Leishmania spp

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Leishmania spp
3 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
liver, lymph node, spleen
Liver cells
Broken piece
is destrained
Spleen
destruction
hyperfunction
Fevering material
Plasma cells
proliferation
Albumin
Destroy WBC,
decrease
RBC and platelet
Central nervous system
Globulin
increase
(3) Anemia
(4)Bleeding
(5)The ratio of albumin to globulin
is inverted(A:G=1:2,
regularly, A:G=2:1)
(1)Fever for a long time
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.
Hemoflagellates
All 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 braziliensis
Leishmania donovani
Trypanosoma cruzi
Trypanosoma gambiense
Trypanosoma 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 gambiense
Trypanosoma 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 rhodesiense
T. 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 separate
Bilateral 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 arthropods
1. Direct harm
a. 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 diseases
Mechanicak 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.
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