Leishmania spp3 species of Leishmania parasitize in human body. They are Leishnania

donovani, Leishmania tropica, Leishmania braziliensis.

1. Leishmania tropica

It causes cutaneous leishmaniasis ( Oriental sore ), this disease is prevalent in Africa, central and south America, western and southern Asia, but not in China. Dogs or rodents are reservoir hosts. The vectors are sand fly or stable fly ( stomoxys calcitrans, may be mechanical transmission ). The sore ruptures to form the ulcer. Contact infection is possible also. The course of disease lasts one year.

2. Leishmania braziliensis

Leishmania braziliensis causes mucocutaneous leishmaniasis (espundia ). It is found in mid and southern America, but not in China. Dogs, cats and horse are reservoir hosts. The vector is sandfly. Besides cutaneous lesion the parasites lead to mucosa lesion in the nose, mouth and pharynx. The ulcers take place in the damaged portion. The course is about 6-15 months.

3. Leishmania donovani

Leishmania donovani causes visceral leishmaniasis ( Kala azar ). Kala azar is an India name, meaning “ black fever ”( darkening of the skin ). It is one of the five major parasitic diseases in China. Its clinical manifestations are irregular fever for long period, massive hypertrophy of spleen and liver, anemia, bleeding, The ratio of albumin to globulin is inverted ( A/G=1:2, but regular ratio is 1.5-2:1 ). The mortality is about 95% without treatment. This disease was prevalent in 16 provinces, cities and autonomous region. There were 600 thousands patients in China in 1949, 300 thousands patients in Shandong. Shandong, Jiangsu, Anhui, Hunan, Hubei, Shanxi, Gansu, Xinjiang were heavily infected districts. But it has been basically eliminated from China since 1958 ( the incidence is less 1% in endemic areas ).I. Morphology

1. Amastigote stage ( Leishmania form or L. D. body ): Oval in shape, 2-3 micrometers in size, has one nucleus and one kinetoplast, a basal body and a rhizoplast. It live in the mononuclear macrophangocytosis system. It is pathogenic stage.

2. Promastigote (Leptomand form ): 14-20 x 2 m in size, fusiform in

shape. It has one nucleus central in position, a flagellum comes from the basal body, which is just as long as its body length. Promastigote is found in the digestive tract of sand fly. It is infective stage.

II. Life cycle

1. In the mammalian host: As female sand fly sucking blood, the infective stage, promastigotes, invade the wound and are engulfed by mononuclear macrophagocytes, in which they multiply by binary fission, until the host cell is destroyed, whereupon new macrophage cells are parasitized. The mammals are considered as the hosts.

2. In the digestive tract of sand fly: As female sand fly sucking blood of a patient, it gets infection. In its intestine, macrophagcyte is digested and amastigotes become promastigotes and then multiply by binary fission. Seven days later, as the sand fly sucking blood again, the final host is infected by the injection of sand fly’s proboscis.

III. Symptomatology and Pathology

Visceral leishmaniasis is due to the mononuclear macrophagocytosis system is parasized by the parasite. The onset of the disease is gradual, and the incubation period may vary from 2 weeks to 18 month ( usually2-4 month). The mortality rate in untreated cases is about 95%, and spontaneous recovery from the diseases is rare, but survivors and cured cases usually have lasting immunity.Clinical manifestation and pathogenic mechanism: see also the diagram of pathogenic mechanism of visceral leishmaniasis.1. Irregular fever for long period is due to the broken piece from parasitized

tissue.2. Massive hypertrophy of spleen and liver are caused by the proliferation

of mononuclear macrophagocytosis system.3. Because bone marrow is involved and spleen is hyperfunction, anemia

take place. The number of red blood cells( RBCs), white blood cells (WBC) and platelet all decrease.

4. Bleeding results from the decrease in blood platelets.5. The decrease of liver function and the proliferation of plasma cells bring

about the ratio of albumin to globulin is inverted (A:G=1:2, regularly, A:G=1.5-2:1 ).

In advanced stage, the patients may be emaciation with ascites, darkened skin, fever, bleeding of the gums, the decrease in immunity. Die of infective complication ( noma, pnuemonia) and bleeding.

6. Past kala arza dermal leishmaniasis It is usually seen in Indian, Sudan, occasionally in China, and

generally occur in 1-2 years after curing visceral leishmaniasis, there are pigmented areas in the skin, occasionally depigmented areas present in Chinese patients’ skin, following nodule formation in which L.D.bodies can be detected. We must pay attention to distinguishing from leprosy.

Diagram of Pathogenic Mechanism of Visceral Leishmaniasis

L.D. bodies live in mononuclear mcrophagocytosis system

Proliferation and destruction of m. m. p. system

(2) Hypertrophy of Bone marrow Broken piece

liver, lymph node, spleen is destrained

Liver cells Spleendestruction hyperfunction Fevering material

Plasma cells proliferation Albumin Destroy WBC, Central nervous systemdecrease RBC and platelet Globulin

increase (3) Anemia (1)Fever for a long time

(4)Bleeding

(5) The ratio of albumin to globulin

is inverted(A:G=1:2,

regularly, A:G=2:1)

Emaciation with ascites, darkened skin, fever, bleeding of the gums, immunity decrease. Die of infective complications( noma, Pneumonia)

IV. Diagnosis

In endemic area, clinical manifestations may lead to a presumptive diagnosis, but the confirmative diagnosis depends on demonstration of amastigotes ( L.D. body ) in direct smear or promastigotes in 3N medium which cultures the parasites from the liver, spleen, bone marrow and lymph node puncture. The bone marrow puncture is usually used because it is safe for the patients. The lymph node puncture is used as evaluation to curative effect. Immunological tests can be used ( water test, complement fixation test, ELISA.).IV. Treatment

Antimony sidium gluconate ( pentavalent ) is very effective to the parasites and is administered intravenously or intramuscularly. Pentamidine is useful to the parasites with resistance to the pentavalent.

V. Epidemiology

This disease is a zoonosis. Transmitting cycle:

Man Man

Animal Animal

1. Geographic distribution: There are 3 major endemic areas in the world.(1) The India, where infection is found among adults, especially young

adults. The infection is from man to man without reservoir host.(2) The Mediterranean region central Asia where infection occurs chiefly in

infants. Dog is the reservoir host.

(3) China, In China there are three endemic areas.A. Man to man form ( Plain form ): is chiefly prevalent in urban and

rural areas, among young adults. The vector is Phlebotomus chinensis, such as Shandong, Jiangsu etc.

B. Dog to man form: is chiefly prevalent in rural mountain, among infants. Dog is reservoir host. The dog that suffers from kala azar is called mangy dog. Because the skin lesion of the dog is obvious, where there are great deal of L.D> bodies, dog serves as an infectve source, it is more important than man does. The vector is Phlebotomus chinensis.

C. Natural foci form (animal to animal form ): is prevalent in desert areas, usually transmitting between wild rodents ( such as Meriones unguiculatus ). It is natural foci disease, can be transmitted to man by Phlebotomus longiductus or P. major wui. Endemic area are Xinjiang, Gansu.

VI. Prevention

Treat all the patients with chemotherapy: control sand flies by spraying insecticide and climate the breeding place of sand flies. The key of controlling kala azar is eradicating sand fly.

Sand flies are easily controlled, because of the following reasons: 1. The breeding places of sand fly are limited.2. The life cycle is long, more than 2 months.3. The reproductive ability is weak, there are two generations at

the most a year.4. The flight ability is feeble, active range is limited.5. They have susceptibility to insecticides.

HemoflagellatesAll genera of the blood and tissue flagellates belong to the family

Trypanosomatidea. Six distinct morphologic types, each representing a genus, have been identified in this family. Of these, four are pf medical significance. The amastigote (leishmanial form) is a small, round or oval body without a fagellum but containing a nucleus and kinetoplast. The promastigote (leptomonal form) is elongated and slender with with a free flagellaum extending from axoneme. The kinetoplast is near the anterior end of the organism. The epimastigote (crithidial form) is somewhat like the

promastigote in body form but less slender and is characterized by the shifting of kinetoplast to a position anterior to the nucleus and the development of an undulating membrane which at the extreme anterior becomes the free flagellum. The trypomastigote (trypanosomal form) is characterized by a shift of the kinetoplast to a posteror position with an undulating membrane extending the full length of the body. A free flagellum may or may not be present. Two genera, Leishmania and Trypanosoma are of medical importance. The species of medical significance are as follow: Leishmania Tropica

Leishmania braziliensisLeishmania donovaniTrypanosoma cruziTrypanosoma gambienseTrypanosoma rhodesiense

Trypanosoma cruzi Trypanosoma cruzi cause America trypanosomiasis or “Chagas” diasease. Confined to the western hemisphere, found chiefly in Mexico, Central Americah America. Various species of triatomid bugs, or kissing bugs, are the vectors or arthropod hosts. Dogs, cats, and other animals may serve as reservoir hosts. Trypanosoma gambienseTrypanosoma gambiense produce Gambian trypanosomiasis or Mid- and West African sleeping sickness. The endemic home of T. gambiense is the tropical heart of Africa. During the early or febrile stage of sleeping sickness. T. gambiense occurs in the blood and lymph nodes, while after development of cerebral symptoms, it is primarily found in cerebrospinal fluid. It does not invade or live within tissue cells but inhabitsconnective tissue spaces of the various organs and the reticular tissue of the lymph nodes and spleen, the intracellular spaces in the brain, and is present in the large numbers in the lymph channels throughout the body. Transmission of T. gambiense from man to man typically occurs through the bites of Glossina (Testes) flies after a cycle of development within the insects. Both male and female flies bite man and may serve as vectors. There is no proof that any of the game animals of Africa act as reservoir of in fection for man, even though various species of antelopes may be experimentally infected; but domestic animals, particularly cattle, pig and goats, carry this infection for long periods of time without apparent symptoms.

The symptoms of diagnostic importance early stages of sleeping sickness are irregular attacks of fever, enlargement of lymph nodes, especially those of the posterior triangle of the neck, erythematous skin eruptions and delayed sensation to pain. The diagnosis of infection with T. gambiense is based on the characteristic symptoms, history of living or having lived in an endemic area, and is established by demonstration of the parasite successively in blood, lymph nodes juice, sternal bone marrow or cerebrospinal fluid. Early diagnosis is essential since early treatment most successful. There two forms of human treypanosomiasis in Africa: one caused by T. gambiense having a much longer, milder, chronoc course and ending fatally with central nervous system involvement after several years duration and the other caused by T. gambiense, having a short course and ending fatally within a year.

Trypanosoma rhodesienseT. rhodesiense produce Rhodesian trypanosomiasis or East African sleeping sickness. This tranpanosome is the cause of a disease which typically runs a rapidly fatal course, often ending in death before the development of the nervous symptoms so typical of T. rhodesiense infections. The morphology of T. rhodesiense both in man and in the transmitting flies is identical with that of T. gambiense. T. rhodesiense inhabits the blood, lymph nodes,cerebrospinal fluid, and tissues of man and is present in the blood of cattle and various of antelope. It alsolives and and multiplies within the intestinal tract, salivary duct and glands of flies belonging to the genus Glossina.

Medical Entomology (Arthropodology) There are more than one million species in the animal kingdom. The

number of Phylum ARTHROPODA constitute the largest assemblage in in the animal kingdom. More than 80% of all animal species belong to the Phylum ARTHROPODA. There are aquatic, terrestrial and aerial.

The athropods are so common that everyone has had some experience with them. For example, you must have been bitten by mosquitoes many times since you were born.

Arthropods play an important role in human health and welfare, both beneficial and destructive: honey bees produce honey and pollinate flowers (fruits). They also serve as food source for other animals. They are very important in the food chain in the animal kingdom. Some of them are plant pests. Locusts destroy crops. Some of arthropods are parasites of man and animals, intermediate hosts of human and animal parasites and vectors of

diseases. Medical entomology deals only with those arthropods of medical importance. Arthropoda are highly organized invertebrates. Characteristics of the Phylum Arthropoda (adult):

Jointed or articulated appendages (arranged in pairs)A chitinized exoskeleton.Hemocele- with hemolymph in an open circulatory system.Sexes are separateBilateral symmetry

Life cycle: the life cycle of arthropods is divided into two main types: 1) complete metamorphosis (holometabola)-egg-larva (several stages)- pupa –adult; 2) incomplete metamorphosis (hemimetabola)-egg(larva)- nymph (several stages)- adult.

Classification: there five classes of medical importance is the phylum arthropoda:Class Insecta (Hexapoda)- flies and mosquitoes.Class arachnida- spiders, scorpins, ticks, and mites.Class Eucrustacea-crabs crayfishes, shrimp.Class chilopoda-centipedes.Class pentastomida (tongue worms) – parasites of vertebrates and occasionally of man. Adults lives in respiratory tract and larva in tissue. Harmful effects of arthropods1. Direct harma. Annoyance-flies interfere with your work and rest.b. Venom-stings of scorpions and spiders may even cause death.c. Parasites-pentastomida are parasites of reptiles, birds, mammals, and sometimes men. Fly larvae may cause myiasis. Scabies and mange are cause by Sarcoptes scabiei. Transmission of diseasesMechanicak transmission. Flies may transmit typhoid bacillus, protozoan cysts and ascaris eggs mechanically. Biological transmission. Pathogens spend a part of their lift cycle in the arthropods.(1) Propagative-arthropods act like culture media for the pathogens. Yersinia pestis multiply in fleas.(2) Cyclopropagative- the pathogenic organisms undergo a developmental

cycle in the arthropod with multiplication and change in form. Plasmodium sp. in anopheline mosquitoes.(3) Cyclodevelopmental- the pathogens undergo a change in form in the arthropod without multiplication. Filaria in mosquitoes. The arthropods involved in both cyclopropagative and cyclodevelopmental transmission are hosts of the pathogens. Without these arthropoda, the pathogens will die.Transovarian- some of the arthropods take only one blood meal in their whole life cycle. The transmission of the disease is accomplished transovarially. That is, the first generation gets the infection and the second generation spreads the disease. Ex. Japenese river fever, a rickettsial in fection.Control: the control of arthropods is complicated procedure. It must combine several methods:1. Reconstruction of environment so that the environment is not fit for their growth. 2. Mechanical-steaming, net (screening).3. Chemical- Most insecticides will kill both harmful and beneficial insects. There many side effects-poisonous to animals and men, food contamination, environmental pollution, etc.4. Biological – includes natural enemies, hereditary measures (sexual interference) etc.