Lutzomyia is present in the tropics of the New World. They display a dorsal hump and wings with a lanceolate oval shape. Only females nourish from blood, usually from mammals but sometimes also from inferior terrestrial vertebrates. Usually they nourish at night; during the day, they hide in dark, humid places.
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Lutzomyia is present in the tropics of the New World. They display a dorsal hump and wings with a lanceolate oval shape. Only females nourish from blood, usually from mammals but sometimes also from inferior terrestrial vertebrates. Usually they nourish at night; during the day, they hide in dark, humid places. Lutzomyia absorb sugars that may have an important role in the development ofLeishmania in the vector species7. Laison and Shaw proposed a classification of leishmaniasis on the basis of their pattern of development in the bowel of the sand fly, which not only assumes evolution of the parasites but also allows their classification into groups such as suprapillary, peripillary, and hypopillary.
In the hypopillary group, infection is limited to the hindgut that is, pylorus ileum and rectum. The peripillary group requires mandatory development of the parasite in the hindgut but migrates to the midgut and foregut. In the suprapillary group, development does not occur in the hindgut, and the parasites are restricted to the midgut and foregut. The host reservoirs are mammals in the Old as well as in the New World species:tropica,major,donovani,mexicana, andhertigi.
Therefore, those parasites are grouped into two subgenera:Leishmania, which includes parasites that develop in the midgut and foregut, andViannia, which develops in thePhlebotomus foregut, midgut, and hindgut.
The subgenusViannia Laison and Shaw, includes the following:L. The species of subgenusLeishmania Saf Janova, includes the following:Leishmania amazonensis, which is responsible for the anergic diffuse cutaneous form and the cutaneous forms with disseminated lesions;Leishmania chagasi, which causes visceral American leishmaniasis and has a wide distribution in Latin America, extending from Mexico to Argentina;L. The duration of the life cycle in the vector varies from 4 to 18 days, depending on the species ofLeishmania; it can be extended at low temperatures or shortened at high temperatures7.
In Mexico, some rodent species have been identified as reservoirs for the parasites. For a species to be considered a reservoir, it must fulfill two criteria: 1 it must carry enough parasites to make it an effective vector at the moment of feeding and 2 in these species the infection must be relatively non-pathogenic or asymptomatic so as not to affect the survival of the reservoir.
In these mammals, the skin and the blood provide adequate environments for the parasite to reproduce. Laboratory studies from Ethiopia suggest that anL. Generally, more than half of reservoirs remain asymptomatic,. Moreover, the demonstration of parasite in the blood of domestic animals using molecular tools such as PCR has suggested that domestic animals could serve as an alternate reservoir for an infection in India. Domestic animals like pets or cattle could increase transmission pressure by virtue of being an untreated reservoir for the parasite, and their proximity to human owners may also increase the transmission ratio because of increased availability of blood meals for the sand fly as well as organic manure for breeding of larvae and resting.
Factors that affect the occurrence of disease include the agent species ofLeishmania , the host genetic susceptibility, degree of immunocompetence, poor nutrition, and other underlying diseases , and environment.
Hypotheses that explain these variations include a differences in the virulence of the parasites, b differences in the cutaneous permeability, c individual variations of genetic susceptibility of the host, and d variations in the attraction of thePhlebotomus toward different individuals,. Parasite transmission from the sand fly to the host depends on how infective the host is, how infective the sand fly is with a single bite, the average rate of biting, and the number of sand flies present.
The biting rate was calculated as 0. The causal agent is an obligatory unicellular protozoan of the familyTrypanosomatidae, suborderTrypanosomatina, and the genusLeishmania. It remains in the gut of the diptera where, within 4 to 25 days, it shows a second stage as an amastigote non-flagellated ; this is an obligatory intracellular parasite that measures from 2.
The infected femalePhlebotomus which is hematophagous , when biting the infected animal, absorbs the amastigote forms from the blood of the reservoir. When the parasite is deposited by regurgitation in the host tegument, it is phagocytized by local macrophages and epidermal Langerhans cells without the involvement of circulating monocytic cells, so this is a local event only in the skin, constituting localized CL LCL.
The host machinery that mediates amastigote uptake is poorly understood; however, it is known that, in the human host, amastigotes bind Fc receptors and enter macrophages primarily through immunoglobulin-mediated phagocytosis. Wetzelet al. Once inside the phagolysosomes, promastigotes differentiate into amastigotes and proliferate extensively by binary fission, evading the immune response.
The biological cycle described is performed in 53 to days1,8,. Pathogen species for humans are classified according to their molecular biology, and in America the predominant complexes areL. In the Old World, the disease is caused byL. According to the type of immune response elicited, the disease can be localized; it can have a tendency to be spontaneously healing or generalized and progressive These can be classified into three main categories: 1 invasive and evasive determinants, such as lipophosphoglycans not found inL.
On the other hand, it has been recognized that different components in the saliva of thePhlebotomus determine the local reaction after the bite. Exclusive to the new Nectar 2 Production Suite, two additional plug-ins are included for perfecting your vocal sound. Explore eleven powerful tools. Nectar 2 production suite torrent. The immune response can vary depending on each clinical form. In the LCL forms, humoral immunity is not triggered; in the muco-cutaneous form, specific IgG antibodies can be detected; and in the diffuse cutaneous form, high levels of IgA are occasionally detected.
In cases of VL, abnormal patterns of resistance, which were related to class II molecules of the major histocompatibility complex, have been identified. In cases of leishmaniasis caused byL. During VL, intracellular parasites are managed via the activation of Th1-associated inflammation.
IL, and eventually programmed death 1-mediated T-cell exhaustion, diminishes pathology caused by inflammation. It is not known which cell types are responsible for initiating T cell—produced IL during VL; however, the population of IgD hi B cells was found to grow threefold during the progression of VL.
Nevertheless, it is clear that CD4 as well as CD8 lymphocytes are activated and required to control the disease The muco-cutaneous form is a variant of the hyperergic spectrum always produced byL.
According to the clinical manifestations, it can be divided into 1 cutaneous localized and disseminated , 2 muco-cutaneous, and 3 visceral or kala-azar2. It is caused byL. In the Mexican Southwest and at its border with Guatemala, the causal agent isL. It occurs in areas of the body exposed to insect bites; in decreasing order of frequency, the most involved regions are the ears areas usually involved are the helix and anti-helix , nose, upper lip, cheeks, legs, hands and forearms, and ankles The incubation period is from 1 to 4 weeks2 but can last for up to several years1.
Patients may refer to previous travel to endemic zones2. It is characterized by a local increase in temperature and swelling. An erythematous asymptomatic papule appears at the site of the bite, although pruritus may be present. The size ranges from 1 to 10 mm in diameter. After 2 days, it turns into a vesicle and later into a pustule, and when it breaks, either spontaneously or by trauma due to scratching, it results in a rounded ulcer with nodular or thick borders with sharp and peaked edges Figure 2.
Such ulcers can last from 3—5 months to 15—20 years. The bottom of the ulcer shows granulation tissue that bleeds when rubbing and a pink periphery and sometimes is covered by a whitish pseudo-membrane Figure 3. In some cases, abundant secretion forms an adherent crust The lesion is not painful if it is not secondarily infected. Ulcers may be solitary or multiple; autoinoculation has been observed with the infection at sites distant to the previous mosquito bite as in the forearms by prolonged contact with ulcerated areas1, The clinical picture is usually afebrile with regional adenopathy2, Early ulcer on the forearm with meliceric crust.
Ulcer on the upper limb with crusts and raised borders. On rare occasions, the initial lesion may not ulcerate and develop vegetating appearance,. LCL can heal spontaneously in 3—9 months in the case ofL. Spontaneous healing in up to 4 years, in which healing progresses from the periphery to the center of the lesion, has been described Spontaneous healing leaves a depressed plaque with uneven pigmentation and telangiectasia, or retractile scars with hypopigmented center and hyperpigmented periphery, as well as local deformity due to large tissue destruction Figure 4.
Atrophic scar on forearm. Diffuse cutaneous leishmaniasis This form is characterized by anergy that is, lack of cellular immune response to parasite antigens.
This allows dissemination through tissue, lymph, and blood pathways, developing lesions in most of the skin, except in the scalp, and sometimes with involvement of mucous membranes. It usually starts with hard erythematous nodules and reddish-brown infiltrative smooth or verrucous plaques. The latter may or may not ulcerate and are present first on the face and afterwards progressively affect the extremities, buttocks, and mucous membranes and in some cases can involve the entire skin surface Figure 7.
Lymphedema, lymphadenopathy, poor general condition, and fever may be observed. When the mucosae such as the oropharynx and nasopharynx are involved, painful nodules may lead to airway obstruction. This clinical form is very difficult to treat, there is no spontaneous resolution, and a long evolution of up to 20 years has been observed1,,. Diffuse cutaneous leishmaniasis anergic clinical form. The causal species of this clinical form belong to the complexL. It causes invasion and destruction of the nasopharyngeal mucosa Figure 8.
Invasion occurs slowly, sometimes causing no initial disturbance, thus allowing the mucosal injury to go unnoticed; on some occasions, it causes only mild local pruritus and swelling,,17,,. Usually, lesions start in the nasal mucosa and spread to the oral and pharynx mucosa, the larynx, and the skin of the nose and lips1.
Lesions of the oral mucosa usually produce symptoms that range from simple discomfort and mild pain or odynophagia to cachexia in extreme cases; the latter is observed only in cases in which the lesion involves the totality of the pharynx, larynx with hoarseness , and esophagus with dysphagia. Early in the disease, there is infiltration of the mucosa with superficial ulcerations; later on, when the ulcers are well developed, their borders have a necrotic appearance and are torn and detached.
The uvula, pillars of the palate roof, and tonsils can be destroyed. Owing to superimposed infections, the regional lymph nodes can become infarcted and become painful. When the infection is in the nasal cavity, atrophy of the nasal turbinates and destruction of the cartilaginous septum with foul smell can occur and in extreme cases can cause death,17,.
Visceral leishmaniasis, or kala-azar black fever The febrile infectious illness known as kala-azar black fever spreads over a large part of south and east Asia mainly in India and China , a large part of Africa, the Mediterranean affecting children and adults , and South America where children are affected.
The incubation period is from 3 to 8 months. The at-risk population includes preschool children and immunocompromised and undernourished individuals.
Recently, this type of leishmaniasis has been seen with increasing frequency in patients who have AIDS or who are intravenous drug users or both, suggesting a potential transmission mechanism through contaminated syringes1.
Lesions in the reticuloendothelial system may follow a subclinical course the minority of cases , or patients may be oligosymptomatic or frankly symptomatic. It is manifested by lymphadenopathy, hepatomegaly, splenomegaly, pallor, anemia, leukopenia, thrombocytopenia, fever, night sweats, weakness, anorexia, asthenia, cutaneous pigmentation, and weight loss, which can progress rapidly in weeks or months.
In addition, affected children present characteristic chronic diarrhea and growth retardation. Typical laboratory abnormalities include pancytopenia and hypergammaglobulinemia.
If the disease progresses in the absence of treatment, cachexia and multisystem failure, hemorrhage due to thrombocytopenia, and superimposed infections can cause death.
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