Plague – Causes, Symptoms, Diagnosis and Treatment

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Plague is disease which is widely prevalent all over the world but is more common in the subtropical region. It is primarily a disease of rodents (sylvitic plague) and is transmitted to humans by the bite of infected rat flea (xenopsylla cheopis). Sporadic cases as well as epidemics of plague occur worldwide.

It is caused by yersenia (Pasteurella) pestis, a pleomorphic gram negative, non-motile, aerobic, rod shaped organism showing bipolar staining. It may remain viable in cool moist conditions for months but can be readily killed by 15 minutes exposure to heat (72°c)

WHO has classified it as

(a) Wild sylvitic plague which mainly afflicts rodents and is independent of human population.

(b) Domestic plague which is spread by rodents living with man. It may present as (i) Bubonic (ii) Pneumonic (iii) Septicaemic or as a (iv) Cutaneous eruption at the site of infection.

Humans become infected from domestic pets when these become infected or catch and return plague infected rodents or their fleas to rural homes. Domestic rats come in contact with wild rats and contract disease. When they die or come in contact with humans the disease spreads.

It is spread by the bite of infected rodent fleas (chief vector). When these feast on dead rats they ingest about 0.5 ml of blood, containing approximately 5,000 or more of its bacteria.

Fleas develop obstruction of the fore gut causing regurgitation of plague bacilli during the next blood meal. In the mean time, the starved flea ravenously bites humans in vain attempt to feed. These bites introduce the plague bacillus into the host and thus spread the disease.

Transmission of disease without fleas may occur by ingestion or handling of infected material possibly through a wound or by inhalation. Human body louse and tics are also capable of inter human transmission.


After inoculation of the organism in the body by flea bite, a primary vesicle may be formed. The organism travels to adjacent lymph nodes where intracellular multiplication results in development of capsular envelopes.

An acute inflammatory response occurs in lymph nodes in 2 to 6 days. The organisms are resistant to phagocytosis because of capsular envelope. The toxins liberated by the organism results in hemorrhagic necrosis of lymph nodes resulting in liberation of large number of bacteria which gain access to the blood stream and along lymphatics involve superficial glands, spleen and other glands in the body (mediastinum and abdomen).

The endothelial lining of the blood vessels is affected giving rise to hemorrhage in the mucous and serous membrane. Liver and kidneys are congested, showing cloudy swelling and fatty change while cardiac muscle shows fatty degeneration.

Spleen which becomes enlarged is hyperaemic and hemorrhagic. Lungs are secondarily infected showing lobar consolidation and hemorrhagic necrosis. Pericarditis with a small seropurulent discharge and meningitis with hemorrhage in the brain may develop.

Clinical features

Plague involves all age group and both sexes. The incubation period of the disease ranges from 2 to 7 days and it may present with sudden onset of fever, chills nausea, vomiting and marked prostration. Earlier on a number of forms of plague were described but now Bubonic, Pneumonic and Septicaemic forms are recognized.

Bubonic plague

It is the commonest form and its incubation period ranges from 2 to 10 days after bite from an infected flea. A single bubo which is tender, erythematic and non-fluctuant develops in lymph glands draining the infected area.

It is commonly in the inguinal region because in majority of cases bite is on the legs. The buboes may appear in the axillary and cervical region reaching full size in 2-5 days. These get matted, suppurate and ulcerate or may even recede.

Buboes are accompanied by prodromal symptoms like headache, malaise and high fever coming with chills. This remains for next 2-5 days and then falls. The patient is mentally dull, apathetic and has slurred speech with unsteady gait. Stupor and coma may develop rapidly. Skin is hot and dry with conjunctival congestion.

Patient may pass into shock, hypo tension, Petechial hemorrhages and subcutaneous bleeding may occur. Disseminated intravascular coagulation may develop. The blood clots in the arterioles may produce gangrene of the fingers and toes giving the disease the term of ‘Black Death’.

Bleeding may take place in other internal organs like gut, etc. Gastrointestinal symptoms in the form of vomiting and bloody diarrhea develops. Spleen and liver may be moderately enlarged. Secondary pneumonia in the lungs may develop. If untreated the patient dies by the 5th day.

Septicemic plague

It is an acute fulminating form of the disease which progresses rapidly with chills, fever, tachycardia severe headache, vomiting and delirium. There is generalized enlargement of lymph glands. Patient may go into septic shock, disseminated intravascular coagulation, cutaneous purpuric lesions and bleeding from internal organs. Soon prostration sets in and patient dies within 24 hours.

Pneumonic plague

It can be divided into two forms Primary pneumonic plague which develops from inhalation of infectious material (droplet infection) or from close proximity to a person infected with pneumonic plague.

Secondary it is due to spread of disease not only from the lymphatics but also via blood stream. Incubation period of this from ranges from 1 to 6 days. It is characterized by high fever, chills, headache, and dizziness, pain in the limbs, cough, tachypnea and tightness in the chest. Symptoms worsen rapidly leading to marked dyspnea, cough and expectoration of copious, bloody or purulent sputum teeming with plague bacilli.

Lungs may show multilobular involvement with consolidation. Primary plague pneumonia is a fulminant illness. Patient may develop respiratory failure and adult respiratory distress syndrome (ARDS). Cardiac failure develops with signs of shock and death occurs within 3-4 days.


A case of it may develop various complications like Plague meningitis, DIC, Acrocyanosis, Pulmonary abscess, digital gangrene, subcutaneous abscesses and cellulitis.

An abortive form of plague is also known where buboe develop which may suppurate or be absorbed without serious symptoms.


Besides typical clinical features, following investigations will help.

1. staining of plague bacillus with gram stain will show a bipolar safety pin appearance.

2. Blood culture from needle aspiration of bubo and grown on blood agar, Mackonkey agar or in an infusion broth. Colonies will be gray white to slightly yellow opaque after 48 hours of incubation.

3. Detection of increased serum antibody titres to yersinia pestis F.I. antigen without a history of plague vaccination. Four fold increases will be diagnostic.

4. Passive haemagglutination test and ELISA.

5. Isolation of yersinia pestis from a clinical specimen.

6. TLC & DLC will show ploy morph leucocytosis. There may be biochemical evidence of DIC (Low platelet count, prolonged partial thromboplastin time and positive fibrin degradation products).

7. X-ray chest: Pulmonary infiltration, patches of consolidation and pneumonia.

Treatment of Plague

Drugs like streptomycin (1 gm I/M twice a day) and gentamicin (5 mg/kg intravenously twice a day) are the drugs of choice. Alternatively drugs like doxycycline (200 mg I/V) ciprofloxacin (500mg I/V twice a day) or chloramphenicol 25 mg/ kg intravenously four times a day) are the drugs which are effective against the disease.

Prevention. In individuals who are liable to be infected in an endemic area, a formalin killed whole bacteria vaccine is administered. It should be read ministered every 6 months.

For individuals in close contact with plague patient; prophylactic oral tetracycline 250 mg four times a day for 7 days should be given.

Prevention shall also depend on the eradication of infection from rodents as well as control of rodent population. (By rat poison and trapping). Insect vectors be destroyed by use of pesticides like DDT, Alderin etc.

Prognosis. Untreated plague carries a very high degree of mortality (70-90%). Prognosis improves if the treatment is instituted early.



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