Mahendra Pal Aklilu Feleke Vol 2(1), 58-67 DOI-
Leptospirosis is an emerging and re-emerging anthropozoonotic disease of major public health and economic importance. The disease is widespread in diverse geo-climatic zones of the world. Human beings acquire leptospirosis from infected domestic animals, rodents, and contaminated water.Various serovars of Leptospira, including Canicola, Icterohaemorrhagiae, and Pomona, can infect humans as well as animals. Several occupational workers such as veterinarians, slaughterhouse workers, and farmers etc are at greater risk of acquiring leptospirosis. In addition, vacationers can also be infected while swimming in water contaminated with urine of infected animals. Leptospirosis is still considered an under-diagnosed clinical condition in human beings. The laboratory diagnosis is imperative to confirm the disease. It is thought that treatment will only affect the course of the disease if it is initiated within four days of onset. The complexity of clinical signs and involvement of multiple host species warrants continuous research on the improvement in the diagnostic techniques. Depopulation of rodents, avoidance of contact with water contaminated with animal urine, provision of protective clothing to occupational groups will certainly help to reduce the incidence of leptospirosis.
Keywords : Anrhropozoonosis Leptospirosis Occupational hazard
Introduction
Leptospirosis (Cane field fever, Canicola fever, Hemorrhagic jaundice, Harvest sickness, Mud fever, Rice field fever, Swampy fever, Swineherd’s disease, Weil’s disease) is a highly infectious bacterial anthropozoonosis with worldwide distribution (Pal, 1996; Acha and Szyfres, 2001; Sambasiva et al., 2003., Pal, 2012). The disease in man was first time described by Adolfo Weil in 1886 in Germany. It is considered as an emerging zoonosis in North India (Chaundhry et al., 2002); and is an important re-emerging disease in many areas of the world including Gujarat, India (Pal, 1996; Meites et al., 2004).
Rodents are considered to be the most important carriers for most serovars of Leptospira, but serovar Pomona and Hardjo are adapted to agricultural animals as carriers. Leptospira organisms is maintained in the kidneys of carrier hosts. Organisms shed in urine contaminate the environment and infect other species, including humans (Pal, 1996; Louvel et al., 2006).
Leptospirosis is acquired by direct or indirect contact with the urine of infected animals such as rodents and domestic animals. Reports have documented that leptospira infect humans through contact of cut or abraded skin or mucous membranes with contaminated urine of infected domestic and wild animals, of which rats are the most common source of infection with a 90 % carriage rate (Esen et al., 2004).
Leptospirosis is widespread in diverse geo-climatic zones of the world, most significantly in countries with hot and humid climate Leptospirosis is predominantly an occupational disease of sewer worker, plumbers, veterinarians, abattoir workers, butchers, sugarcane-field workers and military personnel (Pal, 1996). It has also been increasingly recognized as a recreational hazard to those who swim or wade in contaminated water (Meites et al., 2004). This paper describes the anthropozoonotic significance of leptospirosis.
Etiology
Leptospirosis is caused by different serovars of a spirochete organism known as Leptospira interrogans. In addition to Leptospira interogans, the genus Leptospira includes a free living (non pathogenic) species named as Leptospira biflexa (Esen et al; 2004). At least 300 serovars classified into 23 serogroups and 17 genomospecies have been identified within the pathogenic species (Quinn et al., 2002). The pathogenic species, Leptospira interrogans is a multi-species problem affecting humans, carnivores, ungulates, and rodents (Pal, 1996, Hirsh and Zee, 1999).
Host
Leptospirosis can occur in all mammals, including domestic pets, livestock, wild animals and humans; although in some species it is rare (Pal, 1996). Reptiles and amphibians can also be infected but not as commonly as mammals (Pal, 2007).
Transmission
Leptospira can be carried and excreted by most mammalian species but especially by cattle and rodents; the bacteria multiply in the kidney tubules and are released in the animals’ urine (Senior, 2010).
Man acquires the infection by direct contact with diseased animals or infected tissues; and also from moist soil, water, vegetation contaminated with urine of infected animals (Pal, 2012). Leptospires penetrate through traumatized or injured skin. The organisms can also enter through the mucus membrane of the eye and nasopharynx while bathing in stagnant water particularly the ponds and swimming pool (Pal, 2007).
Pathogenesis
Although the pathogenic mechanisms are not fully known, there is considerable damage to vascular endothelium. Virulent strains produce more cytotoxic protein than avirulent strains. The exact role of this protein in the disease is not clear. The hemolysin of Leptospira appears to be responsible for intravascular hemolysis. Other virulence factors include the organism’s motility, burrowing motility and production of hyaluronidase. After epithelial penetration, there is haematogenous dissemination, with localization and proliferation in parenchymatous organs, particularly the kidney and liver. Leptospiral antibody with complement greatly reduces the number of Leptospira. Kidney infection with multiplication in the convoluted tubules may result in a carrier state; organisms can be shad in the urine for weeks to months (Carter and Wise, 2004).
Clinical Specterum
Man
Although most human leptospirosis infections are self limited, complications are common involving hepatonephric failure, pulmonary hemorrhage and death in 10%-50% of severe cases. Clinically, human leptospirosis is characterized by an acute influenza-like illness, with fever that often reaches 102°F, chills; severe headache, nausea, vomiting and myalgias (Pal, 2007). The eye usually became red on the third or fourth day. In general, two clinical signs have been distinguished as icteric (the serious form or hepatonephric type that has been known as Weil’s disease and less frequent, being estimated to occur in about 10% of cases) and anicteric form which is less severe and known to occur in 85-90% of cases (La Rocque et al., 2005).
Cattle
In cattle, leptospirosis may appear as acute, subacute or chronic forms and usually caused by L. interogans serovares Pomona or Hardjo. The disease is manifested by septicemia with high fever of 40.5 – 41.5°C, anorexia, petechiation of mucosae, depression, dyspnea and acute hemolytic anemia with haemoglobinuria, jaundice and pallor of the mucosa (Pal, 1996; Radostits et al., 1994). In adult cattle, abortion (20% of which may be followed by death) due to systemic reaction is likely to occur at the acute stage of the disease. It has been indicated that placental retention, prenatal mortality, congenital abnormality, loss in milk production and mastitis are common
Sheep and Goat
Leptospirosis in sheep and goats is characterized by fever and anorexia and, in some animals, jaundice, haemoglobinuria or anemia. Abortions, stillbirths, weak lambs or kids and infertility can also be seen, either with or without other clinical signs. Clinical disease is relatively uncommon in sheep (Aiello and Mays, 1998).
Swine
In swine, clinical leptospirosis is most often characterized by reproductive signs including late term abortions, infertility, stillbirths, mummified or macerated fetuses, and increased neonatal mortality. Fever, decreased milk production and jaundice may also been seen (Pal, 1996).
Horses
In horse, the disease has mostly been associated with uveitis or abortion. It has been documented that the serologic prevalence in horses is higher than clinically manifested illness (Aiello and Mays, 1998).
Dog
The dog shows high fever, depression, anorexia, weakness, difficulty in respiration, icterus, rapid dehydration, blood stained faeces, hemorrhagic patches of mouth, lips and conjunctiva and death (Pal, 1996).
Diagnosis
A combination of clinical sign and serological test results provides the most effective diagnostic technique. There are three methods used to diagnose leptopirosis in mammals: demonstration methods, serological techniques, and bacteriological methods.
Isolation
Since, leptospires are fastidious, slow growing organisms for diagnostic purpose has not been routinely relied up on, nevertheless, isolation of the causative agent for leptospirosis are of major importance. Organisms can be isolated from the blood during acute phase and urine during convalescent on special nutrient media such as Korthop’s medium, Fletcher’s medium, Stuart’s medium, EMJH medium with bovine serum albumin (Pal, 2007; Pal, 2012).
Immunoflurescence Techniques
Fluorescent antibody conjugates prepared against leptospiral serovars are employed to demonstrate the presence of leptospires in tissue smears with limited success, as the cross reactivity among different serovars varies (Venkatesha, 2006).
Microscopic Agglutination Test (MAT)
Microscopic agglutination test is widely accepted serological test and is the gold standard for evaluating other tests. Seeing a four-fold rise in convalescent titers in the MAT can make a definitive diagnosis. Observing an antibody titre of equal to or greater than 1:100 in the MAT in conjuction with symptoms consistent with disease can make a presumed diagnosis. MAT is preferably performed on paired serum samples to detect seroconverstion or a rise in titer. The specificity of MAT is very high but it requires the use of a panel of live cultures to be maintained in the laboratory (Ventaesha, 2006).
Enzyme-linked Immunosorbent Assay (ELISA)
Enzyme-linked immunosorbent assay (ELISA) has recently recognized as a useful test for detecting Leptospia antibodies. ELISA also has the advantage to detect a past or recent infection using IgM based-ELISA with accuracy. IgM based dipstick ELISA kit are available commercially in developed countries with limited success, as it is specific to particular serovar depending on antigens used (Venkatesha, 2006).
Lepto dri dot
Lepto Dri Dot is a new card agglutination test developed by the Dutch Royal Tropical Instiitute for rapid diagnosis of leptospirosis. The test does not require special storage or sophisticated equipment and can be performed by relatively low skilled personnel (Vijayachari et al., 2002).
Molecular biological techniques
Molecular diagnosis of leptospirosis includes DNA restriction enzyme analysis (REA), nucleic acid probes and hybridization, polymerase chain reaction (PCR), pulsed field gel electrophoresis (PFGE) and ribotyping (Herrman et al., 1992; Venkatesha and Ramdass; 2001; Levett et al., 2005; Pal; 2007).
Treatment
Human leptospirosis can be treated with different antibiotics such as streptomycin, penicillin, erythromycin, tetracycline, and doxycycline. Generally, early diagnosis and prompt treatment is important (Pal, 2007). Dihydrostreptomycin is effective for termination of carriers or shedder state (Pal, 2012).
Medication of feed with chlortetracycline at 400-800 g/1000 kg for 10 days reduces the number of carriers but does not necessarily eliminate all carriers. Blood transfusion (5-10 litters/450 kg body weight) are indicated as treatment for the haemolytic anemia in acute leptospirosis in cattle (Radostits et al., 2007).
Epidemiology
Leptospirosis is considered to be the most widely prevalent contemporary zoonosis of the world (Pal, 1996). The disease has been recorded in many countries of the globe including India. Leptospirosis is more prevalent in tropical countries as compared to the temperate due to higher humidity rainfall and temperature that promote survival of the organism in such environment. It has major negative impact on people living in urban and rural areas in developing countries with inestimable morbidity and mortality. It occurs wherever there are risks of direct or in direct contact with the urine of infected animals. Because of the importance of water as a means of spreading infection, new cases are most likely to occur in wet seasons and low lying areas, especially when contamination and susceptibility are high. Epidemics diseases recorded during rainy seasons (Pal, 1996).
People at risk are those who have close contact with animals or who are exposed to water, mud, soil, or vegetation that has been contaminated with animal urine. Specific occupational hazards are present when people come into contact with the urine or tissues of infected animals. Butchers, veterinary surgeons, animal breeders, hunters, and freshwater fish farmers are at highest risk (Senior, 2010). Some recreational activities that involve contact with contaminated water or soil can also allow leptospirosis to be transmitted (camping, gardening, bush walking, water rafting, and other water sports) (Acha and Szyfres, 2001; Meites et al., 2004; Lourel et al., 2006). Outbreaks of leptospirosis with pulmonary involvement carrying fatality rate of 10-50 % are reported from India. leptospirosis is essentially a water borne infectious disease, as several outbreaks of disease have been recorded during rainy season (Pal, 2012).
Most of the animals remain asymptomatic carrier and shedder. The contaminated water, therefore, becomes an important source of infection to man. Swimming in leptosires polluted pool is hazardous as many outbreaks of diseases have been traced in swimmers. A person during agricultural operation may receive minor cut or injury in his hand or leg and thereby gives an opportunity to leptospies to enter through abraded skin. Abattoir workers often get the infection while handling the kidney and bladder. Handling of infected organs like kidney and liver may exposed house wives to high risk of leptospirosis. Human infections are most commonly due to Icterohaemorragica, Canicola, Autumnalis and Pomona serogroups (Pal, 1996).
Prevention and Control
Protection of animals against reservoir of leptospires: whenever leptospirosis is endemic under intensive productions. Biosecurity to eliminate or to keep rats and other rodents away from the animals should be put in place. Depopulation of rodents can be achieved by use of rodenticides, rat trapping, fumigation of rat burrows or holes, constriction of rat proof buildings, protection of food, burning of cane field after harvest etc. Furthermore, the accessibility of the animals to potential sources of infection like contaminated water point should be restricted (Pal, 1996).
Protection of people against contagion by available means of hygienic methods such as avoidance of direct and indirect contact with animal urine are recommended as preventive measures. Workers in flooded fields should be cautioned against direct contact with contaminated water or mud and should be advised to use rubber shoes and gloves. In case of any cuts or abrasion on lower extremities of the body, the worker should apply an antiseptic like betadine, dettol, savlon etc before entering the field and after exit. Occupational worker must be provided protective clothing such as apron, gumboot gloves, goggle etc. disinfection of swimming pool with chlorine, and the barn, pen, shed, kennel with cresol or caustic soda, and the cane field, rice field with copper sulfate should be done.
The main preventive measure for leptospirosis is to create awareness about the disease and its prevention by offering health education to occupational group particularly to agricultural farmers, butchers, house wives, and sewage workers about the source of infection, mode of transmission, personnel and environmental hygiene. This has to be carried out by intensive educational campaigns (Pal, 2007).
Conclusions
Leptospirosis, a major zoonotic problem, is widespread in diverse geo-climatic zones of the world. The disease is caused by several serovars of pathogenic species of Leptospira. It is a multi-species problem affecting carnivores, ungulates, and rodents. Rodents act as a reservoir and shed leptospires in the urine throughout their life. Outbreaks of the disease are usually caused by exposure to water contaminated with the urine of infected animals. It is predominately an occupational disease of sewer workers, veterinarians, abattoir workers, butchers, rice-field workers and sugarcane-field growers. The diagnosis of leptosirosis based only on clinical signs is often difficult because clinical signs are not pathognomonic, necessitating laboratory investigation as an essential part of diagnosis. It is emphasized that multidisciplinary approach seems imperative in the control of leptospirosis which is an important global anthropozoonosis.
References
Acha, P. N. and Szyfres, B. 2001: Zoonoses and Communicable Diseases Common to
Man and Animals. 3rd Edition, Pan American Health Organization, Washington
D.C, U.S.A, pp 157-168.
Aiello, S. E. and Mays, A. 1998. Leptospirosis. In: The Merck Veterinary Manual.
8th edition, Co., Inc., Whitehouse Station, U.S.A, pp 474 – 477.
Carter, G.R. and Wise, D.J. 2004. Essentials of Veterinary Bacteriology and Mycology. 6th Edition, Replica, India, pp. 122-123.
Chaudhry, R., Premlatha, M. M., Mahonty, S., Dhawan, B., Singh, K. K. and Dey, A. B. 2002. Emerging leptospirosis, North India. Emerging Infectious Diseases, 18:125-128.
Esen, S., Sunbul, M., Leblebicioglu, H., Eroglu, C. and Turan, D.2004. Impact of clinical and laboratory findings on prognosis in leptospirosis. Swiss Medical Weekly, 134: 347-352.
Herrmann, J. L., Bellenger, E., Perolate, P., Baranton, G. and Girons, I. S. 1992. Pulse-field Gel electeophresis of Notl diagest of leptospiral DNA: a new rapid Methode of serovar identification. Journal of Clinical Microbiology, 3:1696-1702.
Hirsh, D. C. and Zee, Y. C. 1999. Veterinary Microbiology. Black Well Science Ltd, pp 185-189.
La Rocque, R. C., Breiman, R. F, Ari, M. D., Morey, R. E., Janan, F. A., Hayes, J. M., Hossain, M. A., Brooks, W. A. and Levett, P. N. 2005. Leptospirosis during dengue outbreak, Bangladesh. Emerging Infectious Disease: 17:634-645.
Levett, P. N. Morey, R. E., Galloway, R. L., Turner, D. E., Steigerwalt, A. G. and Mayer, L. W. 2005. Detection of pathogenic leptospires by real time quantitative PCR, Journal of Medical Microbiology, 54: 45-49.
Louvel, H., Bommezzadri, S., Zidane, N., Boursaux, C., Creno, S., Magnier, A., Rouy, Z., Medigue, C., Girons, I. S., Bouchier, C. and Picardeau, M. 2006. Leptospirosis. Journal of Bacteriology, 188: 7893-7904.
Meites, E., Jay, M. T., Dersiniski, S., Shieh, W. J., Zaki, S. R., Tompkins, L. and Smith, D. S. 2004. Re-emerging leptospirosis, California. Emerging Infectious Disease, 34:123- 127.
Pal, M. 1996. Leptospirosis: A contemporary zoonosis. Veterinarian, 20: 11- 12.
Pal, M. 2007. Zoonoses. Satyam Publishers, Jaipur, India, 2nd edition, pp 116-117.
Pal, M. 2012. Leptospirosis: An important zoonosis of public health concern. The Ethiopian Herald. 4 January , p.8.
Quinn, P. J., Carter, M. E., Markey, B. K. and Carter, G. R. 2002. Clinical Veterinary Microbiology. Mosby, Spain, pp 295-299.
Radostits, O. M., Blood, D. C. and Gay, C.C. 1994. Veterinary Medicine: A text Book of Diseases of Cattle, Sheep, Pigs, Goats and Horses. 8th Edition, Bailliere Tindal London, pp 884-898.
Sambasiva, R. R., Naveen, G., Bhalla, P. and Agarwal, S. K. 2003. Leptospirosis in india and the rest of the world. Brazilian Journal of Infectious Diseases, 7: 23-25.
Senior, K. 2010. Leptospirosis and Weil’s syndrome: Cause for concern? Lancet infectus Disease, 10: 823-824.
Venkatesha, M. D. 2006. Laboratory techniques in diagnosis of leptospirosis. Intas Polivet, 7:324-336.
Venkatesha, M. D. and Ramadass, P. 2001. Rapid diagnosis of leptospirosis using PCR and DNA hybridization techniques. Indian Journal Animal Sciences, 71: 1104-1106.
Vijayachari, P., Sugunan, A. P. and Segal, S. C. 2002. Evaluation of Lepto Dri Dot as a rapid test for the diagnosis of leptospirosis, Epidemiology and Infection, 129: 617-621.