Emerging Issues in Small Ruminant Health: A Look At A Few Zoonoses Old And New

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1 Emerging Issues in Small Ruminant Health: A Look At A Few Zoonoses Old And New Overview By Stacy H. Tinkler, DVM, Dipl. ACVIM Purdue University Most bacterial diseases associated with sheep and goat abortion have some potential for zoonotic transmission. The main diseases of concern as identified by Edmondson et al (2012) are: Brucella melitensis, C, burnetii (Q fever), Chlamydophila abortus, Salmonella, Toxoplasma gondii and Campylobacter jejuni. Knowledge of abortifacient zoonotic pathogens, their clinical signs, gross lesions and their potential risk to humans is critical to prevent zoonotic disease to veterinarians and small ruminant owners. The focus of these proceedings will be Coxiella burnetii as there has been growing public health concern over the risk to the human population beyond simple occupational exposure, along with a mention of some of the major foodborne zoonotic pathogens and a quick review of Contagious ecthyma (orf). A recent Coxiella/Q fever outbreak in the Netherlands resulted in 4000 human cases and the euthanasia of 50,000 goats (Menzies et al 2013). Coxiellosis, Q fever Coxiella burnetii, the causative agent of coxiellosis in animals or Q fever (Query fever) in humans, is an obligate intracellular gram-negative bacterium and zoonotic pathogen. Ruminants act as a reservoir and are replicating hosts of the organism. Cats, dogs, and wildlife may also serve as reservoirs (Whitney et al 2009). C. burnetii has been identified in fish, wild birds, rodents, marsupials, horses, swine, camels, marine mammals, ducks, turkeys, geese, cats, dogs, and rabbits but was first isolated from a tick and has been identified in ~40 species of tick subsequently (Davis and Cox 1938). The disease is subclinical in most animals, with adverse pregnancy events reportedly the most common clinical sign. These abortion rates can vary from a few cases up to 90% of the herd (Palmer et al 1983, Arricau-Bouvery et al 2005) Recently, C burnetii has been identified as a biological-threat agent due its low infectious dose and high rate of transmission, and is listed as a group B bioterrorism agent by the CDC in the US (Oyston and Davies 2011). This organism is present in ~90% of dairy cattle operations in the United States and a significant number of sheep and goat operations (Plummer 2012). Humans are infected via inhalation of aerosols or contaminated dust from infected ruminants or through exposure to infected animal products (Whitney et al 2009). Exposure and seroconversion may result from consumption of unpasteurized dairy products (Whitney et al 2009). Horizontal human-human transmission is rare but has been reported through sexual contact and aerosol transmission (Whitney et al 2009).

2 Bacteriology and epidemiology C. burnetii occurs in two predominate variants, a large cell variant which replicates in cells, and a small cell variant that survives in the environment. C. burnetii undergoes phase variation, which is associated with alterations in its cell wall components, and have been called phases 1 and 2. The changes in cell surface antigens with subsequent phase variants has clinical implications for serologic testing due to the production of phase 1 and phase 2 antibodies to C. burnetii at different stages of natural infection. Phase 1 is highly virulent and can replicate in immune-competent hosts (Roest et al 2013) and phase 1 bacteria are internalized and survive intracellular killing, whereas phase 2 bacteria are efficiently phagocytized and then killed (Roest et al 2013). The primary route of transmission to both animals and humans is via aerosolization, and the organism is highly infectious; an infectious dose of 1 organism is reported for humans (Jones et al 2006). It has been suggested that the organism is capable of aerosolizing up to 5 km in appropriate environmental conditions. The bacterium is shed from ruminants in fetal membranes, fluids of parturition, vaginal secretions, aborted fetuses, milk, urine and feces (Berri et al. 2001; Arricau-Bouvery et al. 2003, Guatteo et al. 2006), and can be spread from infected carcasses at the time of slaughter (Porter et al., 2011). Bacteria colonize the uterus of the pregnant female, and the trophoblasts in the allanto-chorion of the placenta are the reported target cells of C. burnetii (Roest 2012). Long-term shedding in milk, up to 32 months postinfection, has been reported (Rodolakis et al.2007, Berri et al. 2007; Angelakis and Raoult, 2010). Persistent shedding in urine and feces is reportedly up to 20 days post-partum (Angelakis and Raoult, 2010). Abortion storms are most common in the first year of introduction into herds/flocks when the animals are immunologically naïve with increased herd shedding and fewer abortions observed in later years (Plummer 2012). This is especially true for goats where chronic subclinical shedders often remain in the herd. In sheep, shedding in vaginal secretions, feces and urine has been documented for up to 60 d post-partum (Rousset 2007), with 7-14 d of intermittent milk shedding (Berri 2001, Rodolakis 2007, Astobiza 2010b) but more information regarding excretion of C. burnetii leading to shedding in feces, vaginal secretions, urine and milk is needed. Clinical signs Acute infection is typically asymptomatic in small ruminants (Angelakis and Raoult 2010), and most shedding occurs in the complete absence of clinical signs in infected herds/flocks. Clinical disease is generally associated with adverse pregnancy events (abortions, still-born, weak kids). Rearing of these kids may be complicated by respiratory or GI problems (Wouda and Derksen 2007). Animals that abort generally have no signs of systemic illness and the aborted fetuses/placenta are often grossly unremarkable, although metritis may be present (Wouda and Dercksen 2007). Asymptomatic live born kids may shed high loads of C burnetii into the environment. Up to 98% does in naïve herds have been reported to abort (Berri et al 2007) from

3 Coxiellosis. According to Plummer (2012), C. burnetii is one of the top three causes of goat abortions and is also commonly associated with abortions in sheep; however, Campylobacter, Chlamydophila and toxoplasmosis are more often seen. Diagnosis Abortion is not specific for Coxiellosis. For direct diagnosis of the etiologic agent samples from aborted placental tissue, vaginal discharge or an aborted fetus should be collected and tested, but C. burnetii is capable of being shed in animals without histopathologic evidence of infection (Rousset et al 2007, Plummer 2012). Immunohistochemistry on infected placenta can detect Coxiella to confirm abortion due to coxiellosis. (Roest et al 2013) Coxiella shedding confirms its presence on the farm, and the farm should be considered positive, and a zoonotic Q fever risk. PCR tests are available and validated for use on vaginal fluids, milk, feces and placental tissues (Roest et al 2013). These tests are highly sensitive and specific. There are also a number of indirect diagnostic tests. The World Health Organization for Animal Health (OIE) recommends the complement fixation (CF) test as the preferred serologic assay (OIE 2010) but ELISA and IFA tests are reportedly more sensitive tests (Rousset et al 2007), Plummer. Negative serology tests cannot be used to rule out infection and shedding of an individual animal due to the fact that ~10-15% of infected animals do not develop a measurable immune response. Berri et al. (2001, 2005) found that 57% of parturient ewes shed the organism on vaginal swab PCR despite being ELISA sero-negative. A combination of direct and indirect diagnostic testing methods are recommended, such as PCR of aborted tissue and/or vaginal mucus (2-6 animals) within 8 days of abortion in addition to serology (6-10 animals) from animals that had given birth at least 15 days prior (Roest et al 2013). Increasing the number of samples submitted and repeated sampling around kidding/lambing season will increase the sensitivity for detecting an infected herd, according to Plummer (2012). Bulk tank testing in lambing/kidding season along with herd serology may also be of value in dairy herds. Serology is more cost-effective but PCR gives direct evidence of shedding. A the herd level, serology is helpful to determine if the population is infected; however, individual animal results must be interpreted with caution and negative results do not rule out infection or shedding as shedding is intermittent. According to Roest et al, (2013) PCR is the most sensitive technique to detect C. burnetii, whereas ELISA is the most sensitive technique to detect C. burnetii specific antibodies. Prevention and Control Antibiotic treatment and vaccination are currently the 2 methods available for control of Coxiellosis. The addition of in-feed tetracycline or injectable oxytetracycline pre-partum has not been shown to prevent C. burnetii shedding in milk, feces, and vaginal secretions (Berri et al 2007, Astobiza et al 2010b). Due to the lack of evidence supporting antibiotic efficacy and the

4 fact that prudent use of antibiotics is needed to avoid resistance, they should not be used for treatment of Q fever in animals at this time (Roest et al 2013). Vaccination with a phase 1 C. burnetii, inactivated vaccine is reportedly effective for abortion prevention, and the reduction of bacterial shedding in goats and cattle (Arricau-Bouvery et al 2005, Guatteo at al 2011), and is most effective in primiparous animals. The vaccine is provisionally licensed for cattle and goats in the EU (EFSA 2010a) but there is currently no vaccine in the US. Vaccination may not be effective in animals that are already infected (Guatteo et al 2008, Rousset et al 2009). A phase 1 vaccine is currently available for human use in Australia, and has been recommended for high-risk, occupationally exposed, sero-negative individuals (Arricau-Bouvery and Radolakis 2005). C. burnetii can survive for several weeks outside a host in warm, moist environments (Tissot Dupont et al 1992, Marrie and Raoult, 1997). As ruminants are the main reservoir, controlling endemic Coxiellosis in livestock may play an important role in reducing disease in populations living in close contact with infected animals (Schelling et al 2003). Angelakis and Raoult (2010) suggest that controlling environmental contamination through the control of infected ticks and biosecurity measures may reduce introduction of C. burnetii to naïve farms. Composting is the preferred method for handling manure and bedding and a 90 day minimum decreases the Coxiella burden and risk of spread (Menzies et al 2013). Manure should be covered during transport, stored in a location where water run-off and water contamination is minimal. Transport and spread of manure should be done when wind is minimal to reduce the risk of spread through aerosolization (Tissot-Dupont et al 1999, 2004). Composting carcasses and aborted tissues and contaminated bedding on site is preferred (Menzies et al 2013). Quarantine and mass euthanasia is not recommended for the following reasons: C burnetii is endemic in the US, and is a ubiquitous and persistent organism in the environment. It is thereby almost impossible to completely eliminate infection from a herd and to completely decontaminate, and there is no known treatment to stop shedding in infected animals. (Menzies et al 2013). Zoonotic transmission: the human-animal interface People usually acquire Q fever via inhalation of environmental C. burnetii. Domestic ruminants seem to be the primary source of infection for human Q fever, although companion animals must also be considered a source as several human outbreaks were related to pregnant dogs and cats (Roest et al 2013). The role of horses, ticks and wildlife remains unclear at this time. Outbreaks have been reported frequently, are world-wide and result in approximately labconfirmed human cases/outbreak. Sheep are usually the main source in most outbreaks, and goats are the second most commonly identified source. Contrary to this was the Dutch Q fever outbreak that lasted from , that had mainly dairy goats as the source of infection (Roest et al 2011). 18 reported outbreaks in 12 different countries involving 2 to 289 people were reported between (Angelakis and Raoult, 2010) and were attributed to exposure to sheep, goats, goat and sheep manure, wild animals, and dogs and cats. However, in humans Q

5 fever results from the inhalation of contaminated aerosols. These aerosols can travel up to 5 km and infect humans who have no direct contact with animals, and several outbreaks have demonstrated this (Roest et al 2013). C. burnetii poses a significant zoonotic risk to those exposed to ruminants (veterinarians, farmers, stock-breeders, livestock truck drivers, wool shearers, slaughterhouse workers), medical and paramedical practitioners, laboratory technicians with C. burnetii exposure, rural or semirural residents, and those handling contaminated manure fertilizer (Tissot-Dupont et al. 1999, Berri et al. 2003), and possibly any individuals within a few kilometers distance from infected farms (Plummer 2012). High-risk individuals must be aware of the risks and take necessary precautions such as barrier protection, face masks, and hand-hygiene. Approximately 25% of veterinarians at the 2006 AVMA conference were seropositive for C. burnetii exposure (Whitney et al 2009). The results of this study found that large animal veterinarians or those individuals with contact with standing bodies of water were also at increased risk, but the relationship to standing water was unclear. Consumption of raw milk or the selling of unpasteurized milk to consumers is not recommended as C. burnetii is shed in the milk of infected animals. Pasteurizing milk at 145F for 30 min, or 161F for 15 sec is enough to detroy C. burnetii and many other raw milk pathogens. Clinical presentation of Q fever in humans There are 3 primary clinical presentations: acute Q fever, chronic Q fever, and a post-q fever fatigue syndrome (QFS). The majority of Q fever cases are asymptomatic post-exposure (60%), while 40% will be symptomatic and present with what has been described as a non-specific, selflimiting illness. Fever, headache, chills, pneumonia and hepatitis are observed in more severe acute cases. In the Dutch outbreak, the mortality rate was reportedly low (1.2%) and any fatalities were all patients suffering from severe underlying disease. Chronic Q fever develops in 1-5% patients, and may not be seen for years after primary infection. Symptoms include fatigue, fever, weight-loss, night sweats, hepato-splenomegaly and endocarditis. C. burnetii is not detected in people with QFS and antibody levels are low. Symptoms include: fatigue, arthralgia, myalgia, blurred vision and peripheral lymphadenopathy. Why some people develop long-term presentations of Q fever is unclear but acute Q fever requiring hospitalization was identified as a risk factor (Roest et al 2013). Diagnosis includes combinations of PCR and serologic testing. The treatment of choice is doxycycline.

6 Angelakis E, Raoult D. Q fever: Review. Vet Microbiol 2010:140; Arricau-Bouvery N, Rodolakis A. Is Q-fever an emerging or re-emerging zoonosis? Vet Res 2005:36; Arricau-Bouvery N, Souriau A, Bodier C, Dufour P, Rousset E, Rodolakis A. Effect of vaccination with phase I and phase II Coxiella burnetii vaccines in pregnant goats. Vaccine 2005:23; Astobiza I, Barandika JF, Ruiz-Fons F, Hurtado A, Povedano I, Juste RA, Garcia-Perez AL. Coxiella burnetii shedding and environmental contamination at lambing in two highly naturally infected dairy sheep flocks after vaccination. Res Vet Sci 2010a:91(3);epub Astobiza I, Barandika JF, Hurtado A, Juste RA, Garcia-Perez AL. Kinetics of Coxiella burnetii excretion in a commercial dairy sheep flock after treatment with oxytetracycline. Vet J 2010b:184; Berri M, Rousset E, Champion JL, Russo P, Rodolakis A. Goats may experience reproductive failures and shed Coxiella burnetii at two successive parturitions after a Q fever infection. Res Vet Sci 2007:83(1); Berri M, Rousset E, Champion JL, Arricau-Bouvery N, Russo P, Pepin M, Rodolakis A. Ovine manure used as a garden fertilizer as a suspected source of human Q fever. Vet Rec 2003:153; Davis GE, Cox HR A filter-passing infectious agent isolated from ticks I. Isolation from Dermacentor andersoni, reactions in animals, and filtration experiments. Public Health Rep. 53:9. Berri M, Rousset E, Hechard C, Champion JL, Dufour P, Russo P, Rodolakis A. Progression of Q fever and Coxiella burnetii shedding in milk after an outbreak of enzootic abortion in a goat herd. Veterinary Record 2005:156; Berri M, Crochet D, Santiago S, Rodolakis A. Spread of Coxiella burnetii infection in a flock of sheep after an episode of Q fever. Vet Rec 2005b:157(23); Berri M, Souriau A, Crosby M, Crochet D, Lechopier P,Rodolakis A Relationships between the shedding of Coxiella burnetii, clinical signs and serological responses of 34 sheep. Vet Rec. 148: Davis GE, and Cox HR. A filter-passing infectious agent isolated from ticks. Isolation from D. andersoni, reactions in animals and filtration experiments. Pub. Health Rep.1938;53:

7 Edmondson MA, Roberts JF, Baird AN, Bychawski S, and Pugh DG.Theriogenology of Sheep and Goats. In: Pugh DG, Baird AN, eds. Sheep and Goat Medicine, 2nd Edition. Maryland Heights, MO: Elsevier-Saunders,2012; European Food Safety Authority (EFSA). Application of Systematic Review Methodology to Food and Feed Safety Assessments to Support Decision Making. EFSA J 2010:8(6); Guatteo R, Seegers H, Joly A, Beaudeau F. Prevention of Coxiella burnetii shedding in infected dairy herds using a phase I C. burnetii inactivated vaccine. Vaccine 2008:26; Guatteo R, Seegers H, Taurel AF, Joly A, Beaudeau F. Prevalence of Coxiella burnetii infection in domestic ruminants: a critical review. Vet Microbiol 2011:149(1-2);1-16. Jones RM, Nicas M, Hubbard AE, Reingold AL The infectious dose of Coxiella burnetii (Q fever). Appl Biosafety. 11:10. McQuiston JH, Childs JE. Q fever in humans and animals in the United States. Vector Borne Zoononotic Dis 2002:2; Menzies P et al. Prevention and Control of Coxiella burnetii Infection among Humans and Animals: Guidance for a Coordinated Public Health and Animal Health Response. Available from OIE (Organisation Internationale Epizootic). Q fever. In: OIE Terrestrial Manual Chapter Paris. pp 1-13 Oyston PC, Davies C Q fever: the neglected biothreat agent. J Med Microbiol. 60:9 21 Palmer NC, Kierstead M, Key DW, Williams JC, Peacock MG, Vellend H. Placentitis and abortion in sheep and goats caused by Coxiella burnetii. Can Vet J 1983:24;60-1. Plummer P.Coxiellosis: The disease and clinical presentation,in Proceedings.ACVIM Forum 2012; Porter SR, Czaplicki C, Mainil J, Gutteo R, Saegerman C. Q fever: current state of knowledge and perspectives of research of a neglected zoonosis. Intl J Microbiol, 2011, epub Article ID :22p;doi /2011/ Rodolakis A, Berri M, Hechard C. Comparison of Coxiella burnetii shedding in milk of dairy bovine, caprine, and ovine herds. JDS 2007:90(12); Roest HI, Tilburg JJ, van der Hoek W, Vellema P, van Zijderveld FG, Klaasen CH, Raoult D. The Q fever epidemic in The Netherlands: history, onset, response and reflection. Epidemiol Infect 2011:139(1);1-12.

8 Roest HIJ, van Gelderen B, Dinkla A, Frangoulidis D, van Zijderveld FG, Rebel J, van Keulen L Q fever in pregnant goats: pathogenesis and excretion of Coxiella burnetii. PLoS ONE. 7:14. Roest HI, Bossers A, van Zijderveld FG, Rebel JM. Clinical microbiology of Coxiella burnetii and relevant aspects for the diagnosis and control of the zoonotic disease Q fever. Vet Q 2013;33(3): Rousset E, Durand B, Berri M, Dufour P, Prigent M, Russo P, Delcroix T, Touratier A, Rodolakis A, Aubert M. Comparative diagnostic potential of three serological tests for abortive Q fever in goat herds. Vet Microbiol 2007:124; Rousset E, Durand B, Champion JL, Prigent M, Dufour P, Forfait C, Marois M, Gasnier T, Duquesne V, Thiery R. Efficacy of a phase I vaccine for the reduction of vaginal Coxiella burnetii shedding in a clinically infected goat herd. Clin Microbiol Infect 2009:15(Suppl.2); Schelling E, Diguimbaye C, Daoud S, Nicolet J, Boerlin P, Tanner M, Zinnstag J. Brucellosis and Q fever seroprevalences of nomadic pastoralists and their livestock in Chad. Prev Vet Med 2003:61; Tissot-Dupont H, Torres S, Nezri M, Raoult D. Hyperendemic focus of Q fever related to sheep and wind. Am J Epidemiol 1999:150(1); Tissot-Dupong H, Amadei MA, Nezri M, Raoult D. Wind in November, Q fever in December. Emerg Infect Dis 2004:10(7);available from: Webster D, Haase D, Marrie TJ, Campbell N, Pettipas J, Davidson R, Hatchette TF. Ovineassociated Q fever. Epidemiol Infect 2009:137; Whitney EAS, Massung RF, Candee AJ, Ailes EC, Myers LM, Patterson NE, Berkelman RL. Seroepidemiologic and occupational risk survey for Coxiella burnetii antibodies among US veterinarians. Clin Infect Dis 2009:48(5); Wouda W, Derksen DP. Abortion and stillbirth among dairy goats as a consequence of Coxiella burnetii. Tidjschr Diergeneeskd 2007:132(23);

9 Foodborne zoonotic pathogens The most common zoonotic diseases in the US are gastro-intestinal illnesses. A number of foodborne pathogens have been identified in raw milk that are of clinical significance: Campylobacter jejuni, Shiga toxin-producing E. coli, Listeria monocytogenes and salmonellae (Oliver 2009), with Listeria and Salmonella spp being the most commonly reported. Several studies have assessed the incidence of these organisms in sheep and goat milk and have found the same organisms along with enterotoxigenic Staphylococcus aureus. Raw milk sales are currently allowed in 30 states (Indiana is NOT one of them). Roughly 35-60% of farm families and their employees consume raw milk (Oliver 2009) but consumption in urban communities is unclear. 1. Oliver SP, Boor KJ, Murphy SC and Murinda SE. Food safety hazards associated with consumption of raw milk. Foodborne Pathogens and Disease. 2009;(6)7: Campylobacter Campylobacter jejuni is a leading cause of bacterial food-borne gastroenteritis worldwide and is considered to be a major public health problem. Clinical signs of Campylobacter infections in humans include self-limiting watery/bloody diarrhea, abdominal cramps, nausea, and fever; however, severe neurological disease and sepsis may be seen. Campylobacter is widespread in food animals, and animal products are often contaminated. Campylobacter outbreaks are also commonly associated with consumption of raw milk. Ruminants contribute significantly to sporadic cases and human disease outbreaks. A tetracycline-resistant, highly virulent C. jejuni clone has emerged as the predominant cause of Campylobacter-abortion in sheep which has also been associated with multiple human gastroenteritis outbreaks linked to raw milk consumption. Currently there is no evidence implicating the clone as a cause of human abortion, but it is possible given the virulence of the clone in pregnant animals and the fact that C. jejuni has been implicated in human abortion, stillbirth, and neonatal mortality. This study also supports prior studies that implicate Campylobacter as the most common cause of milk-borne disease outbreaks in the US, with unpasteurized milk and associated dairy products as major sources of human infection. 1. Sahin O et al. Molecular evidence for zoonotic transmission of an emergent highly pathogenic Campylobacter jejuni clone in the United States. J Clin Microbiol.2012;(50)3: Shiga toxin-producing Escherichia coli (STEC) Shiga toxin-producing Escherichia coli (STEC) has emerged as an important zoonotic pathogen, particularly E coli O157:H7 which is responsible for several human diseases, including hemorrhagic colitis (HC), and in children the hemolytic-uremic syndrome (HUS) (Oporto et al 2008). Most outbreaks and sporadic cases of HC and HUS have been attributed to strains of E. coli O157:H7 STEC. Hard cheeses are considered to present a lower risk for growth and survival of pathogens than soft cheeses; however, STEC can survive in hard-ripened raw milk cheeses up

10 to 90 d of ripening (Brooks et al 2012). Cheese may be manufactured in the United States using raw milk, provided the cheese is aged for at least 60 days at temperatures not less than 35 F (1.7 C) (Brooks et al 2012) but there is currently increased concern among regulators regarding the safety of raw milk cheese due to the potential ability of foodborne pathogens to survive the manufacturing and aging processes. A recent study sampled feces from 28 goats and 20 sheep on 7 city hobby farms and found STEC strains in 45/48 (94%) of samples (25/28 goat, 20/20 sheep). Other prior studies cited had found lower prevalence of STEC in sheep (30-67%), and (17-75%) in goats (Schilling et al 2012). While no animals or humans had reportedly shown any clinical signs, silent carriers of this organism can serve as a disease reservoir and are a risk for zoonotic disease. 1. Brooks JC et al. Survey of raw milk cheeses for microbiological quality and prevalence of foodborne pathogens. Food Microbiol. 2012;(31)2: Oporto B et al. Escherichia coli O157:H7 and Non-O157 Shiga Toxin-producing E. coli in healthy cattle, sheep and swine herds in Northern Spain. Zoonoses Public Health. 2008;55: Schilling AK et al. Zoonotic agents in small ruminants kept on city farms in southern Germany. Appl. Environ. Microbiol. 2012;78(11): Listeria monocytogenes (LM) LM is an intracellular, non-spore forming Gram-positive cocco-bacillis that belongs to the genus Listeria. There are 6 species including LM, but only two are considered potentially pathogenic: LM and L. ivanovii. LM is the major pathogen of listeriosis and the only species that poses a serious public health risk. It causes invasive and often fatal CNS infection in ruminants, horses, dogs, pigs, deer, South American camelids, cats, and men. L. ivanovii is considered only mildly pathogenic and seems to affect almost exclusively ruminants, causing abortion, still-births, and neonatal septicemia, but not CNS infections. LM is ubiquitously distributed and grows in soil, water, plant matter, food items, and intestinal tract of mammalian hosts. LM produces a biofilm making it more resistant to hostile environmental conditions such as low ph, high salt concentrations and low temperatures, and food-processing and food-preserving procedures. LM has emerged as an important foodborne pathogen and is a major cause for large food recalls due to bacterial contamination. Although LM is able to infect a wide range of animal species, it occurs primarily in ruminants and humans. The link between ruminant and human listeriosis is not completely understood. Listeriosis is considered to be a zoonosis, but direct transmission between ruminants and humans rarely occurs. Most cases of direct transmission are associated with cutaneous infections via contact with infected cattle or aborted tissue. However, the literature suggests that ruminants may act as a natural reservoir for strains causing human infections given that the same epidemic clone responsible for a large number of human epidemics has been repeatedly isolated from ruminants with listeriosis.

11 1. Oevermann A, Zurbriggen A, and Vandevelde M. Rhombencephalitis Caused by Listeria monocytogenes in Humans and Ruminants: A Zoonosis on the Rise? Interdisciplinary Perspectives on Infectious Diseases.2010; (vol. 2010): Low JC and Donachie W. A review of Listeria monocytogenes and listeriosis. Vet J 1997;153(1): Roberts AJ and Wiedmann M. Pathogen, host and environmental factors contributing to the pathogenesis of listeriosis. Cellular and Molecular Life Sciences 2003;60(5): Regan EJ, Harrison GAJ, Butler S, et al. Primary cutaneous listeriosis in a veterinarian.vet Record 2005;157(7): R. Nappi, E. Bozzetta, R. Serra, et al. Molecular characterization of Listeria monocytogenes strains associated with outbreaks of listeriosis in humans and ruminants and food products by serotyping and automated ribotyping, Vet Res Comm. 2005;29(s2): Staphylococcus aureus food poisoning (SFP) S. aureus is a ubiquitous pathogen found in air, dust, sewage, water, environmental surfaces, and in humans and animals and is associated with both human and animal diseases including mastitis, and staphylococcal food-poisoning (SFP). In rare cases, it has been associated with more life threatening illness such as toxic-shock syndrome (TSS), endocarditis, and necrotizing pneumonia. Clinically and subclinically mastitic animals can be a source of transmission of staphylococcal enterotoxins into milk. Clinical signs of SFP in humans include sudden onset of nausea, vomiting, abdominal cramps and diarrhea, and is caused by ingestion of food containing heat-stable staphylococcal enterotoxins. Other contamination rates in meat products have been reported from % in one study and 96.2% in goat bulk milk and 37.8% in raw milk products in a Norwegian study. Small ruminant owners consuming raw milk, cheese or meat from their animals may be at risk for this disease. 1. Hennekinne JA, De Buyser ML, Dragacci, S. Staphylococcus aureus and its food poisoning toxins: characterization and outbreak investigation. Microbiol Rev. 2012; 36: Contreras A, et al. Mastitis in small ruminants. Small Rumin Res. 2007;68(1-2): Le Loir Y, Baron F, Gautier M. Staphylococcus aureus and food poisoning. Genet. Mol. Res.2003; 2: Lowy, F.D. Staphylococcus aureus infections. N. Engl. J. Med. 1998;339: Balaban N and Rasooly A. Staphylococcal enterotoxins. Int J Food Microbiol. 2000; 61: Normanno G et al,. Coagulase-positive staphylococci and Staphylococcus aureus in food products marketed in Italy. Int. J. Food Microbiol. 2005; 98,

12 7. Jorgensen, HJ, Mork, T, Hogasen HR, Rovik LM. Enterotoxigenic Staphylococcus aureus in bulk milk in Norway. J. Appl. Microbiol. 2005;99: Toxoplasma gondii Toxoplasma gondii infections are highly prevalent in humans and food animals. Felids are the key species in the life cycle of this parasite as they excrete the environmentally resistant oocyst in their feces. Humans become infected via ingestion of tissue cysts from undercooked meat, consuming food contaminated with oocysts, or by accidentally ingesting oocysts from the environment. Clinical toxoplasmosis in humans has been linked to ingestion of T. gondii in food, and foodborne transmission is one of the major sources of T. gondii infection. Clinical disease resulting from T. gondii infection occurs as acquired infection in immune-competent persons (usually mild), disease in immunosuppressed persons usually due to recrudescence, congenital disease, and ocular disease (congenital or acquired). In a recent assessment of foodborne illnesses in the US, toxoplasmosis was identified as the second leading cause of foodborne illness related deaths and fourth leading cause of foodborne illness related hospitalizations). Results of a recent study and previous surveys indicate the prevalence of T. gondii in lambs can be high. Although pasteurization will kill T. gondii in goat s milk, unpasteurized raw milk is sold by small goat farmers and goat cheeses made from raw milk could be a source of T. gondii infection. Little is known of the excretion of T. gondii in goat s milk. Goat meat is also very popular with many ethnic groups in the US. In a recent study, the seroprevalence of T. gondii antibodies in goat meat destined for human consumption in the US was found to be 53.4%. 1. Cenci-Goga BT et al. Toxoplasma in animals, food, and humans: an old parasite of new concern. Foodborne Pathogens and Disease.2011;8(7) Jones JL and Dubey JP. Foodborne toxoplasmosis. Clin Inf Dis.2010;55(6): Centers for Disease Control and Prevention. Parasites, toxoplasmosis, biology. Available at: Accessed January Scallan E, Hoekstra RM, Angulo FJ, et al. Foodborne illness acquired in the United States major pathogens. Emerg Infect Dis 2011; 17:7 15. Salmonella Sheep and goats can be carriers of different Salmonella serovars, including Salmonella enterica serovar Enteritidis and Salmonella enterica serovar Typhimurium, the most important serovars for human infections. However, salmonella prevalence in sheep and goat herds is reportedly very low (Schilling et al 2012). In 2008, 2.25% of the sheep flocks and 1.97% of the individually tested sheep in Germany carried Salmonella spp. The prevalences in goat herds were even lower, at 0.51% of the herds and 0.78% of the individually tested goats. In another study, 1.3% of the sheep carried Salmonella spp., with slightly higher ratios in sheep that were kept on limited pastures and had contact with wild birds. Small ruminants appear to play a minor role in the

13 transmission of Salmonella to human beings, and general hygiene management should be adequate for limiting the risk of acquiring Salmonella infections from sheep and goats. (Schilling et al 2012) 1. Schilling AK et al. Zoonotic agents in small ruminants kept on city farms in southern Germany. Appl. Environ. Microbiol. 2012;78(11): Contagious ecthyma (CE), orf, soremouth, scabby-mouth, contagious pustular dermatitis CE is a contagiuous, zoonotic disease of goats, sheep (and camelids) with a world-wide distribution. It is an epitheliotropic parapox virus that enters the goat via skin abrasions, which then replicates in regenerating epidermal keratonocytes and spreads to lymph nodes, bone marrow and liver during primary viremia. The virus may become generalized and through a secondary viremic phase, spread to the head, extremities, udder, genitals, and lungs. Epidemiology Morbidity in kids can be close to 100%, with a mortality rate from secondary infection and starvation reportedly up to 20% but rarely exceeds 1%. Death is usually due to secondary complications such as pneumonia or starvation and not from CE itself. Persistently infected carrier goats and sheep have been demonstrated as an important source of disease and infection can recrudesce during times of stress. Clinical signs The incubation is 3-8 days post-infection. Papules progress to vesicles, pustules and scabs. Proliferative, crusty lesions typically form on the lips, but can be seen on the face, ears, coronary band, scrotum, teats, or vulva. Other rarer distributions on the neck, chest, and flank and caudal hind legs have also been reported. Scabs may have secondary bacteria and infections can develop. Lesions regress in 3-4 weeks according to Smith and Sherman (2009) or 4-8 weeks (Musser 2012). In more severe cases, lesions have reportedly extended down the respiratory or GI tracts and led to pneumonia or gastro-eneteritis respectively but this is rare. A persistent form referred to as malignant contagious ecthyma has been reported in a small number of sheep flocks. Lesions are found in atypical areas (distal limbs, feet) and fail to regress and may continue to enlarge, making secondary complications more common. Adult goats with lesions on the lips generally continue to eat and milk well, but animals with teat lesions may affect udder health and predispose to mastitis. Painful teats may also lead to rejection of the kid when trying to suckle, or painful lip lesions may prevent adequate suckling. Kids/lambs can also developed more generalized disease and secondary bacterial infections and

14 lesions can also contain maggots if complicated by fly strike. Boer goats and Boer goat crosses seem to develop a more generalized and persistent form of CE, but it is unclear if it is due to a different strain or immunologic response. Diagnosis Diagnosis is usually based on CS but skin biopsy and histopathologic exam can confirm the diagnosis. Electron microscopy, IHC or serology can also aid in diagnosis or distinguish CE from the other differentials. Differential diagnoses include bluetongue, ulcerative dermatoses, capripox (sheep and goat pox) or foot and mouth disease (FMD). Treatment As the disease is typically self-limiting and lesions resolve within 3 weeks, treatment is not often performed. The benefits of treatment must be also weighed against the zoonotic risk of infection. Antibiotics have been used in cases of secondary bacterial infections. If lambs or kids are not suckling well, anesthesia and local debridement of lesions with either electrocautery or cryotherapy have been successfully reported in lambs. Topical astringents or ointments may actually delay resolution of lesions. Zoonotic transmission: the human-animal interface Human lesions are caused by direct inoculation of infected material, through scab contact from either natural disease or from live vaccine and are reportedly very painful. Sheep and goat owners, farmers, and veterinarians are at risk and CE is an occupational disease among sheep shearers, butchers and slaughterhouse workers. CE lesions occur mainly on fingers and are usually seen as large, painful vesiculo-pustular nodules (1 2 cm). A low fever and swelling of the draining lymph nodes may also occur (Grey 1949). Lesions (up to 5 cm) have been observed. Spontaneous recovery occurs in 3 6 weeks but repeat attacks are reportedly common. Diagnosis is confirmed by examination of collected material (from a vesiculo-pustule or a scab) by negative electron microscopy, which shows characteristic virions (LaChapelle 2012). Prevention and control Avoid buying animals from CE-infected farms if possible. Minimize transport stress. Quarantine any new arrivals on the farm until CE infection can be ruled-out. Scabs maintain large amounts of virus and protect it from environmental inactivation from months-years (Musser et al 2008), and provide a source of pasture and shed contamination. Vaccination is generally not recommended in non-infected herds as vaccination with live unattenuated virus will introduce disease. In herds where purchase and introduction of new animals or showing occurs frequently, vaccination may prevent an outbreak during the show

15 season or in milking animals. If vaccination is utilized, it should be done at least 6 weeks prior to the show season so any scabs will not be present, or at least 8 weeks prior to lambing/kidding so the dams are immune when suckling lambs/kids. Vaccinated ewes/does should ideally have all of the scabs fall off before moving them to the lambing/kidding area so neonates are not born into a high viral load. If a CE outbreak occurs on a previously uninfected premise, affected animals should be isolated and vaccinating unaffected animals may limit the duration of the outbreak. Subsequent vaccination of all kids in conjunction with annual revaccination of lategestation does is suggested. It is thought that no colostral antibody transfer occurs with CE for passive immunity in lambs/kids, therefore, timing of vaccination does not appear to be a factor. Commercially available preparations are of un-attenuated, live virus or tissue culture strains marketed as vaccines. Autogenous vaccines are made by crushing scabs in saline, filtration of the suspension through a cheese cloth, along with several drops of antibiotic added to prevent secondary bacterial overgrowth. Skin in a hairless region such as axillae, inner ear pinnae, under the tail is scarified and the vaccine is rubbed in. Scabs should appear in 1-3 days if the inoculation was successful. Lack of response suggests a pre-existing immunity. Most vaccines are not labeled for use in goats and research has shown that the use of sheep vaccine was not protective in goats (de la Concha et al 2003). A goat vaccine was created (Musser et al 2008) and continues to be protective if the vaccine-derived CE strain but is not cross-protective for antigenically distinct strains (Musser et al 2012). Reasons for vaccine failures have historically been attributed to physiologic variability among individual animals and breeds, genetic factors, nutritional differences, environmental conditions, the method of inoculation, viral titers at the time of inoculation and challenge exposure, incorrect vaccine administration, and antigenically distinct strains of the orf virus (Musser et al 2012) but this study suggests it is due to the latter. 1. de la Concha-Bermejillo A, Guo J, Zhang Z, et al. Severe persistent orf in young goats. J Vet Diagn Invest 2003;15: Grey EH. Contagious ecthyma in man. Calif Med May;70(5): La Chapelle JM. Biologic causes of occupational dermatoses. Available at: 3_23/fulltext.html.Accessed January Musser JMB, Taylor CA, Guo J, et al. Development of a contagious ecthyma vaccine for goats. Am J Vet Res 2008;69: Musser JMB, Waldron DF, Taylor C. Evaluation of homologous and heterologous protection induced by a virulent field strain of orf virus and an orf vaccine in goats. Am J Vet Res 2012;73(1):86-90.

16 6. Roberson JR, Baird AN and Pugh DG. Diseases of the integumentary system. In: Pugh DG, Baird AN, eds. Sheep and Goat Medicine, 2 nd Edition. Maryland Heights, MO: Elsevier-Saunders,2012; Smith MC and Sherman DM. Skin. In: Goat Medicine, 2nd Edition.Ames, IA:Wiley- Blackwell, 2009;