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Streptococcus porcinus infections

Streptococcus porcinus infections

M-L PENRITH AND M M HENTON

GENERAL INTRODUCTION: GRAM-POSITIVE COCCI Streptococcus spp. infections

Introduction

Streptococcus porcinus is widely distributed in animals but has a predilection for pigs, in which it sometimes causes disease. The best documented disease manifestation is abscessation, generally of the lymph nodes of the head and neck. The condition was first described in Rumania in 1937, but appears to be rather rare in Europe and only of real significance in North America.27 Septicaemia, pneumonia, meningitis, enteritis, haemorrhagic tracheitis, arthritis and abortions in pigs have been associated with S. porcinus infections.8, 12, 19 Isolates from bovine milk have been associated with mastitis.8 Disease in humans caused by S. porcinus has not been reported. In South Africa, most isolates from pigs are incidental and involve the upper respiratory tract (nasal mucosa and tonsils), but some have been associated with pneumonia, septicaemia, arthritis, and, rarely, abortion.

Aetiology

Streptococcus porcinus comprises Lancefield serological groups E, P, U and V,8 and can be distinguished from other β-haemolytic streptococci that affect pigs by a combination of biochemical tests. Streptococcus porcinus, S. agalactiae and a few strains of S. suis are positive for the Camp test, all other Streptococcus spp. that affect pigs being negative.26 Streptococcus porcinus produces acid from mannitol and sorbitol, whereas S. suis, S. agalactiae and S. dysgalactiae subsp. dysgalactiae (S. equisimilis) are all negative. Streptococcus porcinus, S. dysgalactiae and S. agalactiae produce acid from ribose, whereas S. suis does not, and conversely, inulin is fermented by S. suis but not by S. porcinus, S. dysgalactiae or S. agalactiae. 13 If cross-reactions with Lancefield type B reagents are problematic, the Voges-Proskauer and pyrrolydonylarulamidase tests are used to distinguish between S. porcinus (both positive) and S. agalactiae (both negative).26 Typical growth characteristics include a broader haemolysis zone than that of other porcine species and homogeneous growth in broth,in which other species form a deposit with clear or partially clear supernatant.14

Epidemiology

Streptococcus porcinus is most frequently isolated from pigs. Asymptomatic carrier animals can harbour the organisms in their nasal mucosa and palatine tonsils for as long as 21 months after initial exposure.5, 22 Streptococcus porcinus isolated from various organs, notably the lower respiratory tract and the genital tract of pigs, is not necessarily associated with a disease process.14

Lymphadenitis is the only condition of importance caused by S. porcinus. The serological group most frequently isolated from affected lymph nodes is Lancefield group E.14 Outbreaks may result in large-scale condemnations at abattoirs,28 and condemnation of up to 94 per cent of heads as a result of involvement of mandibular, retropharyngeal and/or parotid lymph nodes in the USA has been reported.17, 22 Association of S. porcinus with abscesses in pigs has been reported rarely in Europe and the Canary Islands.20, 27 Other manifestations have been sporadic or unique. Group P was isolated in pure culture from cases of haemorrhagic tracheitis in pigs observed at slaughter12 and group V from aborted foetuses.19

Transmission is generally via aerosols or drinking water, feed and soil contaminated by oral and nasal secretions.6, 27, 29 Carrier animals have been incriminated in transmission but acutely ill and convalescent pigs are mainly responsible for spread.5, 16, 27 The introduction of healthy adult pigs from herds free of infection into infected herds can result in disease within a few weeks.

Reports on the age at which pigs are most susceptible to infection vary. Pigs younger than eight weeks and older than two-and-a-half years are less susceptible.2, 17, 22 Susceptibility increases from four to five weeks of age,27presumably owing to a decrease in maternally acquired antibodies, and pigs between the ages of 9 and 14 weeks are most susceptible.2, 21 Piglets younger than five days appear to be refractory to infection, even in the absence of maternal antibody.27

Pathogenesis

Bacteria penetrate the tonsillar or pharyngeal mucosa and reach the regional lymph nodes via lymphatics. The mandibular lymph nodes are most commonly affected, but retropharyngeal and parotid lymph nodes are also sometimes involved, and occasionally the inguinal and popliteal lymph nodes.4, 27 In experimentally induced streptococcal lymphadenitis, invasion of lymph nodes by streptococci and neutrophils occurs within two hours of infection and is followed by the development of miliary abscesses in lymph nodes within seven days, after which progressive enlargement of the abscesses occurs.4, 11 Natural infection follows a similar course.27 The course of streptococcal lymphadenitis, from infection to resolution, is approximately two months.27 The pathogenesis of manifestations of disease other than lymphadenitis has not been studied.

Clinical signs and pathology

Pigs infected with S. porcinus develop fever from 8 to 15 days after exposure that may persist for five days.6 A transitory fever may, however, develop as early as 48 hours post-infection, which is accompanied by neutrophilia and decreased feed intake.27 During the febrile period pigs may evidence mild depression, anorexia, and constipation or transitory diarrhoea.6, 27 Lymph node swelling may be felt by deep palpation from 14 days post-infection, with abscesses becoming evident at 21 to 28 days. Necrosis of the skin over the abscesses follows at about five weeks, with rupture at seven to eight weeks and healing after ten weeks.5, 27 Abscesses may be multiple and reach 100 mm in diameter, but in many cases no signs of disease are evident in the herd, and the presence of abscesses is only revealed at slaughter inspection.5, 20

Typical lesions are well encapsulated abscesses that contain greenish, viscous to semi-fluid, non-odorous pus.5, 27 Histopathological examination reveals multifocal necrosis with severe neutrophil infiltration, moderate depletion of lymphoid follicles, and small Gram-positive cocci forming chains.20 Severe haemorrhagic tracheitis, mainly affecting the dorsal tracheal mucosa, has been described in a survey of lesions found in slaughtered pigs.12

In a report on S. porcinus as a cause of abortion, it was stated that foetuses were aborted at 52, 88 and 111 days in a fresh condition. Foetuses aborted at 111 days revealed subcutaneous oedema, and reddish transudate in the thorax; internal organs were normal.19 Streptococcus porcinus was isolated in pure culture from the lungs, liver, spleen, kidneys and stomach.19

Diagnosis

The diagnosis of streptococcal lymphadenitis is based on the clinical signs and pathology, and confirmed by bacteriological isolation of S. porcinus from the pus of abscesses.

The presence of small, chain-forming, Gram-positive cocci in purulent lesions will strengthen the suspicion. A direct fluorescent antibody test may be used not only to identify the organism in smears of cultures and exudates, but also to detect the organism in tonsils of carriers.25 DNA fingerprinting using the 16S ribosomal fingerprint pattern has been suggested as a specific method of identifying S. porcinus. 1 Serological tests, including haemagglutination, tube and plate agglutination, microtitration agglutination, and precipitation have been applied in attempts to detect infected pigs, but none has proved to be a completely reliable diagnostic tool, as cross-reactions with antibodies to other groups of streptococci and other complicating factors occur.3, 16, 18, 28 Cross-reaction with reagents used to identify group B Streptococcus is common.26

Differential diagnosis

Other bacteria which can cause cervical lymphadenitis are: Streptococcus dysgalactiae subsp. dysgalactiae, Rhodococcus equi, Trueperella pyogenes, Pasteurella multocida, Escherichia coli, Mycobacterium spp.,4, 5 and Corynebacterium pseudotuberculosis. 20 Confirmation of S. porcinus infection depends upon the isolation and identification of the organism from abscesses. Bacteriological means are also required to distinguish S. porcinus from more common causes of porcine abortion and other disorders.

Control

Antimicrobial treatment of clinical cases is unrewarding.21, 27 It does not eliminate carriers, and it has been suggested that high levels of tetracyclines in feed, which has proved successful in the prevention of the disease, might, when applied to clinical cases, actually augment development and subsequent rupture of abscesses18 Individual animals suffering from large abscesses can be treated surgically.

Prevention in herds is generally by the addition of antimicrobials, usually tetracyclines, to feed. The addition of chlortetracycline at 125 g/ton of feed for six weeks after weaning will significantly reduce the prevalence of the disease, provided that the strain is not resistant to the medication.10 Simultaneous treatment of all the breeding stock with chlortetracycline at 400 g/ton of feed, and of all the pigs to be marketed with 200 g/ton for one month, also resulted in fewer abscesses in all groups,23, 24 but this régime is expensive and not in line with current tendencies to attempt to reduce the use of antimicrobials in food animals. Early weaning, with the separation of the piglets during the period when full protection from maternally derived antibodies can be expected (i.e. before four weeks of age) probably offers a better option.27 Other managemental procedures, such as reducing the number of pigs in a pen and not mixing pigs of different origin during the postweaning and finishing period, are useful in reducing the prevalence of the disease.17

Vaccination is not widely used,27 but an avirulent, immunogenic oral vaccine (Jowl Vac, Fort Dodge Laboratories, Fort Dodge, Iowa) has been reported to offer protection at a rate of 88 to 100 per cent.7, 9, 15 No vaccine is available in South Africa.

References

  1. ABDULMAWJOOD, A., WEISS, R. & LÄMMLER, C., 1998. Species identification of Streptococcus porcinus by restriction fragment length polymorphism analysis of 16S ribosomal DNA. Research in Veterinary Science, 65, 85–86.
  2. ARMSTRONG, C.H., BOEHM, P.N. & ELLIS, R.P., 1970. Experimental transmission of streptococcic lymphadenitis (jowl abscess) of swine. American Journal of Veterinary Research, 1, 823–829.
  3. ARMSTRONG, C.H., WOOD, R.C. & WESSMANN, G.E., 1982. A microtitration agglutination test for detecting group E Streptococcus infection in swine. Canadian Journal of Comparative Medicine, 46, 201–205.
  4. COLLIER, J.R., 1956. Streptococcic lymphadenitis of the pharyngeal region of swine. Journal of the American Veterinary Medical Association, 129, 543–548.
  5. COLLIER, J.R., 1965. Abscesses of swine. Journal of the American Veterinary Medical Association, 146, 344–347
  6. COLLIER, J.R. & NOEL, J., 1974. Streptococcal lymphadenitis of swine: Prolonged carrier state and bacterial dynamics in the introduction of disease. Journal of the American Veterinary Medical Association, 35, 799–801.
  7. COLLIER, J.R., SHAFFER, H.D. & SCHULTZ, M., 1976. Evaluation of a vaccine for control of streptococcic lymphadenitis of swine. Journal of the American Veterinary Medical Association, 169, 697–699
  8. COLLINS, M.D., FARROW, J.A.E., KATIC, V. & KANDLER, O., 1984. Taxonomic studies on streptococci of serological groups E, P, U and V: Description of Streptococcus porcinus sp. nov. Systematic and Applied Microbiology, 5, 402–413.
  9. ENGELBRECHT, H. & DOLAN, M., 1968. Vaccination of swine for jowl abscesses. Veterinary Medicine/Small Animal Clinician, 63, 872–875.
  10. ERICKSON, E.D., 1993. Streptococcal disease. In: HOWARD, J.L. (ed.). Current Veterinary Therapy: Food Animal Practice 3. Philadelphia: W.B. Saunders Co.
  11. GOSSER, H.S. & OLSON, L.D., 1973. Chronologic development of streptococcic lymphadenitis in swine. American Journal of Veterinary Research, 34, 77–82.
  12. HINTENDORFER, F., KÖFER, J. & HAHN, G., 1990. Streptokokkenisolate aus Untersuchungsmaterial von Schweinen in der Steiermark. Wiener Tierärtzliche Monatschrift, 77, 153–161
  13. HOLT, J.G., KRIEG, N.R., SNEATH, P.H.A., STALEY, J.T. & WILLIAMS, S.T., 1994. Bergey’s Manual of Determinative Bacteriology, 9th ed. Baltimore, Philadelphia, Hong Kong, London, Münich, Sydney, Tokyo: Williams and Wilkins.
  14. HOMMEZ, J., DEVRIESE, L.A., CASTRYCK, F., & MIRY, C., 1991. Beta-haemolytic streptococci from pigs: Bacteriological diagnosis. Journal of Veterinary Medicine B, 38, 441–444.
  15. ISAKI, L.S., BAINEY, M.H. & VAN PATTEN, L.K., 1973. Response of vaccinated swine to group E Streptococcus exposure. Cornell Veterinarian, 63, 578–588.
  16. MILLER, R.B. & OLSON, L.D., 1983. Distribution of abscesses and shedder state of swine inoculated with group E streptococci via routes other than oral. American Journal of Veterinary Research, 44, 937–944.
  17. MILLER, R.B. & OLSON, L.D., 1983. Frequency of jowl abscesses in feeder and market swine exposed to group E streptococci as nursing pigs. American Journal of Veterinary Research, 44, 945–948
  18. OLSON, L.D., MILLER, R.B. & SCHLINK, G.T., 1994. Treatment of group E streptococci-induced lymphadenitis in swine by feeding various concentrations of chlortetracycline: Relation of antibody with prevalence of abscesses. American Journal of Veterinary Research, 55, 650–653
  19. PLAGEMANN, O., 1988. Streptococcus porcinus ? als Abortursache beim Schwein. Journal of Veterinary Medicine B, 35, 770–772.
  20. REAL, F., FERRER, O. & RODRIGUEZ, J.L., 1992. Purulent streptococcal lymphadenitis in swine. The Veterinary Record, 131, 151–152
  21. SCHMITZ, J.A. & OLSON, L.D., 1972. Susceptibility of swine of various ages to streptococcic lymphadenitis. American Journal of Research, 33, 1995–2001.
  22. SCHMITZ, J.A. & OLSON, L.D., 1973. Transmission of streptococcic lymphadenitis by carrier swine. American Journal of Veterinary Research, 34, 189–190
  23. SCHMITZ, J.A. & OLSON, L.D., 1973. Prevention of streptococcal lymphadenitis in swine. Effectiveness of medication with chlortetracycline and isolation from other swine in an infected herd. Journal of the American Veterinary Medical Association, 162, 55–57.
  24. SCHMITZ, J.A. & OLSON, L.D., 1973. Prevention of streptococcal lymphadenitis in swine: Effectiveness of selected antibiotics and a modified live-GES vaccine. Journal of the American Veterinary Medical Association, 162, 58–60.
  25. SCHUELER, R.L., MOREHOUSE, L.G. & OLSON, L.D., 1973. A direct fluorescent antibody test for identification of group E streptococci. Canadian Journal of Comparative Medicine, 37, 327–329.
  26. THOMPSON, T. & FACKLAM, R., 1997. Cross-reactions of reagents from streptococcal grouping kits with Streptococcus porcinus. Journal of Clinical Microbiology, 35, 1885–1886.
  27. WESSMANN, G.E., 1986. Biology of the group E streptococci: A review. Veterinary Microbiology, 12, 297–328.
  28. WESSMANN, G.E., SHUMAN, R.D., WOOD, R.L. & NORD, N., 1971. Swine abscesses caused by Lancefield’s group E streptococci. IX. Comparison of the precipitation, haemagglutination and agglutination tests for their detection. Cornell Veterinarian, 61, 400–415.
  29. WOOD, R.L. & WESSMANN G.E., 1984. Immune response of swine vaccinated with a group E Streptococcus whole-culture bacterin. American Journal of Veterinary Research, 45, 1933–1936.