The genus Yersinia is a member of the family Enterobacteriaceae, which is presented in Chapter 12. The most clinically notorious member of this genus is Yersinia pestis, which causes plague, rather than enteric disease and, therefore, is being discussed separately from the rest of the family. In common with other Yersiniae, Y. pestis is a small rod that stains bipolarly (see Figure 3). Y. pestis produces a variety of plasmid-encoded virulence factors that are immunosuppressive or antiphagocytic. These virulence factors include the Yop proteins, which are secreted by a type III secretion system; the Pla protease, which is a plasminogen activator that prevents blood clotting; and a proteinacious capsule (F1 antigen), which is antiphagocytic.

A. Epidemiology

Plague is predominantly a zoonosis with worldwide distribution. In the United States, the Southwest has been a primary focus of Y.pestis infection, although the distribution of human cases has been expanding into the Northwest and south-central states. The organism can infect a variety of mammals. For example, rats are common reservoirs in urban areas of some countries (urban plague). However, in the United States, plague is predominantly found in the wild, where prairie dogs and ground squirrels are the most important reservoirs (sylvatic plague). Household pets, particularly cats allowed to roam in plague-enzootic areas, may also become infected. Wild carnivores that ingest infected rodents can also be a source of transmission to humans who hunt or come into contact with these animals. Plague is characteristically transmitted by fleas, which serve to maintain the infection within the animal reservoir. Humans are generally accidental and dead-end hosts. Plague can also be transmitted by ingestion of contaminated animal tissue or via the respiratory route (pneumonic plague). [Note: The latter occurs either when organisms reach the lung via the blood stream and establish a secondary pneumonia or following inhalation exposure to respiratory secretions from a patient or animal with plague pneumonia (Figure 1).]

Fig1. Epidemiology and pathology of plague.

B. Pathogenesis

Organisms are carried by the lymphatic system from the site of inoculation to regional lymph nodes. The Yersinae have a tropism for lymphoid tissue. However, the organisms are resistant to intra cellular killing by phagocytes and, instead, may multiply within these cells. Furthermore, the bacteria released from lysed phagocytes are resistant to subsequent phagocytosis by virtue of expression of a type III secretion system that deploys effector proteins (Yops) into host cells to paralyze them. The affected lymph nodes display hemorrhagic necrosis accompanied by high concentrations of both polymorphonuclear leukocytes and extracellular bacteria. Hematogenous spread of bacteria to other organs or tissues may occur, resulting in additional hemorrhagic lesions at these sites.

 C. Clinical significance

 Plague may present several clinically different pictures. Most common is the bubonic/septicemic form. Pneumonic plague may develop as a result of spread to the lungs during septicemic plague or may be spread person-to-person via the respiratory route. Less common presentations include plague meningitis (typically a secondary focus resulting from hematogenous spread of the organ isms), cutaneous plague, and pharyngitis (the latter two generally acquired by handling or ingesting contaminated animal tissue).

1. Bubonic (septicemic) plague: The infectious cycle begins when a flea ingests a blood meal from an animal that is infected and bacteremic. Y. pestis produces a biofilm that blocks the flea's midgut. This blockage prevents the flea from digesting the blood meal so it is consequently starved and voraciously feeds searching for a productive meal. Y. pestis multiplies in this environment. When the flea next attempts to feed, it regurgitates these bacteria from its foregut into the new animal's skin. The incubation period (from flea bite to development of symptoms) is generally 2 to 8 days. Onset of nonspecific symptoms, such as high fever, chills, headache, myalgia, and weakness that proceeds to prostration, is characteristically sudden. Within a short time, a characteristic, painful bubo develops (Figure 2). Buboes (pronounced swellings comprised of one or more infected nodes and surrounding edema that led to the term “bubonic plague”) are typically located in the groin but may also occur in axillae or on the neck. As the disease proceeds, blood pressure generally drops, potentially leading to septic shock and death. Mortality of untreated bubonic plague generally exceeds 50 percent, with untreated and highly contagious pneumonic plague being invariably fatal unless promptly treated. Other manifestations associated with bubonic plague include pustules or vesicles containing leukocytes and Y. pestis. Purpura and necrosis of extremities may occur during systemic disease. [Note: Ingestion of contaminated meat or expo sure to airborne bacilli can result in primary lesions in the pharynx. These produce a severe tonsillitis and cervical buboes.] Septicemic plague is a variation in which the patient is over whelmed by massive bacteremia before the characteristic buboes develop.

Fig2. Bubo characteristic of infections due to Yersinia pestis.  

2. Pneumonic plague: If plague bacilli reach the lungs, they cause hemorrhagic pneumonia that, if untreated, is rapidly fatal. It is also highly contagious person to person. The organisms can cause pneumonic plague directly if inhaled.

3. Plague meningitis: This results from hematogenous dissemination of organisms to the meninges. It may occur following inadequately treated bubonic plague or, like septicemic plague, may occur without, or prior to, development of a bubo. Organisms can be demonstrated in the CSF.

 D. Laboratory identification

Diagnosis of Y. pestis infection may be made presumptively on the basis of clinical presentation. Laboratory identification can be initiated by a gram-stained smear, and culture of an aspirate from a bubo (or from CSF or sputum in the case of meningitis or pneumonic presentations). Blood cultures should be sent to the laboratory. The organism grows on both MacConkey and blood agar media, although colonies grow somewhat more slowly than those of other Enterobacteriaceae.

E. Treatment and prevention

Streptomycin is the drug of choice, but gentamicin and doxycycline are acceptable alternatives (Figure 3). For plague meningitis, chloramphenicol offers good penetration into the CSF. Because of the potential for overwhelming septicemia, rapid institution of antibiotic therapy is crucial. Supportive therapy is essential for patients with signs of shock. A formalin-killed vaccine is available for those at high risk of acquiring plague. For individuals in enzootic areas, efforts to minimize exposure to rodents and fleas are important. Sick or dead rodents should never be touched with bare hands because infected fleas will seek attachment to a warm, living animal.

Fig3. Summary of Yersinia pestis disease. 1   Indicates first-line drugs. CIN = cefsulodin-Irgasan-novobiocin.

اخر الاخبار

اخبار العتبة العباسية المقدسة

قسم الشؤون الفكرية يختتم المرحلة الثالثة من مشروع استعادة مكتبة جامعة الموصل

جامعة الكفيل تنظّم دورة حول نظام (كوها) العالمي لإدارة المكتبات الجامعية في النجف

مجموعة مشاتل الكفيل: إضافة نحو 70 نوعًا جديدًا من المغروسات تتناسب مع الظروف المناخية المحلية

المجمَع العلمي يطلق الدورة التطويرية الخامسة لمعلمي التربية الإسلامية ومدرسيها في النجف الأشرف

المزيد

الآخبار الصحية

اختراق علمي.. دواء يؤخر ظهور السكري من النوع الأول لسنوات

هذا ما يحدث لجسمك إن أهملت نظافة فراشك

لماذا تعتبر النساء أكثر عرضة للإصابة بألزهايمر من الرجال؟

لماذا يحذر الخبراء من الإفراط في تناول الفراولة؟

المزيد

الآخبار التكنلوجية

السيارات الكهربائية أنظف بنسبة 73% من سيارات الوقود

سيارة لوسِد الكهربائية تدخل "غينيس" بأطول مدى في العالم

نظرية جديدة تنسف كل ما نعرفه عن تشكل أول قارة في الأرض

منذ 37 ألف عام.. دراسة تكشف "أقدم أمراض" أصابت البشر

المزيد

مواضيع ذات صلة

Brucella

Legionella

Expanded-Spectrum Cephalosporin Resistance and Carbapenemase Resistance

Extended Spectrum β-Lactamase (ESBL) Producing Enterobacteriaceae

Approach to Identification of Enterobacteriaceae

Bordetella

Hemophilus

Yersinia

Cultivation of Enterobacteriaceae

Primary Intestinal Pathogens of Enterobacteriaceae

Opportunistic Human Pathogens of Enterobacteriaceae

Vibrio