Yersinia pestis infection

 

The Yersinia pestis infection guidelines were first published in the J Feline Med Surg 2013; 15: 582-584 by Maria Grazia Pennisi.

 

 

Agent properties

 

Yersinia pestis is a gram-negative nonmotile, rod-shaped, facultative anaerobe with bipolar staining (giving it a safety pin appearance; Fig. 1) that belongs to the family Enterobacteriaceae. It is the causative agent of plague, a rare but often fatal zoonosis of historical significance in Europe (Black Death). Y. pestis is resistant to low temperatures and freezing, and sensitive to high temperatures (Chomel, 2012).

 

Fig. 1. Yersinia pestis is a nonmotile, rod-shaped, facultative anaerobe with bipolar staining (giving it a safety pin appearance - arrow)

Fig. 1. Yersinia pestis is a nonmotile, rod-shaped, facultative anaerobe with bipolar staining (giving it a safety pin appearance – arrow)

 

Epidemiology and vectors

 

Plague occurs in Asia, Africa and the Americas in semiarid areas, where fleas are active all year round and rodent reservoirs abundant. Epizootics in rodents expose humans and domestic animals to plague (Chomel, 2012). Transmission occurs via flea bite or ingestion of infected rodents or lagomorphs (Eidson et al., 1991). Less common is transmission through mucous membranes, skin lesions or inhalation of infected aerosols from individuals suffering from the pulmonary form. Fleas as Xenopsylla cheopis that had fed on bacteraemic rodents are efficient transmitters of the infection – for more than one year – to nearly all mammals (Fig. 2). However, not all flea species are efficient vectors: Ctenocephalides spp. are considered poor transmitters of plague (Chomel, 2012).

 

 

Fig. 2. Oriental rat flea (Xenopsylla cheopis) infected with the Yersinia pestis bacterium which appears as a dark mass in the gut: The foregut (proventriculus) of this flea is blocked by a Y. pestis biofilm; when the flea attempts to feed on an uninfected host, Y. pestis is regurgitated into the wound, causing infection. Source: https://en.wikipedia.org/wiki/Yersinia_pestis

Fig. 2. Oriental rat flea (Xenopsylla cheopis) infected with the Yersinia pestis bacterium which appears as a dark mass in the gut: The foregut (proventriculus) of this flea is blocked by a Y. pestis biofilm; when the flea attempts to feed on an uninfected host, Y. pestis is regurgitated into the wound, causing infection. Source: https://en.wikipedia.org/wiki/Yersinia_pestis

 

 

Clinical signs

 

In humans

 

An infected flea bite leaves no lesion at the site of inoculation; mononuclear cells carry Y. pestis to the regional lymph node, where the ”bubo“ develops – a swelling with necrosis and suppuration with fistulous tracts (bubonic form). Subsequent dissemination to the lungs may follow in a few days (pulmonary form) and to other lymph nodes and tissues, which may show similar lesions (septicaemic form). In cases of ingestion or inhalation, the incubation period is even shorter. The clinical course may be rapid because of the development of endotoxic shock and DIC, otherwise it lasts for 2-3 weeks (Chomel, 2012; Craven et al., 1991). Any delay in the diagnosis and treatment enhances the risk of mortality (Gage et al., 2000).

 

 

In cats

 

The prognosis for a cat with high and continual fever is poor (Gasper et al., 1993). The bubonic form is most common and usually involves the mouth (necrotic stomatitis) and mandibular or sublingual lymph nodes (Fig. 3), when the infection is acquired by preying on infected rodents; drainage of abscesses is a favourable prognostic factor. Septicaemic forms may involve any organ (mainly the lungs), with a clinical presentation of endotoxic septic shock and death in 48 hours. The pneumonic form has the worst prognosis and may derive from one of the previous forms or, rarely in the cat, occur as the primary form (Eidson et al., 1991; Carlson, 1996). The overall mortality rate is about 50% (Chomel, 2012).

 

Fig. 3. Cat recovering from plague and submandibular bubo. (source Centers for Disease Control and Prevention, www.bt.cdc.gov; http://emergency.cdc.gov/agent/plague/trainingmodule/7/02cat.htm)

Fig. 3. Cat recovering from plague and submandibular bubo. (source Centers for Disease Control and Prevention, www.bt.cdc.gov; http://emergency.cdc.gov/agent/plague/trainingmodule/7/02cat.htm)

 

Diagnosis

 

Clinical suspicion is confirmed by cytology on smears from draining lesions, where only gram negative organisms with a bipolar safety-pin shape are seen (Chomel, 2012). Bacteria can be isolated from the tonsils, blood or other infected tissues by reference laboratories; transportation is subject to class II precautions (hazardous agents). A fourfold rise of antibody titre confirms an acute infection by serology (Chomel, 2012).

 

 

Treatment

 

Gentamicin is the drug of choice; doxycycline is used in less severe cases (bubonic form) or for prevention (Orloski and Lathrop, 2003).

 

 

Recommendations to avoid zoonotic transmission from the cat

 

Between 1977 and 1988, several human cases were reported from the USA, in veterinarians, their technicians and in owners of sick cats (Chomel, 2012). Cats are considered the most important domestic animal involved in plague transmission to humans. Outdoor cats in endemic areas may transmit the infection to their owners or to people caring for sick cats (veterinarians and veterinary nurses). Close contacts (like sharing the bed) are associated with a higher risk for human plague (Gould et al., 2008; von Reyn et al., 1977). Standard hygiene measures and strict flea control should be implemented in endemic areas. Suspected cases must be kept in isolation and protective gloves, clothes, goggles and face masks must be used by the clinic staff.

Vaccines are available for humans only.

 

 

References

 

 

Carlson ME. Yersinia pestis infection in cats. Feline Pract 1996; 24:22-24.

 

Chomel B. In: Greene CE (ed). Infectious diseases od the dog and cat. IV ed. Philadelplhia: Saunders WB 2012, pp. 469-476.

 

Craven RB, Maupin GO, Beard ML, Quan TJ, Barnes AM. Reported cases of human plague infection in the United States 1970-1991. J Med Entomol 1991; 30:758-761

 

Eidson M, Thilsted JP, Rollag OJ. Clinical, clinicopathologic, and pathologic features of plague in cats: 119 cases (1977-1988). J Am Vet Med Assoc 1991;199:1191-1197.

 

Gage KL, Dennis DT, Orloski KA, Ettestad P, Brown TL, Reynolds PJ et al. Cases of cat-associated human plague in the Western US, 1977-1998. Clin Infect Dis 2000; 30:893-900.

 

Gasper PW, Barnes AM, Quan TJ, Benziger JP, Carter LG, Beard ML et al. Plague (Yersinia pestis) in cats: description of experimentally induced disease. J Med Entomol 1993; 30:20-6.

 

Gould LH, Pape J, Ettestad P, Griffith KS, Mead PS. Dog-associated risk factors for human plague. Zoonoses Public Health 2008; 55:448-54.

 

Orloski KA, Lathrop SL. (2003) Plague: a veterinary perspective. J Am Vet Med Assoc 2003; 222:444-8.

 

von Reyn CF, Weber NS, Tempest B, Barnes AM, Poland JD, Boyce JM et al., Zalma V. (1977) Epidemiologic and clinical features of an outbreak of bubonic plague in New Mexico. J Infect Dis 1977; 136:489-94.

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