Organism Yersinia pestis, the fragile organism that causes plague is a small oval-shaped bacillus that stains negative with Grams stain. It is sensitive to heat above 55°C, 0.5% phenol for 15min and exposure to sunlight. Y. pestis occurs in three varieties, orientalis, antigua and mediaevalis, separated by their ability to ferment glycerol and reduce nitrates, which can be useful in elucidating the particular organism involved in an epidemic.
Clinical features The disease in humans, due to the bite of an infected flea, is called bubonic plague, after the bubo or swelling that develops at the regional lymph nodes draining the site of inoculation. It is commonest in the groin and secondly in the axilla, while it can also occur in the cervical lymph nodes. This latter site is more likely in the case of sylvatic plague as infection can result from ingesting the organism when eating the reservoir rodent. (Some people eat rodents as a normal item in the diet, while in famine conditions, others may be driven to eat whatever they can find, including rats.)
The bubo is painful and tender, becomes fluctuant and often breaks down to discharge pus. There is an associated high fever, confusion, irritability and signs of haemorrhage may develop. These may be subcutaneous, into the stomach or intestines, leading to prostration and shock with death soon after.
In a few cases, the disease may be overwhelming from the start with septicaemic plague. All the signs are more severe and develop so rapidly that a bubo is not formed and the patient is dead within a few days. In the generalized spread of the organism around the body, it can invade the lungs and should a case of bubonic or septicaemic plague start coughing out bacteria, then
© R. Webber 2005. Communicable Disease Epidemiology and Control, 2nd edition (Roger Webber)
transmission can occur via the respiratory route. This leads to pneumonic plague, where spread is from person-to-person contact and the flea is not involved. It is highly infectious and lethal, so stringent protective action must be taken. About 5% of bubonic patients develop terminal pneumonia and transmit infection via the respiratory route. The onset of pneumonic plague is very quick with shallow, rapid breathing, watery blood-stained sputum, high temperature, pulmonary oedema and shock. Death occurs between the third and the fifth day.
A mild form of the disease with swollen glands and slight rise in temperature can occur as pestis minor, but many cases go undiagnosed and tend to occur towards the latter part of an epidemic. During an epidemic, routine throat swabs may detect Y. pestis, but there is no good evidence that transmission can occur from these cases.
Diagnosis Fresh aspirate from a gland or sputum stained with Gram stain will show the bipolar staining organism in preliminary field investigations. Culture on to blood agar or desoxycholate can be made from blood, throat swabs, sputa and material aspirated from buboes. Fluorescent antibody or antigen-capture ELISA is a specific confirmatory test. Asymptomatic cases of plague are common during epidemics and can be detected near foci by the passive haemagglu-tination test (PHA).
Transmission Figure 16.1 illustrates the different transmission cycles of plague, the trio of bacillus, rodent and flea, into which humans can be fatally drawn. In the established focus of wild rodent plague, infection is maintained in a comparatively resistant colony of animals, which suffer little from the disease. If a person strays into this focus as a hunter or trapper, then fleas from a wild rodent they have killed may bite them and cause plague. This is sylvatic plague and is generally an isolated case with little epi-demiological significance. The more important event is when some change takes place in the wild rodent focus and domestic rodents become involved. Wars of nature are similar to wars of man and a replacement of one group of plague-resistant rodents by another of no resistance could cause a change in the ecological balance. On the other hand, an increase in the domestic rodent population may expand into the wild rodent one. Whichever ofthese alternative mechanisms takes place, the deprived flea seeks a new host and settles on a domestic rodent. The domestic rodent being highly susceptible to plague is rapidly killed, which brings the flea of the domestic rodent in search of a new host and because of their proximity, humans are likely to become the next victims.
In Africa, the multi-mammate rat (Mast-omys natalensis) acts as an intermediary between the feral rodent reservoir and the domestic rat, feeding on the remnants of the harvest. However, when the rains come, it is driven to look for alternative stores of food and enters the home bringing it in contact with the occupants. This makes a seasonal pattern of plague. If there is a drought, the situation is even more serious because there is no food for the desperate multi-mammate rat, which is forced early into conflict with the domestic rat and an epidemic occurs in the dry season as well.
A focus of plague is determined by three factors: (i) the organism, (ii) the reservoir host and (iii) the flea vector. Many fleas have been incriminated as possible vectors, but species of Xenopsylla are the most important (X. cheopis, X. brasiliensis and X. astia). In identifying fleas, they can either have a comb on the top of the head or they are combless. Xenopsylla is combless, differentiating it from Ctenocephalides, which is the common dog and cat flea. The common human flea Pulex is also a combless flea, but lacks the other distinguishing feature of Xenopsylla, i.e. the presence of a meral rod (these important features are illustrated in Fig. 16.1).
Fleas are able to survive for considerable periods without taking a blood meal (6 months) and the larval and pupal stages are well adapted to changing conditions. If there is a limited food supply or low temperature, then the larva may prolong this stage from 2 weeks to more than 200 days
.16.1. Plague vector and life cycles.
Xenopsylla cheopis, the main vector of human plague (note absence of comb but meral rod on second leg)
and the pupae remain cocooned. When vibrations in the habitat, the emission of carbon dioxide or a rise in humidity indicate that an inhabitant has returned, the larva rapidly develops and the emergent flea feeds on the new host. Fleas are not specific, but prefer their normal host species and fertility may be reduced if they cannot feed on them. Fleas rapidly abandon a dead host and use their powerful hind legs to help them hop on to a new one. Once re-established, they tend to crawl around and settle to a regular feeding pattern. If fleas take in Y. pestis with their blood meal, these multiply in the proventriculus and lead to a blockage of the feeding apparatus. When the flea tries to feed again, it regurgitates bacteria into the blood stream while trying to take up blood. It is unsuccessful, so moves to a new host and tries again. Blocked fleas are important in rapidly infecting many people.
Over 340 species of mammals have been found susceptible to plague including rabbits, monkeys, dogs, cats and camels, but the main reservoir is in rodents, particularly rats. They differ in their susceptibility so that a focus will die out where there is a highly susceptible colony, but persist where resistance is high. While it is the resistant rodents that maintain a focus, it is the movement of susceptible animals, which is responsible for extending plague. Where the speed of mortality is high and the pool of susceptible animals limited, then the exacerbation will collapse and the focus return to its original boundary, but when a coincidence of susceptible rodents abuts domestic rodents, then the stage is set for an epidemic in the human population. Foci of infection have been delineated (Fig. 16.2), some of which have given rise to plague outbreaks, while others have all the potential, but human disease has not occurred.
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