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...