The causative agent and its place in the yersiniosis group
Pseudotuberculosis belongs to the group of zoönotic sapronotic bacterial infections. Sapronoses are infections whose primary reservoir is environmental objects (soil, water). In zoönotic sapronoses, both the external environment and animals serve as reservoirs simultaneously.
Yersinioses are caused by microorganisms of the genus Yersinia. Medically significant representatives include:
- Yersinia pestis — the causative agent of plague;
- Yersinia enterocolitica — the causative agent of intestinal yersiniosis;
- Yersinia pseudotuberculosis — the causative agent of pseudotuberculosis.
The name "pseudotuberculosis" is due to the fact that post-mortem examination reveals granulomas in organs rich in macrophage elements that are morphologically similar to tubercular ones, yet the tuberculosis pathogen is not isolated.
Epidemiology and pathogen resistance
The reservoir for Y. pseudotuberculosis consists of soil and wild murid rodents: gophers, voles, and shrews. Animals become infected alimentarily; the pathogen localizes in the gastrointestinal tract and is excreted with feces, contaminating soil and stagnant water bodies. House mice frequently develop a generalized form resulting in the animal's death.
Humans become infected exclusively via the fecal-oral transmission mechanism; the contact route from rodents does not occur. Transmission pathways are waterborne and foodborne. Main transmission factors:
- uncooked vegetables and greens;
- pickles, sauerkraut, salted cucumbers, and tomatoes;
- less commonly, fruits and dairy products.
A distinctive feature of the pathogen is its high resistance in the external environment despite lacking spores and a capsule. The bacterium multiplies across a wide temperature range — from +2 to +10 °C (vegetable stores, refrigerators, basements) and at +25…+37 °C. Multiplication is also possible in saltwater, which explains the spread of the infection in coastal regions. Outbreaks are frequently recorded during the winter-spring period when long-stored vegetables are consumed.
Pathogenesis
The pathogen enters the gastrointestinal tract with infected food or water, overcomes the gastric barrier, and attaches to the lymphoid apparatus of the intestine — the Peyer's patches of the ileum. Next, the microorganisms penetrate the regional mesenteric lymph nodes, causing lymphadenitis. At this stage, clinical manifestations are typically absent.
When the lymphatic barrier fails, bacteremia develops. The massive destruction of bacteria by immune mechanisms is accompanied by the release of endotoxin, which causes fever and intoxication syndrome as well as organ damage. The causative agent is trapped within the mononuclear phagocyte system — cells of the liver, spleen, bone marrow, and loose fibrous connective tissue, forming specific granulomas. These mechanisms determine the potential for systemic dissemination and polymorphism of the clinical picture.
Clinical classification and course
Three main forms of pseudotuberculosis are distinguished:
- Abdominal (about 80% of cases): mesenteric lymphadenitis, terminal ileitis, acute appendicitis. Pain can be so intense that acute surgical pathology must be ruled out.
- Mixed: scarlatiniform and septic variants.
- Secondary focal: reactive arthritis, erythema nodosum, etc.
The disease begins acutely, with the peak of clinical manifestations occurring during the first week. The prodromal period lasts about 3 days: weakness, fatigue, headache, and muscle pain. Then, fever-intoxication syndrome develops with febrile temperature, which subsides starting from the second week. Catarrhal syndrome frequently joins (hyperemia of the oropharynx, rhinitis, slight cough, scleral vessel injection, conjunctival hyperemia), which complicates differential diagnosis with acute respiratory viral infections (ARVI).
Pathognomonic symptoms and rash
In the first 3 days of the illness, the following appear:
- "Hood" sign — hyperemia of the face and neck;
- "Gloves" sign — edematous hyperemia of the hands;
- "Socks" sign — edematous hyperemia of the feet.
Only the combination of all three symptoms is a pathognomonic sign of pseudotuberculosis. A scarlatiniform rash is also characteristic, localized predominantly in natural skin folds (popliteal, elbow creases), bright, followed by desquamation. In 30% of patients, a morbilliform maculopapular rash is possible.
Gastrointestinal tract involvement manifests as abdominal pain, nausea, vomiting, dyspepsia, and alternating constipation and diarrhea. Diarrheal syndrome is not dominant — this is an important differential diagnostic sign. Hepatomegaly, hepatosplenic syndrome are characteristic; skin icterus due to hyperbilirubinemia, joint, pancreatic, and renal involvement are possible.
Diagnostics and treatment
Clinical diagnosis is based on a combination of fever, scarlatiniform rash, abdominal syndrome, and the pathognomonic "hood — gloves — socks" triad.
Laboratory methods:
- Bacteriological — isolation of the pathogen culture;
- Serological — predominantly passive hemagglutination test (PHA);
- PCR;
- Immunoblotting.
Treatment is based on etiotropic antibiotic therapy, which should ideally be started as early as possible (optimally no later than the third day of illness). Drugs of choice:
- Fluoroquinolones (ciprofloxacin);
- Third-generation cephalosporins.
Additionally, detoxification and pathogenetic therapy are administered depending on the leading syndrome and the form of the disease.
Key points
- Pseudotuberculosis is a zoönotic sapronosis caused by Yersinia pseudotuberculosis.
- Reservoir — soil and wild murid rodents; transmission is fecal-oral, main factors are raw vegetables, greens, pickles.
- The pathogen multiplies at +2…+10 °C, which explains winter-spring outbreaks after vegetable storage.
- Key stages in pathogenesis: lymphadenitis of Peyer's patches → mesenteric lymphadenitis → bacteremia → endotoxemia → fixation in the mononuclear phagocyte system with granuloma formation.
- Abdominal, mixed, and secondary focal forms are distinguished; up to 80% of cases are abdominal.
- The pathognomonic triad is "hood — gloves — socks" combined with a scarlatiniform rash in the skin folds.
- Diarrheal syndrome is not dominant, which distinguishes pseudotuberculosis from typical acute intestinal infections.
- Confirmation — PHA, bacteriology, PCR; therapy — fluoroquinolones or third-generation cephalosporins.