Leishmaniasis Life cycle, Treatment, Symptoms, Diagnosis, Prevention, Types, Distribution.

Leishmaniasis are flagellated protists that cause a group of several human diseases collectively called leishmaniasis. Leishmaniasis also known as kala azar.

There are different types of leishmaniasis such as cutaneous (skin associated ulcers that heal), diffuse cutaneous (disseminated and chronic skin lesions), mucocutaneous (ulcers of the skin, mouth, nose, and throat), and visceral (affecting liver, spleen, and blood).

Leishmania donovani

• Leishmania donovani is a species of intracellular parasites within the genus Leishmania, a group of haemoflagellate kinetoplastids that cause leishmaniasis.
• This parasite infects human circulation and causes visceral leishmaniasis or kala-azar, the most severe form of leishmaniasis. It infects the mononuclear phagocyte system, which is comprised of the spleen, liver, and bone marrow.
• Infection is transmitted by Phlebotomus and Lutzomyia sandfly species in the Old World and the New World, respectively.
• It is widespread in tropical and temperate regions, including Africa (primarily in Sudan), China, India, Nepal, southern Europe, Russia, and South America.
• The species complex causes thousands of deaths annually and has spread to 88 countries, with 350 million people at constant risk of infection and 0.5 million new cases each year.
• Two British medical personnel independently discovered L. donovani in 1903: William Boog Leishman in Netley, England, and Charles Donovan in Madras, India. However, Ronald Ross supplied the proper taxonomy.
• The parasite’s life cycle requires two distinct hosts, humans as the definitive host and sandflies as the intermediate host. In certain regions of the globe, other mammals, particularly canines, serve as reservoir hosts. In human cells they exist as small, spherical, nonflagellated amastigotes, whereas in sandflies they are elongated and flagellated as promastigotes.
• In contrast to other parasitic protists, they cannot directly invade the host cell and instead rely on phagocytosis. In 2011, the complete genome sequence of L. donovani, isolated from southeastern Nepal, was published.
• L. donovani sensu stricto belongs to the same species complex as the closely related pathogen L. infantum, which causes the same disease.
• The former is prevalent in East Africa and the Indian subcontinent, whereas the latter is prevalent in Europe, North Africa, and South America.
• 2007 marked the completion of the divide, but references to L. donovani frequently still refer to the entire complex (sensu lato). The parasite will induce between 50,000 and 90,000 infections worldwide by 2022.

Classification of Leishmania

Domain:	Eukaryota
Phylum:	Euglenozoa
Class:	Kinetoplastid
Order:	Trypanosomatida
Genus:	Leishmania

Visceral leishmaniasis

• Visceral leishmaniasis, also known as systemic leishmaniasis or kala-azar, is a severe form of the parasitic disease leishmaniasis. It is sometimes referred to as black fever or Dumdum fever in Asia. This disease primarily affects the reticuloendothelial system, causing damage to internal organs such as the spleen, liver, and bone marrow. The immune system is also affected due to the damage caused by the parasite to these organs. If left untreated, visceral leishmaniasis is usually fatal, making it the most severe form of the disease.
• The transmission of visceral leishmaniasis occurs through the bite of infected sand flies, mainly belonging to the Phlebotomus genus in the Old World and Lutzomyia genus in the New World. Sandflies, which are about one-third the size of mosquitoes, are difficult to see and hear, making them challenging to detect. These sand flies can transmit the parasite from animals to humans or between humans themselves. There are approximately 93 species of sandfly worldwide that have been identified as vectors for Leishmaniasis.
• Leishmaniasis is divided into various groups, with cutaneous leishmaniasis and visceral leishmaniasis being the most common. In visceral leishmaniasis, several internal organs such as the spleen, liver, and bone marrow are affected, whereas cutaneous leishmaniasis causes skin sores. The disease can infect a range of vertebrates, including hyraxes, canids, rodents, and humans.
• Globally, an estimated 50,000 to 90,000 new cases of visceral leishmaniasis occur each year, but only 25% to 45% of cases are reported to the World Health Organization (WHO). It remains one of the top parasitic diseases with the potential for outbreaks and high mortality rates. Visceral leishmaniasis is the second-largest parasitic killer in the world, responsible for an estimated 20,000 to 30,000 deaths annually, following malaria.
• Leishmaniasis is caused by the parasite Leishmania, which belongs to the genus of trypanosomes. There are around 21 species of Leishmania that are responsible for causing the disease. The disease is mainly found in tropical, subtropical, and southern European regions.
• Post-kala-azar dermal leishmaniasis (PKDL) is a condition that may develop after the treatment of visceral leishmaniasis. It usually appears after one month or several years following the treatment. In PKDL, the parasite invades the skin, leading to the development of macular, papular, or nodular rashes, typically on the face, upper arms, trunks, and other parts of the body. Approximately 5% to 10% of kala-azar patients develop PKDL. This condition is mainly observed in East Africa and the Indian subcontinent. Although PKDL is not life-threatening, it is considered a potential source of Leishmania infection.
• In conclusion, visceral leishmaniasis is a severe form of leishmaniasis that primarily affects the internal organs and can be fatal if left untreated. It is transmitted through the bite of infected sand flies, and the parasite Leishmania is responsible for causing the disease. It is important to raise awareness about this condition and improve reporting and treatment efforts to reduce its impact on global health.

Leishmaniasis distribution

Leishmaniasis is a disease that has a widespread distribution, mainly affecting 88 countries around the world where approximately 350 million people reside. The majority of these countries are located in tropical and subtropical regions.

In addition to tropical and subtropical areas, leishmaniasis is also found in the rainforests of Central and South America and in the deserts of West Asia.

When it comes to visceral leishmaniasis, more than 90% of the global cases are reported in India, Bangladesh, Nepal, Sudan, and Brazil. These countries bear a significant burden of the disease.

Leishmaniasis can be found in several regions worldwide, including:

• Mexico
• Central America
• South America: This includes regions from northern Argentina to Texas, excluding Uruguay, Chile, and Canada.
• Southern Europe: Leishmaniasis is not common among travelers to southern Europe.
• Asia: With the exception of Southeast Asia, leishmaniasis is prevalent in various parts of Asia.
• The Middle East
• Africa: Particularly in East and North Africa, although cases can occur in other parts of the continent as well.

This distribution highlights the global reach of leishmaniasis, with varying levels of prevalence and incidence in different regions. It underscores the need for targeted efforts in these areas to prevent, diagnose, and treat the disease effectively.

Habitat of Leishmania Donovani

• Leishmania donovani, similar to Trypanosoma, is a haemoflagellate parasite that primarily resides within specific cells in the human body. It can be found in lymphoid-macrophage (reticuloendothelial) cells of various organs, including the spleen, liver, bone marrow, intestine, and lymph glands.
• Within its vector host, the sand fly of the Phlebotomus genus, Leishmania donovani is present in its Leptomonad form within the intestine. This is the stage of the parasite’s life cycle where it is adapted to survive and multiply within the sand fly.
• Leishmaniasis, also known as Kala-azar, refers to the disease caused by Leishmania parasites. The disease is widespread in the Eastern hemisphere, particularly in regions such as India, southern United States of America, Burma, central China, Iraq, and other areas. These regions have a significant prevalence of Leishmania donovani and are considered hotspots for the disease.
• Understanding the habitat and localization of Leishmania donovani within the human body and its vector host is crucial for studying the transmission, pathogenesis, and treatment of leishmaniasis. Efforts to control and prevent the disease often focus on targeting the specific habitats and life stages of the parasite, both in humans and the sand fly vector.

Causes of Visceral leishmaniasis – Kala-azar

Visceral leishmaniasis, also known as Kala-azar, is caused by several species of the Leishmania parasite. The specific species responsible for visceral leishmaniasis vary based on geographic regions:

1. Leishmania donovani: This species is prevalent in India and Eastern Africa.
2. Leishmania infantum: Found in the Mediterranean area, including parts of Europe, North Africa, and the Middle East.
3. Leishmania chagasi: This species is responsible for causing visceral leishmaniasis in the Americas, particularly in Central and South America. It is commonly known as Leishmania infantum in the New World.

The transmission of the Leishmania parasites occurs through the bite of small blood-sucking sandflies, primarily belonging to the Phlebotomus and Sergentomyia genera in the Old World. In the New World, the species Lutzomyia is notorious for spreading the disease. These sandflies are small insects, measuring less than 3.5 mm in length, approximately one-third the size of a small mosquito.

Sandflies thrive in moist climates as they are unable to withstand dehydration. They are nocturnal creatures and seek shelter in burrows, under rocks, or other suitable hiding places during the day. Both male and female sandflies obtain carbohydrates from plant juices, but females require a blood meal for egg development. It is during this blood meal that the infected female sandfly transmits the Leishmania protozoa to the human host, leading to the development of visceral leishmaniasis.

Understanding the role of sandflies as vectors in transmitting the Leishmania parasites is essential for implementing effective control measures and preventive strategies against visceral leishmaniasis. Efforts to target the sandfly populations and interrupt their contact with human hosts are crucial in reducing the incidence and spread of the disease.

Leishmaniasis Structure/Morphology of Leishmania donovani

There are two varieties of the parasite: amastigote and promastigote.

Amastigote

• The amastogote stage of the parasite is the aflagellar stage.
• The Amastigote stage of the parasite is present in humans and other mammals.
• Inside monocytes, polymorphonuclear leukocytes, and endothelial cells.
• Amastigotes are tiny, spherical to oval structures measuring between 2 and 3 µm in length.
• They are also referred to as Leishman-Donovan (LD) organisms.
• Cell membrane is fragile and can only be observed in fresh specimens.
• The nucleus has a diameter of less than 1 µm, is oval or round, and is typically located in the centre of the cell.
• A rod-shaped kinetoplast is perpendicular to the nucleus. It consists of a body containing DNA as well as a mitochondrial structure.
• The axoneme (rhizoplast) originates from the kinetoplast and extends to the body margin. It represents the flagellum’s foot.
• Alongside the axoneme is a vacuole, which is a transparent, unstained region.
• They are effectively stained with Giemsa or Wright.
• The cytoplasm surrounded by a limiting membrane appears pale blue in a Giemsa-stained sample. The nucleus is comparatively enlarged and reddened. The kinetoplast was pigmented a deep red color.
• At 37°C, amastigote divides via binary fission.

Promastigote

• Promastigotes are found in the digestive tract and culture media of sand flies (vector).
• The mature promastigotes are elongated, slender, and splinter-shaped. They range between 15 and 25 µm in length and 1.5 and 3.5 µm in width.
• A solitary nucleus is centrally located.
• The kinetoplast is located near the anterior end, transversely.
• The flagellum is singular, delicate, and ranges in length from 15 to 28 µm; it may be the same length as the body or even longer, protruding from the front. Since the flagellum does not wrap around the parasite’s body, there is no undulating membrane.
• The Leishman stain causes the cytoplasm to appear blue, the nucleus to appear pink or violet, and the kinetoplast to appear brilliant red.
• At 27°C, promastigote multiplies via binary fission.

Leishmania species

There are different species of Leishmania all of them are listed in below table;

L. aethiopica	L. amazonensis
L. venezuelensis	L. waltoni
L. turanica	L. tropica
L. tarentolae	L. (Viannia) shawi
L. pifanoi (status disputed)	L. (Viannia) peruviana
L. (Viannia) panamensis	L. (Viannia) naiffi
L. mexicana	L. (Mundinia) martiniquensis
L. (Mundinia) macropodum	L. major
L. (Viannia) lainsoni	L. killicki (status disputed)
L. infantum	L. (Viannia) guyanensis
L. gerbili	L. garnhami (status disputed)
L. forattinii (status disputed)	L. (Mundinia) enriettii
L. donovani	L. chagasi (syn. L. infantum)
L. (Viannia) braziliensis	L. aristedesi (status disputed)
L. archibaldi (starus species)	L. arabica

Life cycle of Leishmania donovani

All leishmania undergo a two-host life cycle. Only the amastigote form occurs in humans and a few other mammals (the definitive host), and its ovoid body contains a nucleus and kinetoplast. In the sandfly (intermediate host), the protozoa appear as promastigotes with a spindle-shaped body and a solitary flagellum emerging from the anterior end.

1. Definitive host (Amastigote form)

• Leishmaniasis is typically detected within macrophages, monocytes, neutrophils, or endothelial cells in definitive hosts. Within these cells, they proliferate via binary fission, generating numerous daughter cells that swell and rupture the parent cells.
• Other macrophages and histiocytes, which are also destroyed by the parasites, phagocytose the liberated daughter cells. In this manner, the parasites ultimately cause extensive damage to the reticuloendothelial (RE) system, which plays a crucial role in host defense.
• Intriguingly, Leishmania Donovani amastigotes that are ingested by neutrophils and eosinophils are killed, but in untreated cases, these polymorphonuclear leucocytes have little or no influence on the disease’s eventual outcome. Due to RE system damage, small numbers of amastigotes can be detected in peripheral blood, but only infrequently in feces, urine, and nasal secretions.

2. Intermediate host (Promastigote form)

• When a sandfly vector feeds on an infected individual, the amastigotes present in the peripheral blood and tissue fluids penetrate the insect along with its blood meal. In the sandfly’s midgut (stomach), the amastigotes elongate and transform into the promastigote form.
• Through longitudinal binary fission, the promastigotes multiply to enormous numbers. They resemble enormous rosettes with their flagella intertwined. By the fourth or fifth day after feeding, the parasites have moved to the oesophagus and pharynx, where they accumulate and obstruct the airway.
• When such “blocked fleas” bite a human (host) and attempt to ingest blood, adherent parasite plugs may be expelled from the pharynx and deposited in the punctured wound. These promastigotes are phagocytosed by macrophages, where they transform into amastigotes and begin to propagate.
• These then penetrate the midgut of the sandfly when it bites an infected individual. It takes between 6 and 10 days for the promastigotes to attain sufficient numbers to obstruct the sandfly’s buccal cavity and pharynx. Consequently, this is the extent of the extrinsic incubation period (Figure 6.9).

Pathogenicity of Leishmania Donovani

• The infection is transmitted by the bite of the vector sand fly Phlebotomus argentipes during the incubation period. The disease is not zoonotic in India, as the only host and reservoir is the human population.
• Typically, the incubation period lasts between three and six months, but it can be as brief as ten days or as long as two years. The presence of a cutaneous lesion at the site of a sandfly bite is not observed in Indian patients, but is common in patients from Sudan and the Middle East.

Pathogenesis

• The disease caused by Leishmania Donovani was first identified in India, where it was given the names Kala azar (meaning “black sickness”), Dum Dum fever, Burdwan fever, and Tropical splenomegaly. Typically, the advent of visceral leishmaniasis is gradual. The onset of the clinical illness is fever, which may be intermittent, continuous, or irregular.
• The onset of splenomegaly is progressive and massive. The incidence of post-kala-azar dermal leishmaniasis (PKDL) is estimated to range between 10 and 20% of kala-azar survivors. Typically, the dermal lesions appear about a year or two after the systemic disease has been cured.
• Kala azar is a reticuloendotheliosis caused by L. donovani’s invasion of the reticulo­endothelial system. Multiple organs are impacted, resulting in diverse symptoms.

(i) Splenomegaly

• The most affected organ is the spleen. Due to perisplenitis, the spleen is significantly enlarged and the capsule is frequently thickened. The massive multiplication of amastigotes within the fixed macrophages blocks the RE system.
• To the detriment of red cell production, blood-forming organs such as the spleen endure compensatory production of macrophages and other phagocytes. Consequently, the spleen becomes significantly enlarged while the patient becomes anemic and emaciated.

(ii) Hepatomegaly

• The liver is enlarged, Kuffer cells and endothelial cells of the blood vessels are severely parasitized, but hepatocytes are unaffected. Even though prothrombin production is commonly diminished, liver function is not significantly impaired. Capillaries in the sinusoids are dilated and swollen. Some degree of lipid degeneration is seen.
• The bone marrow is densely infiltrated with parasitized macrophages that may suffocate the haemopoietic tissues. Due to parasitized cell infiltration, peripheral lymph nodes and lymphoid tissues of the nasopharynx and intestine are hypertrophic. During the progression of the disease, periods of apyrexia are followed by bouts of fever.
• The epidermis becomes dry, rough, and pigmented heavily. The hair thins and becomes brittle. Epistaxis and gingival bleeding are prevalent. The majority of untreated patients perish within two years due to secondary pathogen invasion and concurrent diseases, such as dysentery, that the body is unable to combat.

Leishmaniasis prevention

There are no available vaccines or drugs to prevent infection. The most effective way to prevent leishmaniasis is to protect themselves from sand fly bites. Follow the following rules to decrease the risk of being bitten;

When outdoors 

• Wear long-sleeved shirts, long pants, socks, and tuck your shirt into your pants to reduce the amount of exposed (uncovered) skin.
• Use insect repellent special that contain DEET (N,N-diethylmetatoluamide) to exposed skin such as under the ends of sleeves and pant legs.

In indoors

• Sleep in a well-screened or air-conditioned room.
• Spray insecticide in living/sleeping rooms to kill the insects.
• Use higher floors of a building to sleep because they are poor fliers.
• Use fans in sleeping areas which makes it more difficult for the insects to fly.
• Use a bed net and tuck into your mattress.

Leishmaniasis symptoms

Visceral leishmaniasis, also known as Kala-azar, is characterized by a range of symptoms that can manifest at different stages of the disease. Here are the symptoms associated with visceral leishmaniasis:

1. Early symptoms: The incubation period for visceral leishmaniasis is typically between 3 to 6 months, but symptoms may even appear after 2 years. Early symptoms can include:

• Weight loss
• Weakness
• Prolonged fever lasting for weeks or months
• Enlarged spleen (splenomegaly)
• Anemia due to a decrease in the production of blood cells
• Bleeding tendencies
• Darkening of the skin in a peculiar manner
• Swollen lymph nodes

2. Advanced stage symptoms: If left untreated, visceral leishmaniasis can progress to the advanced stage. In this stage, additional symptoms may manifest, such as:

• Dry, rough, and darkened or pigmented skin
• Brittle hair and hair loss

It is important to note that visceral leishmaniasis can be more severe and life-threatening in specific populations, including preschool children, immunocompromised individuals, and those who are undernourished. In recent years, the frequency of visceral leishmaniasis has also increased in individuals with AIDS or those who are intravenous drug users, particularly through the use of contaminated syringes.

Visceral leishmaniasis can be fatal if left untreated. Recognizing the symptoms and seeking prompt medical attention is crucial for diagnosis and appropriate treatment. Effective management of the disease involves addressing the underlying parasitic infection and managing associated complications, such as anemia and other organ dysfunctions.

Visceral leishmaniasis (Kala-azar) Lab diagnosis

Direct Methods

To diagnose visceral leishmaniasis (Kala-azar) in a laboratory setting, several direct methods can be employed. Here are the common direct methods for the lab diagnosis of visceral leishmaniasis:

1. Microscopy: Microscopy is considered the gold standard for diagnosing visceral leishmaniasis. Various samples can be used, including peripheral blood, bone marrow biopsy, splenic aspirates, and enlarged lymph nodes. Smears of these samples are stained with Leishman, Giemsa, or Wright’s stain and examined under a microscope. Amastigote forms of the parasite, which are intracellular within macrophages, can be visualized. A few extracellular forms may also be seen. The sensitivity of microscopy varies, with higher sensitivity observed in spleen samples (93% to 99%) compared to bone marrow (53-86%) or lymph node aspirates (53-65%). It is a classic confirmatory test for visceral leishmaniasis.
2. Culture: Samples such as blood, splenic or bone marrow aspirates, and tissues can be cultured on NNN (Novy-MacNeal-Nicolle) medium or other biphasic media. The cultures are incubated at 22-24°C for 1-4 weeks. Microscopic examination of the culture fluid is performed regularly, looking for motile promastigotes. Positive cultures demonstrate the presence of promastigotes, which are the infective stage of the parasite.
3. Animal inoculation: Animal inoculation is a highly sensitive method but is not used for routine diagnosis due to ethical considerations. In this method, the suspected material is inoculated into the Chinese golden hamster intraperitoneally or intradermally on the skin of the nose and feet. The animals are kept at 23-26°C. In positive cases, amastigotes can be detected in smears taken from ulcers or nodules that develop at the sites of inoculation or from the spleen of the animals.

These direct methods aid in the laboratory diagnosis of visceral leishmaniasis, allowing for the detection and identification of the Leishmania parasite in clinical samples. Each method has its own advantages and limitations, and their utilization depends on factors such as availability, expertise, and specific diagnostic requirements.

Indirect Methods

For the laboratory diagnosis of visceral leishmaniasis (Kala-azar), several indirect methods can be used. These methods focus on detecting specific antigens or antibodies associated with the disease. Here are the commonly used indirect methods:

1. Detection of Antigen:

• ELISA (Enzyme-Linked Immunosorbent Assay) and PCR (Polymerase Chain Reaction) techniques have been developed to detect leishmanial antigens in serum or other body fluids.
• Urine-based antigen detection tests are being evaluated as non-invasive methods for diagnosing visceral leishmaniasis.
• These tests show good specificity but variable sensitivity, ranging from low to moderate (48-87%).

2. Detection of Antibodies: a. Complement Fixation Test:

• This was the first serological test used to detect serum antibodies in visceral leishmaniasis.
• Specific leishmanial antigens prepared from cultures are used in tests such as the Indirect Immunofluorescent Antibody Test (IFAT), Counter Immunoelectrophoresis (CIEP), and ELISA/Western Blot using whole parasite lysate.
• ELISA assays using whole parasite lysate have shown high diagnostic accuracy in most studies, with sensitivity ranging from 80-100% and specificity varying with the antigen used (80-94%).

b. Direct Agglutination Test (DAT):

• The DAT is a widely used serological test for diagnosing visceral leishmaniasis.
• It is based on the antigen-antibody reaction and uses trypsin-treated, stained, and formalin-preserved promastigotes as the antigen.
• Positive reactions occur as agglutination with specific antibodies from VL-positive patients.
• The DAT assay has been found to be 91-100% sensitive and 72-100% specific in various studies.
• The usefulness of this test is limited by variable sensitivity or specificity, the requirement of electricity, refrigeration, or a well-equipped laboratory, and high cost.

c. rk39 Immunochromatographic Test:

• This specific, rapid, and non-invasive test utilizes the recombinant leishmanial antigen rk39.
• The immunochromatographic test (ICT) method detects antibodies using the rk39 antigen.
• The test shows high sensitivity (98%) and specificity (90%).
• It is recommended by the National Vector Borne Disease Control Programme (NVBDCP) in India and provides results within 5 minutes.
• The test is available in lateral flow cassette test (LCT) or dipstick format, which is more suitable for field use.

3. Molecular Diagnosis:

• DNA probe techniques and PCR (Polymerase Chain Reaction) can be used for the molecular diagnosis of visceral leishmaniasis.

4. Nonspecific Serum Tests: a. Napier’s Aldehyde Test:

• This test involves adding formalin to the patient’s serum and observing jellification and opacification reactions.
• The sensitivity of this test is poor, around 34%, and it is considered nonspecific.

b. Chopra’s Antimony Test:

• This test uses serum diluted with distilled water and a solution of urea stilbamine.
• The formation of a white flocculant precipitate indicates a positive test.
• Both the Aldehyde and Antimony tests can give false-positive reactions in various other diseases.

5. Leishmanin Skin Test (Montenegro Test):

• This delayed hypersensitivity test (DHT) is primarily used for the diagnosis of cutaneous leishmaniasis.
• A killed promastigote suspension is injected intradermally, and a positive result is indicated by induration and erythema.
• This test is useful for epidemiological purposes but has limited value in diagnosing acute visceral leishmaniasis.

6. Blood Count:

• Complete blood count may reveal normocytic normochromic anemia and thrombocytopenia.
• Leukocyte count shows leukopenia with a relative increase in lymphocytes and monocytes.
• Eosinophil granulocytes are absent, and the leukocyte count progressively diminishes during the disease.
• Serum analysis shows hypergammaglobulinemia and altered albumin:globulin ratio.
• Liver function tests may show mild elevations.

These indirect methods help in the laboratory diagnosis of visceral leishmaniasis by detecting specific antigens or antibodies associated with the disease. Each method has its own advantages, limitations, and applications in different settings.

Leishmaniasis treatment

Amphotericin B (Ambisome) can be used to treat Leishmaniasis. There are different treatment methods based on the types of diseases such as;

1. Cutaneous leishmaniasis:
   1. It can be healed without any treatment, but treatment can increase the healing speed and reduce scarring. It also decreases the risk of further disease. 
   2. Sometimes required plastic surgery where skin ulcers that cause disfigurement.
2. Mucocutaneous leishmaniasis
   1. Treatment is required for Mucocutaneous leishmaniasis, it doesn’t heal naturally. 
   2. For treatment of mucocutaneous leishmaniasis two Antiparasitic drugs can be used such as Liposomal amphotericin B and paromomycin.
3. Visceral leishmaniasis
   1. Sodium stibogluconate (Pentostam), amphotericin B, paromomycin, and miltefosine (Impavido) is used for the treatment of Visceral leishmaniasis.

Leishmaniasis in dogs

• Leishmaniasis disease in dogs is known as the Canine leishmaniasis. It is a zoonotic disease.
• Canine leishmaniasis is transmitted through the bite of an infected phlebotomine sandfly.
• The disease was first found in Europe in 1903

(i) Symptoms of Leishmaniasis in dogs

Cutaneous Leishmaniasis in dogs

The symptoms of Cutaneous Leishmaniasis in dogs are Alopecia, Skin lesions, Ulcerative or exfoliative dermatitis, 

Visceral Leishmaniasis in dogs

The symptoms are Epistaxis (nose bleeds), Kidney failure > increased urination and drinking, Ocular signs, Progressive loss of weight with decreased appetite, Swollen lymphnodes.

(ii) Causative Agent of Leishmaniasis in dogs

Old World:

In Old World the Leishmaniasis is transmitted through sandflies of the genus Phlebotomus. L. donovani in Sri Lanka and L. infantum in the United States are responsible for Leishmaniasis in dogs.

New World:

In new World the Leishmaniasis is transmitted through Lutzomyia.  Leishmania donovani complex, including L. infantum, L. chagasi and L. donovani are responsible for canine visceral leishmaniasis.

Dogs does not contains any Mexicana (L. mexicana, L. amazonensis, L. venezuelensis, and L.  pifanoi) and Viannia (L. braziliensis, L. guyanensis, L. panamensis and L. peruviana) strains. 

(iii) Transmission of Leishmaniasis in dogs

• The disease is directly transmitted from sandfly to dog.
• A study in the US found L. infantum can be transmitted from dog to dog by direct contamination with blood and secretions.

(iv) Diagnosis of Leishmaniasis in dogs

For detection of Leishmaniasis in dogs different diagnosis tests are performed such as molecular biology and genetic techniques. The results of these techniques are highly specific and accurate.

ELISA and Polymerase Chain Reaction (PCR) are the most commonly employed methods in medical laboratories for detection of Leishmaniasis in dogs.

(vi) Treatment of Leishmaniasis in dogs

There is no cure for canine leishmaniasis, but different treatment methods are used by different countries. Different treatment methods are used based on the geographic area, strain of infection and exhibited symptoms such as;

• L. donovani: Antimony resistant so amphotericin B is recommended
• L. infantum: Amphotericin B, Meglumine antimoniate, Miltefosine, Allopurinol.

FAQ on Leishmaniasis

Further Reading

• Protozoa Definition, Classification, Characteristics, Structure, Diseases, Examples
• Amoeba Cell Characteristics, Structure, Movement, Nutrition, Reproduction, Disease, Habitat.
• Saini P, Kumar NP, Ajithlal PM, Joji A, Rajesh KR, Reena KJ, Kumar A. Visceral Leishmaniasis Caused by Leishmania donovani Zymodeme MON-37, Western Ghats, India. Emerg Infect Dis. 2020 Aug;26(8):1956-1958. doi: 10.3201/eid2608.200557. PMID: 32687040; PMCID: PMC7392465.
• Davidson, R. N. (2017). Leishmaniasis. Infectious Diseases, 1059–1064.e1. doi:10.1016/b978-0-7020-6285-8.00123-4
• https://www.biologydiscussion.com/protozoa-2/leishmania-donovani-habitat-morphology-and-life-cycle/49238
• https://www.biologydiscussion.com/parasitology/parasitic-protozoa/leishmania-donovani-haemoflagellates-parasitology/62145
• https://www.onlinebiologynotes.com/leishmania-donovani-morphology-life-cycle-pathogenesis-clinical-symptoms-lab-diagnosis-treatment-prevention-and-control/
• https://www.notesonzoology.com/parasitology/leishmania-donovani-with-diagram-zoology/4673