Kissing Bugs in the Americas Final

This topic submitted by Ryan Gifford ( Gifforrj@miamioh.edu) at 10:10 PM on 5/15/04.

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Ryan Gifford
Costa Rica Paper
Kissing Bugs in the Americas

Introduction

Insects have inhabited the Earth for 348 million years before man and so far several hundred thousand have been described. These organisms are crucial to natural ecosystemsŐ functions and often are very beneficial to humans; however, this paper will focus on a specific family of insects (triatominae) that can carry protozoas deadly to humans. Of the class Insecta there are three orders which carry diseases that harmful to man, hemiptera, diptera and siphonaptera. The order hemiptera characteristically has a proboscis and four sharp stylets capable of puncturing skin. Of this order, the subfamily triatominae (reduviidae), commonly known as the kissing bug, is particularly interesting because several genera of triatominae; triatoma, rhodnius, and panstrongylus can be the vectors of the deadly protozoon Trypanosoma cruzi (T. cruzi). This Protozoon kills 20,000 Central and Latin Americans per year and approximately 18 million are infected (Smith 1998).

The Bug

There are six commonly found species of reduviidae in Costa Rica; however, the most abundant species is Triatoma dimidiata (commonly called ŇVinchucaÓ in Central America) which are usually found 100-400m above sea level across the country. P. geniculatus is the second most common reduviidae and is found in the Pacific and Caribbean low lands (80-270m). The third most common is the T. dispar which is found in the highlands across the country (600-800m). These three species make up approximately 75% of all the reduviidae bugs in Costa Rica (Zeled—n 1996). About 12% of the population is infected with T.cruzi and 35% of houses are infested with T. dimidiata (Gilles 1998).
Reduviidae bugs can be difficult to identified because their appearance varies greatly between genera and there are over 100 species all of the family redviidae. The family can be distinguished by 4-segmented antennae, two eyes; the distal leg (tarsi) has 3-segments. The beak has 3-segments and the head is elongated with grooves behind the eyes. They are typically 1-3cm in length, are good flyers (Goddard 1999), and become more active at night (Bastien 1998). Reduviid bug can be found in urban and rural communities along with forests uninhabited by humans. Those found in urban dwellings are referred to as domestic species and those found far from human contact are referred to as sylvatic species.
Domestic species often hide in cracks in houses during the day and feed on the inhabitants at night. Poor neighborhoods often are found to be infested with redviidae bugs because housing made of mud and palm leaves provides more places for the bugs to hide. When pesticides are used to prevent infestations, sylvatic species often move in after domestic species have died (Goddard 1999). Infestation rates vary between villages; rates for Costa Rican houses averaged 35% (Gilles 1999) while South American homes ranged from 38.2% to 96.5% (Bastien1998).
All Reduviid bugs feed on vertebrate hosts for their entire life cycle. They have been given many names ranging from assassin bug, vinchuca, kissing bug, barbeiros and chipo; however kissing bug is probably the most appropriate because the bug typically attacks humans near the mouth or eyelids. It is important to note that, thus far, everything has regarded the reduviidae bug, not the protozoon which causes Chagas Disease. The bug feeds off of blood from vertebrates and the protozoon is not passed to the victim through the saliva but rather through the feces. While feeding on a host, the bug often urinates and defecates on the victim near the wound caused from the feeding. It is only when the victim scratches or moves the feces into a wound that Chagas is contracted.

The Parasite

Chagas disease (American trypanosomiasis) is caused by the protozoon mentioned previously, Trypanosomiasis cruzi (T.cruzi). Between the years 1907 and 1912, Carlos Chagas discovered the disease, its life cycle, and possible vectors and hosts (Gilles 1998). This protozoon lives part of its life cycle within the gut of invertebrate vectors, specifically reduviidae bugs. The protozoan can infect eight different mammalian orders in both sylvatic and domestic life cycles (Diesfeld 1997). The protozoan is classified as a protozoan phylum Mastigophora, Class Zoomastigophora, order Kinetoplastida, family Trypanosomatidae.
Because (T.cruzi) has a complicated life cycle, we will begin looking at the point of human contact where the invertebrate vector has defecated on skin. When the protozoan is in insect feces, it is in the trypomastigote stage and is actively moving within the bug feces due to wave like movements in the membrane and a very active flagellum. When they make contact with human tissue they enter into host cells through the cell lining and begin the amastigote stage (Crampton 1997). In the amastigote stage they are 1.5-5 microns long oval shaped and do not have a flagellum (Bastien 1998). Within the amastigote stage they can multiply by binary fission. After approximately five days in the amastigote stage, the host cell lyses and release trypomastigotes. It is this mechanism that allows the protozoan to remain within the host for its lifetime. A single infected cell can release 500 trypomastigotes. Heart cells are the most common victims of trypomastogotes although all tissues can be attacked. It is during this stage when trypomastigotes are in relatively high concentrations that blood feeding reduviidae can acquire the protozoan from humans (Gilles 1998). When T.cruzi enters the insect it uses its flagellum to attach itself to the gut wall. Within the gut T. cruzi enters its final stage called epimastigotes which are about 10-20 microns long in the midgut and reproduce by binary fission (Bastien 1998). When they enter the hind gut the epimastigotes are about 35-40 microns long and become trypomastigotes before leaving the rectum. Within 1-2 weeks this three step transformation can occur within the bug (Bastien 1998).

Effects on Humans

The life cycle previously described is characteristic of Acute Chagas disease. There are three stages of Chagas disease, acute, intermediate and chronic. We will examine the physiological effects on the human body of each stage through the next few paragraphs beginning with the initial bite.
Reduviidae bugs usually bite on exposed skin while a person is sleeping. Generally they will not climb on the body so that the only part of the bug that is in contact with the person is the proboscis (Vetter 2001). The bite is virtually painless, and was first described by Darwin in his diary for April 9 1835 when he allowed one to bite him on the finger (Bastin 1998). (There are some that believe that Darwin died from Chagas disease from this bite). The feeding lasts for approximately 10 min and the bug is able to survive up to 6 months on a single feeding. Several uncommon allergic reactions can occur in response to the bugŐs saliva but rarely are fatal. The bite mark resembles and is often assumed to be a spider bite (Vetter 2001).
Acute ChagasŐ disease is associated with a high fever, enlarged spleen and liver, swollen lymph nodes (Bastin 1998). Inflammation is due to the destruction of tissue as the parasite proceeds through amastigote and trypanosome stages within the host. Symptoms vary greatly from different species and different geographic locations, but almost always present is the ophthalmo-ganglial complex, which is the swelling around the eye, and chagoma, which is a raised hard tumor like development of subcutaneous cells associated with ChagasŐ(Bastin 1998). Not all patients with T. cruzi experience symptoms of an acute infection. However, patients that do can experience convulsions, loss of consciousness, and heart problems. The trypanosomes typically attack heart tissue, resulting in the swelling of the heart, and possible cardiac arrest which is only seen in a small percentage of cases (~ 5%). Cardiac arrest is the number one reason for death due to an acute infection (Diesfeld 1997). The acute stage typically last for less than 6 months, after which about 70-80% of patients never experience any symptoms (Gilles 1998).
After the acute symptoms disappear, there is often a period where no symptoms are experienced, referred to as the indeterminate stage. In this stage, ECG and X-rays of the body may show no infection. It is possible for the infection to remain in this indeterminate stage for extended periods of time, where the patient is experiencing no symptoms and may live a normal healthy lifestyle (Diesfeld 1997). Only about 2-3% of patients with chronic indeterminate stage develop chronic ChagasŐ disease (Gilles 1998), although this varies greatly between regions.
Chronic ChagasŐ is described as irreversible cardiomyopathy and inflammation of the intestinal system and is seen in about 30% of T. Cruzi cases. Inflammation of the heart and esophagus results in cardiac arrest due to pulmonary embolism and suffocation respectively (Diesfeld 1997).

Diagnosis

Two methods are commonly used for diagnosis, first the parasitological which employs lab raised, sterile, kissing bugs to feed off of the patient for approximately 30 minutes. The bugs are then examined ~15 days later for acute cases and ~45 days later for chronic cases. The bugsŐ rectal contents are examined under a microscope and checked for parasites. This test is accurate in acute cases and between 10-50% accurate in chronic cases depending on how many bugs are permitted to feed (Gills 1998). Serological tests detect antibodies to T. cruzi and are 98% accurate; however, these tests are expensive and not frequently used in South American (Diesfeld 1997).

Therapy

The two drugs that are used to treat ChagasŐ (nifurtimox and benznidazole) both are toxic, cause unpleasant side effects (Diesfeld 1997) and the actual drugs themselves provide little suppression of the parasite (Gills 1998). Because of these two reasons, no treatment is recommended for most acute cases; however cases involving children and patents with chronic stages are often prescribed the drugs.
New research has indicated an alternative to reducing the prevalence of ChagasŐ disease through genetic modification of the symbiotic bacteria in the intestinal track of the reduviidae bug so that it would be unable to transmit the ChagasŐ disease. The genetically modified bugs would then be introduced into infested areas, hopefully disabling the parasite by interrupting part of its life cycle (Beard 2002).


Bastien J.
1998 The Kiss of Death ChagasÍ Disease in the Americas. Salt Lake
City, UT: The University Of Utah Press.

Beard C, Cordon-Rosales C, Durvasula R.
Bacterial Symbionts of the Triatominae and Their Potential Use In Control of ChagasŐ Disease Transmission. Annual Review of Entomology January 2002, Vol. 47, pp. 123-141.

Crampton J., Beard C., Louis C.
1997 The Molecular biology of Insect Disease Vectors. London UK: The
University Press, Cambridge.

Diesfeld H.
1997 Historical Aspects of American Trypanosomiasis (ChagasÍ Disease).
Frankfurt am Main: Peter Lang Europaischer Verlag der Vissenschaften.

Gilles H.
1998 Protozoal Diseases. London UK: Arnold, a member of the Hodder
Headline Group.

Goddard J
Kissing Bugs and Chagas' Disease. Infect Med 1999; 16(3):172-180.

Guerrant R, Souza M, Nations M1996 At the Edge of Development Health Crises in a Transitional Society. Durham, NC: Carolina Academic Press.

Smith M
The Kiss of Death
http://www.cocori.com/library/eco/chagas.htm
November 1, 1998

Vetter R
Kissing bugs (Triatoma) and the skin
Dermatology Online Journal 7(1):6 2001

Zeled—n, R, Ugalde J, Paniagua L.
Entomological and Ecological Aspects of Six Sylvatic Species of Triatomines (Hemiptera, Reduviidae) Collection of the National Biodiversity Institute of Costa Rica, Central America; Vol. 96(6): 757-764, August 2001

http://cancerweb.ncl.ac.uk April 15, 2004

On-line Medical Dictionary, © 1997-98 Academic Medical Publishing & CancerWEB


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