1. Blood & Tissue Protozoa
Lange Chapter 52
Faculty: AGUAZIM SAMUEL, M.D.

2. The medically important organisms:
The sporozoans: Plasmodium and Toxoplasma
The flagellates: Trypanosoma and Leishmania

3. Trypanosoma
and
Trypanosomiasis

4. Trypanosoa species Vertebrate host vector disease Epidemiology
Diseases caused by Trypanosoma spp. parasite
Trypanosoa species
Vertebrate host
vector
disease
Epidemiology
T.bruci bruci
Horses, pigs, cattle, rodents
Glossina spp.
Nagana
Tropical Africa
T.bruci gambiense
Human, monkeys, dogs,pigs,etc..
Sleeping sikness
West Africa
T.bruci rhodesiense
Human,pigs.
East Africa
T.crusi
Human, domestic & wild animal.
Reduviid bugs (Triatoma rhodnius)
Chagas’ disease
South America
T.evansi
Horses, dogs.
Tabanus spp.
Surra
India, Africa, Australia, South and central America

5. Trypanosoma cruzi (American Trypansomiasis)
Disease: Chagas’ disease (American trypanosomiasis)
Characteristics: Blood and tissue protozoan.
Life cycle:
1. Trypomastigotes in blood of reservoir host
2. Ingested by reduviid bug ( kissing bug or cone bug)
3. Form epimastigotes
4. Form trypomastigotes in the gut.

6. cone-nose or kissing bug
Riduvid bug, the vector of American trypanosomiasis

7. Trypanosoma cruzi
When the bug bites, it defecates and feces containing trypomastigotes contaminate the wound.
Organisms enter the blood and form amastigotes within cells; these then become trypomastigotes.
Transmission: Transmitted by reduviid bugs. Humans and many animals are reservoirs. Occurs in rural Latin America.
Pathogenesis: Amastigotes kill cells, especially cardiac muscle

8. Pathogenesis (Acute) Acute phase Starts 1 week after infection
Fever, lymph node enlargement, unilateral swelling of the eyelids (Romana’s sign), acute myocarditis, damaged muscle cells and edema.

9. Pathogenesis (Chronic)
Chronic Phases:
Starts 2 months after initial infection.
Indeterminate form: 60-70% of people with Chagas. Completely free of cardiac, gastrointestinal and neurological symptoms but 2-5% of patients convert to cardiac or digestive forms each year (reason not clear).

10. Cardiac manifestation
Cardiac form:
30-40% of people with Chagas. Induces arrhythmia, cardiac failure, thromboembolism, atrioventricular fibrillation, ventricular hypertrophy

11. Gastrointestinal manifestation
Digestive form:
10% of people. Megaoesophagus 3%, megacolon and may be associated with cardiac form. Difficulty in swallowing, regurgitation, aspiration may cause pneumonia and death. Chronic constipation, fecal compacting causes perforation of the colon.

12. Trypanosoma cruzi Laboratory Diagnosis:
Trypomastigotes visible in blood
But bone marrow biopsy, culture in vitro, or serologic tests may be required.
Clinical findings:
facial edema (Ramana’s sign)
nodule (chagoma) near the the bite.
Complications include megacolon and enlarged heart.
DEATH FROM CHRONIC CHAGAS DZ IS USUALLY DUE TO CARDIAC ARRHYTHMIAS AND FAILURE

13. Trypanosoma cruzi, trypomastigote form, in a blood smear (Giemsa stain) CDC

14. Chagoma: raised, non-purulent erythematous plaque surrounded by hard edema

15. Romana's sign: unilateral conjunctivitis and orbital edema 

16. Trypanosoma cruzi
Treatment: Nifurtimox and benznidazole  for acute disease. No effective drug for chronic disease.
Prevention: Protection from bite. Insect control.

17. Trypanosoma Disease: Sleeping sickness (African trypanosomiasis)
Trypanosomiasis is a systemic disease caused by the parasite Trypanosoma brucei.
East African trypanosomiasis: T. rhodesiense
West African trypanosomiasis: T. gambiense.
It is transmitted by the bite of the tsetse fly, a gray-brown insect about the size of a honeybee.

18. Trypanosoma (African Sleeping Sickness)
Characteristics: Blood and tissue protozoan.
Life cycle:
Trypomastigotes in blood of human or animal reservoir, are ingested by tsetse fly.
3. They differentiate in the gut to form epimastigotes
4. Metacyclic trypomastigotes formed in salivary glands.
5. When fly bites, trypomastigotes enter the blood.
6. Repeated variation of surface antigen occurs, which allows the organism to evade the immune response. Recurrent Fever.

19. MOT: metacyclic trypomastigote

20. Tsetse fly. The vector of African trypanosomiasis 

21. Trypanosoma (African Sleeping Sickness)
Transmission: Transmitted by tsetse flies.
Pathogenesis: Trypomastigotes infect brain, causing encephalitis.
Laboratory Diagnosis:
Trypomastigotes visible in blood in early stages and in cerebrospinal fluid in late stages.
Serologic tests useful.
This article is about the African trypanosomiasis. For the encephalitis epidemic of 1917–1928, see encephalitis lethargica.
Sleeping sickness Classification & external resources
Trypanosoma forms in a blood smear. ICD-10 B56. ICD DiseasesDB MedlinePlus eMedicine med/2140  Sleeping sickness or African trypanosomiasis is a parasitic disease in people and animals, caused by protozoa of genus Trypanosoma and transmitted by the tsetse fly. The disease is endemic in certain regions of Sub-Saharan Africa, covering about 36 countries and 60 million people. It is estimated that 50,000 to 70,000 people are currently infected, the number having declined somewhat in recent years.[1] Three major epidemics have occurred in the past hundred years, one from 1896–1906 and the other two in 1920 and 1970.
[hide]
Contents
1 Clinical features
2 History
5 Laboratory diagnosis
4 Life cycle
3 Geographic distribution and epidemiology
6 Treatment
8 See also
7 Prevention and control
6.1 History of treatment for sleeping sickness
9 References
9.1 Numbered references
Symptoms begin with fever, headaches, and joint pains. As the parasites enter through both the blood and lymph systems, lymph nodes often swell up to tremendous sizes. Winterbottom's sign, the telltale swollen lymph glands along the back of the neck may appear. If untreated, the disease slowly overcomes the defenses of the infected person, and symptoms spread to include anemia, endocrine, cardiac, and kidney diseases and disorders. The disease then enters a neurological phase when the parasite passes through the blood-brain barrier. The symptoms of the second phase give the disease its name; besides confusion and reduced coordination, the sleep cycle is disturbed with bouts of fatigue punctuated with manic periods progressing to daytime slumber and nighttime insomnia. Without treatment, the disease is fatal, with progressive mental deterioration leading to coma and death. Damage caused in the neurological phase can be irreversible.
[edit] Clinical features
10 External links
Mother to child infection: the trypanosome can cross the placenta and infect the fetus, causing perinatal death.
In addition to the bite of the tsetse fly, the disease is contractible in the following ways:
[edit] History
Blood transfusion
Laboratories: accidental infections, for example, through the handling of blood of an infected person and organ transplantation, although this is uncommon.
The condition has been present in Africa since at least the 14th century, and probably for thousands of years before that. The causative agent and vector were not identified until 1902–1903 by Sir David Bruce, and the differentiation between protozoa was not made until The first effective treatment, Atoxyl, an arsenic based drug developed by Paul Ehrlich and Kiyoshi Shiga was introduced in 1910 but blindness was a serious side effect. Numerous drugs designed to treat the disease have been introduced since then.
There have been three severe epidemics in Africa over the last century: one between 1896 and 1906, mostly in Uganda and the Congo Basin, one in 1920 in several African countries, and one that began in 1970 and is still in progress. The 1920 epidemic was arrested due to mobile teams systematically screening millions of people at risk. The disease had practically disappeared between 1960 and After that success, screening and effective surveillance were relaxed due to the withdrawal of colonial authorities, and the disease has reappeared in endemic form in several foci over the last thirty years. [2]
The disease is found in two forms, depending on the parasite, either Trypanosoma brucei gambiense or Trypanosoma brucei rhodesiense. T. b. gambiense is found in central and western Africa; it causes a chronic condition that can extend in a passive phase for months or years before symptoms emerge. T. b. rhodesiense, is the acute form of the disease but has a much more limited range. It is found in southern and eastern Africa; its infection emerges in a few weeks and is more virulent and faster developing. According to recent estimates, the disability adjusted life years (9 to 10 years) (DALYs) lost due to sleeping sickness are 2.0 million.[3] Recent estimates indicate that over 60 million people living in some 250 foci are at risk of contracting the disease, and there are about 300,000 new cases each year.[4] The disease has been recorded as occurring in 36 countries, all in sub-Saharan Africa.
[edit] Geographic distribution and epidemiology
Humans are the main reservoir for Trypanosoma brucei gambiense, but this species can also be found in pigs and other animals. Wild game animals and cattle are the main reservoir of T. b. rhodesiense.
Horse-flies (Tabanidae) and Stomoxydinae possibly could play a role by mechanical transmission (in special situations) not only of Nagana (the animal form of sleeping sickness) but also of the human disease form.[5]
The tsetse fly is large, brown and stealthy. The bite feels like a hot needle being stuck into the flesh. While taking blood from a mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream (1). Inside the host, they transform into bloodstream trypomastigotes (2), are carried to other sites throughout the body, reach other blood fluids (e.g., lymph, spinal fluid), and continue the replication by binary fission (3). The entire life cycle of African Trypanosomes is represented by extracellular stages. A tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host (4,5). In the fly's midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission (6), leave the midgut, and transform into epimastigotes (7). The epimastigotes reach the fly's salivary glands and continue multiplication by binary fission (8). The cycle in the fly takes approximately 3 weeks to progress.
Life cycle of the Trypanosoma brucei parasites. Source: CDC
[edit] Life cycle
Two areas from a blood smear from a patient with African trypanosomiasis. Thin blood smear stained with Giemsa. Typical trypomastigote stages (the only stages found in patients), with a posterior kinetoplast, a centrally located nucleus, an undulating membrane, and an anterior flagellum. The two Trypanosoma brucei species that cause human trypanosomiasis, T. b. gambiense and T. b. rhodesiense, are indistinguishable morphologically. The trypanosomes length range is 14 to 33 µm, Source: CDC
[edit] Laboratory diagnosis
The diagnosis rests upon demonstrating trypanosomes by microscopic examination of chancre fluid, lymph node aspirates, blood, bone marrow, or, in the late stages of infection, cerebrospinal fluid. A wet preparation should be examined for the motile trypanosomes, and in addition a smear should be fixed, stained with Giemsa (or Field), and examined. Concentration techniques can be used prior to microscopic examination. For blood samples, these include centrifugation followed by examination of the buffy coat; mini anion-exchange/centrifugation; and the Quantitative Buffy Coat (QBC) technique. For other samples such as spinal fluid, concentration techniques include centrifugation followed by examination of the sediment. Isolation of the parasite by inoculation of rats or mice is a sensitive method, but its use is limited to T. b. rhodesiense. Antibody detection has sensitivity and specificity that are too variable for clinical decisions. In addition, in infections with T. b. rhodesiense, seroconversion occurs after the onset of clinical symptoms and thus is of limited use.
Three similar serological tests are available for detection of the parasite; the micro-CATT, wb-CATT, and wb-LATEX. The first uses dried blood while the other two use whole blood samples. A 2002 study found the wb-CATT to be the most efficient for diagnosis, while the wb-LATEX is a better exam for situations where greater sensitivity is required. PMID
[edit] Treatment
The current standard treatment for first stage disease is:
The current standard treatment for second stage (late stage) disease is:
Intravenous suramin (for T.b. rhodesiense)
Intravenous pentamidine (for T.b. gambiense); or
Alternative first line therapies include:
Intravenous melarsoprol 2.2 mg/kg daily for 10 consecutive days.[6]
In areas with melarsoprol resistance or in patients who have relapsed after melarsoprol monotherapy, the treatment should be:
Intravenous eflornithine 50 mg/kd every six hours for 14 days.[8]
Intravenous melarsoprol 0.6 mg/kg on day 1, 1.2 mg/kg iv melarsoprol on day 2, and 1.2 mg/kg/day iv melarsoprol combined with oral 7.5 mg/kg nifurtimox twice a day on days 3 to 10;[7] or
melarsoprol and nifurtimox, or
(old "standard" 26-day melarsoprol therapy) Intravenous melarsoprol therapy (3 series of 3.6 mg/kg/day intravenously for 3 days, with 7-day breaks between the series) (this regimen is less convenient and patients are less likely to complete therapy)[9];
The following traditional regimens should no longer be used:
eflornithine
(incremental melarsoprol therapy) 10-day incremental-dose melarsoprol therapy (0.6 mg/kg iv on day 1, 1.2 mg/kg iv on day 2, and 1.8 mg/kg iv on days 3–10) (previously thought to reduce the risk of treatment-induced encephalopathy, but now known to be associated with an increased risk of relapse and a higher incidence of encephalopathy)[7][9];
According to a treatment study of Trypanosoma gambiense caused human African trypanosomiasis, use of eflornithine (DMFO) resulted in fewer adverse events than treatment with melaroprol. PMID
Suramin was introduced in 1920 to treat the first stage of the disease. By 1922, Suramin was generally combined with Tryparsamide (another pentavalent organo-arsenic drug) in the treatment of the second stage of the gambiense form. It was used during the grand epidemic in West and Central Africa in millions of people and was the mainstay of therapy until 1969.
[edit] History of treatment for sleeping sickness
All patients should be followed up for two years with lumbar punctures every six months to look for relapse.
The organo-arsenical melarsoprol (Arsobal) was developed in the 1940s, and is effective for patients with second stage sleeping sickness. However, % of those injected have reactive encephalopathy (convulsions, progressive coma, or psychotic reactions), and % die; it can cause brain damage in those that survive the encephalopathy. However, due to its effectiveness, melarsoprol is still used today. Resistance to melarsoprol is increasing, and combination therapy with nifurtimox is currently under research.
Pentamidine, a highly effective drug for the first stage of the disease, has been used since During the fifties, it was widely used as a prophylactic agent in Western Africa, leading to a sharp decline in infection rates. At the time, it was thought that eradication of the disease was at hand.
Eflornithine (difluoromethylornithine or DFMO), the most modern treatment, was developed in the 1970s by Albert Sjoerdsmanot and underwent clinical trials in the 1980s. The drug was approved by the United States Food and Drug Administration in 1990, but Aventis, the company responsible for its manufacture, halted production in In 2001, however, Aventis, in association with Médecins Sans Frontières and the World Health Organization, signed a long-term agreement to manufacture and donate the drug.
The genome of the parasite has been decoded and several proteins have been identified as potential targets for drug treatment. The decoded DNA also revealed the reason why generating a vaccine for this disease has been so difficult. T. brucei has over 800 genes that manufacture proteins that the disease mixes and matches to evade immune system detection. (Berriman, et al., 2005)
An international research team working in the Democratic Republic of the Congo, New Sudan and Angola involving Immtech International and University of North Carolina at Chapel Hill have completed a Phase IIb clinical trial and commenced a Phase III trial in 2005 testing the efficacy of the first oral treatment for Sleeping Sickness, known at this point as "DB289". [10] [11]
Recent findings indicate that the parasite is unable to survive in the bloodstream without its flagellum. This insight gives researchers a new angle with which to attack the parasite.[12]
Prevention and control focus on, where it is possible, the eradication of the parasitic host, the tsetse fly. Two alternative strategies have been used in the attempts to reduce the African trypanosomiases. One tactic is primarily medical or veterinary and targets the disease directly using monitoring, prophylaxis, treatment, and surveillance to reduce the number of organisms which carry the disease. The second strategy is generally entomological and intends to disrupt the cycle of transmission by reducing the number of flies. For in depth information on prevention of the disease via tsetse fly control see Tsetse fly control
[edit] Prevention and control
Regular active surveillance, involving case detection and treatment, in addition to tsetse fly control, is the backbone of the strategy for control of sleeping sickness. Systematic screening of communities in identified foci is the best approach as case-by-case screening is not practically possible in highly endemic regions. Systematic screening may be in the form of mobile clinics or fixed screening centres where teams travel daily to the foci. The nature of gambiense disease is such that patients don't seek treatment early enough because the symptoms at that stage are not evident or serious enough to warrant seeking medical attention, considering the remoteness of some affected areas. Also, diagnosis of the disease is difficult and most health workers may not be able to detect it. Systematic screening allows early-stage disease to be detected and treated before the disease progresses, and removes the potential human reservoir.[13]
Instances of sleeping sickness are being reduced by the use of the sterile insect technique.
The cover story of the August 25, 2006 issue of Cell journal describes an advance; Dr. Lee Soo Hee and colleagues, working at Johns Hopkins, have investigated the pathway by which the organism makes myristate, a 14-carbon length fatty acid. Myristate is a component of the variant surface glycoprotein (VSG), the molecule that makes up the trypanosome's outer layer. This outer surface coat of VSG is vital to the trypanosome's avoidance of immunological capture. Dr. Lee and colleagues discovered trypanosomes use a novel fatty acid synthesis pathway involving fatty acid elongases to make myrsitate and other fatty acids.
There is a single case report of sexual transmission of West African sleeping sickness.[14] This is not believed to be an important route of transmission. A case of sexually transmitted sleeping sickness was the focus of an episode of House.
David Bruce (microbiologist)
Drugs for Neglected Diseases Initiative
[edit] See also
The other important human tropical disease caused by Trypanosomes is Chagas-disease, occurring in America.
Sleep disorder

22. METACYCLIC TRYPOMASTIGOTE
Blood smear from a patient (a U.S. traveler) with Trypanosoma

23. Pathogenesis (2 stages)
Stage 1: Haemolymphatic stage (ACUTE)
Most patients do not notice this stage of infection.
Small papule from bite may develop exciting local inflammation.
When trypomastigotes enter the haemo-lymphatic system to multiply,clinical symptoms include:
Fever, headache and joint pain
Winterbottom’s sign: swelling of lymph nodes at the posterior neck region.

24. Stage 2: Meningoencephaltic stage (CHRONIC)
Sleeping sickness stage because trypanosomes have crossed the blood-brain barrier
Personality changes, headaches and withdrawal from the environment.
Simple tasks become harder to accomplish as individual experience nocturnal insomnia and daytime lethargy, apathy and ultimately succumb to secondary infections such as pneumonia.

25. Trypanosoma African Sleeping Sickness
Clinical Finding: Important!!!
Indurated skin ulcer (trypanosomal chancre) at the site of fly bite
Fever for 1 wk./ no fever 2 wks./fever again
Enlargement of the glands of the posterior cervical region (Winterbottom's sign)
Neurological complications can occur as a result of infection.
Wasting and skin damage caused as a result of the intense itching which can accompany late-stage disease.
Coma

26. The leg of a teenage girl who has sleeping sickness, showing the chancre at the site of the tsetse fly bite

27. Parasitemia 2-3 WEEKS after the bite fever malaise, lassitude
insomnia, headache
lymphadenopathy and edema
Kerandel's sign : painful sensitivity of palms and ulnar region to pressure
Febrile episodes:
few months- Rhodesian disease
several years - Gambian disease

28. Very characteristic of Gambian disease is visible enlargement of the glands of the posterior cervical region (Winterbottom's sign)

29. CNS Stage changes in character and personality
lack of interest and disinclination to work
avoidance of acquaintances
morose and melancholic attitude alternating with exaltation
mental retardation and lethargy
low and tremulous speech
tremors of tongue and limbs
slow and shuffling gait
altered reflexes
males become impotent

30. Neuropathology of Human African Trypanosomiasis Acute hemorrhagic leucoencephalopathy

31. Why do they call it sleeping sickness?
DAYTIME SOMNOLENCE
NIGHTTIME INSOMNIA
Micro class
Ziggy’s

32. DOC:
1. Pentamidine–inhibiting dihydrofolate reductase enzyme, interfering with aerobic glycolysis
2. Suramin – trypanocidal; inhibiting parasitic enzymes ,growth factors
3. Melarsoprol – CNS; trypanocidal, inhibiting parasitic glycolysis ; late disease

33. PREVENTION
Protection against the fly bite, using netting and protective clothing.
Clearing forest around villages
Irradiation of male flies technique
Chemical sprays( insecticides)

34. LEISHMANIASIS

35. Introduction
In the Middle East L. major and L. tropica are the most common species
L. major causes skin infection
L. tropica causes skin and visceral infection and rarely causes mucocutaneous infection
About 1.5 million new cases of cutaneous leishmaniasis in the world each year
500,000 new cases of visceral leishmaniasis estimated to occur each year also
20 cases of cutaneous leishmaniasis from L. major/ L tropica and twelve cases of visceral infection caused by L. tropica were reported in soldiers from Desert Storm

36. Endemic Areas for Leishmaniasis
Highlighted areas are parts of the world where leishmaniasis has been reported.
Taken from British Medical Journal :378
BMJ 2003;326:378

37. Leishmaniasis in the Middle East
90% of cutaneous leishmaniasis occurs in Afghanistan, Iran, Saudi Arabia, Syria, Brazil and Peru
8,779 cases were reported in Iraq in 1992
Sore is commonly called the Baghdad boil
At least 20 cases of cutaneous leishmaniasis were reported in Americans from Desert Storm
90% of all visceral leishmaniasis occurs in Bangladesh, Brazil, India, and the Sudan
2893 cases were reported in Iraq in 2001
12 visceral leish cases were reported in Americans in Desert Storm
90% of mucocutaneous leishmaniasis occurs in Bolivia, Brazil and Peru
Rarely associated with L tropica which is found in Middle East
Data on leishmaniasis is based on voluntary reporting by countries so true incidence may be higher in countries that are not likely to report.
Numbers of cases in Iraq come from recent Promed messages (authors Desjeux and Deresinki)

39. LEISHMANIASIS: Leishmania 2nd largest parasitic killer in the world
L. donovani: visceral leishmaniasis
(Kala-azar, black disease, dumdum fever)
L. tropica: cutaneous leishmaniasis
(oriental sore, Delhi ulcer, Aleppo, Delhi or Baghdad boil)
L. braziliensis: mucocutaneous leishmaniasis (espundia, Uta, chiclero ulcer)

40. LEISHMANIASIS prevalent world wide south east Asia Indo-Pakistan
Mediterranean
north and central Africa
south and central America

41. MOT: bite of Sandfly (Phlebotomus) aka sandflea, no-see-um, no-see-em, noseeum, sand gnats, chitras, punkie, or punky

42. Infective form: promastigote Intracellular form: amastigote

43. Leishmania donovani
Disease: Kala-azar

44. Two children with visceral leishmaniasis
Two children with visceral leishmaniasis. The size of the spleen is marked on the abdomen. Normally the spleen does not protrude below the bottom rib.
Photograph provided by COL Charles Oster

45. Leishmania donovani Characteristics: Blood and tissue protozoan
Life cycle:
Human macrophages containing amastigotes are ingested by sandfly.
2. Amastigotes differentiate in fly gut to promastigotes
3. Migrate to pharynx which can be transmitted during next bite.
4. When fly bites, promastigotes enter blood and engulfed by macrophages and form amastigotes.
5. These can infect other reticuloendothelial cells, especially in spleen and liver.
Amastigotes: without flagella
Promastigotes: with flagella

46. Leishmania donovani Transmission: Transmitted by sandflies.
Animal reservoir (chiefly dogs, small carnivores, and rodents) in Africa, Middle East, and parts of China.
Human reservoir in India.

47. Laboratory Diagnosis:
Leishmania donovani
Pathogenesis: Amastigotes kill reticuloendothelial cells, especially in liver, spleen, and bone marrow.
Laboratory Diagnosis:
Amastigotes visible in bone marrow smear
Serologic tests useful.
Skin test indicates prior infection.

48. Clinical Finding: Leishmania donovani Severe muscle wasting.
visceral leishmaniasis develop a noticeable thickening, stiffening and darkening of the eyelashes and eyebrows
Jaundice
Enlarged spleen and liver
Skin ulcer

49. Profile view of a teenage boy suffering from visceral leishmaniasis(dumdum fever). The boy exhibits splenomegaly, distended abdomen and severe muscle wasting.  CDC

50. Many children suffering from visceral leishmaniasis develop a noticeable thickening, stiffening and darkening of the eyelashes and eyebrows

51. A 12-year-old boy suffering from visceral leishmaniasis
A 12-year-old boy suffering from visceral leishmaniasis. The boy exhibits splenomegaly and severe muscle wasting.

52. Jaundiced hands of a visceral leishmaniasis patient

53. Enlarged spleen and liver in an autopsy of an infant dying of visceral leishmaniasis.

54. Skin ulcer due to leishmaniasis, hand of Central American adult. CDC
Skin ulcer is called an “oriental sore”
Skin ulcer due to leishmaniasis, hand of Central American adult. CDC

55. Cutaneous leishmaniasis (Oriental sore, Delhi ulcer, Baghdad boil)
L. tropica
multiplies locally
encrusted ulcer with satellite papules
disfiguring scar

56. Cutaneous Leishmaniasis
Most common form
Characterized by one or more sores, papules or nodules on the skin
Sores can change in size and appearance over time
Often described as looking somewhat like a volcano with a raised edge and central crater
Sores are usually painless but can become painful if secondarily infected
Swollen lymph nodes may be present near the sores (under the arm if the sores are on the arm or hand…)
Some sores are covered by a scab or have not yet ulcerated so they may look like red raised plaques- sometimes with dry crust/scale

57. Cutaneous Leishmaniasis
Most sores develop within a few weeks of the sandfly bite, however they can appear up to months later
Skin sores of cutaneous leishmaniasis can heal on their own, but this can take months or even years
Sores can leave significant scars and be disfiguring if they occur on the face
If infection is from L. tropica it can spread to contiguous mucous membranes (upper lip to nose)

58. Cutaneous leishmaniasis of the face.

59. A cutaneous leishmaniasis lesion on the arm.

60. Depigmented scar
Scar on skin of upper leg representing healed lesion of leishmaniasis CDC 

61. Girl with diffuse cutaneous leishmaniasis of the face which is responding to treatment 

62. Multiple lesions on arm with a variety of appearances.
Photograph provided by COL Naomi Aronson

63. Both lesions are leishmaniasis
Note the raised border and wet appearance of the sore on the back of the hand.
Sores over joints are very concerning as scarring with healing can lead to limited movement of joint.
Photograph provided by COL Charles Oster

64. Upper Eyelid.
Note the dry, crusted/scabbed appearance which is different than previous sores shown.
Photograph provided by COL Naomi Aronson

65. Back of hand.
Note raised border and wet appearance. Patient has bacitracin ointment applied to lesion.
Photograph provided by COL Naomi Aronson

66. Close up of another dry, crusted lesion with concentric surrounding scale. This is a typical appearance for Old World Leishmaniasis.
Photograph provided by COL Charles Oster

67. Mucocutaneous Leishmaniasis L. braziliensis
begins with a papule at the bite site, but then metastatic lesions form, usually
at the mucocutaneous junction of the nose and
mouth.
Disfiguring granulomatous, ulcerating lesions destroy nasal cartilage but not adjacent hone.
These lesions heal slowly, if at all. Death can occur from secondary infection.

68. Photograph provided courtesy of COL Donald Skillman

69. Treatment and Prevention
DOC: Sodium stibogluconate
-potent inhibitor of parasitic enzymes ,enhancer of cytokines
Amphotericin B: resistant strains
PREVENTION
Protection from sandflies using netting, protective clothing and insect repellents and insecticide spraying.

70. The Highest form of Deception is to Think or Believe…
The Highest form of Deception is to Think or Believe….Everybody is Doing It!!!!!!
General Bison