Plague diagnosis pathology and management

Plague diagnosis pathology and management

An acute severe infection caused by Y. pestis manifests byeither lymphadenitis with suppuration (bubonic plague) orby necrotizing pneumonitis (pneumonic plague). It is azoonosis.

Aetiology The organism is a Gram-negative aerobic bacillus of theparvobacteria family. It grows well at 28C. At 37C itproduces an antigen which inhibits phagocytosis. It has alipopolysaccharide capsular endotoxin.

Distribution and incidence Asia, Africa, the Middle East and the Americas (SouthAmerica and the southern states of the USA) are endemic areas with comparatively small numbers of reported caseseach year. The disease is probably under-reported. Plagueis considered a re-emerging disease because the number ofcases being reported to the WHO is increasing, and since1994 it has reappeared in several countries such as Malawi,Madagascar, Mozambique and India, where it had not beenexperienced for 15-30 years. Also, the number of foci haveincreased in some countries, including the United States.The last pandemic started in 1894, and by the middle of thetwentieth century public health measures had led to itbeing purely sporadic.

Transmission The infection is transmitted to man by the bite of the rat flea. The natural hosts are rodents and thevector is the rat flea, Xenopsylla cheopis, which takes bloodmeals from its rodent hosts. Infected rats die and the fleasleave the dead rats for other hosts. The organisms producea coagulant which prevents the flea taking a full bloodmeal. The flea bites the host repeatedly, encouragingtransmission. The coagulant is inactive above 28C andtransmission diminishes.

Pathology Necrosis and haemorrhage are the main features, togetherwith marked inflammatory changes. An eschar is occasionallyfound at the bite site. Buboes are grossly enlarged,inflamed lymph nodes draining the site of the flea bite. Thenormal lymph node architecture is destroyed and necrotic,with large numbers of bacilli. The pathological changes inpneumonic plague are very similar, with haemorrhagicnecrosis of lung tissue.

Clinical featuresThe incubation period is 2-8 days before the onset ofsystemic upset, fever, chills and headache. Within 24 hoursof this the patient finds a bubo, which is exquisitely tender.Any group of lymph glands can be involved. Tachycardia and high fever are usual, with hypotension and shock inseverely affected patients. Purpura may occur.Pneumonic plague results from haematogenous spread of organisms to the lungs. Cough, chest pain and haemoptysisin a severely ill patient are usual features. Patchy shadowing is seen on the chest X-ray. Aerosol spread canoccur from patients with pneumonic plague. Septicaemicplague has a high mortality.There is a neutrophil leukocytosis. Some degree of disseminated intravascular coagulation is common,although spontaneous bleeding is uncommon.

Diagnosis The organism may be found in material aspirated fromthe necrotic centre of buboes and in blood films. Smearsmade on slides can be stained with Giemsa stain, whichshows the Gram-negative coccobacilli. The organism growsreadily on standard media. Antigen (F1) can be detected insputum by the second day of symptoms using a dipstick testwhich is simple and highly practical.

Management The high mortality in untreated plague (over 50%) has been altered by antibiotics. Streptomycin 15mg/kg twice daily i.m. for 10 days is the treatment of choice. Defervescence occurs by the third or fourth day. Tetracycline and chloramphenicol are alternative choices but there arereports of multiple resistance to antibiotics mediated by aplasmid. Supportive treatment is needed in those with lowblood pressure and shock, with volume replacement usingsaline or plasma. Buboes should be aspirated.

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