days or 7 days fever. There are two important manifestations, namely dengue haemorrhagic fever (DHF) and dengue shock syndrome (DSS) which are responsible for heavy morbidity and mortality every year causing serious concern to health. It is an important disease caused by an arbovirus worldwide especially in the tropical and subtropical regions. The severity of the disease can be judged from simple statistics that over 40 per cent (2.5 billion) of the world's population in 100 countries continue to live under threat of contracting dengue infection. Annually, dengue virus infections are responsible for up to 100 million cases of dengue fever and more than 500,000 cases of haemorrhagic fever. Besides, every year the disease forces nearly 500,000 people to hospitalization of which 90% are children and causing 24,000 deaths. Mostly these deaths are due to lack of early diagnosis of dengue virus infection. In DHF case fatality rate generally exceeds 20 per cent in a non-endemic population and it can be reduced to less than 1 per cent with the aid of modern supportive therapy based on early diagnosis of the type of viral infection.

Dengue fever (DF) is an acute febrile viral disease characterized by headaches, bone or joint and muscular pains, rash and leucopenia as symptoms. Dengue haemorrhagic fever (DHF) is characterized by four major clinical manifestations: high fever, haemorrhagic phenomena, 73 often with hepatomegaly and in severe cases, signs of circulatory failure. Such patients may develop hypovolaemic shock resulting from plasma leakage. This is called dengue shock syndrome (DSS) and can be fatal.

The year 2001 witnessed unprecedented global dengue epidemic activity in the American hemisphere, the Pacific Islands and continental Asia. During 2002, more than 30 Latin American countries reported over 1 million DF cases with large number of DHF cases. This has been followed by extensive epidemics of DHF in several parts of India during 2003.

Dengue fever (DF) is caused by ingestion of viraemic blood containing dengue virus by mosquitoes of Aedes sp. followed by passage to a second human host. An extrinsic incubation period is required before the virus appears in the saliva of the transmitting female Aedes mosquitoes. After the bite, there is an incubation period of 3 to 14 days (average 4 to 7 days) followed by the onset of fever and nonspecific signs and symptoms (frontal headache, retro-orbital pain, body aches, nausea and vomiting, joint pains, weakness and rash). The febrile phase is self limiting and may last for 2 to 10 days followed by remission of fever in most cases. Laboratory abnormalities include neutropenia followed by a lymphocytosis and thrombocytopenia.

Swine influenza (Swineflu) is a highly contagious viral disease of pigs. It is an upper respiratory tract disease of pigs that causes outbreaks in herds. Swineflu infects people every year and is found typically in people who have been in contact with pigs although there have been person to person transmission of the disease. Influenza A virus subtypes namely H1N1, H1N2 and H3N2 are circulating around the world. In US, H1N1 subtype was exclusively prevalent among swine population before 1998 however since late August 1998, H3N2 subtype has been isolated from pigs. Most of the H3N2 virus isolates are triple assortants containing genes from human (HA, NA and PB1), swine (NS, NP and M) and avian (PB2 and PA) lineages. Influenza viruses are generally species specific i.e. avian influenza virus will infect only birds, swine influenza virus pigs, human influenza virus humans and so on. Although interspecies transmission of influenza viruses are reported, the transmission of influenza virus from one species to another is not always possible. Again, influenza A virus isolated from pigs can acquire the pandemic potential but not isolated from other species. Further, recent outbreaks of swineflu affecting human beings in Mexico, USA, UK,Canada, Asia etc with a death toll of 49 persons resulted in high alert in all the countries and compulsory checking of all the persons coming from the affected countries to other counties. The causative agent of swineflu is H1N1. So, it is the prime time to create awareness about the disease among the public which in turn help in tackling the disease in an effective and efficient manner and to prevent its transmission to human beings from swine species.

Etiology: Swineflu is caused by a virus under the genus Influenza A virus and family Orthomyxoviridae. Influenza A viruses are spherical with a diameter of 80-120 nm and may be filamentous. There are two types of surface glycoproteins namely haemagglutinin (HA) and neuraminidase (NA) present on the virus particles. A total of 17HA and 10NA types have been reported in influenza A viruses. It contains 8 copies single stranded negative sense RNA molecules as genome which encode 12 proteins: 3 subunits of the viral RNA polymerase complex, PB1 (encoding 3 proteins PB1, PB1-F2 and N-40), PB2 and PA; a nucleoprotein (NP), two surface glycoproteins, HA and NA, a matrix protein (M1), an ion channel protein (M2), a nonstructural protein (NS1) and a nuclear export protein (NEP- also known as NS2). There are 170 combinations of two surface glycoproteins, 17 HA and 10 NA that determine the antigenic properties and subtype classification of virus. However, human disease historically has been caused by 3 subtypes of HA (H1, H2 and H3) and two types of N (N1 and N2). Further in 1997, the outbreak of avianflu/birdflu in Hong Kong affected 18 persons with a death of 6 persons. The avian influenza virus responsible for that outbreak was H5N1. From that time H5, H7 and H9 ( all from avian origin) have been implicated in causing disease in human beings.

Avian influenza (AI) is a listed disease of the World Organization for Animal Health (OIE) that has become a disease of great concern for both animal and human health. Avian influenza (AI) or 'bird flu' is an infectious disease of birds ranging from a mild to a severe form of illness. It is caused by influenza A virus under the family Orthomyxoviridae. It is an enveloped virus with two types of surface projections haemagglutinin (H) and neuraminidase (N). The haemagglutinin is a rod shaped homotrimer which agglutinates RBCs and neuraminidase is a mushroom shaped homotetramer which releases the virus from cells because of its sialidase activity. There are 17 different H antigens (H1 to H17) and 10 neuraminidase antigens (N1 to N10). The virus also contains 8 single stranded negative sense RNA segments each of which encodes for a protein. Avian influenza virus is generally limited to poultry but an unprecedented epizootic of avian influenza A (H5N1) that is highly pathogenic has crossed the species barrier in Asia to cause many human fatalities and likely to possess an increasing pandemic threat. Zoonotic potential of AI virus was first recorded in 1997 with hospitalization of 18 people (six died) following the infection with HPAI (H5N1) in Hong Kong. This provided the evidence that HPAI strains of chicken can adapt, multiply and even cause death in affected individuals. So, it is the prime time to create awareness about the HPAI and its transmission to human beings so that necessary precautionary measures can be taken to prevent and control the disease efficiently and effectively.

Etiology: Influenza viruses are under the Orthomyxoviridae family and belong to either influenza A or influenza B or influenza C genus. The virus particles are enveloped with glycoprotein projections having haemagglutinin or neuraminidase activity and contain 8 negative sense single stranded RNA. Influenza A viruses are classified into subtypes based on these two surface antigens, haemagglutinin (H) and neuraminidase (N ). The haemagglutinin is a rod shaped trimer which agglutinates RBCs and neuraminidase is a mushroom shaped tetramer which releases the virus from cells because of its sialidase activity. Beneath the lipid envelope there is a membrane or matrix (M) protein which surrounds a helical complex containing the nucleoprotein (NP) and polymerases (PB1, PB2, P) protein. There are also two nonstructural protein (NS) present in the virus. There are 17 haemagglutinin antigen (H1 to H17) and 10 neuraminidase antigens (N1 to N10) present in influenza A viruses. Each RNA strand of AI virus code for at least one protein. The H glycoprotein of influenza virus has two important functions which are imperative for the infectivity of the virus (i) it is responsible for attachment of the virus to the host cell receptors of glycoprotein or gangliosides containing sialic acid. (ii) it possesses fusion activity between the host cell membrane and the virus membrane so that virus genetic material is introduced into the host cell. The glycoprotein is produced as a precursor, HAo which requires post translational cleavage to HA1 and HA2, by host proteases before it is able to induce membrane fusion. Then only the B virus particles becomes infectious. Type A viruses include the avian, swine, equine and human influenza A viruses. The large number of subtypes present in the type A influenza viruses are due to fact that viruses often undergo antigenic shift by the process of genetic reassortment.

Synonyms: Hydrophobia, Lyssa, Jalatanka

This is an acute highly fatal viral disease of all warm blooded animals including man characterized by signs of abnormal behaviour, nervous symptoms (increased excitability and irritability), impairment of consciousness ascending paralysis and death. The disease was variously known as lytta or lyssa coming from the belief that the disease was caused by a worm under the tongue (lytta) or hydrophobia, which describes the thirst and fear of water associated with the disease. The English name rabies derived from Latin word ‘Rabere’ which has been derived from Sanskrit word ‘Rabhas’ meaning raging, furious, savage, madness or to do violence whereas Greek term hydrophobia is now specifically used for rabies in man. The symptom hydrophobia (fear of water) is developed due to painful spasm of muscles of deglutition.

Distribution: The disease is known since ancient time. The disease has been recorded in various parts of the world in different species of animals. Australia, Britain, Scandinavian, New Zealand, Singapore, Hong Kong, Hawaii and some other Islands are free from rabies. This was possible due to strict quarantine measures and restriction on import of animal and animal products from disease prone areas. Lot of outbreaks are reported in India throughout the year causing 30,000 death annually and number of death toll may be higher as many cases go unnoticed. India accounts for the 80% casualties from rabies worldwide.

1. Introduction

India is a land of large varieties of fruits and vegetables due to its vast soil and climatic diversity. India is the second largest producer of fruits and vegetables in the world, with an annual production of fruits 45.5 Million tonnes and vegetables 90.8 Million tonnes. It contributes 10.23% and 14.45% of the total world production of fruits and vegetables (F&V) respectively (NHB, 2010). Though fruits and vegetables are grown only on 7–8% of gross cultivated area, these contribute more than 18.8% of the gross value of agricultural output and 52% export earnings from total agricultural produce. These have a high export potential of 20-30 times more foreign exchange per unit area than cereals due to higher yields and higher price available in the international market (Sen et al., 2012). According to estimates, the per capita consumption of fruits and vegetables in India is only around 46g and 130g which are far below the stipulation of a minimum of 92g and 300g respectively as recommended by the Indian Council of Medical Research and National Institute of Nutrition. The low availability is mainly due to considerably high post-harvest losses. About 15-20% of the fruits and vegetables are wasted every year in the country, due to poor post-harvest management and lack of infrastructural facilities for processing and storage, amounting to a revenue loss of over Rs. 625 billion.

The sensorial, nutritional, and organoleptic quality of fresh produce starts deteriorating after harvest as a result of soon after harvest the altered plant metabolism and microbial growth. The quality deterioration is the result of produce respiration and transpiration, senescence, ripening-associated processes, wound-initiated reactions, development of postharvest disorders, microbial proliferation leading to postharvest quality loss. Therefore, it is necessary to understand the respiration and ripening processes and the physiological and biochemical changes during ripening. The best way to reduce respiratory metabolism is to reduce the storage temperature. All biological processes proceed more slowly at lower temperature (Yahia, 2007). In general, O₂ levels must be reduced to less than 10 % to see a reduction in the rate of respiration. Respiration rate is temperature dependent; so, as the temperature reduces the amount of oxygen required also drops. Therefore, oxygen levels must be substantially reduced at low temperature for it to affect the rate of respiration. It must however, be ensured that O₂ levels do not fall below extinction point as anaerobic respiration and decay may occur. Tolerance to low O₂ varies between species and cultivars and is also time dependent. Commodities may be able to tolerate low O₂ for short periods of time. Low O₂ can also be tolerated when CO₂ is low.

1. The Aflatoxin Molecule

Aflatoxins are chemically difuro-coumarin derivatives. Presently, 18 different types of aflatoxins have been identified with aflatoxin B₁, B₂, G₁, G₂, M₁ and M₂ being the most common. Of these Aflatoxin B₁ (AFB₁) and G₁ occur most frequently, with AFB₁ being the most potent. Physicochemical and biochemical characteristics of the AFB₁ molecule reveal two important sites for toxicological activity (Heathcote and Hibbert, 1978). The first site is the double bond in position 8,9 of the furofuran ring (Figure 1). The interactions of aflatoxin, DNA and proteins, which occur at this site alter the normal biochemical functions of these macromolecules and leads to deleterious effects at the cellular level.Monteiro et al. (1966) studied the in vitro interaction of groundnut proteins namely arachin and conarachins with AFB₁ molecule. The second reactive group is the lactone ring in the coumarin moiety (Lee et al., 1981). The lactone ring is easily hydrolyzed and is therefore vulnerable to degradation.