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Streptococcus suis infections

Streptococcus suis infections

M-L PENRITH AND M M HENTON

GENERAL INTRODUCTION: GRAM-POSITIVE COCCI Streptococcus spp. infections

Introduction

Streptococcus suis is a common and potentially pathogenic commensal organism in pigs that can cause septicaemia, meningitis, purulent arthritis and valvular endocarditis, and is also associated with bronchopneumonia, genital infections and abortions. Sporadic infections with S. suis have been reported in other species including humans.

Outbreaks of disease associated with an alpha-haemolytic Streptococcus were first described in the Netherlands in 1951, followed by the UK in 1954.10, 28 Disease caused by S. suis has been described in most countries where pig production is highly developed, and is regarded as a major problem in the pork industry. Disease incidence is rising,35, 42 apparently in response to increased intensification of pig production. The infection can cause unacceptably high mortality levels among neonates and weaners, but the major economic loss results from high medication costs and reduced growth.

Aetiology

Early isolates were assigned to Lancefield groups R, S, R/S and T, as well as Lancefield group D; groups R, S and R/S were designated as serotypes 1, 2 and 1/2 respectively on the basis of capsular antigens.55 In 1987 the organism was formally described as a species genetically distinct from other streptococci, including Lancefield group D.32 Thirty-four capsular serotypes have subsequently been recognized,14, 15, 16, 23 as well as two intermediate serotypes, 1/255 and 1/14.19 Many more strains within these serotypes have been identified.3, 35 Serotyping, based on capsular antigens, is not possible in all laboratories owing to the complexity of the organism. Not all of the serotypes have been associated with disease.

Streptococcus suis is a catalase negative, facultatively anaerobic, Gram-positive coccus, usually occurring in pairs. It is weakly beta-haemolytic on blood agar. No haemolysis or alpha-haemolysis may be seen after 24 hours of culture, but beta-haemolysis is usually evident after 48 hours of growth. In some cases it may be necessary to scrape away the small grey colonies to observe the haemolysis on the underlying agar.

Streptococcus suis ferments lactose, salicin, trehalose and inulin, but not arabinose, mannitol and sorbitol. Rattinose fermentation is variable. Arginine, esculin and starch are hydrolysed. Growth occurs at 37 °C, but not at 10 °C or 45 °C.

Epidemiology

Disease caused by S. suis has been reported in Europe, North and South America, the Far East, Australia, New Zealand45 and South Africa.20 Most of the serotypes are apparently widespread. Owing to the complexity of the organism, detailed epidemiological studies are unusual. Serotyping of isolates from target organs of diseased pigs, in particular the brain, has indicated that serotype 2 is most often implicated in epidemics worldwide. However, several other serotypes have also been demonstrated to cause epidemics, notably 1, 1/2, 3–8, 9, 10, 14, 15, 17 and 27.12, 19, 33, 34, 39, 49 Serotypes 2, 4 and 14 have been associated with disease in humans.16 Although some serotypes are apparently isolated more frequently from particular age groups, considerable overlap occurs.39 Clinical and pathological manifestations of infection with different strains and serotypes do not differ materially,40 although differences in the frequency and distribution of lesions have been reported.49 During an epidemic, in order to establish the aetiology, it is necessary to isolate the bacterium from diseased organs. Genomic fingerprinting has revealed that clusters of several closely related strains within a serotype may be involved in an epidemic.35 Epidemic strains may persist for long periods in a herd.46 Other strains, and even other serotypes, may be isolated from non-target organs, especially tonsils and nasal cavity, of sick and healthy pigs in the same herd.35 However, infection of herds with multiple serotypes has rarely been reported.42

Intensive pig farming, where large numbers of pigs are in close contact, appears to favour outbreaks of disease caused by S. suis. Early weaning, accompanied by strategic medication, has proved effective in the prevention of many important diseases of pigs1, 4 but does not eliminate S. suis infection.4, 42 The removal of piglets weaned before three weeks of age to another site and the mixing of litters may precipitate S. suis infection,4, 39, 42 because piglets are exposed to different serotypes or strains when litters are mixed at a time when they lose maternally conferred immunity and lack active immunity.47

It is generally supposed that the disease is introduced into herds by carrier pigs.7, 42, 45 Isolation of epidemic strains of a serotype from healthy pigs in an affected herd is, however, apparently rare.35 Horizontal transmission, via the oronasal route, appears to be usual, but some evidence exists for vertical transmission.43

During epidemics, younger pigs are usually affected. Septicaemic S. suis infection has been reported in both neonates and pigs from one to six months of age, with higher mortality among neonates. On ‘high health’ farms where early weaning is practised, mortality among neonates is often between 4 and 14 per cent.46 The organism is usually the primary or sole pathogen in cases of septicaemia and meningoencephalitis. Respiratory infections associated with it occur more commonly in growers and finishers, and are generally mixed infections with other pathogenic bacteria, usually Escherichia coli and Pasteurella multocida. It has been demonstrated that infection with porcine reproductive and respiratory (PRRS) virus can predispose to infection with S. suis type 2.13 Persistent infections are indicated by a relatively high incidence of isolation from lesions of septic arthritis, vegetative valvular endocarditis and pneumonia in apparently healthy slaughter pigs.18, 31 In one abattoir survey, however, isolation of S. suis from healthy as well as diseased lung tissue suggested that this organism had not necessarily caused the lesions observed.36

No clear seasonal pattern of disease is evident, but cold weather has been reported to favour outbreaks.45 Reams et al., in a retrospective study of disease caused by several serotypes, considered seasonal variance to be negligible.39 Their survey indicated a slightly higher overall incidence in autumn and winter, but the most important cause of outbreaks, S. suis serotype 2, was recovered at a constant rate throughout the year. Since the highest incidence of streptococcal infection is in totally enclosed operations, where temperature is usually fairly well controlled, this is perhaps not surprising.

Occurrence of S. suis in other species is sporadic. Streptococcus suis infection in humans appears to be an occupational hazard of pig farmers and handlers, and butchers.11, 25 It usually manifests as meningitis, but death due to recurrent septic shock 11 years after the initial infection has been reported.11 In other species, infection has only rarely been associated with close contact with pigs. Out of 18 cases of extramammary suppurative lesions in ruminants from which S. suis was isolated, only one occurred on a farm on which there were pigs.25 In horses, S. suis isolated from cases of meningitis, septic polyarthritis, subclinical guttural pouch infection, and pneumonia with pleuritis appeared likely to be the primary pathogen, while it also has occurred in mixed infections in cases of pneumonia and dermatitis in cats.9

In these cases there was no known association with pigs. It has also been associated with septicaemia and peritonitis in fallow deer,24 and as a mixed infection with E. coli, causing pneumonia in a young wild boar.8

Pathogenesis

The pathogenesis of S. suis infection has not been fully elucidated. The throat is considered to be the primary site of infection,54 and bacteria apparently colonize the tonsils. Bacteraemia may develop and result in septicaemia, meningitis and interstitial pneumonia, or localization of the bacteria in various sites, leading to such lesions as polyarthritis or vegetative valvular endocarditis. The possibility that meningitis does not always result from septicaemia, but might also occur by extension from the cribriform plate after nasal infection has been raised.6 The balance of evidence, however, favours the role that septicaemia plays in the pathogenesis of the meningitis. In many cases of meningitis, suppurative interstitial pneumonia was also present, which suggests that bacteraemia or septicaemia might have played a role.40 A study in which the pigs were infected intravenously, and were therefore bacteraemic or septicaemic, indicated that S. suis enters the brain in monocytes, and that meningitis induced by S. suis is usually accompanied by choroiditis, which points to the choroid plexus as a possible portal of entry.53 This conclusion is supported by the finding that meningoencephalitic lesions are more severe in the caudal part of the brain after natural infection.40

In the lungs, predisposing or concurrent infections with PRRS virus, Aujeszky’s disease virus or bacteria other than S. suis, including Bordetella bronchiseptica, P. multocida, E. coli and Actinobacillus pleuropneumoniae, appear to be necessary for S. suis to cause bronchopneumonia, although cases of pneumonia from which only S. suis could be isolated have been reported.41

Little is known about the determinants of virulence in S. suis, although a number of potential virulence factors have been recognized.2 One of these, a recently discovered haemolytic factor named suilysin, has been found to confer protection against the development of clinical signs in pigs challenged with homologous strains,26, 27 but is evidently more prevalent in European than in North American strains of S. suis type 2.17 Certain anti-phagocytic factors are believed to occur, and an unidentified factor that inhibits neutrophil activity has been reported.2 Isolates of S. suis serotype 2 that were positive for muramidase-released proteins (MRP) were shown to be more virulent than a MRPnegative strain.50, 51, 52

Clinical signs and pathology

An outbreak of streptococcal infection may be heralded by peracute deaths before clinical signs of disease develop. Piglets that survive longer frequently show fever, anorexia and the nervous signs typical of meningitis, such as incoordination, opisthotonus, nystagmus and paddling in lateral recumbency. In older pigs, the most prominent sign of infection may be pneumonia. Neurological and respiratory signs are rarely combined.40 Joints may be painful and swollen. Reproductive disorders, characterized by returns to service, vulval discharge, and late abortions without mummified foetuses have been reported.33 Vegetative valvular endocarditis is often asymptomatic but may result in heart failure.

At necropsy, the most frequently described lesions are suppurative meningitis, fibrinous to fibrinopurulent polyserositis and fibrinohaemorrhagic bronchopneumonia. Vegetative valvular endocarditis, myocarditis and purulent polyarthritis may also be observed, but these lesions are not consistently present. Arthritis was reported to be the most frequently observed lesion of natural infection with serotype 9, followed by meningitis and pneumonia, mainly interstitial; endocarditis was less frequent.49 The only macroscopically visible lesion in pigs that die suddenly may be meningeal congestion.35 Histopathology reveals exudation of fibrin and neutrophils in the leptomeninges and choroid membranes. In more chronic cases, lymphocytic meningitis is not uncommon,40 but was found in a study to be five times more likely to occur in pigs co-infected with Aujeszky’s disease virus.40 Endothelial lesions of the choroid plexus and vasculitis are generally absent.53 However, pulmonary and cardiac vasculitis have been described.40, 41 Histopathological lesions in organs other than the brain are indicative of purulent inflammation but have mostly been found to be non-diagnostic and correspond with the lesions caused by a variety of other pyogenic bacteria.40 In one study, optic perineuritis was observed.49 Multifocal necrosis in various organs and interstitial nephritis, due to septic embolism, may sometimes occur.40, 49

Diagnosis

A preliminary diagnosis is based on clinical signs and lesions, including histopathological examination that might demonstrate the presence of the organism. Confirmation of the diagnosis depends upon isolation and identification of S. suis from target organs of pigs that have died. Useful specimens for bacteriological examination are brain, cerebrospinal fluid, blood, peritoneal and pleural effusions, internal organs, and synovial membranes and fluid.5 Identification of S. suis is performed by demonstrating the type-specific polysaccharide capsule using hyperimmune rabbit serum, or by direct or indirect immunofluorescent antibody tests on smears.5, 44 The methods of identfication of S. suis have been reviewed.22 Recently, a species-specific polymerase chain reaction (PCR) assay to detect S. suis has been described.38

Serotyping is of value, particularly if vaccination is to be used as a control measure, as cross-reactivity between serotypes is variable and protection is limited. It is also essential for detection of carriers, since nasal and tonsillar swabs will frequently yield isolates of S. suis, but these may be of no significance.

Where more precise data are required, techniques such as genomic fingerprinting are used.3, 35 An enzymelinked immunosorbent assay (ELISA) for the detection of antibodies against serotype 2 has been described.30

Differential diagnosis

Streptococcus suis infections cause a wide variety of clinical signs and lesions, and the differential diagnoses of each manifestation need to be considered. In general, other bacterial septicaemias, especially those that cause polyserositis, polyarthritis and meningitis, as well as bronchopneumonia, are the most important differential diagnoses. The organisms that should be considered are therefore Haemophilus parasuis, E. coli, Mycoplasma hyopneumoniae and P. multocida. The lesions caused by S. suis are more purulent than those of H. parasuis and E. coli. Mycoplasma hyopneumoniae generally produces milder and more chronic lesions. In slaughtered pigs, erysipelas is often incriminated when arthritis and endocarditis are present. In cases of fibrinohaemorrhagic bronchopneumonia, co-infection is likely with other bacteria or with an underlying viral disease, specifically PRRS and Aujeszky’s disease. In South Africa, S. suis has been isolated from lesions of necrohaemorrhagic pneumonia macroscopically suggestive of infection with A. pleuropneumoniae. The lesions were histologically non-specific, and A. pleuropneumoniae was not isolated.21

In cases of acute death, before lesions have developed, a wide variety of viral and bacterial diseases should be considered.

Control

Control is generally effected by prophylactic and therapeutic medication. Prophylactic medication has not been successful in early weaning operations.42 In-feed medication has been postulated as the most cost-effective way of reducing the incidence of streptococcal meningitis in a herd.29 Penicillin is usually the drug of choice for treatment and control, but resistance has increasingly been reported.37, 39, 48 In a comparative study, trimethoprim-sulphamethoxazole was found to be effective against most isolates.48

Vaccination may be effective, but problems have been encountered because of the wide variety of serotypes and strains involved. Autogenous vaccines can limit outbreaks, but may fail unless they are prepared from the epidemic strains involved. Failure of autogenous bacterins to elicit an appropriate immune response has also been recorded.42 As knowledge of the organism increases, the possibilities for improved vaccines based on virulence factors, for example suilysin, should emerge.26, 27 Studies so far, however, indicate that such virulence factors may vary from one region to another. Suilysin was found to be far more prevalent in European than in North American isolates.17

References

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