Journal of ISSN: 2469 - 2786 JBMOA

Bacteriology & Mycology: Open Access
Review Article
Volume 2 Issue 6 - 2016
The Relationship between Human Campylobacteriosis and Broilers
Roy D Sleator1, Brigid Lucey1, James SG Dooley2 and William J Snelling2*
1Department of Biological Sciences, Cork Institute of Technology, Ireland
2School of Biomedical Sciences, Ulster University, UK
Received: September 13, 2016 | Published: November 07, 2016
*Corresponding author: William J Snelling, School of Biomedical Sciences, Biomedical Sciences Research Institute, Ulster University, Cromore Road, Northern Ireland, BT52 1SA, UK, Email:
Citation: Sleator RD, Lucey B, Dooley JSG, Snelling WJ (2016) The Relationship between Human Campylobacteriosis and Broilers. J Bacteriol Mycol Open Access 2(6): 00047. DOI: 10.15406/jbmoa.2016.02.00047


Campylobacter is the leading cause of bacterial foodborne diarrhoeal disease in the developed world, with raw and undercooked broilers (chicken meat) the primary source of sporadic infection. In this review we provide an update of the significance of Campylobacter infection and broilers.

Keywords: Campylobacter jejuni; Broilers; Poultry; Illness; Epidemiology


DALYs: Disability-Adjusted Life-Years, FQ: Fluoroquinolones; GBS: Guillain-Barré Syndrome; GLP: Good Laboratory Practice; HACCP: Hazard Analysis Critical Control Point; HPA: Health Protection Agency; IBS: Irritable Bowel Syndrome; LMIC: Low- and Middle-Income Countries; MLBs: Multilamellar Bodies, MLST: Multilocus Sequence Typing; OMVs: Outer Membrane Vesicles; PCR: Polymerase Chain Reaction, ReA: Reactive Arthritis


Campylobacteriosis has been the most frequently reported zoonotic disease in humans in the EU since 2005 [1] (Table 1). The true frequency of gastroenteritis caused Campylobacter spp. is difficult to accurately determine due to underreporting, particularly in Low- and Middle-income countries (LMIC) [2]. Several surveys have calculated the annual incidence to be between 4.4 and 9.3 per 1,000 population in high-income countries [2]. Recorded Campylobacter species in these studies are mostly the thermotolerant species C. jejuni and C. coli [1]. In general, reported Campylobacter infections are markedly higher in specific age groups; young children in particular (<5 years of age) [3]. There are probably varied risk factors with different age groups [3-5]. Outside areas other than Europe and North America, incidence reports are relatively rare, and frequently show low detection rates from human samples [6]. In temperate regions human campylobacteriosis exhibits particular seasonality trends [7]. Environmental sources, e.g. livestock & wild birds, cause a higher incidence in young rural children in late spring [3]. An extended summer peak linked with chicken strains has been found in adult populations [3], partially because of barbeques and summer holidays. International trade and travel influence public health globally by affecting patterns of antimicrobial use and resistance selection [2].































Table 1: Campylobactercases: 2000 to 2012 for England and Wales [40,41]. Figures shown are for Campylobacter sp cases reported to the Health Protection Agency (HPA) for England and Wales. It includes patients with enteric and non-enteric infections and includes isolates from all body sites.
Source: Laboratory Reports in England and Wales reported to HPA.

Campylobacter and Illness

Antimicrobial treatment is usually not needed with human campylobacteriosis, as it is normally self-limiting [8]. The exceptions are severe cases with patients who are generally young, old, pregnant or immunocommpromised. Human campylobacteriosis is normally associated with watery and occasionally bloody diarrhoea, fever, abdominal cramps and vomiting lasting for roughly 5-7 days. These symptoms usually develop 1-5 days after exposure. Guillain-Barré syndrome (GBS) is a severe demyelinating neuropathy and campylobacteriosis is the most common infection proceeding the onset of post-infectious GBS [6]. Roughly 33% of global GBS cases are attributed with campylobacteriosis [2]. Around 20% of GBS cases require intensive care and case-fatality rates in high income countries are 3-10% [2]. Campylobacter disease burden is also significantly increased by irritable bowel syndrome (IBS) and reactive arthritis (ReA) sequelae [9]. Studies indicate that ReA occurs with 1-5% of campylobacteriosis cases. A shortage of clear diagnostic and classification criteria make the true extent of ReA challenging to accurately determine. Around 25% of ReA cases can develop into chronic spondyloarthropathy. People with more severe acute enteric disease are more likely to develop IBS within 1-2 years after having campylobacteriosis; IBS develops in up to 36% of patients [2]. The median estimated costs to patients and the National Health Service in the UK from 2008-2009 were; Campylobacter £50 million (£33m-£75m), norovirus £81 million (£63m-£106m), rotavirus £25m (£18m-£35m) [10]. The costs per case were approximately £30 for norovirus and rotavirus, and £85 for Campylobacter, which was mostly borne by patients and caregivers via lost income or out-of-pocket expenditure. Campylobacter-related GBS hospitalisation cost around £1.26 million (£0.4m-£4.2m). The number of years lost due to disability caused by Campylobacter related sequelae [disability-adjusted life-years (DALYs)] are also used to calculate disease burden[6,9,11]. Recent estimates range from 1,568 DALYs in New Zealand [12], 3,633 in The Netherlands [9], 18,222 in Australia [11] and 22,500 in the USA [6]. The economic costs of efforts to control Campylobacter in agriculture, food production are also significant and need to be considered [10].

Poultry and Campylobacter

Many sources of campylobacterisos have been identified, e.g. raw milk and pets, but broilers and broiler meat are the most important [13-16]. Campylobacteriosis in urban areas has been associated with broilers, but less so in the countryside [8]. The European Food Safety Authority estimated that chicken meat consumption accounts for 20%-30% of campylobacteriosis in the EU, with 50%-80% of cases linked to the chicken reservoir as a whole [17]. Between 2000-2014, global chicken meat production rose from 58.5 million tonnes to 95.5 million tonnes [8], and has continued to increase, putting more pressure on public health agencies and the poultry industry to lower poultry/ chicken-associated human campylobacteriosis [8]. To survive under environmental conditions encountered along the food chain, i.e., from poultry digestive tract its natural reservoir to the consumer's plate, Campylobacter has developed adaptation mechanisms [18]. Among those, biofilm lifestyle has been suggested as a strategy to survive in the food environment and under atmospheric conditions [18]. Campylobacter prevalence in poultry, as well as the contamination level of poultry products, varies between different countries; from 0.6% to 13.1% in the Finland, Norway and Sweden, and up to 74.2%-80% in several other countries [19]; one Northern Ireland study from 2009 showed a prevalence on poultry meat of 91% [20].

The stages in the broiler production and processing chain consist of primary production at rearing farms, transport to slaughter, the slaughter process, followed by the processing of chicken meat products, selling products at the retail level, and handling and consumption of chicken meat products at home and in public places such as restaurants [6]. In order to implement effective interventions that reduce the probability of Campylobacter colonisation of broiler flocks, it is essential to understand the risk factors involved [16]. All of these different phases have a role in the transmission of Campylobacter from farm to fork. Production chain conditions vary between countries, and this is also reflected in the annual number of Campylobacter-positive chicken flocks [8]. Contamination and resulting colonisation of broiler flocks in farms normally results in the transmission of Campylobacter along the poultry production chain and in contamination of poultry meat at retail [8]. During the slaughter process, plucking and evisceration can lead to carcasses contamination, whilst transport appears to have a lesser effect on the contamination of carcasses [17]. A large variety of poultry products ranging from fresh, frozen, cooked, whole carcasses and smaller portions with different infection risks are globally commercially available. Lower Campylobacter counts have been recorded from skinless portions of meat, e.g. breast fillets [17]. Good hygienic practices and applying control measures based on Hazard Analysis Critical Control Point (HACCP) principles are important for effective post-harvest control [2]. Decontamination of carcass by chemical or physical methods as part of these measures have proved successful [2]. Quality surveillance data is vital to identify disease outbreaks, to detect sporadic cases for case–control studies, to provide isolates that can be used in attribution models based on isolate subtyping, and to furnish data for constructing and calibrating risk assessment models and to document the success of control programmes [2]. Surveillance data also advises national decision-making by: determining the relative importance of campylobacteriosis compared with other enteric infections; showing which animals are the primary reservoirs for infection; and helping to identify the most common transmission pathways. Campylobacteriosis surveillance is practised more in countries with higher incomes [2].

Farm Epidemiology

In developed countries, each broiler rearing house in farms generally contains between 10,000-30,000 birds, with several houses usually present in each farm [8]. These high numbers facilitate high levels of Campylobacter amplification, the rapid spread between broilers within houses, [8] and cross-contamination between separate houses on farms. Even with improving farm biosecurity levels the Campylobacter colonisation of broilers is extremely difficult to prevent [20-21]. After approximately two weeks poultry flocks are frequently colonised with C. jejuni without any apparent symptoms [1]. Vertical transmission, from parents to progeny, is not a significant Campylobacter source [8]. Better biosecurity intervention strategies in farms have reduced broiler Campylobacter colonisation, decreasing subsequent campylobacteriosis cases in several countries [8]. In broiler farms, longer downtimes between flocks, older broiler houses (> five years), no separate ante-room or barrier in houses, and the use of the drinker nipples with cups or bells compared with nipples without cups, have all increased the risk of Campylobacter colonisation [16]. Increasing the slaughter age of birds (from 36 days, to >40 days), laughtering in summer months (June, July and August), thinning broiler flocks, and an increasing amount of rearing houses on farms are all significant factors for producing Campylobacter positive broilers [19,22,23]. Farms with poorer biosecurity measures have been linked with having broilers with more strains of Campylobacter [24]. There is limited knowledge about how Campylobacter persists in broiler litter and faeces [25]. C. jejuni survives significantly longer in faeces, with a minimum survival time of 48 hours, compared with 4 hours in used broiler litter. C. jejuni survival is significantly enhanced at 20ËšC in all environmental conditions in both broiler litter and faeces, compared with survival at 25ËšC and 30ËšC. Survival is greater in microaerophilic compared with aerobic conditions in both sample matrices. The persistence of Campylobacter in broiler litter and faeces under various environmental conditions has implications for farm litter management, hygiene, and disinfection practices [25].

The colonisation of broilers with Campylobacter in drinking water may be partly due to Campylobacter resisting disinfection inside waterborne protozoa [26]. Campylobacter jejuni inside amoeba can infect broilers [27]. Campylobacter survive for prolonged periods of time both within, and in the presence of, different protozoa, including amoeba and ciliates [26]. Some protozoa package and excrete bacteria into multilamellar bodies (MLBs), increasing the risk of persistence of C. jejunu in the environment and possible transmission between different reservoirs in food and potable water through packaging [28]. The protection of Campylobacter from disinfection within protozoa and/or biofilms has important implications for water safety [29]. Whilst Campylobacter is present in the faeces of wild mammals (mice, rats, badgers, foxes, and rabbits), pets (dogs and cats), insects, and wild birds, are all frequently present in the vicinity of farms, the evidence of actual transmission, either direct source contamination from house entry or via environmental faecal contamination, to broilers is contradictory, sparse and unclear [30]. Relatively low Campylobacter isolation rates have been recorded from Dipteran flies [21]. However, in the summer the potential of broiler Campylobacter colonisation from this potential reservoir could in theory rise when fly populations increase [21]. Certain investigations have shown no significant overlaps in the Campylobacter populations in poultry and wildlife [30]. The incorporation of ecological data into studies of C. jejuni in wild birds has the potential to resolve when and how wild birds contribute to domestic animal and human C. jejuni infection, leading to the improved control of initial poultry contamination [31]. The antibiotic resistance of C. jejuni and C. coli, particularly with macrolides and fluoroquinolones (FQ), has raised concerns about the evolution of antibiotic resistance and has major implications for animal and human treatment [14]. Using FQ to treat poultry correlates with high levels of resistance to these drugs [2]. Resistant bacteria may transfer between farms, as farms with no record of using FQ have had FQ-resistant Campylobacter detected on them [15].

Dangerous Consumer Behaviour

There is a high prevalence of unsafe behaviours (undercooking and poor hand washing technique) when cooking poultry and eggs, and a great need for improvement in consumer behaviour and education [32]. Many consumers still do not follow recommended food safety practices for cooking poultry and eggs, which can lead to exposure of pathogenic Salmonella and Campylobacter [32]. In the USA, nearly 70% of consumers rinse raw poultry before cooking it and the majority of consumers (>80%) incorrectly store raw poultry in refrigerators [33]. This is extremely unsafe behaviour because of the potential cross-contamination of Campylobacter to other kitchen surfaces and other foods, especially ready-to-eat foods [33]. In the UK, outbreaks of Campylobacter infection are increasingly attributed to undercooked chicken livers, yet many recipes, including those of top chefs, advocate short cooking times and serving livers pink [34]. It is estimated that 19%-52% of livers served commercially in the UK fail to reach 70ËšC, and that predicted Campylobacter survival rates are 48%-98%. These findings indicate that cooking trends are linked to increasing Campylobacter infection case numbers [34]. Collectively, using information from research studies and effectively monitoring and examining consumer behaviour will improve the effectiveness of science-based education of schemes to lower the frequency of human campylobacteriosis cases [33].

Conclusion & Future Approaches

Chicken meat is the main global source of Campylobacter [1]. Reducing Campylobacter colonisation, carriage and transmission in broiler chickens, and related products, would lower human campylobacteriosis levels. Because of the epidemiological complexity of this problem, including geographical variations, the solution cannot be achieved by a few simple intervention strategies [2]. Campylobacter control and intervention strategies need to be tailored to reflect and adapt to regional variations, possibilities, practicalities and preferences, by the effective implementation of multiple stepwise interventions on the farms and in processing facilities [2,8]. From an epidemiological and risk assessment perspective, further knowledge should be obtained on Campylobacter prevalence and genotype distribution in primary production [35]. Effective quality assurance schemes, including Good Laboratory Practice (GLP), which includes continuous monitoring and improvement, are vital for cogent diagnostic laboratories [2]. In developed countries molecular methods, e.g. real-time PCR, could be applied to quantify Campylobacter spp. directly from chicken droppings and thus avoid culture-associated bias resulting from failure of recovery from viable but non-culturable states previously described in Campylobacter [36]. Intervention methods which are effective in the pre-harvest stages in farms include application of strict biosecurity measures, good animal husbandry, and health measures [34]. The elucidation of the seasonal components of human campylobacteriosis epidemiology would improve with increasing the integration molecular subtyping [3]. Temporal patterns in human infections do not always correlate with those found in poultry [8]. Community socioeconomic and environmental factors are important to consider when assessing the relationship between possible risk factors and Campylobacter infection [7]. Overseas travel has been linked as being a significant source of the disease, especially for northern European residents [8].

Despite numerous trails and studies, there are currently no available vaccines commercially available to remove or reduce Campylobacter intestinal load in poultry [37]. Feed additives (pre and probiotics) have potential to reduce Campylobacter infection in flocks [35]. Probiotics, e.g. Lactobacillus salivarius SMXD5, may exhibit an anti-Campylobacter activity in vivo and partially prevent the impact of Campylobacter on the avian gut microbiota [1]. In future it will be important to identify, characterise, develop and promote new vaccine antigens, with more robust economics funding models which enable vaccine developers to hedge against the risks of market volatility [37,38]. The oral vaccination of poultry with modified outer membrane vesicles (OMVs) could be a promising option for future vaccine development [39]. With well organised and multidisciplinary and coordinated approaches between countries in these and other areas, the disease burden on Campylobacter should hopefully be reduced in the future.


  1. Saint Cyr MJ, Haddad N, Taminiau B, Poezevara T, Quesne S, et al. (2016) Use of the potential probiotic strain Lactobacillus salivarius SMXD51 to control Campylobacter jejuni in broilers. Int J Food Microbiol.
  2. Anonymous (2012) FOOD SAFETY. The global view of campylobacteriosis report of an expert consultation. World Health Organisation, Utrecht, Netherlands, pp. 9-11.
  3. Strachan NJ, Rotariu O, Smith Palmer A, Cowden J, Sheppard SK, et al. (2013) Identifying the seasonal origins of human campylobacteriosis. Epidemiol Infect 141(6): 1267-1275.
  4. Roux F, Sproston E, Rotariu O, Macrae M, Sheppard SK, et al. (2013) Elucidating the aetiology of human Campylobacter coli infections. PloS One 8(5): e64504.
  5. Buettner S, Wieland B, Staerk KDC, Regula G (2010) Risk attribution of Campylobacter infection by age group using exposure modelling. Epidemiol Infect 138(12): 1748-1761.
  6. Scallan E, Hoekstra RM, Mahon BE, Jones TF, Griffin PM (2015) An assessment of the human health impact of seven leading foodborne pathogens in the United States using disability adjusted life years. Epidemiol Infect 143(13): 2795-2804.
  7. Rosenberg Goldstein RE, Cruz Cano R, Jiang C, Palmer A, Blythe D, et al. (2016) Association between community socioeconomic factors, animal feeding operations, and campylobacteriosis incidence rates: Foodborne Diseases Active Surveillance Network (FoodNet), 2004-2010. BMC Infect Dis 16: 354.
  8. Skarp CP, Hänninen ML, Rautelin HI (2016) Campylobacteriosis: the role of poultry meat. Clin Microbiol Infect 22(2): 103-109.
  9. Mangen M JJ, Bouwknegt M, Friesema IHM, Haagsma JA, Kortbeek LM, et al. (2015) Cost-of-illness and disease burden of food-related pathogens in the Netherlands, 2011. Int J Food Microbiol 196: 84-93.
  10. Tam CC, O'Brien SJ (2016) Economic Cost of Campylobacter, Norovirus and Rotavirus Disease in the United Kingdom. PLoS One 11(2): e0138526.
  11. Gibney KB, O’Toole J, Sinclair M, Leder K (2014) Disease burden of selected gastrointestinal pathogens in Australia, 2010. Int J Infect Dis 28: 176-185.
  12. Lake RJ, Cressey PJ, Campbell DM, Oakley E (2010) Risk ranking for food borne microbial hazards in New Zealand: burden of disease estimates. Risk Anal 30(5): 743-752.
  13. Tam CC, Higgins CD, Neal KR, Rodrigues LC, Millership SE, et al. (2009) Chicken consumption and use of acid-suppressing medications as risk factors forCampylobacter enteritis, England. Emerg Infect Dis 15(9): 1402-1408.
  14. Moore JE, Barton MD, Blair IS, Corcoran D, Dooley JS, et al. (2006) The epidemiology of antibiotic resistance in Campylobacter. Microbes Infect 8(7): 1955-1966.
  15. Taylor NM, Wales AD, Ridley AM, Davies RH (2016) Farm level risk factors for fluoroquinolone resistance in E. coli and thermophilic Campylobacter spp. on poultry farms. Avian Pathol 45(5): 559-568.
  16. Borck Høg B, Sommer HM, Larsen LS, Sørensen AI, David B, et al. (2016) Farm specific risk factors forCampylobactercolonisation in Danish and Norwegian broilers. Prev Vet Med 130: 137-145.
  17. Anonymous. (2011) Scientific opinion on campylobacter in broiler meat production: control options and performance objectives and/or targets at different stages of the food chain. EFSA J 9(4): 2105-2246.
  18. Bronnec V, Turoňová H, Bouju A, Cruveiller S, Rodrigues R, et al. (2016) Adhesion, biofilm formation, and genomic features of campylobacter jejuni Bf, an atypical strain able to grow under aerobic conditions. Front Microbiol 7: 1002.
  19. Anonymous (2015) The European Union summary report on trends and sources of zoonoses, zoonotic agents and food-borne outbreaks in 2013. EFSA J 13: 51-58.
  20. Moran L, Scates P, Madden RH (2009) Prevalence of Campylobacter spp. in raw retail poultry on sale in northern ireland. J Food Prot 72(9): 1830-1835.
  21. Royden A, Wedley A, Merga JY, Rushton S, Hald B, et al. (2016) A role for flies (Diptera) in the transmission of Campylobacter to broilers? Epidemiol Infect 144(15): 3326-3334.
  22. Lawes JR, Vidal A, Clifton Hadley FA, Sayers R, Rodgers J, et al. (2012) Investigation of prevalence and risk factors for Campylobacter in broiler flocks at slaughter: results from a UK survey. Epidemiol Infect 140(10): 1725-1737.
  23. Agunos A, Waddell L, Léger D, Taboada E (2014) A systematic review characterizing on-farm sources of Campylobacter spp. for broiler chickens. PLoS ONE 9(8): e104905.  
  24. Jorgensen F, Ellis Iversen J, Rushton S, Bull SA, Harris SA, et al. (2011) Influence of season and geography on Campylobacter jejuni and C. coli subtypes in housed broiler flocks reared in Great Britain. Appl Environ Microbiol 77(11): 3741-3748.
  25. Smith S, Meade J, Gibbons J, McGill K, Bolton D, et al. (2016) The impact of environmental conditions on Campylobacter jejuni survival in broiler faeces and litter. Infect Ecol Epidemiol 6: 31685.
  26. Snelling WJ, McKenna JP, Lecky DM, Dooley JS (2005) Survival of Campylobacter jejuni in waterborne protozoa. Appl Environ Microbiol 71(9): 5560-5571.
  27. Snelling WJ, Stern NJ, Lowery CJ, Moore JE, Gibbons E, et al. (2008) Colonization of broilers by Campylobacter jejuni internalized within Acanthamoeba castellanii. Arch Microbiol 189(2): 175-179.
  28. Trigui H, Paquet VE, Charette SJ, Faucher SP (2016) Packaging of Campylobacter jejuni into Multilamellar Bodies by the Ciliate Tetrahymena pyriformis. Appl Environ Microbiol 82(9): 2783-2790.
  29. Snelling WJ, Moore JE, McKenna JP, Lecky DM, Dooley JS (2006) Bacterial-protozoa interactions; an update on the role these phenomena play towards human illness. Microbes Infect 8(2): 578-587.
  30. Newell DG, Elvers KT, Dopfer D, Hansson I, Jones P, et al. (2011) Biosecurity-based interventions and strategies to reduce Campylobacter spp. on poultry farms. Appl Environ Microbiol 77(24): 8605-8614.
  31. Taff CC, Weis AM, Wheeler S, Hinton MG, Weimer BC, et al. (2016) Influence of Host Ecology and Behavior on Campylobacter jejuni Prevalence and Environmental Contamination Risk in a Synanthropic Wild Bird Species. Appl Environ Microbiol 82(158): 4811-4820.
  32. Maughan C, Chambers Iv E, Godwin S, Chambers D, Cates S, et al. (2016) Food handling behaviors observed in consumers when cooking poultry and eggs. J Food Prot 79(6): 970-977.
  33. Kosa KM, Cates SC, Bradley S, Chambers E 4th, Godwin S (2015) Consumer-reported handling of raw poultry products at home: results from a national survey. J Food Prot 78(1): 180-186.
  34. Jones AK, Rigby D, Burton M, Millman C, Williams NJ, et al. (2016) Cross P; ENIGMA Consortium. Restaurant Cooking Trends and Increased Risk for Campylobacter Infection. Emerg Infect Dis 22(7): 1208-1215.
  35. Schallegger G, Muri-Klinger S, Brugger K, Lindhardt C, John L, et al. (2016) Combined Campylobacter jejuni and Campylobacter coli Rapid Testing and Molecular Epidemiology in Conventional Broiler Flocks. Zoonoses Public Health
  36. Guyard-Nicodème M, Keita A, Quesne S, Amelot M, Poezevara T, et al. (2016) Efficacy of feed additives against Campylobacterin live broilers during the entire rearing period. Poult Sci 95(2): 298-305.
  37. Tholozan JL, Cappelier JM, Tissier JP, Delattre G, Federighi M (1999) Physiological characterization of viable-but-nonculturableCampylobacter jejuni cells. Appl Environ Microbiol 65(3): 1110-1116.
  38. Meunier M, Guyard-Nicodème M, Hirchaud E, Parra A, Chemaly M, et al. (2016) Identification of Novel Vaccine Candidates againstCampylobacter through Reverse Vaccinology. J Immunol Res 5715790.
  39. Lund M, Jensen JD (2016) A real options approach to biotechnology investment policy-the case of developing a Campylobacter vaccine to poultry. Prev Vet Med 128: 58-69.
  40. Godlewska R, Kuczkowski M, Wyszyńska A, Klim J, Derlatka K, et al. (2016) Evaluation of a protective effect of in ovo delivered Campylobacter jejuni OMVs. Appl Microbiol Biotechnol 100(20): 8855-8864.
  41. Anonymous (2013) Research and analysis Campylobacter cases: 2000 to 2012. Campylobacter infections: figures for England and Wales. Published by Public Health England.
© 2014-2018 MedCrave Group, All rights reserved. No part of this content may be reproduced or transmitted in any form or by any means as per the standard guidelines of fair use.
Creative Commons License Open Access by MedCrave Group is licensed under a Creative Commons Attribution 4.0 International License.
Based on a work at
Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version | Opera |Privacy Policy