Leishmaniasis is a complex of sand fly-borne diseases widely distributed in tropical and subtropical areas of North and South America, Europe, Asia, and Africa (Fig. 9.6). The ecology of leishmaniasis varies widely in different areas. In central Asia it occurs in semiarid and arid situations. In the American tropics it is primarily a

FIGURE 9.9 Mucocutaneous form of leishmaniasis, destruction of oral and nasal tissues of man in Bolivia. (From Walton and Valverde, 1979)

FIGURE 9.8 Cutaneous Leishmaniasis, granulomatous and necrotic lesion on the face of a 16-year-old girl in Kenya. (From Mehbrahtu etal., 1992)

granulomatous ulcers that discharge necrotic material (Fig. 9.8). New areas of the body become involved by extension of the primary lesions or by metastasis via the blood or lymph (disseminated cutaneous leishmaniasis). Lesions of the mucous membranes of the nose, mouth, and pharynx (mucocutaneous or nasopharyngeal leishmaniasis) may develop after the primary lesion has healed or in the absence of a recognized primary lesion ( Fig. 9.9). Species with known potential to produce mucocutaneous infections are indicated in Table I. The term diffuse cutaneous leishmaniasis is applied to a progressive, anergic, nonulcerative condition due to defective cell-mediated immunity.

Several clinical manifestations of cutaneous leishmaniasis have acquired specific common names: In the Old World, the condition characterized by single or multiple cutaneous ulcers due to L. tropica or L. major has been called oriental sore, tropical sore, Aleppo boil, Baghdad boil, Jericho boil, or Delhi boil. The form of lesion caused by L. tropica in the Mediterranean region and eastward to India has been called the classical form or dry form, and the form of lesion caused by L. major in Central Asia has been called the wet form. In Central America, the

FIGURE 9.9 Mucocutaneous form of leishmaniasis, destruction of oral and nasal tissues of man in Bolivia. (From Walton and Valverde, 1979)

condition characterized by single or multiple ulcers on the face or ears due to L. mexicana is known as chiclero ulcer. In French Guiana, the condition characterized by moderate ulcers due to L. amazonensis or L.guyanensis is known as pian bois. In Peru and Ecuador, the condition characterized by numerous, small, benign lesions due to L. peruviana is known as uta. In South America, mucocutaneous leishmaniasis due to L. amazonensis or L. braziliensis is known as espundia.

Cutaneous leishmaniasis may be self-limiting or chronic. Mucocutaneous leishmaniasis persists for many years and ultimately may be fatal. Chiclero ulcer and diffuse cutaneous leishmaniasis are also chronic, and diffuse cutaneous leishmaniasis is resistant to treatment. Infections of L. tropica may recur at or near the site of the healed ulcer after apparent cure, a condition clinically known as leishmaniasis recidivans or chronic relapsing leishmaniasis. Skin lesions of leishmaniasis are prone to secondary infections by bacteria and fungi, and infestation by fly larvae (myiasis) may occur. Disfiguring scars remain after healing.

Known and suspected vectors and reservoirs of cutaneous leishmaniasis are shown in Table I. Transmission of L. major by P. caucasicus in semiarid regions of central Asia is a classic example of an endemic zoonosis.

In this area, P. caucasicus breeds in burrows of gerbils (Rhombomys opimus) and ground squirrels (Spermophilop-sis leptodactylus) and transmits the agents of cutaneous leishmaniasis from animal to animal and from animals to humans. When gerbils were eradicated from the vicinity of a construction camp in Turkestan, leishmaniasis disappeared from the construction workers.

Cutaneous leishmaniasis due to L. mexicana occurs rarely, but widely, in south-central Texas (Bexar, Cameron, Gonzales, Uvalde, and Wells counties) and the adjoining states of Coahuila, Nuevo Leon, and Tamaulipas in Mexico. Typical and diffuse forms have been reported. Lutzomyia anthophora is believed to transmit the disease among woodrats (Neotoma micropus), and L. diabolica is suspected of transmission from woodrats to humans. Seropositive coyotes and an infected cat have been found in southern Texas.

Visceral Leishmaniasis

Visceral leishmaniasis is also known as kala-azar (from the Hindi for "black fever") and dumdum fever (from Dum Dum, the location of a former British arsenal near Calcutta). It is a chronic systemic disease that begins with an inconspicuous cutaneous lesion at the site of inoculation by the bite of an infective sand fly. From this site the parasites are distributed through the body in the bloodstream, producing chronic fever, wasting, marked hepatosplenomegaly (especially splenomegaly), pancytopenia, and hypergammaglobulinemia. Incomplete syndromes are common, and early clinical manifestations are variable. Untreated visceral leishmaniasis is usually fatal. Leishmania tropica, however, may produce inapparent or subclinical visceral infections, a condition called vis-cerotropic leishmaniasis. The intrinsic incubation period is usually 2 to 4 months. Cutaneous lesions may appear after apparent recovery or cure and may persist for up to 20 years in the absence of treatment. Such lesions are known as post-kala-azar cutaneous leishmaniasis or dermal leishmanoid.

Known and suspected vectors and reservoirs of viscera] leishmaniasis are shown in Table I. In India, Nepal, and Bangladesh, humans and sand flies are the only known hosts. Transmission of L. donovani by P. argentipes in India is a classic example of an epidemic disease. An epidemic in Assam State in the 1890s depopulated whole villages and decimated populations over large areas. Subsequently, large epidemics occurred in Assam State, Bihar State, and the Bengal region. A resurgence of visceral leishmaniasis occurred in the 1970s when the World Health Organization program of spraying homes with dichlorodiphenyltrichloroethane (DDT) for eradication of malaria was discontinued. In Bihar State, 100,000 cases were reported in 1977.

The Psychodinae have no known veterinary importance. The Phlebotominae are undoubtedly pests of livestock, pets, and wildlife in places where they are abundant, although their contribution to the overall economic loss caused by biting arthropods has not been determined. In addition, they are known to transmit leishmanial agents that infect dogs and cats and may play a role in the transmission of vesicular stomatitis virus among livestock.


The veterinary forms of leishmaniasis are canine leishmaniasis and feline leishmaniasis. Both domestic dogs and cats are susceptible to cutaneous leishmaniasis. The lesions usually occur on the nose and ears. Dogs are also susceptible to visceral leishmaniasis and may be important reservoirs, but cats are rarely infected and do not show signs of disease. The incubation period may be months or years. Infection in dogs is prevalent in Brazil, China, and the Mediterranean region.

In the United States, autochthonous cases in dogs have been reported from Oklahoma, Kansas, and Ohio. The parasites have been variously identified as L. chagasi, L. infantum, and L. mexicana. The sand fly vectors are unknown.

Beginning in 1999 an outbreak of visceral leishmaniasis occurred among foxhounds in a foxhunting club in New York, eventually resulting in 20 fatalities. Inquiry uncovered a prior outbreak among foxhounds in a foxhunting club in Michigan in 1989. Subsequent investigation found seropositive dogs in clubs located in 21 US states and the province of Ontario, Canada. Since known cases have been limited to foxhounds, it has been suggested that direct dog-to-dog transmission occurs during annual foxhound shows.

Vesicular Stomatitis

Vesicular stomatitis is an acute, febrile, weakening, viral disease of horses, cattle, swine, and occasionally sheep and goats. It is characterized by small, superficial, erosive blisters that form in and about the mouth and on the feet, teats, and occasionally other parts of the body. Because the symptoms closely resemble those of foot-and-mouth disease, vesicular stomatitis also is known as pseudo foot-and-mouth disease. Susceptibility depends on the host animal's immune status. Nonimmune animals are 100% susceptible, and up to 90% develop clinical disease. The intrinsic incubation period is 2—8 days. The disease is usually self-limiting, with recovery in about 2 weeks, but recrudescence or reinfection may occur. Economic losses are due to the reduced condition of infected animals, reduced meat and milk production, and secondary bacterial infections. In the 1950s vesicular stomatitis virus was regarded as a potential biological warfare agent to incapacitate draft animals.

The Indiana, New Jersey, and Alagoas serotypes of the vesicular stomatitis virus are known to cause disease in domestic animals in North and South America. Vesicular stomatitis is endemic in tropical regions, but it tends to be epidemic in temperate regions. In tropical regions it occurs year-round, but in the United States it occurs primarily in late summer and early fall. Opossums, monkeys, porcupines, raccoons, bobcats, and pronghorns are suspected reservoirs. Antibodies occur in domestic and wild dogs.

Lutzomyia shannoni is a proved vector of the New Jersey serotype among feral pigs on Ossabaw Island, GA, and L. shannoni, L. trapidoi, and L. ylephiletor are suspected vectors in other areas. Vesicular stomatitis virus has been isolated from a number of biting and nonbiting insects, in addition to sand flies. Repeated isolations have been made from black flies (Simuliidae), and outbreaks of the disease in cattle have been associated with high populations of black flies. Laboratory-infected Simulium vit-tatum transmit the virus to mice experimentally.

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