2. Epidemiology
– Neglected of the tropical diseases
– 2 million new cases every year
– 350 million people are considered to be at risk.
– 80,000 deaths annually
– Affects the poorest populations in 88 countries
– 90 %of CL =seven countries :Afghanistan, Algeria, Brazil,
Iran, Peru, Saudi Arabia and Syria
– Four countries: Brazil, India, South Sudan and Sudan,
reported >2000 VL cases, representing 73% of cases
globally ; with Ethiopia, Kenya and Somalia, 90% of VL
cases reported worldwide (2015 WHO report)
3.
4.
5. Three syndromes associated with Leishmania
infection in humans
• Variability of the clinical features results from both the
diversify of the leishmania species and the immune
response of the hosts
• Visceral leishmaniasis (VL), (kala azar)
• The most severe form of the disease.
• Mortality rate of almost 100%
– Leishmania donovani
– Leishmania infantum/ chagasi
6. Three syndromes associated with Leishmania
infection in humans cont..
•Cutaneous leishmaniasis (CL)
–large numbers of skin ulcers on the exposed parts of the body.
–Often self-healing but it can create permanent scars.
–After recovery or successful treatment, induces immunity to
re-infection by the species that caused the disease.
– Represent 50-75% of all new cases.
• Leishmania tropica
•Leishmania major
•Leishmania aethiopica
7. Three syndromes associated with Leishmania
infection in humans cont..
Mucocutaneous leishmaniasis (MCL)
lesions can lead to extensive and disfiguring destruction
of mucous membranes of the nose, mouth and throat
cavities.
Leishmania braziliensis
Leishmania mexicana
Leishmania amazonensis
Diffuse cutaneous leishmaniasis
Post kalazar dermal leishmaniasis
8. Epidimiology In Ethiopia
• Information on the epidemiology is incomplete as no surveillance
system is yet in place, but reports of VL endemicity date back to the
1940s.
• VL is prevalent mostly in arid lowland areas, and the principal
parasite involved L. donovani, with an estimated annual incidence
of 4000 cases.
• 4.0 million people living in areas with risk of VL transmission
(FMOH, 2008).
• Sporadic epidemiological surveys showed the presence of VL in
more than 40 isolated localities in Ethiopia
9. Epidimiology In Ethiopia
• VL is spreading to previously non-endemic areas, as
exemplified by the recent outbreak in Libo-Kemekem and
Fogera districts (south Gondar), Segen Zone
• Cutaneous leishmaniasis is endemic in the highlands; the
predominant parasite is L. aethiopica with the rock hyrax
as reservoir.
• The sandfly vector is thought to be phlebotomus orientalis
in the northwest, phlebotomus martini in the south.
10. Epidimiology In Ethiopia
• Endemic areas :VL
• North-West
– Metema, Humera, Wolkayit =60%
– Libo/Fogera
• North-East
– Awash valley
– Ethiopia–Djibouti border
• South and South-West
• Dawa, Genale, , Segen, Woito, Konso and Omo river valley
• Kenya border
• Gambella–Sudan border
12. Life Cycle of Leshimaniasis
• Transmitted by the bite of an infected female phlebotomine
Sand fly
• Two forms
– Leishmanial form:- ( amastogote ) this is non flagellate
form seen in man and extra human vertebrate reservoir
– Leptomonad forms (also called promastigotes) are
flagellated forms
• Animal Reservoirs: include
– Rodents - Commonly in East Africa, Ethiopia, the Sudan
and Kenya and
– Canines -Mediterranean and Asia.
13. Life Cycle of Leshimaniasis
• As the sandfly feeds, promastigote forms of the
leishmanial parasite enter the human host
• Within the human host, the promastigote forms of the
parasite are ingested by macrophage where they
metamorphose into amastigote
• They increase in number until the cell eventually bursts,
then infect other phagocyctic cells and continue the
cycle.
• The infected host is bitten by another female sandfly.
• The parasites are transformed inside the fly and
delivered to a new host, and the life-cycle continues
14. Immuno -pathology of Leishmaniasis
Establishing a Leishmania Infection .
Some surface membrane molecules:
• Protect Leishmania from the host immune response
• Increase infectivity
• The two major molecules are
– Lipophosphoglycan (LPG)
– gp63.
15. IP of L. ct..
• Other outer membrane molecules
– Membrane – bound acid phosphatase
– ATP ase
– Glucose transport protein
– gp 48
– PSA 2 glycoprotein
16. IP of L. ct..
• Evasion of complement lysis.
• Promastigotes are inoculated into the blood of
a bite wound when a female sandfly feeds on
humans
• Are exposed to complement immediately after
inoculation
• Must avoid destruction by complement before
they can successfully parasite host mΦs
17. IP of L. ct..
Use complement deposition to enhance their ability to
invade mΦs
Leishmania may avoid complement by the use of
intracellular enzyme
Invasion of the Host Cells
Promastigotes that are not destroyed by complement
rapidly invade mΦs by inducing phagocytosis.
Attachment to the surface of the mΦs is an important
part of this process and facilitates entry in to the mΦ
18. IP of L. ct..
• The promastgotes transform in to
amastigotes with in macrophages
• Amastigotes with in the phygolysosome can
resist destruction and increase in number until
eventually the mΦ bursts.
• Released amastigotes can reinfect other mΦs.
19. The early granuloma.
A Leishmania infection may;
• Remain localized at the site of infection
• Disseminate to various tissues and organs
• Infected mΦ accumulate in to a granuloma,
which Is an inflammatory lesion.
• Arises when an intracellular organism cannot
be totally eliminated
20. granuloma ct.
• Is associated with infiltration of other cells,
especially plasma cells, T. lymphocyte.
• Has a central zone of infected mΦs
surrounded by lymphocytes.
• Efficiently ‘walls off’ the infection site to
prevent the spread of infection.
21. T cell activation
With infected macrophages
• Some leishmania are broken down.
• Leshmania proteins are associated with MHC
molecules
• MHC class II molecules present leishmania
antigen on the mΦ cell surface and CD4 + Th 1
cells
22. T cell activation Ct…
• Bind the presented Leishmania antigen
• Become activated to:
– Multiply
– Release interleukin 2 (IL-2)
– Release IF-γ
– Others
• Specialized antigen presenting cells called dendritic cells
may present Leishmaina antigens to T cells.
23. Activation of macrophages
Activated CD4+ Th 1 cells stimulate mΦ
stimulated mΦ:
• Are known as activated mΦs.
• Have a more motile cell membrane.
• Have an increased ability to kill parasites
• Release TNF- and IL -12.
• Show alterations in surface molecules .
• Show more effective killing by
– ROIs
– RNIs
CD4 + Th 1 cells have a very important role in coordinating the mΦ
responses
24. Effect on mΦ and T cell function
• Leishmania parasites are able to disrupt mΦ and T-cell
function, some species of Leishmania can:
– Block amastigotes antigen from presentation on mΦs
– Decrease level of MHC –molecules on mΦs so that
antigen presentation is inhibited.
– Suppress secretion of IL-2 and IFN-γ from activated T
cells.
– Impair TNF and production by infected mΦ
25. Effect on Ct…
– Induce production of cytokines which inhibit mΦ
function.
– For example L.aethiopica can induce IL -10 which
inhibit IFN-γ
26. Outcome of infection
The outcome of Leishmania infection depends upon a balance
between subsets of CD4+T cells.
A Th 1 Cell response
•Stimulates cell-mediated
responses (phagocyte-dependent
immunity)
•Protects against Leishmania
infection
•Results in the release of
IFN- γ
IL-2
Cytotoxic molecules
A Th 2 response
•Activates phagocyte
Independent immunity (humoral
immunity).
•Is not effective at controlling
the spread of infection and leads
to progressive disease.
•Results in release of cytokines
which inhibit cell mediated
response.
27. Cytokine pattern
Some correlations between cytokines and forms of the
disease have been found but evidence is not conclusive.
The following patterns have been observed.
• Localized simple CL lesions have high levels of IFN -γ
while diffuse CL lesions have relatively low.
• IL-4 and IL-10 are increased in patients with diffuse CL
• IL-10 is high in patients with VL and decreases after
treatment.
28. Immunology of VL
• In VL the parasites migrate from the site of inoculation to
the Viscera
• With in the viscera, the parasitized phagocytic cells
– Proliferate
– Form small granules
• Some VL patients do spontaneously heal
• But established disease is associated with
– A failure of specific cell-mediated immunity to
Leishmania
– High levels of antibody
29. Cell-mediated immunity
• Patents with progressive VL show:
– Uncontrolled parasitization of mΦs
– Reduced lymphocyte proliferation to Leishmnia antigens
– Decrease level of IL-2, IFN-γ
– Increased level of IL-4, IL-10
30. Failure of cell mediated immunity
why?
• Reduced ability of mΦ to present antigen to T cells,
Kill intracellular paraistes
• Failure to activate a CD4+ Th 1 cell response
• Macrophage production of deactivating cytokines
(eg. IL-10 TGF-B)
31. Clinical Features,VL
Symptom
• I.P. is difficult to evaluate precisely.
• It is generally 2-6 months, but can range from 10
days to many years. ≈10 years
• Onset sudden or gradual
• Protuberent abd, and muscle wasting of limbs
• A general syndrome including fever, asthenia weight
loss, anaemia, splenomegally, hepatomegally and
some times LAP dominates the clinical presentation.
32. Clinical Features VL Ct…
Splenomegally appears early and is almost invariably
present.
It is firm, smooth, mobile and painless, spleen size increases
regularly, in relation to the duration of the disease.
Hepatomegally less frequent .
Diarrhea, pulm. involvment, bleeding tendencies .
During evolution the clinical picture progressively
worsens.
33. Post Kala-Azar Dermal Leishmaniasis
• Sequel of VL & first described in India.
• Can develop before therapy, during therapy or within a
few months after therapy ( eg, in E/Africa) or can
develop years later (eg in India)
• Manifested by skin lesions (including macules,
papules, nodules, or patches) that typically are more
prominent on the face but it may involve other parts
of the body.
• Lesions are not painful and ulcerations are uncommon.
• may contain parasites in great numbers
• Can serve as a reservoir of infection.
• Relapse of visceral infection can occur
• Should be differentiated from syphilis, yaws and
leprosy.
34.
35.
36.
37. PKDL is considered to be triggered immunologically &
follows apparently successful treatment of VL in a
proportion of patients.
ART during HIV co-infection can lead to PKDL.
• It is almost always associated with L.donovani
38. Clinical Features CL
• Following the bite of sand flies, leishmania multiply
in the macrophages of the skin.
• Single or multiple painless nodules occur on exposed
areas (mainly the face) within one week to 3 months
of the bite.
• The nodules may enlarge and ulcerate with
erythematous raised border and overlying crust
which may spontaneously heal over months to years.
39. Clinical Features MCL
• In the early stage it affects the skin, but in secondary stage of
the disease it involves the upper respiratory mucosa.
• Initially painful, itchy nodules appear on the lower limbs and
then ulcerate with lymphangitis.
• The lesion may heal spontaneously in 6 months
• In about 40% of patients, secondary lesions appear several
years later at the mucocutaneous junctions of nasopharynx.
• This leads to nasal obstruction, ulceration , septal
perforations and destruction of the nasal cartilage called
Espundia.
40. Clinical case definition
• VL Case definition:
– fever > 2 weeks, with malaria excluded.
– plus either splenomegaly or lymphadenopathy.
– plus either of wt. loss, anemia, or leukopenia.
• If a patient does not fit the clinical case definition, then
– positive serology is not specific enough to diagnose VL.; as 5-
10% of adults in the endemic area will have +ve anti-
Leishmania antibodies
41. Case definition vs VL cases
2. Case definition
4. VL Cases
1. Population
3. DAT +
42. Diagnosis
• Once differential diagnoses have been ruled out, a
clinically suspected case can be confirmed by
– 1.Parasitological Tests
– 2.Imunological Tests
2 A. Serological Diagnosis (Antibody
detection or humoral response Assay)
2 B. Cell Mediated Immune Response Assay
43. Frequent S & S Common S & S Less common S&S
•Splenomegally
•Fever, prolonged
•Weakness
•Weight loss
•Pallor/anemia
•Leukopenia
•Hepatomegally
•Loss of appetite
•Diarrhea
•Cough
•Lymphadenopathy
•Ascites
•edema
•Jaundice
•Epistaxis
•Vomiting
•Skin darkening
The frequency of signs and symptoms of VL/HIV negative Ethiopian
VL patients.
Approximately 30-50% of patients meeting the clinical case def. of VL
are found to have the disease.
44. 1.Parsitological Tests
• Splenic Aspirate
– highly sensitive - 96%
– risky leading to life threatening internal bleeding
(the risk of mortality from aspiration may happen
1/1000 cases)
– Contraindications
• patient with bleeding tendency and jaundiced
• platelet count < 40,000/mm3 or
• protrombin time is >5 seconds
• spleen <3cm
• Patient critical and vital signs are derranged
• Children if restless or unable to lie
• advanced stage of pregnancy
45. • Bone marrow aspirate
- sensitivity is 70-80%
• Lymph node aspirate
- Sensitivity 60%
- Palpable lymph nodes(> 1x1 cm) can be used
- Convenient site: Inguinal and epitrochlear
• Skin slit smear/ biopsy
– Tissue sample (scraping, aspirate or punch biopsy)
for smear and culture
• Sensitivity 75-90%
• PCR
.Buffy coat smear
46. 2.Immunological tests
- Serological Test
Types of serological tests
I. Direct Agglutination Test (DAT)
II. Rk39 Dipstick Test (rk39)
III. Formol Gel Test
IV. Immuno Fluorescent Antibody Test (IFAT)
V. Enzyme Linked Immunosorbent Assay (ELISA)
- Cell Mediated Immune Response Assay
47. Direct Agglutination Test (DAT)
detects the presence of Leishmania antibodies using
Leishmania antigen
Used to confirm diagnosis with clinical case
definition strictly followed
for primary VL, never for relapse
cases
highly sensitive (95%) and specific (>85%)
plates incubated for 8-12 hours and then read
takes 2-3 days
48. 100 12800 25600 51200
800 1600 3200 6400
200 400 102400
0 1 2 3 4 5 6 7 8 9 10 control
Titers
DAT Titer Designation
by integer
49. Rk39 test
qualitative membrane based immunoassay
detection of Leishmania antibodies
rapid and easy diagnostic test
results available with in 10-15 minutes
highly sensitive and specific
easy to use in the field settings during outbreak
50. Leishmainin skin Test (Montenegro Reaction)
• test used for epidemiological
/prevalence study
• Indicates the number of persons that
had infection with Leishmania at some
point in their life
• intradermal injection of Leishmania Ag
(inner surface of the forearm)
• reading: 48-72 hrs after test
• positive reaction indurations with
diameter >5mm
• - associated with clinical cure
51.
52. Additional Investigations for VL patients
Hematology tests
HIV Counseling and Testing
CXR, sputum exam
ECG
Organs Function Tests –liver enzymes, LFT
- Serum amylase
- RFT (urea/creatinine)
53. General principle of Management
• General aspect
– Establish diagnosis
• Clinical
• Laboratory
– Asses for complications and co-infections
– Outline management options
• Specific drug management
• Supportive
– Nutritional support and feeding
– Correction of co-morbid conditions
• Anemia, bleeding,super-infection and co-infection etc
• In HIV/VL co-infection: start ART
54. Specific drug management
aims for Kalazar
• Reduce the parasite burden
• Prevent resistance
• Avoid toxic drug effect
• Improve complications: anemia, malnutrition &
secondary infections, etc
– ultimately the cell mediated immunity can return which
helps to clear the remaining Leishmania as ‘sterile cure’ by
drug/s is not possible to date.
55.
56. Management after drug interruption
Scenarios:
i) If it’s discontinued for less than 5days, resume treatment where
patient has left off and continue till normal number of doses of Rx has
been given
ii) if 5-15 days of interruption, continue Rx till normal number of doses has
been given but do TOC at the end of treatment
iii) If a 15 days or more interruption, the patient needs readmission, for
parasitological testing:
=if positive, restart Rx as day 1 and do TOC before discharge.
=If test is negative, give Rx till normal number of doses has been given
57. Treatment Out come
Clinical response-
• Cure: Initial Vs definitive
Initial cure: initial parasitological cure (TOC)
Definitive cure: free of relapse by 6 months after initial
clinical or parasitological cure; decided clinically ;TOC may not
be needed
• Relapse: 1st, 2nd, 3rd,etc
• unresponsive:
no decrease in parasitological load after adequate treatment; or
TOC 4+ parasitological load if not done at diagnosis
• Death-
• After treatment the patient should be
– reviewed at 1, 3, 6 and 12 months.
– Patients should be told to report if they develop symptoms of VL
or a skin rash (PKDL).
58. How can cure be evaluated?
• Clinical assessment
– Fever disappearing, Pt. look stronger, good
appetite (7-10days)
– regressing spleen, Hgb improved, weight gained
(14days)
• Parasitological confirmation of cure
– not routinely necessary and may be reserved for
cases where response is in doubt.
– is essential, however, in the treatment of relapses.
59. Relapse
• Definition- If a person returns with symptoms, after
having been treated and discharged with a negative TOC
• Impossible to differentiate new infection from
relapse All cases are considered relapses
• Occurs in up to 5% of treated patients
• Could be as high as 50-80% in HIV/VL Co-infected
patients.
- Most occur in the first 6 Months of initial discharge
60. Relapse cont’d
- diagnosed parasitologically
- higher chance of second relapse & failing to respond to Rx
=> due to host factors (HIV,Tb etc) and because of parasitic
drug resistance
- there should be two –ve TOC before discharging relapsed
patient at each relapse
- the likelihood of having +ve TOC after treating a relapse is
as high as 10%
- any further relapse is difficult to treat and cure
61. Relapse cont’d
• Rx of 1st Relapse:
– SSG for 40-60 days;
1st TOC to be done at day 33 and 2nd TOC by day 40
– If still has parasite at day 60,consider unresponsiveness and use
Amphoterecin B
• 1st TOC day 23, 2nd TOC by day 30
– ?Combination therapy preferred
– Always consider the possibility of Co-infection with HIV, and
others like TB
62. • Bad prognosis criteria
– AIDS
– severe concomitant opportunistic infection
– low CD4+
– thrombocytopenia
– relapsing course
– Severe anemia
– no secondary prophylaxis
– Duration of illness >5 months
– Extremes age groups >45 and <2 yrs
– Very low BMI <13 or Wt/Ht <60%
– Those in a state of collapse
Prognosis of VL
63. HIV-VL co-infection
• Leish - HIV co-infection rate is reported to reach up
to 40% in Ethiopia-Humera
– In Libo, 15–18% of all VL patients are HIV positive
• A retrospective review of 791 cases in Tigray
indicated that more than 4x CFR in HIV + VL patients
64. HIV-VL risk groups in Ethiopia
• Sex workers
• Seasonal migrant laborers
• Young adults and new settlers in the endemic areas
(in the North west & along Sudan border)
• Truck and other public transport drivers
• Military personnel deployed in the border areas
65. Peculiarities of HIV-VL co-infection
• Parasites can be in unusual sites
• Presentations may be atypical
• Mortality is high (3.5-4 times higher)
• Lower response rate for treatment
• Serious side effects with treatment
• Relapse rate is very high
66. • Treatment after relapse may be refractory
• HIV increases the chance to develop clinical VL rather
than sub-clinical self healing infection
• Highly infectious reservoirs
• A few cases of the first occurrence of VL (Berry et al.
2004) and PKDL as an IRIS after initiation of HAART
have been reported (Gilad et al. 2001).
67. HIV-VL on survival
• 30 % of HIV/VL patients will die during treatment or
within a month after treatment.
• Death is seldom due to VL alone.
• The average time to relapse is
– usually 3 - 6mons, with successive relapses becoming
less typical and less acute, but occurring more
frequently.
68. Diagnosis of VL in HIV co-infection
• Parasitologic diagnosis has high sensitivity.
Sensitivity of bone marrow aspirate microscopy is
reported to be 94 % and culture 100 %.
Microscopy of blood films may be useful and is said
to be positive in 50 % of patients.
• Serology has low sensitivity
Over 40% of co-infected patients have no detectable
specific antibody levels against Leishmania
69. HIV-VL Co-infection - Treatment
• Treatment principle is similar to HIV-ve VL
• All VL drugs are less effective in HIV patients
• ?AmBisone 1st line drug for primary kalazar.
• Second line= Miltefosine, Pentavalent antimonials,
Paramomycine sulfate
• ??? Combination Therapy
• Treat relapse if only symptoms are severe
• Treat other OIs if diagnosed.
• HAART is the key to postpone relapse
70. Suggested Drug combinations for the treatment of visceral leishmaniasis associated
with HIV/AIDS
Based on discussion and recommendations made by a “Drug combinations for the treatment of visceral leishmaniasis“ Working Group that met
on the 15-16th of February 2005 at DNDi, Geneva.
• Antimonials: 20 mg/kg/d x 28 d + Paromomycin: 15 mg/kg/d x 28 d
• Antimonials: 20 mg/kg/d x 28 d + Amphotericin-B: 1 mg/kg/d x 28 d
• Antimonials: 20 mg/kg/d x 28 d + Allopurinol: 20 mg/kg/d x 28 d
• Antimonials: 20 mg/kg/d x 28 d + Miltefosine: 2.5 mg/kg/d x 28 d
• Miltefosine: 2.5 mg/kg/d x 28 d + Amphotericin-B: 1 mg/kg/d x 28 d
• Miltefosine: 2.5 mg/kg/d x 28 d + Paromomycin: 15 mg/kg/d x 14-28 d
• Pentamidine: 4 mg/kg/d x 28 d + Paromomycin: 15 mg/kg/d x 28 d
72. Leishmania sp. → HIV infected
• Increase viral load, decrease CD4+ count
• Progression to AIDS
• Respond poorly, relapse repeatedly
• Suffering and death
• Treatment toxicity
– Sb: 15% cardiotoxicity, 31% pancreatitis, 5%
nephrotoxicity
– Ampho B: 36% nephrotoxicity
73. •modifies VL-relapsing pattern
- longer time between VL-episodes
- mainly if CD4+ <200 cells/L, but even if very low
HIV-viral load is achieved.
•Decreases incidence of new VL
(overall reduction 50-65%)
•HAART increases survival of co-infected patients
HAART effect on co-infected patients
74. PKDL
• Who needs treatment?
- Grade 2 & 3
- SSG 20mg/kg/d for 30days
- continue for 40-60days if no response.
• Toxicity due to SSG is very rare in PKDL.
• Miltefosine has been used in certain cases of
unresponsive PKDL in HIV/VL infection
75. VL and Pregnancy
Safety of the drug has to be considered during
treatment of VL in pregnancy
Under Category B= AmBisome and Amph.B.
Probably category C= Paromomycin
Probably Category X= Miltefosine
Unknown for SSG
Rx: AmBisome or Amphoterecin B
• Risk-benefit has to be outweighed in using SSG
specially during the first trimester.
76. VL and Malaria
• Malaria is a severe complication of VL because patients
are already weak, have ineffective spleen function, and
are already anemic.
• B/F or RDT needs to be done on every patients at
admission from endemic areas.
• No reliable data up to the rate of co-infection
• Treatment of both at a time needs care and attention
because of overlap of drug side effects.
Quinine and SSG results in QT prolongation and have
similarity in other CV side effects
77. Malaria/VL cont’d
• Rx:
– In uncomplicated pf malaria, Coartem has to be used and
the patient can get his SSG
– In severe malaria ,IM Artemether has to be used
– If treatment with quinine is inevitable, stop SSG while
quinine is being used.
– After treatment with quinine is finished, resume SSG
starting 24hrs after the last dose of quinine
80. Epidemiology
• The disease is prevalent in 75 countries and more
than 650 million people live in endemic areas
• 200 million people infected; 85% in sub-Saharan
Africa.
• Yearly estimated deaths of 200000 - 800000
deaths/year.
• Exposure to water (while planting, fishing,
washing, swimming and so on) containing the free
living infective stage of the parasite (cercariea)
released from the intermediate host (snail)
82. Epidemiology in Ethiopia
• S. mansoni is widespread in all regions and is rapidly
spreading in connection with water resource
development and intensive population Movements .
• S. haematobium is restricted to lowland areas so far
reported from the Awash and Wabeshebele river basins
and from Kurmuk at the Ethiopia/Sudan border.
• Lower altitudes ranging from 300 to 700 meters were
suitable for the establishment of snails and
maintenance of the parasite in S. haematobium
83.
84.
85.
86. Clinical Schistosomiasis
1. Cercarial penetration
Cercarial dermatitis (Swimmers itch)
• Associated with the death of cercariae in the skin.
• In unexposed people, the invasion causes a
transient immediate hypersensitivity reaction
with intense itching.
87. • Within 12 to 24 h it is followed by a delayed reaction
characterized by a small, red, pruritic, macular rash
progressing to papules after 24 h.
• The rash may persist for up to 15 days and residual
pigmentation may persist for months.
• Repeated exposure, the signs and symptoms increase
dramatically and start earlier.
• Treatment, if needed, is symptomatic.
89. o Marked in non-immune adults, but acute S. japonicum infection
can occur in re-exposed individuals and is SEVERE.
o 2 to 6 weeks after exposure.
o The clinical picture resembles an AFI with fever as a prime
characteristic.
o P/E may reveal , an enlarged tender liver, and, sometimes, and
an urticarial rash .
o Patients may become confused or stuporose or present with
visual impairment or papilloedema.
o Severe cerebral or spinal cord manifestations may occur, and this
is an indication for urgent investigative measures.
o light infections may cause severe illness and the syndrome can, in
rare cases, be fatal.
94. Diagnosis: intestinal schistosomiasis
• History of freshwater exposure
• History of freshwater exposure
• History of freshwater exposure
• Stool for O&P (egg counts and viability)
• Serology-- Elisa and Western Blot
• Eosinophilia
• Rectal snips or biopsies
• Liver biopsy
• Ultrasound or CT of abdomen
97. Diagnosis: urinary schistosomiasis
• History of freshwater exposure
• Screening for blood and protein in urine
• Urine for eggs
• Ultrasound, CT or IVP
• Serology-- Elisa and Western Blot
• Eosinophilia
• Cystoscopy-trigone appearance
98. Treatment
• Praziquantel drug of first choice for all species…
20 mg/kg po bid x 1 day
• Oxamniquine (second line) for S. mansoni
15-20 mg/kg daily x 1-3 days
• Metrifonate (second line) for S. haematobium
7.5-10 mg/kg every 2 weeks x 3 doses
• Artesunate (anti-schistosomule) 6 mg/kgm weekly x 3
