Yersinia 

Y. pestis is the causative pathogen of plague (black death, bubonic plague). Plague is a classic rodent zoonosis. It occurred in epidemic proportions in the Middle Ages, but is seen today only sporadically in persons who have had direct contact with diseased wild rodents. The pathogens penetrate into the skin through microtraumata, from where they reach regional lymph nodes in which they proliferate, resulting in the characteristic buboes. In the next stage, the pathogens may enter the bloodstream or the infection may generalize to affect other organs. Laboratory diagnosis involves isolation and identification of the organism in pus, blood, or other material. Therapy requires use of antibiotics.

Y. enterocolitica and Y. pseudotuberculosis cause generalized zoonoses in wild animals and livestock. Diseased animals contaminate their surroundings. Humans then take up the pathogens orally in water or food. The organisms penetrate the mucosa of the lower intestinal tract, causing enteritis accompanied by mesenteric lymphadenitis.

Extramesenteric forms are observed in 20% of infected persons (sepsis, lymphadenopathies, various focal infections). Secondary immunopathological complications include arthritis and erythema nodosum. Diagnosis involves identification of the pathogen by means of selective culturing.

To date, 10 different species have been classified in the genus Yersinia. The species most frequently isolated is Y. enterocolitica. Y. pestis, the “black death" pathogen responsible for epidemics in the Middle Ages, today no longer presents a significant threat.

Yersinia pestis

Morphology and culture. Y. pestis is a nonflagellated, short, encapsulated, Gram-negative rod bacteria that often shows bipolar staining. This bacterium is readily cultured on standard nutrient mediums at 30 °C.

Pathogenesis and clinical picture. The plague is primarily a disease of rodents (rats). It spreads among them by direct contact or via the rat flea. Earlier

plague epidemics in humans resulted from these same transmission pathways. The rare human infections seen today result from contact with rodents that are infected with or have died of plague. The pathogen breaches the skin through dermal injuries. From such a location, the bacteria reach regional lymph nodes in which they proliferate. Two to five days after infection, hem-orrhagically altered, blue, and swollen lymph nodes (buboes) are observed. Over 90 % of pestis infections show the “bubonic plague” course. In 50-90 % of untreated cases, the organisms break out into the bloodstream to cause a clinical sepsis, in the course of which they may invade many different organs. Dissemination into the pulmonary circulation results in secondary pulmonary plague with bloody, bacteria-rich, highly infectious sputum. Contact with such patients can result in primary pulmonary plague infections due to direct, aerogenic transmission. Left untreated, this form of plague is lethal in nearly 100% of cases.

Diagnosis. The pathogen must be identified in bubo punctate, sputum, or blood by means of microscopy and culturing.

Therapy. In addition to symptomatic treatment, antibiotics are the primary method (streptomycin, tetracycline, in the case of meningitis, chloramphenicol). Incision of the buboes is contraindicated.

Epidemiology and prevention. Plague still occurs endemically in wild rodents over large areas of Asia, Africa, South America, and North America. Human plague infections have been reduced to sporadic instances. The sources of infection are mainly diseased rodents. Transmission of the disease is mainly via direct contact with such animals.

Prevention involves exposure prophylactic measures. Persons with manifest disease, in particular the pulmonary form, must be isolated. Contact persons must be quarantined for six days (= incubation period). Cases of plague infection must be reported to health authorities.

Yersinia enterocolitica and Yersinia pseudotuberculosis

Occurrence and significance. Y. enterocolitica and Y. pseudotuberculosis cause generalized infections in domestic and wild animals, especially rodents. The pathogens can be transmitted from animals to humans. Y. enterocolitica is responsible for about 1% of acute enteritis cases in Europe. Y. pseudotuberculosis is insignificant in terms of human pathology.

Morphology, culture, and antigen structure. These are pleomorphic, short rods with peritrichous flagellation. They can be cultured on all standard mediums. These Yersinia bacteria grow better at 20-30 °C than at 37 °C.

Pathogenesis and clinical pictures. All of the strains isolated as human pathogens bear a 70 kb virulence plasmid with several vir determinants. They code for polypeptides that direct the functions cell adhesion, phagocytosis resistance, serum resistance, and cytotoxicity. Yersiniae also have chromosomal virulence genes, for example markers for invasins, enterotoxins, and an iron capturing system. Exactly how these virulence factors interact to produce the disease is too complex to be described in detail here.

Yersiniae are usually ingested indirectly with food. Although much less frequent, infections can also occur by way of direct contact with diseased animals or animal carriers. The bacteria enter the lower intestinal tract, penetrate the mucosa and are transported with the macrophages into the mesenteric lymph nodes. A simplified overview of the resulting clinical pictures follows:

- Intestinal yersinioses. The clinically dominant symptom is enteritis together with mesenteric lymphadenitis. This form is frequently observed in youths and children. Other enteric forms include pseudo appendicitis in youths and children, ileitis (pseudo Crohn disease), and colitis in adults.

- Extraintestinal yersinioses. These infections account for about 20% of cases, usually adults. Notable features of the clinical picture include sepsis, lymphadenopathy, rarely hepatitis, and various local infections (pleuritis, en-docarditis, osteomyelitis, cholecystitis, localized abscesses).

- Other sequelae. The immunopathological complications observed in about 20% of acutely infected patients one to six weeks after onset of the intestinal symptoms include reactive arthritis and erythema nodosum.

Diagnosis. A confirmed diagnosis is only possible with identification of the pathogen in a culture based on physiological characteristics. Special mediums are used to isolate the pathogen from stool. The agglutination reaction, an ELISA or immunoblot assay can be used to detect the antibodies.

Therapy. Generally, favorable courses require no chemotherapy. Clinically difficult cases can be treated with cotrimoxazole, second- or third-generation cephalosporins, or fluorinated 4-quinolones.

Epidemiology and prevention. Prevalence of Y. enterocolitica and Y. pseudo-tuberculosis in animals is widespread. The most important reservoirs in epi-demiological terms are mammals that are diseased or carry latent infections. From these sources, vegetation, soil, and surface water are contaminated. Transmission is by the oral pathway in food. Contact zoonosis is possible, but rare. There are no specific prophylactic measures.