WEEKLY EPIDEMIOLOGICAL REPORT

A publication of the Epidemiology Unit

Ministry of Health
231, de Saram Place, Colombo 01000, Sri Lanka
Tele: + 94 11 2695112, Fax: +94 11 2696583, E mail: [email protected]
Epidemiologist: +94 11 2681548, E mail: [email protected]
Web: http://www.epid.gov.lk

Vol. 39 No.02 07th – 13th January 2012

Leishmaniasis
Background Local lymphadenopathy can occur, especially with
Outbreaks of Leishmaniasis have been reported in Sri species of the L. braziliensis complex. Spontaneous
Lanka, mainly from Matara, Anuradhapura and Ham- healing is common, but requires months to years. The
banthota districts. Most of these were cutaneous proportion that heals without treatment and length of
leishmaniasis, but the first case of visceral Leishmani- time required for healing vary by species.
asis was reported from Anuradhapaura in 2006.
Mucocutaneous leishmaniasis usually occurs months
Leishmaniasis comprises a complex of vector-borne or years after healing of primary cutaneous leishmani-
diseases, caused by more than 20 species of the proto- asis, most commonly due to parasites of the L. bra-
zoan genus Leishmania and ranging from localized ziliensis complex and can cause destruction of the
skin ulcers to lethal systemic disease. The most com- nasal septum, palate and other mucosal structures
mon syndrome is localized cutaneous leishmaniasis. leading to devastating facial mutilation and rarely death
Other forms of leishmaniasis are mucocutaneous from airway involvement. Factors associated with
leishmaniasis, disseminated cutaneous leishmaniasis, higher risk of mucocutaneous leishmaniasis include
leishmaniasis recidivans and visceral leishmaniasis. malnutrition and delay in treatment of the antecedent
Visceral leishmaniasis is a systemic disease, typical localized cutaneous lesion. Other complicated forms
features of which include fever, wasting, splenomegaly, include disseminated cutaneous leishmaniasis (diffuse
hepatomegaly and bone marrow suppression. Full nodular non-ulcerating disease) and leishmaniasis re-
blown clinical visceral leishmaniasis (sometimes called cidivans (localized slowly progressive non-healing or
kala-azar) is lethal in nearly all untreated cases. relapsing lesions). These forms of the disease are rare,
The Disease difficult to treat and can be severe.
Dozens of different sand fly vectors, adapted to differ- Visceral leishmaniasis is usually caused by L. donovani
ent ecological settings where leishmaniasis occurs, are and L. infantum. The time from an infective sand fly
known to transmit some form of leishmaniasis. bite to the onset of visceral leishmaniasis is typically 2
Leishmaniasis, especially the visceral form, can also be to 6 months but can range from 2 weeks to more than
transmitted by blood transfusion or sharing of contami- 2 years. The onset is usually insidious with worsening
nated needles. Congenital transmission has been re- symptoms over a period of weeks to months. The
ported, but appears to be rare. typical patient presents with fever lasting at least 2
In sylvatic cycles, animal reservoir hosts can maintain weeks, malaise, weight loss and may complain of ab-
transmission indefinitely without human disease. Spo- dominal fullness related to organomegaly. Common
radic or epidemic leishmaniasis occurs when humans clinical features include fever, wasting, splenomegaly,
enter the sylvatic habitat for economic or military pur- hepatomegaly, hypergammaglobulinemia and pancyto-
poses or when human habitation encroaches on the penia. Hepatomegaly is usually less prominent than
sylvatic setting. In domestic cycles, humans or dogs splenomegaly. The course is complicated by immuno-
form the predominant or sole infection reservoir. In suppression and secondary bacterial infections, hemor-
some areas, leishmaniasis transmission is zoonotic (dog rhage, anemia and when kala-azar occurs during preg-
-sand fly - human), while in other areas, it may be an- nancy, foetal wastage or congenital leishmaniasis. Kala-
throponotic (human -sand fly -human). azar is lethal in nearly all untreated cases. Even in
The most common syndrome is localized cutaneous treated patients, case-fatality rates are often 10% or
leishmaniasis, most frequently caused by L. major and higher. Jaundice, wasting, severe anemia and HIV co-
L. tropica in the Old World (Europe, Asia and Africa) infection are associated with increased risk of mortality.
and L. braziliensis, L. mexicana and related species in Post-kala-azar dermal leishmaniasis (PKDL) is a
the New World (Americas). The incubation period chronic rash seen in apparently cured kala-azar pa-
ranges from a few weeks to several years. The lesion tients, presenting with erythematous or hypopigmented
may start as a nodule but eventually ulcerates in most macules, sometimes progressing to plaques or nodules.
cases. Growth is usually fairly gradual but continues Sometimes it resolves without treatment in most mild
over a period of months. In the absence of secondary cases, while the condition is said to require treatment
bacterial infection, lesions are usually non-painful. in some areas.

Contents Page
1. Leading Article – Leishmaniasis 1
2. Surveillance of vaccine preventable diseases & AFP (31st December – 06th January 2012) 3
3. Summary of newly introduced notifiable diseases (31 December – 06 January 2012)
st th 3
4. Summary of selected notifiable diseases reported (31st December – 06th January 2012) 4
WER Sri Lanka - Vol. 39 No. 02 07th – 13th January 2012
Diagnosis Visceral leishmaniasis (Kala-
(Kala-azar)
The diagnosis of cutaneous leishmaniasis relies on the demonstration Patients with VL should be evaluated for HIV co-infection; if found,
of Leishmania in tissue biopsy, scraping or impression preparations by HIV should be treated aggressively. In the absence of treatment, the
microscopy and/or culture in a specialized medium. Species identifica- case-fatality rate of visceral leishmaniasis is >90%. Mortality is often
tion is recommended because management may vary depending on due to hemorrhagic or infectious complications. Supportive therapy to
the infecting species. Recently, assays based on the use of polymerase address nutritional status, concomitant anemia, hemorrhagic complica-
chain reaction (PCR), including multiplex assays that can distinguish tions and secondary infections is therefore essential to optimize treat-
among several species simultaneously, have become more widely avail- ment outcomes and maximize survival.
able.
For visceral leishmaniasis, definitive diagnosis requires the demonstra-
• Liposomal amphotericin B is the drug with the highest therapeutic
efficacy and the most favourable safety profile
tion of the parasite by smear or culture in tissue, usually bone marrow
or spleen and thus entails an invasive procedure. Splenic aspirate has • The pentavalent antimonial drugs, sodium stibogluconate and
the highest sensitivity of available tissue sampling techniques, but car- meglumine antimoniate, remain the most widely used antileishma-
ries a risk of serious hemorrhage. Bone marrow aspirates are safer, but nial drugs.
have substantially lower sensitivity. Parasites can be detected in tissue • New drugs such as parenteral paromomycin and miltefosine are
samples by light microscopy of stained slides, culture in a specialized not readily available.
medium or by specific PCR assays. Serological tests (for example,
immunofluorescent antibody tests or enzyme linked immunosorbent Prevention & Control
assays) can be used to demonstrate anti-leishmania antibodies. These Prevention and control of leishmaniasis is based on two major modali-
assays have high sensitivity for visceral leishmaniasis in patients without ties: to decrease human exposure to sand fly bites and interventions to
HIV infection, but may show positive results due to subclinical infec- decrease the infection reservoir of Leishmania species. However, the
tion or cross-reactions and are therefore less specific than tissue sam- strategy for a given location must be tailored to the local epidemiology
pling. Sensitivity of serology was low among patients with HIV-visceral and ecology. Specifically, the best control modalities depend on the
leishmaniasis co-infection. Therefore, parasitological diagnosis is advis- ecology of transmission (sylvatic or domestic), local sand fly behaviour
able. (sylvatic versus peridomestic; resting in houses versus resting in out-
door niches); and the local reservoir hosts (wild animal, domestic ani-
Treatment
mal or human).
Cutaneous leishmaniasis
Decreasing the Reservoir of Infection
Localized cutaneous leishmaniasis is not a life-threatening condition.
Treatment decisions should take into account the degree of morbidity For anthroponotic leishmaniasis, rapid diagnosis and effective treat-
balanced against the potential side effects of therapy options. The ment of patients decreases the infection reservoir. Theoretically, ca-
choice of treatment is dependent on Leishmania species (especially for nine reservoir reduction should decrease transmission of zoonotic VL,
New World cutaneous leishmaniasis), number, size and location of but programmes that are focused on the culling of infected dogs have
lesions and the availability of specific treatment modalities. not proved highly effective, possibly due to inadequate sensitivity of
diagnostic testing to detect infected dogs and time delays between diag-
Cutaneous leishmaniasis ulcers from several Leishmania species may nosis and culling. For sylvatic foci of cutaneous leishmaniasis, eliminat-
heal without treatment, although healing usually takes months and will ing rodent reservoir hosts in a buffer zone around human dwellings
leave a scar. For one or a few small lesions not on the face or over a may decrease transmission.
joint, careful follow-up without drug treatment may be appropriate.
The exceptions are ulcers due to L. braziliensis and L. panamensis, Vector Control
which tend not to heal spontaneously and are associated with a small Indoor residual insecticide spraying (e.g. Pyrethroid insecticides) may
risk (<5%) of subsequent mucocutaneous leishmaniasis. be an effective intervention for sand fly vector species that rest inside
human dwellings. Spraying usually needs to be repeated every 6
• The pentavalent antimonial drugs, sodium stibogluconate and months. Use of insecticide-treated nets and other materials can be
meglumine antimoniate remain the most widely used anti- highly effective when the peak period of vector activity is late evening.
leishmanial agents, but are increasingly being replaced by safer Long-lasting insecticide-treated nets avoid the need for re-treatment,
drugs. but the duration of their effect against sand flies under field conditions
• Oral antifungal drugs (fluconazole, ketoconazole, itraconazole) in endemic areas has not been evaluated. In areas of zoonotic leishma-
have been used to treat cutaneous leishmaniasis with variable re- niasis with a canine reservoir (e.g. L. infantum), treated dog collars and
sults depending on the Leishmania species and geographic loca- other modalities to decrease sand fly biting show promise as interven-
tion. tions to decrease infection exposure for humans.
• Liposomal amphotericin B appears to have efficacy against several
The use of insect repellent and insecticide treated clothing is advisable
for travellers, but is usually not feasible for the populations at highest
cutaneous leishmanial species, but data are limited and the optimal
risk.
dose regimen has not been established.
Source
• Other treatment modalities that have shown some efficacy for
cutaneous leishmaniasis due to some Leishmania species include Leishmaniasis, available from
topical paromomycin ointment, oral miltefosine, thermotherapy http://www.cdc.gov/parasites/leishmaniasis/health_professionals/
and intralesional pentavalent antimonial drugs. index.html

Compiled by Dr. Madhava Gunasekera of the Epidemiology Unit

Page 2
WER Sri Lanka - Vol. 39 No. 02 07th – 13th January 2012
Table 1: Vaccine-preventable Diseases & AFP 31st December – 06th January 2012 (01st Week)
Disease No. of Cases by Province Number of Number of Total Total num- Difference
cases cases number of ber of between the
during during cases to cases to number of
current same date in date in cases to date
week in week in 2012 2011 in 2012 & 2011
W C S N E NW NC U Sab
2012 2011

Acute Flaccid 00 00 00 00 00 00 00 00 00 00 01 00 01 - 100.0 %

Paralysis

Diphtheria 00 00 00 00 00 00 00 00 00 - - - - -

Measles 00 00 00 00 00 00 00 00 00 00 01 00 01 -100.0 %

Tetanus 00 00 00 00 00 00 00 00 00 00 01 00 01 -100.0 %

Whooping 00 00 00 00 00 00 00 00 00 00 00 00 00 00 %
Cough

Tuberculosis 68 41 90 24 58 13 24 07 28 353 140 353 140 152.1 %

Table 2: Newly Introduced Notifiable Disease 31st December – 06th January 2012 (01st Week)
Disease No. of Cases by Province Number of Number of Total Total num- Difference
cases cases number of ber of between the
W C S N E NW NC U Sab during during cases to cases to number of
current same date in date in cases to date
week in week in 2012 2011 in 2012 & 2011
2012 2011

Chickenpox 11 02 07 03 13 05 02 06 06 55 76 55 76 - 37.5 %

Meningitis 02 00 00 00 00 08 01 01 01 13 12 13 12 + 8.3 %
KL=2 KR=7 AP=1 MO=1 RP=1
PU=1

Mumps 14 05 06 04 17 04 15 04 11 80 42 80 42 + 90.5 %

Leishmaniasis 00 00 02 00 00 00 04 00 00 06 01 06 01 + 500.0 %
HB=2 AP=3
Po=1

Key to Table 1 & 2

Provinces: W: Western, C: Central, S: Southern, N: North, E: East, NC: North Central, NW: North Western, U: Uva, Sab: Sabaragamuwa.
DPDHS Divisions: CB: Colombo, GM: Gampaha, KL: Kalutara, KD: Kandy, ML: Matale, NE: Nuwara Eliya, GL: Galle, HB: Hambantota, MT: Matara, JF: Jaffna,
KN: Killinochchi, MN: Mannar, VA: Vavuniya, MU: Mullaitivu, BT: Batticaloa, AM: Ampara, TR: Trincomalee, KM: Kalmunai, KR: Kurunegala, PU: Puttalam,
AP: Anuradhapura, PO: Polonnaruwa, BD: Badulla, MO: Moneragala, RP: Ratnapura, KG: Kegalle.
Data Sources:
Weekly Return of Communicable Diseases: Diphtheria, Measles, Tetanus, Whooping Cough, Chickenpox, Meningitis, Mumps.
Special Surveillance: Acute Flaccid Paralysis.
Leishmaniasis is notifiable only after the General Circular No: 02/102/2008 issued on 23 September 2008. .

Dengue Prevention and Control Health Messages

You have a duty and a responsibility in preventing dengue
fever. Make sure that your environment is free from water
collections where the dengue mosquito could breed.

Page 3
WER Sri Lanka - Vol. 39 No. 02 07th – 13th January 2012
Table 4: Selected notifiable diseases reported by Medical Officers of Health
31st December – 06th January 2012 (01st Week)
DPDHS Dengue Fe- Dysentery Encephali Enteric Food Leptospiro Typhus Viral Human Returns
Division ver / DHF* tis Fever Poisoning sis Fever Hepatitis Rabies Re-
ceived

A B A B A B A B A B A B A B A B A B %
Colombo 219 219 3 3 0 0 9 9 0 0 2 2 0 0 0 0 0 0 92
Gampaha 117 117 3 3 0 0 1 1 0 0 3 3 0 0 6 6 0 0 73

Kalutara 36 36 6 6 0 0 3 3 0 0 5 5 0 0 1 1 0 0 85

Kandy 60 60 4 4 0 0 0 0 0 0 4 4 4 4 0 0 0 0 87

Matale 9 9 3 3 1 1 0 0 0 0 2 2 0 0 0 0 0 0 92

Nuwara 5 5 1 1 0 0 0 0 0 0 2 2 2 2 1 1 0 0 77

Galle 26 26 3 3 0 0 1 1 1 1 1 1 0 0 0 0 0 0 79

Hambantota 8 8 2 2 0 0 0 0 0 0 2 2 1 1 0 0 0 0 75

Matara 30 30 2 2 0 0 3 3 0 0 3 3 3 3 4 4 0 0 100

Jaffna 14 14 7 7 1 1 14 14 2 2 2 2 34 34 1 1 0 0 92

Kilinochchi 6 6 1 1 0 0 1 1 0 0 0 0 4 4 0 0 1 1 75

Mannar 15 15 1 1 0 0 2 2 0 0 1 1 0 0 0 0 0 0 100

Vavuniya 4 4 0 0 2 2 0 0 2 2 2 2 0 0 0 0 0 0 100
Mullaitivu 2 2 0 0 0 0 0 0 0 0 1 1 0 0 0 0 0 0 100

Batticaloa 40 40 4 4 0 0 1 1 0 0 0 0 0 0 0 0 0 0 86

Ampara 1 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 71

Trincomalee 11 11 4 4 0 0 2 2 0 0 0 0 0 0 0 0 0 0 83

Kurunegala 42 42 3 3 1 1 2 2 0 0 3 3 1 1 3 3 0 0 87

Puttalam 19 19 2 2 0 0 1 1 0 0 2 2 1 1 0 0 00 00 83

Anuradhapu 7 7 2 2 0 0 0 0 1 1 4 4 1 1 1 1 0 0 68

Polonnaruw 3 3 0 0 0 0 0 0 0 0 1 1 0 0 1 1 0 0 86

Badulla 5 5 2 2 0 0 1 1 0 0 0 0 0 0 1 1 0 0 76

Monaragala 5 5 3 3 1 1 2 2 0 0 7 7 0 0 1 1 1 1 82

Ratnapura 24 24 5 5 2 2 0 0 2 2 6 6 0 0 0 0 0 0 67
Kegalle 22 22 0 0 0 0 2 2 4 4 1 1 0 0 12 12 0 0 91

Kalmune 4 4 8 8 0 0 1 1 0 0 0 0 0 0 0 0 0 0 92
SRI LANKA 734 734 69 69 08 08 46 46 12 12 54 54 51 51 32 32 02 02 83

Source: Weekly Returns of Communicable Diseases WRCD).

*Dengue Fever / DHF refers to Dengue Fever / Dengue Haemorrhagic Fever.
**Timely refers to returns received on or before 06th January, 2012 Total number of reporting units 329. Number of reporting units data provided for the current week: 275
A = Cases reported during the current week. B = Cumulative cases for the year.

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ON STATE SERVICE

Dr. P. PALIHAWADANA
CHIEF EPIDEMIOLOGIST
EPIDEMIOLOGY UNIT
231, DE SARAM PLACE
COLOMBO 10