Plague Etiology.The disease is due to Yersinia pestis, the bacillus of the genus Yersinia, the family Enterobacteriaceae. It is a barrel-shaped gram-negative nonmotile bacillus. Its pathogenicity toward humansand animals is very high. The bacillus remains viable outside the macroorganism for a long time. In dead rodents, Yersinia pestis can live 5 months (at 0°C); in dead (frozen) humans the bacillus cansurvive from 7 to 12 months. In the sputum the bacillus remains viable from several days to 5 months, in pus, to 40 days, and in water,to 3 months. Its stability toward disinfectants is low. At 100 °C the plague agent is killed in few seconds. Epidemiology.Plague is a typical disease of rodents which are the primary source of the disease among humans. Rodents such as marmots, sousliks, hamsters, field mice and voles, brown and grey rats, house mice, etc. are highly susceptible to plague. The primary reservoir of plague infection are sousliks, voles, marmots and rats. Anthropozoonotic Rodents usually develop an acute form of plague and die. But some of them (hibernating sousliks, marmots) develop the latent disease which remains in them till next year. Other animals are also involved in the epizootics. Spontaneous infection with plague has been observed in 300 species of rodents and 29 species of other animals (camels, monkeys, jackals, hedgehogs, etc.). Ectoparasites, such as fleas are involved in the spread of plague and its maintenance in nature. Fleas are the main vector of infection. They leave dead animals and attack another host. Fleas can survive in burrows of the dead for a year until the hole is occupied by a new animal. Humans are a great danger to the surrounding as a source of infection. These are patients with primary and secondary pneumonic types of the disease and the septicemic form. Patients with uncomplicated bubonic forms are practically not dangerous.The main route of infection transmission from an infected rodent to a human being is through a bite of an infected flea. The flea isinfected through ingestion of blood of a bacteremia animal. As the bacillus multiplies in the intestinal tract of the flea, a Jell is formed at the entrance to the stomach that prevents the passage of subsequentmeals. As a result, the bacilli are regurgitated when the infected flea attempts to ingest another blood meal. The flea remains hungry and its activity increases. In the absence of rats, the flea attacks humans to infect them. If a human being hunts in the focus of plague he may getcontaminated by direct contacts with marmots, hares or otherinfected animals, either dead or captured. If an individual damages the skin when removing the pelt, or touches the mucosa with thecontaminated hands, he gets infected. People also get infected during funeral ceremonies because the fluid issuing from the mouth or nose of the dead contains the plague agent. Ingestion of contaminated food also leads to penetration of the plague bacillus into the gastrointestinal mucosa.Susceptibility of humans to plague is extremely high. When infected from an animal, the patient usually develops the bubonic form. Bubonic plague is characterized by slowly increasing incidence. In primary or secondary pneumonic plague, the infection is transmitted from person to person by air-borne route which is agreat epidemiologic danger because the disease can spread widelywithin a short period of time. Pulmonic plague usually follows thebubonic form and very soon it becomes the main clinical form. Theimmunity developed in the plague patient is rather stable and repeated infections are rare. Pathogenesis.The pathogenesis depends on the route by which the plague agent penetrates the body. If the infection gains entrance through the skin, the bacillus is carried to the regional lymph nodeswhere the microbes propagate to cause various inflammations with hemorrhagic infiltration. The whole group of the lymph nodes and the adjacent subcutaneous fat are involved in the inflammation. A primary bubo is thus formed. From the bubo, the microbes enter the blood stream to cause bacteremia. The microbes enter the internal organs and lymph nodes that are remote from the portal of entry;secondary buboes are thus formed. Secondary plague pneumonia isespecially dangerous. Less frequently, a papule or vesicle (thattransforms later into a pustule, filled with sanguine purulent exudate)is formed at the portal of entry of the infection. The pustule turns into an ulcer with raised margins. The regional lymph nodes are alsoinvolved in the process. If a person is infected by the air-borne route, hemorrhagic pneumonia and sepsis occur (primary pulmonic and secondary septicemic forms). In alimentary infection, the disease is manifestedby hemorrhagic enteritis and sepsis (intestinal and secondarysepticaemic forms). In primary septicemia, the lymphatic barrier isweak (usually due to incomplete phagocytosis of the plague agent,and due to the massive dose of infection and low body reactivity). Carried by the blood stream, the plague agent therefore generalizesthe process. The plague microbe forms exo- and end toxins which cause toxemia. The cardiovascular and the nervous systems are first of all involved: the pulse changes, arterial pressure falls, the patient ise xcited and delirious. Vascular changes are manifested by necrosis, infiltration and serous impregnation of the vascular walls. Clinical picture.The incubation period lasts from 2 to 6 days. It is shorter in the pulmonic form while in the vaccinated it can be as longas 8-10 days. Plague begins suddenly with a severe chill and rapid elevation of temperature to 39 °C and higher. Toxemia rapidly develops in all clinical forms. It is manifested by severe headache andvertigo, insomnia, myalgia, weakness, nausea and vomiting. Thepatient is first excited. His face and conjunctiva are hyperemic, the tongue is white and swollen, speech becomes inarticulate. All these symptoms (unsteady gait included) resemble those of alcoholic intoxication. Circulatory disorder is marked; tachycardia develops(120-160 beats per minute); arterial pressure falls; arrhythmia occursin severe cases. Severe cases are also characterized by cyanosis,pointedness , The diuresis decreases Nervous system:- of the features (expression of fright on the face of some patients), delirium and hallucinations. Blood anaylysis:- Neutrophilic leukocytosis witha shift to the left and accelerated ESR are seen in the blood. The diuresis decreases; the urine contains protein, granular and hyalinecasts and red blood cells. In addition to the symptoms that arecommon for all forms of plague, each particular form is alsocharacterized by its specific symptoms. Depending on the route of infection transmission, the patient maydevelop either a localized form of plague, such as cutaneous,bubonic, cutaneous-bubonic, or tonsillar (pharyngeal), or a generalized form, such as primary septicaemic, secondary septicaemic,primary pulmonic, secondary pulmonic or intestinal plague. In the cutaneous-bubonic form, a spot is first seen at the portal of entry, which is then converted into a papule, a vesicle, a pustule, and an ulcer. The ulcer is surrounded by a zone of red, later it becomes covered with a dark crust and does not heal for a long time. Asdistinct from anthrax, a plague carbuncle is painful. The regionallymph nodes are almost always involved. Lymphadenitis (plague bubo) develops on the first or second dayof the bubonic form. The bubo is tender not only during movement but also at rest. The patient is therefore motionless. Pain makes him assume a forced position. If the bubo is the inguinal area, the patient flexes his leg. In the presence of an axillary bubo, the patient lies on his back with the arm set apart from the trunk. The bubo fuses with the subcutaneous cellular tissue; the overlying skin is tense and cyanotic. The bubo either resolves spontaneously or purulates and scleroses. Cutaneous-bubonic forms can be complicated by secondary buboes, secondary pulmonic and secondary septicaemic plague. The tonsillar (pharyngeal) plague lasts 2-3 days. The toxemia is weak, the body temperature rises to 38 °C, the submandibular and neck lymph nodes are enlarged. The primary septicaemic form is characterized by delirious hyperactivity or complete adynamia, dyspnea, rapid and weak pulse, Hemorrhagic rash and hemorrhages into the skin and mucosa develop, hematemesis and bleeding can be seen. Untreated patientdies during first days of the disease. The intestinal form is characterized by high body temperature, extreme weakness, loss of appetite, nausea, recurrent vomiting, ample liquid stools with streaks of blood and mucus, severe abdominal pain during the defecation. Primary pulmonic plague is characterized by a fulminating course with dyspnea (40-60 breaths a minute), severe chest pain, cough with liberation of liquid blood-stained foaming sputum. Cardiovascular failure develops on the very first days of the disease. In the pre-antibiotic era, pulmonic plague transformed into it ssecondary septicaemic form in 1-2 days and the patient died. The prognosis is more favorable today. Diagnosis.The diagnosis is based on clinical, epidemiologic andlaboratory findings. Special precautions must be observed whentaking infected material, its transportation and further handling inthe laboratory. The following specimens are taken: bubo contents, spontaneously draining exudate from ruptured buboes, vesicles,pustules, carbuncles and ulcers; sputum is taken from patients with the pulmonic form; if sputum is absent, faucial mucus is taken. Faeces should be taken from patients with intestinal lesions. Blood specimens of patients with all forms of the disease are studied. The dead should be autopsied and pieces of the buboes, cutaneous lesions, lymph nodes and the parenchymatous organs (spleen, liver,lung), as well as blood from the heart or large vessels should beexamined in the laboratory. Exudates from buboes, vesicles, or pustules should be taken by asterile syringe. Since the amount of the material is small, about 0.5 mlof a sterile broth is taken in the same syringe and the contents are wide-mouth bottles with ground-in stoppers. Blood (10 ml) is takenfrom the cubital vein. Several smears (4-5) are prepared at thepatient's bedside. A 5-ml portion of blood is inoculated in a vialcontaining 50 ml of broth, while the remaining blood is placed in asterile test tube. If the laboratory is remote, the blood is placed intwo 5-ml test tubes and examined in the laboratory not later than 5-6hours (in the absence of a refrigerator). In the laboratory, the smearsare stained with Gram's stain and methylene blue (Loeffler). Theserologic luminescence analysis should be conducted if a luminescentmicroscope is available. Hottinger's or Martin's culture mediacontaining sodium sulphite and gentian violet are inoculated. Theremaining material is used for infection of guinea pigs and albinomice. The serologic method is used for retrospective diagnosis inthose who sustained a suspected plague, in patients to whomantibiotics were given, and in studies on the material taken fromdecaying corpses. Indirect hemagglutination and indirect agglutinationinhibition tests are commonly used. The latter test with anantigen diagnosticum is used to control specificity of the positiveindirect haemagglutination test. Serologic reactions should be conductedon the 5th day of the disease and then at 5-day intervals tillthe patient is discharged from hospital. The reaction of fluorescentantibodies can be used to detect the plague agent within 2 hours. Fleas and rodents, and also dead animals, especially camels, shouldbe examined bacteriologically in the focus of infection. Treatment.Treatment of the patient must be complex. Specific treatment includes the tetracyclines (tetracycline, doxycycline, oxycycline,methacycline) 0.2 g 6 times a day. In order to prevent complications due to the antibiotics, dimedrol,0.03 g 2-3 times a day, and vitamins (B1; B6, B12, C, K) should begiven. A 40 per cent glucose solution should be infused to patients with marked toxemia. It should be given in the amount of 20-40 ml. A 5 per cent glucose should be given in the amount of 500-1000 ml.Isotonic sodium chloride solution or sodium hydrocarbonate shouldbe given in marked acidosis. Haemodez, rheopolyglucin and plasmacan also be given. Lasix, furosemide and other diuretics should be given if liquid is retained in the patient. Cordiamine, camphor, caffeine, ephedrine,adrenaline and strophanthin should be used to correct cardio vasculardisorders. Prevention and control. Quarantine is necessary. The presence of natural nidi in various countries and reports of plague cases in them indicate possible export of the disease to other countries. The anti-plague measures should be taken in airports, sea ports,and railway border posts in accordance with the international requirements. Persons with plague should be detected and isolated.Those suspected for plague should also be isolated and observed. Allpersons who had contacts with plague patients should be observed. Objects suspected for contamination should be examined bacteriologically. Vaccination is necessary. Current and final disinfection,disinsection, deratization and quarantine measures are necessary. Special anti-plague institutions should be involved in prevention andantiepidemic measures in natural nidi of plague. Measures in the focus.Plague patients and people suspected for plague are placed in special hospitals. Any room is suitable for preliminary isolation. Allpeople must be removed from the room where the patient was present. The plague case should immediately be reported to higher medical authorities. Each hospitalized patient must be placed in aseparate room or at least screened from the other patients in theroom. The hospital must be guarded. The personnel must wear special anti-plague overalls. Persons who had contacts with plague patients should be isolatedfor 6 days. Persons who had contacts with pulmonic plague patientsshould be isolated in individual rooms. All persons who had contactswith patients or the dead (with pediculosis) must have their bodytemperature measured at least twice a day and must be givenpreventive treatment for 5 days with doxycycline (0.2 g once a day\=intramuscularly) or tetracycline (0.5 g three times a day). The dead must be buried in coffins (or without coffins) to a depthof 1.5-2 meters. Dry chlorinated lime should be placed on the bottomof the grave. The dead can be burned. If hospitalization of all contacts is impossible in view of theirmultitude, observation is especially important. People should beobserved at home with obligatory thermometry. Patients with fevershould be examined by the physician (who must establish thepreliminary diagnosis) and sent to the corresponding hospital. Whenever necessary, observation should be combined with vaccinationand health education of population. Current disinfection in the focus should be conducted when takingcare of patients, during evacuation of patients and persons who hadcontacts with them. Final disinfection should be conducted inresidential houses after evacuation of the patients and contacts, andalso after burying the dead. Disinsection and deratization shouldalso be conducted.
