Bubonic plague Made by

Adel Mohamed Mohie Under supervision of:

Dr.Nehal Elgendy

Bubonic PlagueThe term bubonic plague is derived from the Greek word βουβών, meaning "groin". Swollen lymph nodes (buboes) Bubonic plague is a zoonotic disease.caused by Yersinia pestis.Around the Mediterranean Region, summers seemed to be the season when the disease took place. In northern Europe, the disease had its most frequent outbreaks in the autumn.

i. resulting from the bite of an infected flea (the rat flea) In very rare circumstances ,the fleas are often found on rodents such as rats and mice, and seek out other prey when their rodent hosts die.

ii. The bacteria began its life harmlessly living in the digestive tracts of mammals.

iii. The bacteria remained harmless to the flea, allowing the new host to spread the bacteria. The bacteria form aggregates in the gut of infected fleas and this results in the flea regurgitating ingested blood, which is now infected, into the bite site of a rodent or human host. Once established, bacteria rapidly spread to the lymph nodes and multiply.

Causes

Oriental rat flea (Xenopsylla cheopis), also known as the tropical rat flea, is a parasite of rodents, and is a primary  vector for bubonic plague. This occurs when the flea has fed on an infected rodent, and then bites a human.

The Disease

Cycle

Flea drinks rat blood that carries the

bacteria.

Flea’s gut cloggedwith bacteria.

Bacteriamultiply inflea’s gut.

Flea bites human and regurgitates blood into human wound.

Human is infected!

Signs and symptomsThe most infamous symptom of bubonic plague is an infection of the lymph glands (lymphadenitis), known as buboes, which become swollen and painful. After being transmitted via the bite of an infected flea, the Y. pestis bacteria become localized in an inflamed lymph node, where they begin to colonize and reproduce. Buboes associated with the bubonic plague are commonly found in the armpits, upper femoral, groin and neck region. Acral gangrene (i.e., of the fingers, toes, lips and nose) is another common symptom.

Bubonic plague symptoms appear suddenly, usually 2–5 days after exposure to the bacteria. Symptoms include:•Gangrene of the extremities such as toes, fingers, lips and tip of the nose.•Chills•General ill feeling (malaise)•High fever (39 °C; 102 °F)•Muscle cramps•Seizures•Smooth, painful lymph gland swelling called a bubo, commonly found in the groin, but may occur in the armpits or neck, most often at the site of the initial infection (bite or scratch)Pain may occur in the area before the swelling appearsSkin color changes to a pink hue in some very extreme cases

Pathogenesis due to Y. pestis  infection of mammalian hosts is due to several factors, including an ability of these bacteria to suppress and avoid normal immune system responses such as phagocytosis and antibody production. Flea bites allow for the bacteria to pass the skin barrier. Y. pestis expresses the yadBC  gene, which is similar to adhesins in other Yersinia  species allowing for adherence and invasion of epithelial cells. Y. pestis expresses a plasminogen activator that is an important virulence factor and that might degrade on blood clots to facilitate systematic invasion. 

Many of the bacteria's virulence factors are anti-phagocytic in nature. Two important anti-phagocytic antigens, named F1 (Fraction 1) and V or LcrV, are both important for virulence.These antigens are produced by the bacterium at normal human body temperature. Furthermore, Y. pestis  survives and produces F1 and V antigens while it is residing within white blood cells such as monocytes, but not in neutrophils. Natural or induced immunity is achieved by the production of specific opsonic antibodies against F1 and V antigens; antibodies against F1& V induce phagocytosis by neutrophils.

In addition, the type-III secretion system (T3SS) allows Y.pestis  to inject proteins into macrophages and other immune cells. These T3SS-injected proteins, called Yersinia  outer proteins (Yops), include Yop B/D, which form pores in the host cell membrane and have been linked to cytolysis. The YopO, YopH, YopM, YopT, YopJ, and YopE are injected into the cytoplasm of host cells by T3SS into the pore created in part by YopB and YopD. The injected Yops limit phagocytosis and cell signaling pathways important in the innate immune system, In addition, some Y. pestis  strains are capable of interfering with immune signaling (e.g., by preventing the release of some cytokines).

Diagnosis

Laboratory testing is required in order to diagnose and confirm plague. Ideally, confirmation is through the identification of Y. pestis  culture from a patient sample.Confirmation of infection can be done by examining serum taken during the early and late stages of infection.

TreatmentSeveral classes of antibiotics are effective in treating bubonic plague. These include aminoglycosides such as streptomycin and gentamicin, tetracyclines (especially doxycycline), and the fluoroquinolone ciprofloxacin.People potentially infected with the plague need immediate treatment and should be given antibiotics within 24 hours of the first symptoms to prevent death. Other treatments include oxygen, intravenous fluids, 

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