The presentation slide consists the description of Reduviid bug, and the disease it cause: chagas disease.

1. REDUVIID BUG AND
ASSOCIATED DISEASE
KAPIL SHARMA NEUPANE
MBBS 1st YEAR
DEVDAHA MEDICAL COLLEGE
KATHMANDU UNIVERSITY

2. CLASSIFICATION
• Kingdom : Animalia
• Phylum :Arthropoda
• Class : Insecta
• Order : Hemiptera
• Family : Reduviidae

3. MORPHOLOGY
• 4-40 mm in length depending upon species
• Have elongated head with distinct narrow
neck
• Have long limbs
• Have prominent mouthparts called
proboscis(rostrum)
• May be brown, black or red

4. FEEDING
• May be blood sucking or predators
• Feeds on cockroach, millipedes, ants, human
blood etc
• Inject lethal saliva in prey
• Saliva digest tissues and liquifies the inside of
prey.
• DISEASES TRANSMITTED: American
trypanosomiasis (Chagas diseases) caused by
Trypanosoma cruzi.

6. Life cycle of T. cruzi
• T. cruzi passes its life cycle in 2 hosts:
• Definitive host- man.
• Intermediate host- reduviid bug.
• Extrinsic incubation period: 8-10 days
• Intrinsic incubation period:1 week
• Infective form- Metacyclic trypomastigote form found in
feces of Reduviid bug.
• Reduviid bug are large, night biting bugs, which typically
defecate while feeding. Feces contain metacyclic
Trypomastigote.

7. Development In Human
• Transmitted to human host by contamination of
ulcerated skin lesion by feces of Reduviid bug
containing metacyclic trypomastigote form of T.
cruzi.
• Development in human- Trypomastigote form
invade the reticuloendothelial system and spread
to other tissues.
• Passing through promastigote & epimastigote
forms, they again become trypomastigotes which
get released into the blood stream- infective stage
for Reduviid bug.

8. Development in Reduviid bug
• Bug acquire infection by feeding on an
infected human host.
• The trypomastigote are transformed into
epimastigote in the midgut in the from where
they migrate to hindgut and multiply.
• After multiplication, develops into non
dividing metacyclic trypomastigotes which is
excreted in feces- infective stage for human.

10. CHAGAS DISEASE
• Infection caused by Trypanosoma cruzi, transmitted
by Reduviig bug.
• Result in acute inflammatory changes in skin
(chagomas), eye & many other body tissues,
especially those of the heart and intestinal tract.
• First described by Carlos Chagos in 1909 in Brazil.
• Not contagious.

11. EPIDEMIOLOGY
• About 8-11 million people are infected worldwide(2016).
• Highly prevalent countries: (WHO 2010)
• Endemic in Mexico, Argentina, South America and Central
America
• Sporadic in Amazon.
• Mostly prevalent in rural areas.

12. ROUTES OF TRANSMISSION
1. Bite of Reduviig bug.
2. Consumption of food contaminated with
faeces from infected bugs.
3. Blood transfusion from infected donors.
4. Passage from mother to new born during
pregnancy and child birth.
5. Organ transplant from infected donors.
6. Laboratory accidents.

13. TRANSMISSION
Bug live in mud, thatch or huts. They hide in walls
or roof during day and come out during night.
Bite human during sleeping hours. During feeding,
they defecate & leave T. cruzi parasites on skin.
Parasites enters into body through eyes, mouth, cut
or scratch or the wound from the bug bite site.
Once entered inside body the parasite multiply and
spread.

14. PHASES OF DISEASE
1. Acute phase
2. Intermediate phase
3. Chronic phase

15. SIGNS AND SYMPTOMS
1. Acute phase
Histologic changes- presence of parasite within
leucocytes cells of subcutaneous tissue and
development of interstitial edema,
lymphocytic infiltration and
hyperplasia of lymph nodes.
• Ramona sign- Unilateral painless
edema of palpebrae and
periocular tissues.

16. SIGNS AND SYMPTOMS
Acute phase (Continue…)
• Chagoma-Swelling and redness at the site of
infection
• Rashes & Fever
• Head and body aches
• Fatigue
• Nausea & Vomiting
• Hepatomegaly & splenomegaly

17. SIGNS AND SYMPTOMS
2. Intermediate phase
• Subpatent parasitemia
• Easily detectable antibodies to T. cruzi
• Asymptomatic.

18. SIGNS AND SYMPTOMS
3. Chronic phase
a. Heart
• Thinning of ventricular walls
• Biventricular failure
• Mural thrombi
• Arrhythmias
• Conduction system abnormalities
• Lymphatic infiltration, diffuse interstitial
fibrosis & atrophy of myocardial cells.

19. SIGNS AND SYMPTOMS
b. GIT
• Dilation of esophagus and colons
• Abdominal pain and constipation.
• Focal inflammation lesions with lymphocytic
infiltration.
• Reduced number of neurons in myoenteric plexus.

20. PREVENTION AND CONTROL
1. Primordial prevention
Mass education
 We should aware the people about kissing
bug because it seems friendly but it can
transmit the parasite named Trypanosoma
cruzi.

21. PREVENTION AND CONTROL
2. Primary prevention
Synthetic pesticide sprays.
 Personnel protection using mosquito net.
 Remove wood, brush, rock and piles near
the house.
Modification of house structure.

22. PREVENTION AND CONTROL
3. Secondary prevention
Screening of blood is done;
Transfusion control
Mother-Child transmission control
Treatment of Chagas disease[Acute phase]
Benznidazole
Nifurtimox

23. PREVENTION AND CONTROL
4. Tertiary prevention
If disease progress to chronic phase: it is no
longer curable so require management of
symptoms.
Cardiomyopathy; Pacemaker placement, Heart
transplant.
Megaesophagous; Esophagocardiomyectomy.
Megacolon; Duhamel-Haddad operation.