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Home , Burkholderiaceae, Burkholderia mallei, Pasteurellaceae, Taylorella, Taylorella equigenitalis

18 Bacterial diseases Bacterial diseases 19

Burkholderia mallei: ‘’ Clinical presentation 13 Hypopyon, suppurative uveitis. The anterior eye chamber 13 Phylum BXVII Clinical signs include febrile episodes, cough, blood- is blurred with specks of a fibrinopurulent exudate. From Class II /Family encrusted material on nostrils, inflammatory nodules this foal cepacia was isolated. Members of the / I Burkholderia: Gram- and ulcers developed in the nasal passages with a B. cepacia complex are regarded as opportunistic . negative aerobic rods and cocci sticky yellow discharge, characteristic stellate scars in the nasal septum, purulent nasal discharge, Definition/Overview enlargement of submaxillary lymph nodes, chronic Glanders is an ancient, highly fatal, and usually lymphangitis, skin abscessation, progressive debility, chronic respiratory disease of solipeds caused orchitis, and dyspnoea associated with interstitial by (formerly . Furthermore, apparent neurological mallei) with being accidental hosts. The degeneration is seen in acute glanders (Lopez et al. diagnosis is based on the presence of characteristic 2003). Life expectancy was judged likely to have stellate scars in the nasal septum and a positive been less than 12 hours in B. mallei inoculated reaction to the mallein test, combined with a positive due to subsequent pulmonary oedema (Lopez culture of B. mallei. infections are often fatal et al. 2003). if untreated. Differential diagnosis Hydrolysis probe-based real-time PCR using the Public health significance Aetiology The differential diagnosis includes various causes of uneven distribution of type III Humans are accidental hosts of B. mallei and the B. mallei is a facultative rod-shaped Gram-negative and dyspnoea (see p. 262). system genes afforded considerable improvements majority of cases have been the result of nonspore-forming, nonmotile, intracellular in the specificity and rapidity of the diagnosis of occupational contact with infected horses. Whereas that can invade, survive, and replicate in epithelial Diagnosis B. pseudomallei, B. mallei, and B. thailandensis, equines are generally infected orally, the primary and phagocytic cell lines (Ribot & Ulrich 2006). It is The presence of stellate scars in the nasal septum is and allows rapid discrimination from opportunistic route of infection in humans is contamination of skin an obligate pathogen whose natural hosts are regarded as pathognomonic. B. mallei can be pathogens such as members of the B. cepacia abrasions or mucous membranes with nasal horses, donkeys, and , but infections can also cultured easily from purulent nasal discharge and the complex (13), that routine diagnostic laboratories discharge or skin lesion exudate from an infected occur in felines, camels, and goats. in complement fixation test can be used for serology. are more likely to encounter (Thibault et al. 2004). animal (Schell et al. 2007). Person-to-person spread B. mallei is multifactorial and several virulence Furthermore, the mallein test can also be used to of B. mallei is extremely rare. In humans, glanders determinants have been identified and characterized identify infected horses; purulent exudate in the eye Pathology is characterized by initial onset of fever, rigors and (Schell et al. 2007). Seventeen distinct ribotypes were associated with blepharospasm of a glanderous B. mallei infection results in pyogranulomatous and malaise, culminating in a rapid onset of pneumonia, identified from human and equine infections (Harvey animal 24–48 hours following subconjunctival necrotic pulmonary nodules, and ulcerative nodular bacteraemia, pustules and , leading to death & Minter 2005). inoculation is regarded as a positive test result. skin and respiratory mucosal lesions with in 7–10 days without treatment. The Alternatively, the intracutaneous mallein test can be characteristic white stellate scars in the nasal septum. course of infection is dependent on the route of Epidemiology used with an increase in rectal temperature and a Histologically, lung lesions comprise liquefactive exposure. Direct contact with the skin can lead to a Glanders is endemic in Africa, Asia, the Middle East, swelling at the point of injection regarded as a necrosis including and surrounding localized cutaneous infection. Inhalation of aerosol and Central and South America. Carriers that have positive test result (Arun et al. 1999). When tested epithelioid and fibrosis. The dermal or dust containing B. mallei can lead to septicaemic, made an apparent recovery from the disease are the comparatively with Dutch PPD mallein as standard, disease of ulcerations including lymphangitis is pulmonary, or chronic infections of the muscle, liver, most important source of infection, as the pathogen trichloroacetic acid-precipitated proteins were named ‘farcy’ (Jubb et al. 2007). Remarkably, and spleen. The disease has a 95% case fatality rate does not survive for more than 6 weeks outside the comparable to Dutch PPD mallein in potency and Streptococcus equi subsp. zooepidemicus was for untreated septicaemia infections and a 50% case (Lehavi et al. 2002). innocuity, whereas ammonium sulphate-precipitated isolated from the brain of all B. mallei inoculated fatality rate in antibiotic-treated individuals proteins elicited nonspecific reactions (Verma et al. horses (Lopez et al. 2003). (Mandell et al. 1995). Burkholderia infections are Pathophysiology 1994). difficult to treat with and no Equines are generally infected orally (Schell et al. Competitive enzyme-linked immunosorbent assay Management/Treatment exists (Whitlock et al. 2007). 2007). Following penetration of the mucosae, the (cELISA) test specificity for B. mallei was 99%. Horses with a tentative diagnosis of glanders should pathogen is spread via the lymphatic tissues. Concordance and kappa value between the be isolated to prevent possible human exposure. complement fixation (CF) and the cELISA Treatment should not be attempted as the pathogen Incubation period procedures for the serodiagnosis of B. mallei has important public health significance and The incubation period varies from 1 to 2 days infection in experimentally exposed horses were glanders is a reportable disease. following intratracheal deposition, with rectal 70% and 0.44, respectively (Katz et al. 2000). The temperatures increased to above 40°C (Lopez et al. cELISA offers the possibility for automatization, can 2003). be applied to noncomplement fixing sera, and used for various host although the complement fixation test (CFT) is internationally mandatory for testing of equine sera for the absence of glanders to date (Sprague et al. 2009). 20 Bacterial diseases Bacterial diseases 21

Burkholderia pseudomallei: Incubation period Hydrolysis probe-based real-time PCR methods 15 Phylum BXVII Spirochaetes This is not established in the equine species yet. The using the uneven distribution of type III secretion Class II Betaproteobacteria/Family incubation period in man from defined inoculating system genes afford considerable improvements Burkholderiaceae/Genus I Burkholderia: Gram- events was previously ascertained as 1–21 (mean 9) in the specificity and rapidity of the diagnosis of negative aerobic rods and cocci days (Currie et al. 2000b). B. pseudomallei, B. mallei, and B. thailandensis and allow rapid discrimination from opportunistic Definition/Overview Clinical presentation pathogens, such as members of the B. cepacia Melioidosis is a rare disease caused by Burkholderia Clinical signs include fever, septicaemia, oedema, complex (15, 16), that routine diagnostic labora - pseudomallei (formerly Pseudomonas pseudomallei) colic, diarrhoea, and lymphangitis of the legs. A case tories are more likely to encounter (Thibault et al. characterized by an intracellular life cycle. Both of acute meningoencephalomyelitis caused by 2004). humans and (including birds, crocodiles, infection with B. pseudomallei has been described and kangaroos) are susceptible to melioidosis with associated with inability to stand, opisthotonus, Pathology both latency and a wide range of clinical facial paralysis (14) and nystagmus, rapidly Multiple abscesses in most organs are characteristic manifestations. Some species may develop progressing to violent struggling (Ladds et al. 1981). of the disease. The encapsulated nodules with 15 Necrosuppurative bronchopneumonia in a foal. The melioidosis only if immunocompromised. Sheep, caseous centres are composed of necrosis, cranioventral lung field is hyperaemic, consolidated, and firm. goats, and horses are particularly susceptible, Differential diagnosis neutrophils, lymphocytes, and epithelioid macro - Lesions resemble pulmonary lesions in melioidosis. From this but zoonotic transmission to humans is The differential diagnosis includes various causes of phages. In a case of acute meningoencephalo myelitis foal Burkholderia cepacia was isolated. extremely unusual (Neubauer et al. 1997, Choy et al. internal abscessation (without characteristic stellate gross examination revealed malacia and 2000). Melioidosis has important public health scars in the nasal septum as seen in B. mallei) (see p. haemorrhage in the medulla oblongata and adjacent significance and is a reportable disease. 262). Listeriosis should be considered in a case of spinal cord. Microscopically there were disseminated . focal neutrophilic accumulations in affected areas, 16 Aetiology perivascular cuffing with mononuclear cells and B. pseudomallei is a Gram-negative, bipolar-staining, Diagnosis lymphocytes, and marked oedema. Intracellular pleomorphic, motile , which is principally an B. pseudomallei can be cultured easily from purulent were identified in sections stained by the environmental saprophyte responsible for nasal discharge. The diagnosis is based on a positive Giemsa method (Ladds et al. 1981). melioidosis. reaction to the mallein test combined with a positive culture. Management/Treatment Epidemiology Horses with a tentative diagnosis of melioidosis This saprophyte inhabitant of telluric environments should be isolated to prevent possible human is mainly encountered in southeast Asia and northern exposure. Treatment should not be attempted as the Australia, but is sporadically isolated in subtropical disease has important public health significance. and temperate countries (White 2003). Melioidosis Furthermore, the ubiquitous bacterium is has become an increasingly important disease in characterized by remarkable insensitivity to endemic areas such as northern Thailand and antimicrobial drugs. For instance, B. pseudomallei is 16 Necrosuppurative bronchopneumonia in a foal. The Australia (Currie et al. 2000a). In endemic areas, the intrinsically resistant to and cranioventral lung lobes show on cut section a well-delineated positive rates of antibodies against B. pseudomallei macrolides, mostly due to AmrAB-OprA efflux hyperaemic area enclosing pale yellow, variably sized, in humans, horses, oxen, and pigs were 4–15%, 9– 14 pump expression (Trunck et al. 2009). caseating, coagulative, necrosuppurative sequesters of 18%, 7–33%, and 35%, respectively (Li et al. 1994). Immunization with heat-inactivated B. pseudo- remnant pulmonary parenchyma. Lesions resemble mallei cells provided the highest levels of protection pulmonary lesions in melioidosis. From this foal Burkholderia Pathophysiology against either melioidosis or glanders, indicating cepacia was isolated. Following ingestion via contaminated soil or faeces, longer-term potential for heat-inactivated bacteria a diverse assortment of virulence factors (quorum to be developed as against melioidosis and sensing, type III secretion system, glanders (Sarkar-Tyson et al. 2009). and other surface ) allows B. pseudomallei to become an effective opportunistic Public health significance pathogen; its intracellular life cycle also allows it to Melioidosis has important public health significance avoid or subvert the host (Adler et and is a reportable disease. It is a life-threatening al. 2009, Wiersinga & van der Poll 2009). The BoaA disease that is mainly acquired through skin and BoaB genes specify adhesins that mediate inoculation or pulmonary contamination, although adherence to epithelial cells of the human respiratory other routes have been documented (Neubauer et al. tract. The BoaA gene product is shared by B. 1997). Primary skin melioidosis occurred in 12% of (Gibney et al. 2008). Severe septicaemia secondary pseudomallei and B. mallei, whereas BoaB appears human patients. Secondary skin melioidosis to melioidosis carries a high mortality. Although to be a B. pseudomallei-specific adherence factor (multiple pustules from haematogenous spread) was melioidosis can involve most tissues and organs, (Balder et al. 2010). present in 2%. Patients with primary skin pericardial involvement is rare (De Keulenaer et al. melioidosis were more likely to have chronic 2008). Of human cases, 46% were bacteraemic and 14 Facial paralysis is associated with equine melioidosis. presentations (duration of a minimum of 2 months) 19% died (Currie et al. 2000a). 22 Bacterial diseases Bacterial diseases 23

Bordetella bronchiseptica Incubation period Phylum BXVII Spirochaetes Not established in the equine species yet. Class II Betaproteobacteria/Family III Alcanigenaceae/Genus III Bordetella: Gram- Clinical presentation negative aerobic rods and cocci Clinical presentation includes respiratory disease in 17 foals (17) (Koehne et al. 1981), coughing in Definition/Overview Thoroughbred racehorses (Christley et al. 2001), The opportunistic bacterium Bordetella bronchi - bronchopneumonia (Saxegaard et al. 1971), septica is a rare cause of acute respiratory disease abortion (Mohan & Obwolo 1991), and infertility and abortion/infertility. (Mather et al. 1973). B. parapertussis did not grow in tracheobronchial washing from a (Porter & Aetiology Wardlaw 1994). are Gram-negative bacteria with an important role as primary or opportunistic, mainly Differential diagnosis respiratory, pathogens in domestic and wild animals. The differential diagnosis includes various causes of Some species of Pasteurellaceae cause severe diseases fever and dyspnoea (see p. 262). with high economic losses in commercial animal husbandry and are of great diagnostic concern Diagnosis (Dousse et al. 2008). Sixteen distinct ribotypes were Diagnosis primarily depends on culture of the identified in B. bronchiseptica strains (Register et al. bacterium from tracheobronchial washing samples 1997). Four main types of variation of the combined with clinical signs. Analysis of B. bronchiseptica lipopolysaccharide (LPS) are tracheobronchial washing samples for known apparent: (1) heterogeneity of the core, (2) presence Bordetella nutrients revealed concentrations of 17 Suppurative bronchopneumonia in a foal. Cranioventral pulmonary hyperaemia and or absence of 0-chains, (3) differences at the level of amino acids and nicotinic acid averaging 0.35 mM consolidation. A primary viral respiratory infection (herpesvirus, influenza virus) can be the hinge region between the 0-chain and the core, and 0.56 µg/ml, respectively (Porter & Wardlaw complicated by opportunistic bacteria like Streptococcus spp., , Klebsiella and (4) differences in the association with other cell 1994). pneumoniae, Rhodococcus equi, and Bordetella bronchiseptica. surface constituents. Isolates from different animal species did not show significant differences in their Pathology patterns of reactivity with monoclonal antibodies Common lesions caused by B. bronchiseptica include (LeBlay et al. 1997). a catarrhal to suppurative bronchopneumonia and a (sero)fibrinous pleuropneumonia. These are usually Epidemiology opportunistic secondary infections preceded by viral Glucose nonfermenting Gram-negative bacilli have infections in juvenile animals. been recognized as opportunistic pathogens of humans. The most common veterinary glucose Management/Treatment nonfermenting Gram-negative bacilli were Treatment of diseased animals is supportive and , Acinetobacter calcoaceticus, specific treatment should be based on in-vitro B. bronchiseptica, and Pseudomonas pseudoalcaligenes. antimicrobial susceptibility testing. Of all clinical veterinary specimens submitted for cultures, 10% contained nonfermenters (Mathewson Public health significance & Simpson 1982). B. bronchiseptica was isolated The absence of smooth-type LPSs appears to be from bronchial lavage specimens in distal respiratory rather frequent in human isolates, since long-chain tract disease (nasal discharge, cough, pneumonia) in LPSs were detectable in only 52% of human isolates, 13% of foals (1–8 months old) (Hoffman et al. whereas 94% of animal isolates contained molecules 1993). of that type (Le Blay et al. 1997). B. bronchiseptica might have some public health significance and its Pathophysiology zoonotic risk should be minimized. Either B. bronchiseptica does not persist inside animals or susceptible animals possess specific receptors for smooth-type LPSs, in contrast to man (Le Blay et al. 1997). 24 Bacterial diseases Bacterial diseases 25

Taylorella equigenitalis: CONTAGIOUS latest CEM occurrence was warranted (Timoney 18 19 EQUINE METRITIS 2011). Among stallions examined in Slovenia, 92% Phylum BXVII Spirochaetes were negative to T. equigenitalis by either PCR or Class II Betaproteobacteria/Family III culture (Zdovc et al. 2005). In comparison, from Alcanigenaceae/Genus XI : Gram- 1999 through 2001, four out of 120 imported negative, microaerophilic, fastidious slow-growing European stallions tested positive for CEM at a coccobacilli quarantine facility in Darlington, MD, USA (Kristula & Smith 2004). Samples from mares with no clinical Definition/Overview signs of CEM submitted for conventional culture Contagious equine metritis (CEM) caused by were negative for T. equigenitalis, but in the PCR is a highly contagious disease assay 49% were positive for Taylorella DNA. The that is transmitted venereally. The carrier state high incidence of Taylorella in horse populations occurs in the mare and the stallion and carrier without apparent clinical signs of CEM, the animals are frequently the source of infection for occurrence of incidental clinical cases, and the new outbreaks (Timoney 1996). known variability between strains indicate that Taylorella was endemic in the horse population Aetiology (Parlevliet et al. 1997). T. equigenitalis is a Gram-negative, microaerophilic, 18, 19 Taylorella asinigenitalis resembling T. equigenitalis fastidious slow-growing with Pathophysiology might be isolated from the urethral fossa (arrow) in horses. -sensitive and -resistant biotypes CEM is transmitted by direct or indirect venereal (Timoney 1996). Isolates of T. equigenitalis obtained contact. The invasiveness of T. equigenitalis strains from European horses analysed by pulsed-field gel seemed to be associated with the contagiousness of electrophoresis (PFGE) were classified into 18 the infection, whereas the replication index seemed genotypes (Kagawa et al. 2001). High sequence to be associated with the severity of the symptoms similarity (99.5% or more) was observed throughout of contagious equine metritis (Bleumink-Pluym et al. isolates from Japan, Australia, and France, except 1996). from nucleotide positions 138 to 501 where substitutions and deletions were noted (Matsuda et Incubation period al. 2006). A phylogenetic analysis revealed a position Horses challenged with T. equigenitalis showed as for identification of these species. The cervical swabs of 84% (Wood et al. 2005). of T. equigenitalis in the beta subclass of the class seroconversion from day 11 post-inoculation (Katz T. asinigenitalis had a low minimum inhibitory There was close agreement between CFT and apart from the position of Haemo - & Geer 2001). concentration (MIC) of (≤1 µg/ml) but a ELISA methodologies during the post-exposure philus influenzae, which belongs in the gamma high MIC of streptomycin (>16 µg/ml) (Båverud et time period used to detect CEM serodiagnostically subclass of Proteobacteria. A close phylogenetic Clinical presentation al. 2006). in regulatory animal health testing programmes. relationship among T. equigenitalis, Alcaligenes CEM can be the cause of short-term infertility Unlike the CFT, which requires an overnight xylosoxidans, and Bordetella bronchi septica was sometimes associated with mucopurulent discharge Diagnosis incubation step, the ELISAs are more convenient detected (Bleumink-Pluym et al. 1993). Lipo - and, very rarely, abortion in mares (Fontijne et al. Diagnosis is based primarily on culture of and can be completed in 3 hours (Katz & Geer O-PS could be a specific marker for 1989). Unlike the mare, stallions exposed to T. the bacterium from its predilection sites in 2001). identification and differentiation of T. equigenitalis equigenitalis do not develop clinical signs of disease the reproductive tract of the mare and the stallion and T. asinigenitalis, and provide the basis for the (Timoney 1996). It has been concluded that T. (18, 19) (Timoney 1996). However, the rate of Pathology development of specific detection assays for equigenitalis is of limited significance in horse T. equigenitalis detection was higher with PCR than Macroscopically no vaginal lesions are apparent; the T. equigenitalis (Brooks et al. 2010). breeding (Parlevliet et al. 1997). with the classic bacteriological examination. PCR is endometrial mucosa may be swollen and corrugated especially valuable in cases of intensive bacterial and with a scant mucopurulent exudate. Histology of Epidemiology Differential diagnosis fungal contamination of swabs where the isolation uterine biopsies might reveal a mild endometritis, CEM has given rise to international concern since it Atypical (-origin) Taylorella spp. infections of T. equigenitalis usually fails (Zdovc et al. 2005). A characterized by interstitial mucosal oedema and a was first recognized as a novel venereal disease of should be considered as a differential diagnosis direct-PCR assay was developed for the rapid mild inflammatory infiltrate composed of equids in 1977. The first known outbreak of CEM in of equine infertility in mares (Katz et al. 2000). detection of T. equigenitalis in equine genital swabs neutrophils; later plasma cells may be more evident the USA was in Kentucky in 1978. For some time T. asinigenitalis, resembling T. equigenitalis, was without need for a preliminary step of DNA (Jubb et al. 2007). none of the subsequent outbreaks impacted recently isolated from the urethral fossa, urethra, extraction or bacterial isolation (Duquesne et al. significantly on the horse industry. That changed and penile sheath of a 3-year-old stallion of the 2007). The assay is also able to discriminate between Management/Treatment dramatically in 2008, however, after the discovery of Ardennes breed when it was routinely tested for T. equigenitalis and T. asinigenitalis (Wakeley et al. Aggressive systemic antibiotic therapy accompanied some 1,005 exposed and carrier stallions and mares CEM. However, the colony appearance, the slow 2006). by routine topical therapy might be required to treat in 48 states. Neither clinical evidence of CEM nor growth rate, and the results in the API ZYM test In chronically infected mares, the organism was CEM-positive stallions (Kristula & Smith 2004). decreased pregnancy rates were reportedly a feature differed slightly from those of T. equigenitalis. detectable in the clitoral swabs of nearly 93%, but in infected or exposed mares. In light of these Sequence analysis of 16S rRNA genes was shown to in the cervical swabs of only 31%. In contrast, in Public health significance findings, the question arose as to whether or not the be a reliable tool for differentiation of donkey- acutely infected mares, the organism was detectable Not convincing yet. considerable expense incurred in investigating the related T. asinigenitalis from T. equigenitalis, as well in the clitoral swabs of nearly 69%, but in the