Detailed Explanation of Prevention and Treatment Methods for Streptococcus suis Disease, Pig Farmers Should Save This

Streptococcus suis disease is a zoonosis caused by infection with various pathogenic Streptococcus suis bacteria. Among these, pigs are the main source of infection. The disease is uncommon in humans but the population is generally susceptible, mainly manifesting as fever and severe toxemic symptoms. With early diagnosis and timely treatment, most patients can be cured, but some patients may be left with sequelae.

The Harm of Streptococcus suis Disease

Streptococcus suis has a relatively high prevalence in pigs, is uncommon in humans, but the illness is very serious. The population is generally susceptible, with butchers, slaughterhouse workers and farmers having a high incidence. Other groups such as those who transport or clean up sick/dead pigs, such as drivers, are also susceptible to infection with Streptococcus suis and developing the disease. Slaughterhouse workers can carry the bacteria in their pharynx; they may appear healthy but pose a potential danger. The disease first breaks out and spreads among pig herds, after which slaughterers and those involved in handling sick and dead pigs develop the disease. In particular, modern intensive pig farming makes the disease more prone to spreading. The onset time is relatively concentrated in the high-temperature season from June to August. Cases of human infection with Streptococcus suis were reported as early as 1968 in the Netherlands and Denmark, and subsequently cases have also been reported in Sweden, France, the United Kingdom, Belgium, Italy, Germany, New Zealand, Canada and China, among others. Currently, more than 450 cases of Streptococcus suis infection have been reported globally, mainly in some countries and regions in Northern Europe and South Asia where pigs are farmed and pork is consumed. In 1998, in the Nantong area of Jiangsu, China, an outbreak of Streptococcus suis occurred, with 25 cases, of which 16 presented with toxic shock syndrome (13 deaths) and 9 presented with meningitis (1 death). According to a notification from the Ministry of Health, from June to August 2005, Sichuan Province reported a cumulative total of 204 human cases of Streptococcus suis infection, including 38 deaths and 166 cured and discharged. The cases were distributed across 12 cities, 37 counties, 131 townships and 195 villages, including Ziyang, Neijiang and Chengdu. In fact, in vast rural areas, sporadic cases occur every year; due to insufficient diagnostic capability, or failure to identify the pathogen, deaths from delayed treatment occur from time to time.

Causes of Streptococcus suis Disease

Pigs are the main source of infection; in particular, sick pigs and carrier pigs are the main sources of infection for this disease, followed by sheep, horses, deer, birds and poultry (such as ducks and chickens). The carrier rate of Streptococcus suis in pigs is about 20%-40%, and under normal circumstances it does not cause disease. If the bacteria undergo virulence variation and cause disease in pigs, the bacteria and toxins in the dead pigs are then transmitted to humans, causing human disease. So far, no human-to-human transmission with humans as a source of infection has been found.

The natural sites of Streptococcus suis infection in pigs are the upper respiratory tract (especially the tonsils and nasal cavity), reproductive tract and digestive tract. It is mainly transmitted through open wounds, such as when wounds on human skin or mucous membranes come into contact with the blood and body fluids of dead pigs, causing disease, so the incidence rate among butchers and slaughterhouse workers is relatively high. In some patients, disease is caused by eating unclean cold-dressed sick/dead pork or eating raw pork meatballs, or by washing, cutting, processing and handling sick/dead pork; processing frozen pork can also cause sporadic cases. Some patients can also be infected through respiratory transmission. Between pigs, it is transmitted through the respiratory tract and close contact, but there is no evidence suggesting transmission to humans through the pig respiratory tract.

Pathogenesis of Streptococcus suis Disease

The mechanism by which humans develop Streptococcus suis disease has not yet been fully elucidated, and there is very little research on the pathogenesis of human infection with Streptococcus suis.

The occurrence of Streptococcus suis disease is related to the immune status of pigs, environmental factors and the virulence of pathogenic strains. Streptococcus suis that causes meningitis, septicemia and arthritis syndrome requires virulence factors that increase bacterial invasiveness, including capsular polysaccharide (CPS), muramidase-released protein (MRP), extracellular factor (EF) and hemolysin (SLY). The acapsular mutant strain of Streptococcus suis type 2 and untypeable (NT) Streptococcus suis show strong adhesion and invasiveness. Studies have shown that Streptococcus suis type 2 can induce human monocytes to produce tumor necrosis factor α (TNFα), IL-1, IL-6, IL-8 and monocyte chemoattractant protein 1 (MCP-1), and these cytokines can cause systemic inflammatory responses. The capsular lipopolysaccharide of Streptococcus suis type 2 is related to bacterial adhesion and invasion; encapsulated strains can resist phagocytosis, so capsular lipopolysaccharide plays an important role in the pathogenic mechanism, leading to a decrease in the body's phagocytosis of Streptococcus suis.

When the bacteria enter the blood from the tonsils and are phagocytosed by monocytes, they pass through the choroid plexus into the cerebrospinal fluid, stimulating monocytes or macrophages to produce cytokines and toxins, thereby causing inflammatory cell infiltration in the blood and cerebrospinal fluid. The pathogenesis of Streptococcus suis pneumonia may be due to the bacteria entering through the respiratory tract, colonizing and multiplying in large numbers, and producing toxins and various proteases, hemolytic toxins, etc., which cause cell lysis, leading to destruction of the epithelial cell barrier and causing pulmonary infection, while also facilitating the pathogen's invasion into the bloodstream and dissemination throughout the body. In addition, the effects of cytokines and toxins increase blood-brain barrier (BBB) permeability in patients with bacterial meningitis, leading to the occurrence of cerebral edema, increased intracranial pressure and interruption of cerebral blood flow. After Streptococcus suis directly infects through wounds, the bacteria multiply in large numbers in the body and produce toxins that cause hematogenous infection, leading to septicemia and multiple organ failure; this situation is similar to septicemia caused by ordinary bacteria.

Pathological changes mainly involve multiple organs throughout the body. In septicemia, congestion or hemorrhage often occurs in the systemic organs. In some pigs presenting with meningitis, congestion can be seen in the meninges, lymph nodes and lungs. The most typical histopathological feature of meningitis is diffuse infiltration of neutrophils, fibrinous exudation, edema and inflammatory cell infiltration in the meninges and choroid plexus. The lungs often show parenchymal lesions, including fibrinous hemorrhagic and interstitial fibrinous pneumonia, fibrinous or suppurative bronchopneumonia, alveolar hemorrhage, interlobular emphysema and fibrinous suppurative pleurisy. Cardiac damage includes fibrinous suppurative pericarditis, mechanical valvular endocarditis and hemorrhagic myocarditis. The histopathological changes are punctate or patchy diffuse hemorrhage or necrosis in the myocardium, with fibrinous suppurative liquefaction. The pericardial fluid often contains eosinophils, a small number of neutrophils, monocytes and a large amount of fibrin.

The above is the mechanism by which pigs develop disease after infection with Streptococcus suis. Whether the process of occurrence and development after human infection with Streptococcus suis is the same as in pigs, or what differences there are, is currently poorly studied or absent.