PARASITES 
ON
PARADE!!
 (Updated September 30, 2009)

 

 Dr. Stan Eisen
Biology Department
Christian Brothers University
650 East Parkway South
Memphis, TN 38104

 

To the course schedule: http://www.cbu.edu/~seisen/BIOL413LcLbDesc.htm

          TABLE OF CONTENTS

Articles You May Not Want to Read Before Lunch

Studies in mutualism

Parasitology-Related Web Sites
The West Nile Portfolio


Some Basic Concepts in Parasitology
Helminth Infections in Humans
Protozoan Infections in Humans
Definitions
Specialized Terms For Protozoa
Adaptations To Parasitic Existence
Six Essential Aspects To A Parasite Life Cycle
Diagnostic Methods
Candidates For Parasitic Infections

A Rogue's Gallery of Parasites:

Parasitic Protists
Entamoeba histolytica
Entamoeba coli
Entamoeba gingivalis
Endolimax nana
Iodamoeba butschlii
Naegleria fowleri
Giardia lamblia (intestinalis)
Chilomastix mesnili
Trichomonas vaginalis
Leishmania donovani
Leishmania tropica
Leishmania braziliensis
Trypanosoma gambiense and rhodesiense (African trypanosomiasis)
Trypanosoma cruzi (American trypanosomiasis)
Plasmodium spp. (Malaria)
Toxoplasma gondii
Pneumocystis carinii
CryptosporidiumSpp spp.
Balantidium coli

Parasitic Platyhelminthes
Clonorchis sinensis
Fasciola hepatica
Fasciolopsis buski
Paragonimus westermanni
Schistosoma haematobium
Schistosoma mansoni
Schistosoma japonicum
Diphyllobothrium latum
Taenia solium
Taeniarhynchus saginata
Hymenolepis diminuta
Vampirolepis nana
Dipylidium caninum
Echinococcus granulosus

Parasitic Nematoda
Trichuris trichiura
Trichinella spiralis
Strongyloides stercoralis
Ancyclostoma duodenale
Necator americanus
Comparison of hookworm species
Correlation between Necator worm burden and patient status
Ancylostoma caninum
Ascaris lumbricoides
ToxocaraSpp spp.
Enterobius vermicularis
Wuchereria bancrofti
Onchocerca volvulus
Dirofilaria immitis
Dracunculus medinensis

Acanthocephala
Macracanthorhynchus hirudinaceus
Moniliformis moniliformis
Polymorphus paradoxus

Mollusca

Parasitic Arthropods
Importance of Arthropods in Parasitology
Types of Biological Transmission  

Insect life cyles
http://www.kendall-bioresearch.co.uk/life.htm

Order Hymenoptera

Order Diptera (true flies)
Glossina spp. (Tsetse flies)
Chrysops spp. (Deerfly)
Culicidae (Mosquitos)
Simulium sp. (Blackflies)
Phlebotomus sp. (Sandflies)
Lutzomyia spp. (New World Sandflies)

Order Hemiptera (true bugs)
Triatoma infestans
Rhodnius prolixus
Cimex spp.

Order Siphonoptera (fleas)
Pulex irritans
Ctenocephalides spp. (dog & cat fleas)
Tunga penetrans
Xenopsylla cheopis (rat flea)

Order Anoplura (biting lice)
Pediculus humanus
Phthirus pubis

Acarina (ticks, mites)
Dermacentor andersoni
Ixodes spp. and other hard ticks
Trombicula alfreddugesi (chiggers)
Sarcoptes scabiei
Demodex spp.

Vertebrates
Cuckoos
Petromyzon marinus (sea lamprey)
Vandellia cirrhosa (candiru catfish)

Plants

Rafflesia tuan-mudae (carrion plant)
Indian pipes 

 

 

 

 

Drugs Used for Treatment 

Articles, Web Pages or Books You May Not Want To Read Before Lunch

          Stone, Richard. 2001. Down to the Wire on Bioweapons Talks. Science 293:414-416.

          Colwell, Strant T., Jr. 1998. Prevalence of Helminths in Fecal Deposits of Dogs in Anderson County, Tennessee. Journal of the Tennessee Academy of Science 73(3-4):104-105.

Bwire, Robert. Bugs in Armor: A Tale of Malaria and Soldiering,

Peterson, R.K.D. 1995. Insects, Disease, and Military History: The Napoleonic Campaigns and Historical Perception. This article is reprinted and adapted from Peterson, R. K. D. 1995. Insects,disease, and military history: the Napoleonic campaigns and historical perception. American Entomologist. 41:147-160.
http://scarab.msu.montana.edu/historybug/napoleon/past_present.htm

Tongue-eating bug found in fish
http://news.bbc.co.uk/cbbcnews/hi/newsid_4200000/newsid_4209000/4209004.stm

 

Medscape:  Severe Abdominal Pain in a Young Girl After a Hug CME/CE: 
http://cme.medscape.com/viewarticle/704048?src=cmemp

You have to be just a little twisted to buy one of these:

Parasitological gifts for yourself or really significant others:
www.parasitepals.com

Studies in mutualism

 

I.  Introduction

          Mutualism is one of several potential interactions or relationships which may occur when representatives of two species interact or encounter each other.  They can be summarized by the following chart:

                   + = enhances survival of symbiont

                   0 = does not affect survival of symbiont

                   - = decreases survival of symbiont

 

 

Symbiont 2

 

 

+

0

-

 

+

Mutualism, which may be either obligate or facultative, e.g. clownfish and sea anemones

 

 

Symbiont 1

0

Commensalism, e.g. barnacles on the skin of whales. 

 

 

 

-

Predation, if symbiont 1, as prey, gets eaten by symbiont 2, as predator;

Parasitism, if symbiont 2 lives in or on symbiont 1. 

 

Competition, in which symbiont 1 and symbiont 2 require the same limited resource.  Over time, character displacement or specialization reduces the severity of direct competition

 

 

A.  Termite intestinal flagellates

Introduction

          Trichonympha spp. and Pyrrsonympha  spp. are two genera of  symbiotic flagellates that live in the intestines of  some termites.  Although termites can bite off pieces of wood and swallow them, they are incapable of chemically digestine the cellulose into monosaccharides because they cannot synthesize cellulose.  This enzyme is produced by these and other flagellates in the termite gut, enabling the termite to survive.  In fact, when termites are exposed to an environment with enriched oxygen, will die of starvation because the increased oxygen concentration kills off the flagellate population in the gut.  These flagellate protozoa are found nowhere else except in the termite gut.  Therefore, this is an example of obligate mutualism. 

          The flagellates themselves possess mutualistic bacteria which adhere to the pellicle of the flagellate.  These bacteria engage in a synchronized movement, thereby providing locomotion to the flagellate cell. 

          Vertical transfer of the flagellates is by regurgitation of food to each other.  The regurgitated food contains the active flagellates.  Termites have to be re-infected with digestive flagellates after each molt, because their hind guts (where the flagellates live) get shed with the skin.

 

Procedure

1.Place 2-3 drops of Invertebrate Ringer’s on a clean slide;

2.Pick up a  living termite with forceps and place it in the Invertebrate Ringer’s;

3.Use sharp probes to tease apart and spread the intestinal contents into the Invertebrate Ringer’s solution.  (There is nothing delicate to this part of the procedure.   Just smush their little bodies apart.);

4.Cover with a cover slip, and scan the slide under 100x, and then look carefully under the 400x. 

 

Images:

http://workforce.cup.edu/buckelew/Trichonympha_sp_400x_other_termi.htm

 

http://bioweb.uwlax.edu/zoolab/Table_of_Contents/Lab-2b/Termite_Gut_Flagellates/termite_gut_flagellates.htm

 

http://www.stcsc.edu/ecology/TermSymb.htm

 

Why the study of parasites is an integral part of ecology:

Pesticides and flawed frogs: Researchers reveal first signs linking land runoff to deformities
Carl T. Hall, Chronicle Science Writer
Tuesday, July 9, 2002
©2002 San Francisco Chronicle.

URL: http://www.sfgate.com/cgi-bin/article.cgi?file=/chronicle/archive/2002/07/09/MN79035.DTL

Raising new questions about the environmental risks of some widely used farm chemicals, scientists are reporting today the first evidence linking agricultural runoff to grotesque hind-limb deformities in frogs.

Researchers said frogs appear to be made more vulnerable to a common parasite when exposed to the pesticides atrazine and malathion. The parasite, a burrowing trematode worm, tends to infect the hindquarters of developing tadpoles.

Atrazine is part of a family of chemicals that rank among the world's most widely used weed killers. Malathion is commonly applied to control mosquitoes and other insects, and pharmaceutical grades are approved for killing head lice. Both products are controversial but considered safe for commercial use in the United States.

Now, effects of these and other chemicals on the environment are coming under new scrutiny. Research is driven partly by keen public and scientific interest in the declining health of amphibian populations, often portrayed as a sentinel for environmental decline and a possible early warning of health problems affecting humans.

At last count, wild frogs with missing or extra hind limbs have been observed in at least 43 states and five Canadian provinces. Earlier studies clearly implicated the trematode parasite but left open the question of what might be causing the apparent increase in the problem.

The latest study, by ecologist Joseph Kiesecker at Pennsylvania State University and edited by UC Berkeley amphibian specialist David Wake, tries to fit in the key remaining puzzle piece. The study appears in the early edition of this week's Proceedings of the National Academy of Sciences.

Kiesecker said his observations of the common wood frog Rana sylvatica in the wild, followed by controlled studies in his laboratory, produced "compelling" evidence that pesticides can weaken the immune system of exposed amphibians -- even at very low concentrations -- making the frogs more vulnerable to parasites.

The field studies showed "considerably higher rates of limb deformities where there was pesticide exposure," Kiesecker said in an interview. "Then the lab experiments helped support the mechanism for what we saw in the field."

He also looked at another pesticide, a synthetic chemical called esfenvalerate, but did not find the same links to growth anomalies as seen with malathion and atrazine.

For the latter two chemicals, significant effects were seen even at concentrations considered safe for drinking water by the Environmental Protection Agency.

Even these very low levels of exposure could produce "dramatic effects on the immune response" of the animals. And that, in turn, led to significantly more growth defects.

Kiesecker stopped short of endorsing any effort to further restrict use of atrazine and malathion. But he said his results underscored the importance of studying toxic chemical effects in a context approaching the complexity found in natural ecosystems.

In this case, he explained, the two farm chemicals "disturbed host-pathogen interactions" with sometimes devastating effects. But all that would be missed in traditional studies examining only the chemicals and the frogs in isolation.

Some other scientists, backed by the farm-chemical industry, challenged Kiesecker's results. Although they said the new study was intriguing, they suggested the details couldn't be trusted until corroborated independently.

©2002 San Francisco Chronicle. Page A - 2

 The following images came from the March 2003 image of Scientific American, and they demonstrate the severity of effects that are possible as a result of parasitic infection.

Close-up of malformed frogs. Deformations are associated with infestations of Ribeiroia ondotrae.

 

Life cycle of Ribeiroia ondotrae. The definitive hosts are carnivorous shore birds, but the intermediate hosts, frogs, are easily infected with the cercariae of this parasite.

 Although there was no positive diagnosis, the following image appeared in:  Scott, A.F.  (1999).  Malformed Southern Leopard Frogs (Rana sphenocephala utricularius) Discovered in North-Central Tennessee.  Journal of the Tennessee Academy of Science 74(3-4):61-63.

XRayOfSixLeggedRanaTNEN150

 

Parasitology-Related Websites and Resources

Professional Societies:

American Society of Parasitologists
c/o D
aniel R. Brooks, Secretary-Treasurer
Department of Zoology
University of Toronto
Toronto, Ontario
Canada M5S 3G5
(416) 978-3509
Fax: (416) 971-2381
E-mail:
parasite@zoo.toronto.edu
World Wide Web Site:
         
http://www-museum.unl.edu/asp/

Journal: Journal of Parasitology

American Society of Tropical Medicine and Hygiene
60 Revere Drive, Suite 500
Northbrook, Ill. 60062

(847) 480-9592
Fax: (847) 480-9283
E-Mail:
astmh@aol.com

Journal: American Journal of Tropical Medicine and Hygiene

 

Internet Sites:

"Batch of Bug Sites"
http://www.microbes.info

Merck Veterinary Manual
http://www.merckvetmanual.com

Home page for the journal Molecular and Biochemical Parasitology http://www.elsevier.nl/cas/estoc/contents/SA1/01666851.html


World Health Organization Web Page (Contains WHO documents on tropical health)
http://www/who.ch

 Directory of Parasitologists: Lists scientists working in the field
URL <ftp://magnus.acs.ohio-state.edu/pub/zoology>

Parasite Genome Projects: Provides descriptions of projects and links to other genome projects http://woodland.bio.ic.ac.uk/fgn/parasite-genome/parasite-genome.html

Center for Disease Control - Atlanta, GA
http://www.dpd.cdc.gov/DPDx

USENET groups:

Newsgroups for parasitology-related areas, including bionet.parasitology, bionet.molbio, and bionet.protista

Visit http://www.bio.net/ for all bionet postings

 

SOME BASIC CONCEPTS 

A Picture Painted with a Broad Brush

Parasitic infections are relatively rare in the United States. Why? Because most Americans:

1.     Can afford shoes;

2.     Have adequate nutrition, at least relative to calories and protein;

3.     Have access to a water supply that is not contaminated with raw sewage;

4.     Have adequate access to health care resources (medical professionals, nearby hospitals, antibiotics, drugs, vaccines);

5.     Use synthetic fertilizers to grow crops, as opposed to human nightsoil;

6.     Life in the temperate zone, where there is a season during which insect vectors are absent.

So? People live long enough to show diseases of degeneration, such as:

  • Cancer: ~ 400,000 deaths per year
  • Heart disease: ~ 800,000 deaths per year

This is NOT the case in 3rd World Countries:

World Life Expectancy
http://www.worldlifeexpectancy.com/

HELMINTH INFECTIONS IN HUMANS.(ADAPTED FROM PETERS AND GILLES, 1977; PETERS, 1978; and Schmidt & Roberts, Foundations of Parasitology, edition 5, 1996)

 INTESTINAL NEMATODES

Human Infections

Deaths per year

All Helminths

3.5 Billion

 

Ascaris lumbricoides

1 Billion

20,000

Hookworm (Necator sp., Ancylostoma spp.)

900 million

50,000-60,000

Trichuris trichiura

700 million

 

Enterobius vermicularis

 

 

Strongyloides stercoralis

 

 


TISSUE NEMATODES

Human Infections

Deaths per Year

Wuchereria bancrofti

350 million

 

Dracunculus medinensis

80 million

 

Trichinella spiralis

50 million

 

Onchocerca volvulus

40 million

 

Loa loa

20 million

 


TREMATODES

Human Infections

Deaths per year

Schistosoma spp.

300 million

 

Clonorchis sinensis

40 million

 

Fasciolopsis buski 

15 million

 

Paragonimus westermanni

5 million

 


CESTODES

Human Infections

Deaths per year

Taenia spp.

80 million

 

Hymenolepis spp.

40 million

 

Diphyllobothrium latum

15 million

 

 

 

 

PROTOZOAN INFECTIONS IN HUMANS (From Markell & Voge: Medical Parasitology and Schmidt & Roberts, Foundations of Parasitology, ed.5, 1996)

SPECIES

Human Infections

Deaths per year

Entamoeba histolytica

600 million

 

Plasmodium spp.

489 million

1-2 million

African trypanosomiasis

35 million

 

American trypanosomiasis

10 million

 


In 1986, there were an estimated 60 million deaths, of which 30 million were children < 5 years old. Half of the deaths among children were due to a combination of malnutrition and intestinal infection.
 

 

DEFINITIONS:

PARASITE: An organism which derives sustenance or benefit at the expense of its host.

  • ENDOPARASITE = internal
  • ECTOPARASITE = external
  • OBLIGATE: Parasite stage necessary for completion of life cycle. e.g., Trichuris trichiura, Entamoeba histolytica.
  • FACULTATIVE: Normally free-living, but can exist as a parasite, e.g., Strongyloides stercoralis.
  • ACCIDENTAL: A parasite found in an abnormal host, e.g., Naegleria fowleri.

HOST: That organism which is necessary for the development of a parasite.

  • DEFINITIVE: Parasite reaches sexual maturity, e.g., Humans for Clonorchis sinensis
  • INTERMEDIATE: Necessary for development, but parasite does not reach sexual maturity, e.g., cyprinid fishes for Clonorchis sinensis
  • PARATENIC: A host which is not necessary for the physiological development of the parasite, but which facilitates transferral from the intermediate host to the definitive host to the definitive host.
  • VECTOR: Any agent, e.g. an arthropod, that transmits a disease organism.

HYPERPARASITISM: Parasite serving as a host for another parasitic species.

SPECIALIZED TERMS FOR PROTOZOA:

TROPHOZOITE: Metabolically active form of protozoan parasites,
within the appropriate organ of the host.

CYST: Metabolically inactive form of protozoan parasites,
adapted for transmission.

 

ADAPTATIONS TO PARASITIC EXISTENCE

I. SPECIALIZATION

  • Certain sensory organs are highly developed.
  • Resistant stage (e.g. cyst or egg) for transferral to new hosts.

 II. DEGENERATION    

  • "Unnecessary" organs become vestigial or disappear.
  • Loss of capacity to synthesize enzymes, nutrients.

 III. HIGH BIOTIC POTENTIAL, facilitated by

  • Hermaphroditism: Adults have functional male and female reproductive systems. In parasitic organisms, this hermaphroditism is simultaneous, as opposed to sequential.
  • Parthenogenesis: Development of an egg without fertilization by a sperm cell. Common among insects, e.g. aphids.
  • Polyembryony: Larval forms undergo a form of budding in the intermediate host. This is observed in digenetic trematodes (flukes) and some wasps.
  • Strobilization: Segments (proglottids) develop behind a holdfast organ (scolex). Each proglottid develops within it complete male and female reproductive systems. Following self- or cross-fertilization, the male reproductive structures deteriorate and eggs mature mature. Proglottids which are furthest away from the scolex are gravid, and will release eggs when the proglottid is shed.

 SIX ESSENTIAL ASPECTS TO A PARASITE LIFE CYCLE

 1. Find a Host

 2. Enter a Host

  • Active: Infective stage may burrow into skin, as cercariae of blood flukes do.
  • Passive: Host will ingest or inhale infective forms.

 3. Overcome Host Defenses: Mechanisms include

  • Antigen Shielding: Surface of parasite adsorbs host derived antigen, so that parasite is recognized as "self". (Documented among adult blood flukes)
  • Surface Antigen Shifting: Proteins forming protein surface change so that immune reactions lag behind development of the parasites. (Documented in Trypanosoma gambiense and T. rhodesiense (African trypanosomiasis.)

 4. Derive Nutrients From Host

  • Aerobic Metabolism
  • Obligate Anaerobic Metabolism

5. Reproduce More Individuals

  • Hermaphroditism
  • Polyembrony
  • Very high egg output: among some tapeworms, daily output can be in millions.

6. Disperse Young to New Hosts

  • Presence of Obligate Free-living Stage: Needs to tolerate changes in temperature, osmotic pressure, desiccation.
  • Passive or Active Dispersal: Cercariae of digenetic trematodes burrow out of snail host in search of 2nd intermediate host or of definitive host.
  • Parasite-Induced Change in Host Behavior: Intermediate stages will induce qualitative changes in the intermediate host such that the infected intermediate host is more likely to be captured by a predator which is the definitive host.

DIAGNOSTIC METHODS

Diagnostic Method

Example

FECAL EXAMINATION

Intestinal Helminths, e.g.:  Hookworm ova

HookwormEggs.gif

 Intestinal Protozoa, Giardia lamblia cysts

GiardiaCyst.jpg

BLOOD SMEAR

Plasmodium sp. (Malaria)

PlasmodiumVivax.jpeg

URINALYSIS

Schistosoma haematobium

SchistosomaHaematobiumOvum.jpg

IMMUNOASSAY

Pneumocystis carinii, Cysticercosis (Taenia solium), Echinococcus granulosus Cysts, Giardia lamblia

OCULAR EXAMINATION

Toxoplasma gondii,

OcularToxoplasmosis03.jpg

Toxocara spp.

ocularToxocariasis03.jpg

BIOPSY

Onchocerca volvulus, Trichinella spiralis

VAGINAL SMEAR

Trichomonas vaginalis

TrichomonasBest.JPG

IMMUNOBLOT

Plasmodium falciparum

XENODIAGNOSIS                  

Trichinella spiralis

ADHESIVE TAPE ACROSS PERIANAL FOLDS

Enterobius vermicularis

Enterobius_eggA.jpg

 

CANDIDATES FOR PARASITIC INFECTIONS

 I.      IMMIGRANTS  (From Emma Lazarus’ The New Colossus, 1883 - "Give me your tired, your poor,

Your huddled masses yearning to breathe free,

The wretched refuse of your teeming shore.

Send these, the homeless, tempest-tost to me,

I lift my lamp beside the golden door!"

 Malaria, Amoebiasis, Schistosomiasis, Clonorchiasis

 II.     TOURISTS & SERVICEMEN (NOT NECESSARILY OVERSEAS)

 Same As Above Plus Giardiasis

 III.    CHILDREN

Enterobius (Pinworm), Hydatid Cyst (Echinococcus), Ascariasis, Trichuriasis, Hookworms, Lice, Toxoplasmosis, Dermal Larva Migrans, Visceral Larva Migrans, Naegleria/Acanthomoeba

IV.     IMMUNOSUPPRESSED

 Pneumocystis, Toxoplasma, Strongyloides, Cryptosporidium

V.      RURAL AND INDIGENT

 Trichinella, Strongyloides, Giardia, Entamoeba, Hookworms, Ascariasis

VI.     PEOPLE WHOSE DIETS INCLUDE RAW MEATS

Trichinella (pork), Diphyllobothrium (freshwater fish), Anisakis (marine fish), Taenia (pork), Taeniarhynchus (beef)

From: http://www.Dribbleglass.com/subpages/billboards57b.htm

VIII.  PROMISCUOUS (through not necessarily)

Trichomonas vaginalis


Comparative morphology of the amebas of man and schematic representation of their nuclei. Adapted from Figure 3-1 and Table 3-1 of Brown & Neva (1983), Basic Clinical Parasitology, Appleton-Century-Crofts, Norwalk, Connecticut.

  

PARASITIC PROTISTS

 Entamoeba histolytica (amebic dysentery)

Images:  http://www.k-state.edu/parasitology/625tutorials/Ehistolytica.html

Life cycle:

EntamoebaHistolyticaLifeCycle

Phylogeny:
Superclass Sarcodina

Preferred definitive host:
Humans

Reservoir hosts:
Dogs, Pigs, Monkeys

Vector/intermediate hosts:
None are necessary, but transport by filth flies is possible

 Geographical location:    Cosmopolitan

Organs affected:
Coecum, appendix, colon. Advanced disease may include the liver and lungs.

Symptoms and clinical signs:
Mucosal destruction, perforated colons, peritonitis, abscesses in liver, lesions in lungs.

 Treatment:
Metronidazole, Dehydroemetine, Chloroquine

 

 Entamoeba coli

 Images:  http://www.k-state.edu/parasitology/625tutorials/Entamoebacoli.html

Phylogeny:
Superclass Sarcodina

Preferred definitive host:
Humans

Reservoir hosts:
None

Vector/intermediate hosts:
None

Geographical location:
Cosmopolitan

Organs affected: Cecum and general colon

 Symptoms and clinical signs:
Symptomless, since E. coli feeds on bacteria, yeast, and on rare occasions, blood cells. This species is frequently mistaken for E. histolytica.

 Treatment:  None required

  

Entamoeba gingivalis

Images:  http://www.k-state.edu/parasitology/625tutorials/Egingivalis.html

Phylogeny:
Superclass Sarcodina

Preferred definitive host:
Humans

Reservoir hosts:
None
, but it will infest primates, dogs, and cats. Transfer is possible among avid pet lovers.


Vector/intermediate host:
None

Geographical location:
Cosmopolitan

 

Organs affected:
Surface of teeth and gums, gingival pockets near the base of the teeth, and sometimes in the crypts of the tonsils.

Symptoms and clinical signs:
None

Treatment:
None required


Endolimax nana

Images:  http://www.k-state.edu/parasitology/625tutorials/Endolimax.html

Phylogeny
Superclass Sarcodina

Preferred definite host:
Humans

Reservoir hosts:
None

Vector/Intermediate host:
None

Geographical location:
Cosmopolitan

Organs affected:
Lives in the large intestine, mainly at the level of the cecum and feeds on bacteria.

Symptoms and clinical signs:
None. This organism is a commensal which can be confused for pathogenic species

Treatment:
None required

Iodamoeba butschlii

Images:  http://www.k-state.edu/parasitology/625tutorials/Iodamoeba.html  

Phylogeny:
Superclass Sarcodina

Preferred definitive host:
Humans

Reservoir hosts:
Other primates and pigs

Vector/intermediate host:
None

Geographical location:
Cosmopolitan

Organs affected:
Large intestine, mainly in the cecal area

Symptoms and clinical signs:
Generally none, but in a few cases it has induced ectopic abscesses like those of E. histolytica.

 Treatment:
None required


Naegleria fowleri

Images:  http://www.k-state.edu/parasitology/625tutorials/Naegleria.html

Phylogeny:
Superclass Sarcodina

Preferred definitive host:
Humans are an accidental host for Naegleria.

 Reservoir hosts:
None

Vector/intermediate host:
None

Geographical location:
Cosmopolitan. Cases have been documented in Europe, North America, Africa, New Zealand, and Australia.

 Organs affected:
Brain tissue

Symptoms and clinical signs:
Meningoencephalitis, involving convulsions leading to death.

 Treatment:
None are available. Infection with Naegleria is always fatal.

Deadly amoeba lurks in Florida lakes

*       Story Highlights

*       3 boys die from deadly amoeba in Orlando-area lakes this summer

*       Bathers warned to stay out of water warmer than 80 degrees Fahrenheit

*       Officials: Flu-like symptoms after swimming in a lake should spark alarm

By John Zarrella and Patrick Oppman
CNN

ORLANDO, Florida (CNN) -- Something in the lakes around Orlando, Florida, has claimed the lives of three boys this summer.

"This thing is just there. It's lurking like some deadly thing in the water which can take our children's lives and we all have to be aware," said Orange County Health Department Director Dr. Kevin Sherin.

The "thing" isn't a fish or alligator. It is so small it cannot be seen with the naked eye. The killer that lives in the hot, fresh water is a single cell amoeba that once exposed to the human brain through the nasal passages is almost always fatal.

At first people exposed to the amoeba, naegleria fowleri, suffer from flu-like symptoms. Very quickly, in from one to 14 days, the symptoms worsen, Sherin said. "There's a downhill course. Folks lapse into a coma; there are abnormal movements of the eyes and a terrible cascade of events leading to the actual death of parts of the brain."

Sherin said exposure to the amoeba can be detected by an MRI and it can be treated with antibiotics if caught early enough, but Sherin said he believes medical personnel are not in the habit of looking for the disease.

That is because the amoeba is very rare. The Centers for Disease Control in Atlanta, Georgia, has documented 24 cases in the United States since 1989.

Health officials do not know what caused three cases in Orlando in one summer. Theories range from warmer temperatures to a drought that has lowered lake levels. Sherin said officials considered closing access to the lakes, but concluded they did not have the authority. Even if public lakes had been closed, private lakes would have remained open.

So, at 15 parks and lakes around the city, warnings about the amoeba have been posted. The signs urge bathers to wear nose clips or stay out of water warmer than 80 degrees Fahrenheit, which can be a breeding ground for the amoeba.

The warnings provide little solace for Steve Sellars.

Health investigators said they believe Sellars' 11-year old son, Will, was exposed to the amoeba during an August weekend spent learning to wakeboard on Orlando's Lake Jessamine.

"You think it won't happen to me, it won't happen to my family." Sellars said. "You're wrong"

"[Will's] symptoms were like a flu bug," Sellars said, "We rushed him to the hospital and two days later he's passed away. It's like a nightmare."

A month later, a 10-year-old boy died from exposure to the amoeba. Investigators have not determined where he was exposed. The death of a 14 year-old boy in June in the Orlando area also is being blamed on the amoeba.

As he investigates the deaths of the three boys from the amoeba, Sherin is concerned these type of deaths may be underreported. Health departments in Florida are not required to report amoeba infections to the state. The illness is so rare, he said, it may be commonly misdiagnosed in the United States and internationally.

He said anyone who exhibits flu-like symptoms who has been in a lake recently should see a doctor immediately.

Speaking in Will's old bedroom, which Steve Sellars has decorated with photographs of his son, Sellars said he hopes he can help get the word out. He does not want anyone to lose a family member as quickly and mysteriously as he did.

"It's the worst thing we ever had to go through and I hate to see any other parent go through this and another child lose his life," Sellars said.

All AboutCenters for Disease Control and PreventionOrlando (Florida)

 

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Find this article at:
http://www.cnn.com/2007/HEALTH/09/18/zarrella.killerlakes/index.html?eref=rss_mostpopular

 

 

 

 Giardia lamblia (intestinalis)

 Images:

 Cysts:  http://www.k-state.edu/parasitology/625tutorials/Protozoa04.html 
 Trophozoites: 
http://www.k-state.edu/parasitology/625tutorials/Protozoa02.html

Giardia_lamblia_life_cycle

Phylogeny:
Order Diplomonadida

Preferred definitive host:
Humans

Reservoir hosts:
Possibly dogs, cats, rodents, cattle, beaver

Vector/intermediate host:
None

Geographical location:
Cosmopolitan, but occurs most frequently in warm climates among children.

 Organ affected:
Duodenum, jejunum, and upper ileum.

Symptoms and clinical signs:
Mucus in stools, diarrhea, dehydration, intestinal pain, flatulence, and weight loss.

(I mean, we're talkin' explosive diarrhea here, man!)

 

 Treatment:
Quinacrine, Metronidazole

 Note: European travel agents are advising THEIR customers who arrange visits to the United States, "Don't drink the water! It's infected with G. lamblia!"

Chilomastix mesnili

 Images:  http://www.k-state.edu/parasitology/625tutorials/Protozoa05.html

Phylogeny:
Order Retortamonadida

Preferred definitive host:
Humans

Reservoir hosts:
Other hosts include chimpanzees, orangutans, monkeys, and pigs

Vector/intermediate host:
None

Geographical location:
Cosmopolitan

Organs affected:
Cecum and colon

Symptoms and clinical signs:
May cause watery stools

Treatment:
None required


Trichomonas vaginalis

Images:  (lower two)  http://www.k-state.edu/parasitology/625tutorials/Protozoa01.html

Phylogeny:
Order Trichomonadida

Preferred definitive host:
Humans

Reservoir hosts:
None

Vector/intermediate host:
None

Geographical location:
Cosmopolitan

Organs Affected:
Vagina and urethra of women and in the prostate, seminal vesicles, and urethra of men

Symptoms and clinical signs:
Frequently symptomless among males,
but some strains cause inflammation, with itching and a copious white discharge swarming with trichomonads. Vaginal secretions may become greenish and condition may become chronic and/or recurrent.

This is what the book means by a copious white (frothy) discharge, swarming with trichomonads.

 

Treatment:
Metronidazole      

 

Medscape from WebMD

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Trichomoniasis Increases Risk of HIV Infection



Reuters Health Information 2007. © 2007 Reuters Ltd.
Republication or redistribution of Reuters content, including by framing or similar means, is expressly prohibited without the prior written consent of Reuters. Reuters shall not be liable for any errors or delays in the content, or for any actions taken in reliance thereon. Reuters and the Reuters sphere logo are registered trademarks and trademarks of the Reuters group of companies around the world.

NEW YORK (Reuters Health) Feb 06 - Women with trichomoniasis have about a 50% greater risk of acquiring HIV infection compared with women who do not have this common sexually transmitted infection, according to a study in the March 1 issue of The Journal of Infectious Diseases, now available online.

This is one of the first studies to demonstrate a statistically significant link between Trichomonas vaginalis and HIV infection, the study team notes.

Among 1335 HIV-seronegative female sex workers in Mombasa, Kenya, who were followed for a median of 566 days, researchers documented 806 cases of T. vaginalis infection and 265 women became infected with HIV.

According to Dr. R. Scott McClelland of the University of Washington, Seattle and colleagues there and in Kenya, trichomoniasis was associated with a 1.52-fold increased risk of HIV-1 infection after adjustment for condom use and number of sex partners.

A causal association between vaginal trichomoniasis and increased risk of HIV infection is biologically plausible, the authors say, noting that T. vaginalis "leads to an inflammatory response with recruitment of CD4-bearing lymphocytes and macrophages to the vaginal and cervical mucosa."

Mucosal hemorrhages can occur with trichomoniasis, which could provide a physical pathway for HIV-1 infection. Trichomoniasis may also render women more susceptible to bacterial vaginosis or persistent abnormal vaginal flora.

"Interventions to prevent and treat trichomoniasis and to improve vaginal health in general," conclude Dr. McClelland and colleagues, "could provide important female-controlled methods for reducing the risk of HIV-1 transmission to women."

J Infect Dis 2007;195:698-702.

Trichomonas vaginalis is a risk factor for Preterm Delivery.  Figure from Roush, W.  (1996).  Science 271:  139-140.

PathogenicCausesPreTermBirth

 

 

 

 

Leishmania donovani

Images:  http://www.k-state.edu/parasitology/625tutorials/Kinetoplastids01.html

LeishmaniaAmastigotes

In the context of military parasitology --
http://www.cdc.gov/epo/mmwr/preview/mmwrhtml/00016144.htm
http://www.pdhealth.mil/deployments/gulfwar/leish.asp

Generalized life cycle:

Leishmania_LifeCycle

Phylogeny:
Order Kinetoplastida

Preferred definitive host:
Humans

Reservoir hosts:
Dogs, jackals, foxes

Intermediate/vector hosts:
Phlebotomus spp. sandflies

Geographical location:
Southern Russia, China, Northeast India, Bangladesh, Central and South America

 Organs affected:
Reticuloendothelial system

Symptoms:
Fever, anemia, edema, difficulty breathing,
diarrhea, emaciation, hepatosplenomegaly as compensation for anemia

Treatment:
Antimony sodium gluconate, Pentamidine

 

Leishmania tropica

Images:
Skin lesions:
LeishmaniasisCutaneous


Rhinophymous Leishmaniasis: A New Variant – from Medscape Infectious Diseases
http://www.medscape.com/viewarticle/704662?src=mp&spon=3&uac=40240FX

Phylogeny:
Order Kinetoplastida

Preferred definitive host:
Humans

Reservoir hosts:
Dogs, rodents

Intermediate/vector hosts:
Phlebotomus spp. sandflies

Geographical location:
West-Central Africa, Mediterranean region, India, South America, Central America, Ethiopia


Organs affected:
Reticuloendothelial system, skin

Symptoms:
Ulcers and sores on skin

Treatment:
Antimony sodium gluconate. Frequently self-healing with lasting immunity.

From: Newsday.com

Skin Disease Strikes U.S. Troops in Iraq

December 8, 2003, 7:37 AM EST

BAGHDAD, Iraq -- The Army's 101st Airborne Division has sent 20 soldiers to Walter Reed Army Medical Center in Washington for treatment for a skin disease transmitted by bites from sand flies in Iraq, the military said.

Another 10 to 20 soldiers from the division stationed in Mosul in northern Iraq are under observation for the illness, called leishmaniasis, said Maj. Trey Cate, a division spokesman. The 101st Airborne Division is based at Fort Campbell, Ky.

"We are concerned about the health and welfare of the soldiers, hence we have evacuated them to a major medical center where this disease that does not exist in the U.S. can be treated by the experts and studied in ways that are impossible in the field," Cate said Sunday in an e-mail to The Associated Press.

The disease is known as "Baghdad Boil" to U.S. soldiers in Iraq, and can leave disfiguring lesions on the skin for months.

Cate said the U.S. military took measures against the sand flies before deploying soldiers in Iraq, issuing insect repellent to soldiers and impregnating their uniforms and insect netting with permethrin, an insecticide.

Leishmaniasis is more common in rural than urban areas, but is found on the outskirts of some cities, according to the Centers for Disease Control and Prevention in Atlanta. Risk is highest between dusk and dawn. Vaccines and drugs for preventing infections are not currently available.

About 150 U.S. soldiers serving in Iraq have been diagnosed with leishmaniasis and more may have been infected with the disease, according to U.S. newspaper reports. The disease can take months to incubate.

Copyright © 2003, The Associated Press

 

 

  

Leishmania braziliensis

 Images:

Phylogeny:
Order Kinetoplastida

Preferred definitive host:
Humans

Reservoir hosts:
Dogs, rodents, cats, kinkajou

Intermediate/vector hosts:
Lutzomyia spp. sandflies

Geographical location:
Central and South America

Organs affected:
Nasal system and buccal mucosa

Symptoms:
Destruction of cartilaginous and soft tissue, ulceration of lips, palate, pharynx leading to deformity.

 Treatment:
Antimony sodium gluconate, Amphotericin B, cycloguanil pamoate

  

Trypanosoma gambiense and T. rhodesiense (African trypanosomiasis) 

Life cycle of African (sleeping sickness) species:

TrypanosomaAfricanLifeCycle.gif

Winterbottom’s sign:  Enlargement of lymph nodes in the neck, a sign of early trypanosomiasis infection:

WinterbottomsSignForSleepingSickness.jpg

 

From the July 18, 2005 issue of SciAm.com:

Analysis Identifies Common Genetic Core for Trio of Parasites:

Scientists have successfully sequenced the genomes of three deadly parasites that together threaten half a billion people annually around the globe. According to reports published in the current issue of the journal Science, the parasites responsible for African sleeping sickness, Chagas disease and leishmaniasis--illnesses with very different symptoms--share a core of a few thousand genes. Scientists hope that the results will prove useful for identifying novel drug or vaccine targets.

The three parasites, which are passed on to humans through very different vectors, are from the family Trypanosomatidae and look similar under a microscope. In addition, the new genetic analyses identified 6,200 core genes that the so-called TriTryps share, which represent about 70 percent of their total DNA. But the international research teams also identified important ways in which they differ and discovered that the genes unique to each organism are mostly located near the ends of chromosomes. "Thanks to these studies, scientists are now much closer than they were five years ago to developing effective drugs against these terrible diseases, " remarks Najib El-Sayed of the Institute for Genomic Research in Rockville, Md. For therapeutic purposes, the scientists say their focus will be on genes that are similar for all three, but different from human genes.

The results indicate that T. brucei, which causes sleeping sickness, has the least overall metabolic capacity, whereas Leishmania major has the greatest. The Chagas disease parasite T. cruzi, meanwhile, has some 1,300 genes that may help it better evade a host's immune system. "Now that the genes of parasites are mapped out, it's much easier to identify genes that are critical for parasite survival," explains co-author Peter J. Myler of the Seattle Biomedical Research Institute. "Genes encoding proteins that are involved in critical biological processes often serve as drug targets."

Images:  http://www.k-state.edu/parasitology/625tutorials/Protozoa06.html

Phylogeny:
Order Kinetoplastida

Preferred definitive host:
Humans

Vector/intermediate host:
Tsetse flies (genus Glossina spp.)

Geographical location:
Central and East central Africa

Organs affected:
Blood, central nervous system.

Symptoms and clinical signs:
Lymph nodes swell, increasing apathy, mental dullness, tremor of the tongue, hands and trunk, anemia due to lysis of rbc's, somnambulism.

Treatment: Arsenic drugs, suramin, pentamidine, Berenil.

  

Trypanosoma cruzi (American trypanosomiasis - Chagas’ Disease)

Images:
http://www.k-state.edu/parasitology/625tutorials/Kinetoplastids01.html

Life cycle of American trypanosomiasis:

TrypanosomaCruziLifeCycle

From: Cohen, Joel E. and Gurtler, Ricardo E., 2001. Modeling Household Transmission of American Trypanosomiasis. Science 293:694-698. "American trypanosomiasis, or Chagas disease, caused by the protozoan parasite Trypanosoma cruzi and transmitted by blood-feeling triatomine bugs, is a chronic, frequently fatal infection that is common in Latin America. Neither adequate drugs nor a vaccine is available. A mathematical model calibrated to detailed household data from three villages in northwest Argentina shows that householders could greatly reduce the risk of human infection by excluding domestic animals, especially infected dogs, from bedrooms; removing potential refuges for bugs from walls and ceilings; and using domestically applied insecticides. Low-cost, locally practicable environmental management combined with intermittent use of insecticides can sustainably control transmission of T. cruzi to humans in rural Argentina and probably elsewhere."

 

Medscape from WebMD

www.medscape.com

 

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Blood Donor Screening for Chagas Disease --- United States, 2006-2007

 

MMWR.  2007;56(7):141-143.  ©2007 Centers for Disease Control and Prevention (CDC)

Posted 03/09/2007
NOTE: To view the article with Web enhancements, go to:
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Content

Chagas disease, a zoonotic disease caused by the bloodborne parasite Trypanosoma cruzi, affects an estimated 11 million persons throughout much of Latin America. In endemic areas, T. cruzi is transmitted primarily by triatomine insects (i.e., kissing bugs); infection also can occur via blood transfusion, congenital transmission, organ transplantation, laboratory incident, and ingestion of triatomine-contaminated food or drink.[1] To evaluate an investigational assay for detecting T. cruzi infection in blood donations, the American Red Cross conducted a clinical trial during August 2006-January 2007, screening 148,969 blood samples at three blood-collection centers in the United States. In January 2007, after the new assay was licensed by the Food and Drug Administration (FDA), other centers began screening donors for T. cruzi. This report describes the results of the American Red Cross study, which identified 32 donations (approximately one in 4,655) as confirmed positive for T. cruzi antibodies. As blood-donation screening for Chagas disease becomes more widespread, public health officials and health-care providers should anticipate increased numbers of questions regarding the diagnosis, evaluation, and management of Chagas disease.

Chagas disease has an acute stage, typically asymptomatic or with mild symptoms (e.g., fever, malaise, swelling at the site of innoculation and lymphadenopathy) during the first 6-8 weeks after infection. If not treated, infection is lifelong with low-level, intermittent parasitemia. The majority of infected persons remain asymptomatic in the chronic indeterminate phase (i.e., a prolonged period of clinically silent infection that follows acute primary infection). However, an estimated 30% will have onset of chronic symptomatic disease, usually decades after the initial infection, with cardiac manifestations (e.g., cardiomyopathy, arrhythmias, and sudden death) or gastrointestinal involvement (e.g., megaesophagus or megacolon).

In the United States, vector-borne transmission of Chagas disease is rare.[2] However, one study revealed an increasing Chagas seroprevalence among blood donors in Los Angeles County, California, from 1996 (one in 9,850 donors) to 1998 (one in 5,400 donors).[7] In 1991, a questionnaire was introduced to screen blood donors; those reporting a history of Chagas disease are deferred, but most persons with Chagas disease likely are unaware of their infections. Seven cases of transfusion-associated transmission have been documented in the United States and Canada during the past 20 years; all occurred in immunosuppressed recipients.[3-6] Because acute infections often are asymptomatic and the level of awareness of Chagas disease among clinicians is low, cases of transfusion-associated transmission can go undetected.

In 2005, a new commercial test for blood-donation screening for Chagas disease was developed. The test, manufactured by Ortho-Clinical Diagnostics (Raritan, New Jersey), is an enzyme-linked immunosorbent assay (ELISA) that uses epimastigote lysate antigens for detection of antibodies to T. cruzi in serum and plasma.[8] In clinical trials evaluating the test, including the American Red Cross study, blood donor specimens with initially reactive results were retested twice and considered repeat reactive if one or both of the repeat tests were reactive. Repeat reactive specimens from the clinical trials underwent further testing using a radioimmunoprecipitation assay (RIPA); those with positive RIPA results were considered confirmed positive. However, FDA has not licensed a supplemental test as a confirmatory assay in blood donation screening for T. cruzi antibodies.

After a clinical trial in 2005 with approximately 40,000 blood donors resulted in only one repeat reactive specimen (which tested negative with RIPA),[8] the American Red Cross conducted a larger study of the new screening assay in areas where Chagas was expected to be more prevalent. The study was conducted in three collection facilities of the American Red Cross, including the Southern California Region (Los Angeles, California), the Northern California Region (Oakland, California), and the Arizona Region (Tucson, Arizona). Blood donations collected during August 28, 2006-January 28, 2007, were tested with the screening assay for those blood donors willing to participate in the study. All donors were asked to participate; 78.5% agreed, and their specimens were tested.

A total of 148,969 blood-donation specimens were tested; 63 specimens from 61 donors were repeat reactive for T. cruzi antibodies (approximately one in 2,365 donations). Among the 61 donors with repeat reactive speciments, 40 (66%) were male; the age range was 17-84 years, with a mean age of 47 years and a median of 50 years. Of the 63 repeat reactive specimens, 50 (79%; one in 1,993 donations) were collected from the Los Angeles center, nine (14%; one in 3,258 donations) were collected from the Oakland center, and four (6%; one in 5,995 donations) were collected from the Tucson center. Fifty-five (90%) of the 61 donors were allogeneic donors; the remaining six included five autologous donors (two with two reactive donations each) and one directed donor. Of the 55 allogeneic donors, 18 (33%) were first-time donors, and 37 (67%) had donated blood previously. All of the 63 repeat reactive donations were tested with RIPA, of which 32 (51%) were positive and 31 (49%) were negative.

On December 13, 2006, based in part on preliminary results from the American Red Cross study, FDA licensed the Ortho T. cruzi ELISA Test System to screen blood donors in the United States. The new assay also is labeled for testing plasma and serum samples from living cell and tissue donors and from heart-beating organ donors, but is not labeled for general clinical diagnostic use.

Reported by: SL Stramer, PhD, American Red Cross, Gaithersburg; RY Dodd, PhD, DA Leiby, PhD, American Red Cross, Rockville, Maryland. RM Herron, MD, American Red Cross, Los Angeles; L Mascola, MD, Los Angeles County Dept of Public Health; LJ Rosenberg, MD, California State Health Dept. S Caglioti, Blood Systems Laboratories, Tempe; E Lawaczeck, DVM, RH Sunenshine, MD, Arizona Dept of Health Svcs. MJ Kuehnert, MD, Div of Health Care Quality Promotion, National Center for Preparedness, Detection, and Control of Infectious Diseases (proposed); S Montgomery, DVM, C Bern, MD, A Moore, MD, B Herwaldt, MD, Div of Parasitic Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases (proposed); H Kun, PhD, JR Verani, MD, EIS officers, CDC.

Editorial Note

Findings from the American Red Cross study described in this report provided evidence to support FDA approval of the first blood donor screening test for Chagas disease in the United States. Use of this test by blood centers to screen for T. cruzi antibodies is not required. However, both the American Red Cross and Blood Systems, Inc., blood-collection organizations that are responsible for approximately 65% of the U.S. blood supply, began screening all donations for T. cruzi on January 29, 2007, and providing testing services for smaller blood-collection centers and hospitals that requested testing. FDA is expected to recommend implementation of the test by all blood-collection establishments.

The AABB (formerly known as the American Association of Blood Banks) has issued recommendations to its member facilities regarding how to use the new test.* AABB recommends that all components from blood donations that are repeat reactive by the ELISA test should be quarantined and removed from distribution, and the donor should be deferred from making donations indefinitely. Recipient tracing should be conducted to identify and test recipients of blood components collected previously from donors who are confirmed positive (i.e., repeat reactive by ELISA and positive by RIPA). AABB also suggests testing at-risk family members of donors who are confirmed positive or family members with a similar history of exposure to vectors in an endemic area (e.g., the children of seropositive women). Deferred donors, at-risk family members, and potentially infected recipients should be referred to health-care providers for evaluation and management.

Screening blood donations for T. cruzi antibodies can identify persons with previously undiagnosed Chagas disease and further enhance the safety of the U.S. blood supply. However, as with any screening test, limitations exist. Although available data regarding the performance of the new assay have suggested high sensitivity and specificity,[8,9] some false-negative results have occurred with this assay[8] and with other assays used to screen for T. cruzi antibodies.[10] In addition, when a screening assay is used in a population with low disease prevalence, a greater proportion of false-positive results can be expected. Donors with reactive screening assay results require further clinical diagnostic testing to verify T. cruzi infection and to guide clinical management.

For clinical purposes, no single laboratory test is adequately sensitive and specific to diagnose Chagas disease. Diagnosis generally is made by using at least two different serologic tests (e.g., diagnostic ELISA tests, immunofluorescence assay, or indirect hemagglutination)[1] and by considering clinical findings and exposure risk. Clinical diagnostic testing for Chagas disease is available through commercial laboratories and the Division of Parasitic Diseases (DPD) at CDC. After diagnosis, health-care providers should conduct a thorough clinical evaluation to determine the stage of disease, develop an appropriate treatment plan, and provide information regarding prognosis. CDC is preparing guidance for the clinical evaluation, staging, management, and treatment of patients with Chagas disease.

Cases of Chagas disease likely will be increasingly identified as a result of screening blood donors for infection with T. cruzi. In addition, requests for diagnostic testing might become more frequent as awareness of Chagas disease increases among clinicians and the general public. Most identified cases likely will represent chronic infections that were acquired years earlier.

Chagas treatment options are limited and are most effective during the acute stage of infection. However, increasing evidence suggests that treatment of persons with chronic infections can result in seroreversion and prevent progression of cardiac morbidity.[1] Treatment of women of childbearing age with Chagas disease can decrease the risk for congenital transmission. Antitrypanosomal medication in the United States is currently available only through CDC under an investigational new drug protocol.

Questions regarding laboratory diagnosis, evaluation, and management of Chagas disease can be posed to DPD by telephone, 770-488-7775. Additional information regarding Chagas disease is available at http://www.cdc.gov/ncidod/dpd/parasites/chagasdisease/default.htm.

* Available at http://www.aabb.org/content/members_area/association_bulletins/ab06-08.htm.

References

1.    WHO Expert Committee. Control of Chagas disease. World Health Organ Tech Rep Ser 2002;905:i-vi,1-109.

2.    Herwaldt BL, Grijalva MJ, Newsome AL, et al. Use of polymerase chain reaction to diagnose the fifth reported US case of autochthonous transmission of Trypanosoma cruzi, in Tennessee, 1998. J Infect Dis 2000;181:395-9.

3.    Cimo PL, Luper WE, Scouros MA. Transfusion-associated Chagas' disease in Texas: report of a case. Tex Med 1993;89:48-50.

4.    Lane DJ, Sher G, Ward B, Ndao M, Leiby D, Hewlett B. Investigation of the second case of transfusion transmitted Chagas disease in Canada. Presented at: 42nd Annual Meeting of the American Society of Hematology, San Francisco, California; December 1-5, 2000.

5.    Leiby DA, Lenes BA, Tibbals MA, Tames-Olmedo MT. Prospective evaluation of a patient with Trypanosoma cruzi infection transmitted by transfusion. N Engl J Med 1999;341:1237-9.

6.    Saulnier Sholler GL, Kalkunte S, Greenlaw C, McCarten K, Forman E. Antitumor activity of nifurtimox observed in a patient with neuroblastoma. J Pediatr Hematol Oncol 2006;28:693-5.

7.    Leiby DA, Herron RM Jr, Read EJ, Lenes BA, Stumpf RJ. Trypanosoma cruzi in Los Angeles and Miami blood donors: impact of evolving donor demographics on seroprevalence and implications for transfusion transmission. Transfusion 2002;42:549-55.

8.    Food and Drug Administration. Product approval information licensing action. ORTHO T. cruzi ELISA Test System. Available at http://www.fda.gov/cber/products/tryorth121306.htm.

9.    Tobler LH, Contestable P, Pitina L, et al. Evaluation of a new enzyme-linked immunosorbent assay for detection of Chagas antibody in US blood donors. Transfusion 2007;47:90-6.

10. Leiby DA, Wendel S, Takaoka DT, Fachini RM, Oliveira LC, Tibbals MA. Serologic testing for Trypanosoma cruzi: comparison of radioimmunoprecipitation assay with commercially available indirect immunofluorescence assay, indirect hemagglutination assay, and enzyme-linked immunosorbent assay kits. J Clin Microbiol 2000; 38:639-42.

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 Phylogeny:
Order Kinetoplastida

Preferred definitive hosts:
Humans

Reservoir hosts:
Dogs, cast, opossums, armadillos, wood rat

Intermediate/vector hosts:
Triatoma bugs in Uruguay, Chili, Argentina, Rhodnius prolixus in northern South America and Central America

Geographical location:
Central and South America

Organs affected:
Lymph node, nervous tissue, heart muscle

Symptoms and clinical signs:
Swelling of lymph nodes, progressive deterioration of nervous tissue, resulting in loss of strength, nervous disorders, heart failure, megaesophagus or megacolon

 Treatment:
No effective drug

 

Plasmodium spp., including P. falciparum, P. malariae, P. ovale, and P. vivax (malaria)

Images: 
Plasmodium falciparum: 
http://www.k-state.edu/parasitology/625tutorials/Plasmodium01.html
Plasmodium lophurae exflagellation: 
http://www.k-state.edu/parasitology/625tutorials/Apicomplexa05.html
Plasmodium malariae: 
http://www.k-state.edu/parasitology/625tutorials/Plasmodium04.html
http://www.cbu.edu/~seisen/Malaria_files/frame.htm

Generalized Life cycle of Plasmodium spp.

MalariaLifeCycle03

World Malaria Report 2005:  http://rbm.who.int/wmr2005/html/exsummary_en.htm

Timeline, adapted from Maher, B.A.  (2005).  Fever Pitch.  The Scientist 18(10):25.

Year

Discovery

400 BC

Susruta, A Brahmin priest, describes malarial fever that he attributes to mosquito bites.

95 BC

Lucretius suggests that an organism rather than poisonous air or miasma might cause malaria, which means “bad air” in Italian.

450 AD

A widespread epidemic occurs in Lugnano, north of Rome, according to forensic DNA evidence.

1638

Juan del Vego uses a tincture from bark of a tree to treat the Countess of Chinchon in Peru; the remedy is later named quinine.

1716

Giovanni Maria Lancisi, physician to three popes, notes that draining swamps curbs malaria; he suggests an insect origin.

1880

French army surgeon Charles Louis Alfonse Laveran identifies malaria parasite; wins Nobel Prize in 1907.

1894

Patrick Manson hypothesizes that an external vector transmits malaria.

1897

Ronald Ross, military physician in India, observes malaria parasite in Anopheline mosquito guts, wins Nobel Prize in 1902.

1934

Chemist Hans Andersag at Bayer laboratories in Germany discovers chloroquine (resochin), but the compound is largely forgotten.  It won’t be recognized as a safe effective antimalarial drug until 1946.

1939

Paul Muller in Switzerland notes insecticidal properties of DDT, synthesized nearly a 100 years earlier by Othmar Zeidler, a German chemistry student.

1947-1951

National Malaria Eradication Program established by state and federal agencies essentially eradicates malaria in the United States.

1956

World Health Organization (WHO) launches Global Malaria Eradication Program.

1960’s

Widespread drug-resistant parasites and DDT-resistant mosquitoes are noted

1962

Rachel Carson publishes Silent Spring, about the environmental effects of DDT.

1967

WHO abandons malaria eradication in favor of control.

1972

The US Environmental Protection Agency bans the use of DDT

1979

Chinese researchers describe artemisinin, a wormword-derived treatment noted in ancient texts.

1983

First Plasmodium gene is cloned

1998

WHO initiates Roll Back Malaria program with the goal of halving the burden of malaria by 2010.

2000

UK researchers produce the first transgenic mosquitoes.

2002

International consortia publish the sequence of Plasmodium falciparum and a draft sequence of Anopheles gambiae.

Phylogeny:
Subphylum Apicomplexa

Preferred definitive host:
Technically, mosquitos are the definitive host since the parasite undergoes sexual reproduction in the mosquito. By convention, mosquitos are considered the "vectors" to humans.

Reservoir hosts:
None

Vector/intermediate host:
Mosquitos, particularly those of the genus Anopheles.

Geographical location:
Central and South America, Africa, Middle East, Asia, Pacific Islands

Organs affected:
Liver, blood, kidney

Symptoms and clinical signs:
Most symptoms are associated with its effects on erythrocytes. Symptoms commonly include chills, fever, and anemia. Other symptoms include muscle pain, headache, loss of appetite, nausea, vomiting, jaundice, and renal failure.

Treatment: Chloroquine, Primaquine, Sulfamethoxine, Pyrimethamine, Sulfadiazine, Quinine, Amodiaquine.

Some drugs used in the treatment of malaria are nasty, and have psychological effects. Here is the text of an e-mail distributed, requesting information regarding Lariam:

From: "Dan Olmsted" <DOlmsted@upi.com
To: <info@rpcv-wa.org>
Sent: Wednesday, June 05, 2002 1:14 PM
Subject: Lariam query from UPI

We would appreciate it if you could post this and/or send to volunteers. If you have any questions feel free to contact me at 202 302 3753 or via e-mail. Thanks, Dan Olmsted, Washington Bureau Chief, United Press International. United Press International is investigating the anti-malaria drug Lariam and is interested in hearing from Peace Corps volunteers about any problems they may have experienced.

If you experienced psychiatric or other reactions to the drug either during or after your Peace Corps years, we would like to hear from you. We also are interested in hearing about any reports of volunteers not taking the drug because of side effects; what kind of warnings you received; whether your complaints about side effects were taken seriously, and how Peace Corps medical officers dealt with the issue of side effects. We also would like to find former medical officers or Peace Corps officials who would talk to us. Also, we are interested in any information about suicidal thinking or behavior, or actual suicides or unexplained deaths, that might be connected with the drug. UPI published an article on side effects including suicide on May 21; you can read it by going to UPI.com and typing in Lariam, or going to Newsday.com and doing the same thing (that is a shorter version).

You can e-mail me at dolmsted@upi.com. Please include a phone number and indicate whether you would be willing to be quoted by name (we only use named sources in our reporting). Also, if you are attending the Peace Corps convention in Washington in June, please let us know.

We are taking the issue of side effects very seriously and are committed to full and accurate reporting about the situation.

Sincerely,

Dan Olmsted
Washington Bureau Chief
United Press International

New Study of Malaria Finds Many New Cases:  From a Reuters article released March 11, 2005

More than half a billion people, nearly double previous estimates, were affected by the deadliest form of malaria in 2002, according to a new estimate by scientists.

.

Most of the cases were in sub-Saharan Africa but nearly 25 percent of them occurred in Southeast Asia and the Western Pacific.

.

There are 515 million clinical attacks of Plasmodium falciparum malaria a year on the planet, said Robert Snow, professor of public health at the Kenyan Medical Research Institute in Nairobi and one of the authors of the study.

.

"We have taken a conservative approach to estimating how many attacks occur globally each year," Snow said, "but even so the problem is far bigger than we previously thought."

.

The figures, which were reported in a letter to the science journal Nature, published Thursday, are almost twice those of the World Health Organization, which estimated the global incidence at 273 million cases in 1998, with 90 percent of cases in Africa.

.

"It is quite substantially higher than the WHO estimate," Snow said. In the new study, it was estimated that there were 365 million cases of malaria in Africa alone in 2002.

.

Malaria is an infectious disease caused by parasites transmitted to humans by the bite of an infected mosquito. The disease occurs in more than 100 countries and kills more than one million people each year - mostly young children in sub-Saharan Africa.

.

The new research suggests that 2.2 billion people are at risk of malaria.

.

Although the scientists did not estimate deaths from the disease, the risk of severe life-threatening complications was estimated to be approximately 10 times higher in Africa than in Southeast Asia and the Western Pacific.

.

"Getting the numbers right is important," Snow said. "Not knowing the size of the problem limits our ability to articulate how much money we need to tackle the problem - not knowing where the problem is located means you can't spend wisely."

.

Groovy Web site(s):

Malaria Foundation International
http://www.malaria.org

 Note: A number of genetic conditions have evolved among human populations in response to malaria. The best known are sickle-cell anemia and favism, a deficiency of gluose-6-phosphate dehydrogenase.

From the Abstract of Aluoch, JR, 19997. Higher resistance to Plasmodium falciparum infection in patients with homozygous sickle cell disease in western Kenya. Trop. Med. Int. Health 1997 Jun;2(6):468-71.

"Sickle haemoglobin (HbS) is considered to be protective against malaria. Malaria is fatal in homozygous sickle cell (HbSS) disease. In a cross-sectional survey…of 766 residents of Western Kenya…, 20 were found to have HbSS disease, `120 sickle cell trait (HbAS) and 626 the normal genotype (HbAA). Blood slides for malarial parasites (MPs) were performed in 728 cases, i.e. 592 HbAAs, 116 HbASs and all 20 HbSSs. Malaria parasites were found in 261 (35.8%) HbAAs, 42 (5.8%) HbAss, and 20% (4 out of 20) in HbSSs. The relative risk of malarial infection was 0.33 in the HbSSs compared to both HbAAs and HbASs. It seems that the protection conferred by HbS against malaria is more marked in HbSS disease than in HbAS and is HbS-content related, and that the balanced polymorphism in the HbS-malaria relationship is maintained-by higher mortality risk due to malaria and high mortality risk of HbSSs caused by complications of HbSS."

 

 

Medscape from WebMD

www.medscape.com

 

http://images.medscape.com/pi/global/ornaments/spacer.gif

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WHO Urges Free Distribution of Anti-Malaria Nets



Reuters Health Information 2007. © 2007 Reuters Ltd.
Republication or redistribution of Reuters content, including by framing or similar means, is expressly prohibited without the prior written consent of Reuters. Reuters shall not be liable for any errors or delays in the content, or for any actions taken in reliance thereon. Reuters and the Reuters sphere logo are registered trademarks and trademarks of the Reuters group of companies around the world.

By Stephanie Nebehay

GENEVA (Reuters) Aug 16 - The World Health Organisation on Thursday recommended that malaria endemic countries widely distribute free insecticide-treated mosquito nets that give long-term protection against the disease which kills more than one million people a year.

The new guidance from the United Nations agency follows "impressive results" in Kenya, where mortality was reduced by 44 percent among children sleeping under long-lasting nets that cost $5.

"For the first time, WHO recommends that insecticidal nets be long-lasting and distributed either free or highly subsidised and used by all community members," it said in a statement.

Free mass distribution of the nets, which are efficient for at least three years and also kill the mosquitoes, is a "powerful way to quickly and dramatically increase coverage, particularly among the poorest people".

Malaria kills a child every 30 seconds, mainly African children under 5 years old, WHO says. Some 114 countries in Africa, Asia and Latin America are endemic.

The disease, which makes more than 500 million people a year severely ill, is caused by a parasite transmitted via bites from infected mosquitoes.

Conventional nets need to be re-treated regularly and many people fail to wash them properly or replace them when torn.

WHO director-general Margaret Chan said the new guidance provided "a road map for ensuring that life-saving long-lasting insecticidal nets are more widely available".

"Long-lasting insecticidal nets, with longer useful life, are cheaper to use, even if they are more expensive to buy," the WHO said in a paper sent to its 193 member states.

WHO's previous guidelines recommended providing insecticide-treated mosquito nets for use by children under five and pregnant women.

"However, recent studies have shown that by expanding the use of these nets to all people in targeted areas, increased coverage and enhanced protection of vulnerable groups can be achieved while protecting all community members," it said.

In Kenya, between 2004 and 2006, a near tenfold increase in the number of children sleeping under insecticide-treated nets resulted in 44 percent fewer deaths than among children not protected by nets, according to preliminary government data.

President Mwai Kibaki last year launched an effort to distribute 3.4 million long-lasting insecticidal nets free of charge to children in 45 of Kenya's 70 districts, the WHO said.

"Seven lives were saved for every 1,000 nets given out," Peter Olumese, a medical officer with WHO's Global Malaria Programme, told Reuters on Thursday.

<hr size=1 width="100%" noshade color=gray align=center>

 

http://bi.medscape.com/pi/global/medscape-1x1.gif

 

 

'Happy' Malaria Awareness Day

Today on campuses around the country students with the Student Campaign for Child Survival are demanding concrete US action to prevent the deadly impact of malaria.  On lawns, in their homes, in dining halls, around the dinner table and as a part of the "Malaria Bites, Bite Back" nation-wide house party students are coming together, preparing foods from malaria regions, learning about the devastating impact of the disease, and sending a bold message to their elected officials in DCs – WE ARE BITING BACK! 

·        Students from California to New York, from Wisconsin to Texas will be taking part. 

·        Stanford:  Students will be tabling on campus, hosting a speaker and screening a film – all on African malaria

·        Cornell:  Campaign members are hosting house parties and taking pictures of all the partygoers who are 'biting back.'

·        St. Scholastica:  Students participating in the Mayfest Fun Run will be sporting "I'm Biting Back" stickers.  Non-runners can pose for pictures in the student union or make a fee call to their elected officials in DC. 

·        Beloit College:  At this small school in Southern Wisconsin students are taking over their entire (and only) dining hall with a school-wide game of Malaria Trivia. 

·        Texas A&M:  Students are gathering for a more intimate roundtable discussion on the US response to the deadly disease.

·        And many more!

Photos of students participating in their events and holding signs that read "I'm biting back" will be compiled by students at SCCS's DC headquarters and presented to Representative Obey (D-WI) with our semester's primary request - fully fund the Global Fund and PMI. 

Our press release is attached, updates on how everything panned out will follow, and the house-party action kit, if you are curious, is still online
here

Keep up the good work everyone,

Simon Stumpf  |  SCCS National Organizer
The  Student  Campaign  for  Child Survival
c: 320 420 0959  | 
supportchildsurvival.org

          CHARACTERISTICS OF PLASMODIUM SPP.

 

 PARAMETER

            VIVAX

            FALCIPARUM

            OVALE

            MALARIAE

CIRCADIAN CYCLE OF FEVERS

 

          48 hours

 

          IRREGULAR -

          48 hours

 

          72 hours

 

          72 hours

OCCURRENCE

Temperate zone & North Africa & Vietnam

 

Tropical: Accounts For 50% of cases

 

Africa, S.E. Asia, New World

Tropics: Java & New Guinea

CELLULAR MARKINGS

Schuffner's Dots

          Maurer's

          Cleft

Schuffner's Dots

          Absent

EXOERYTH-

ROCYTIC GENERA-

TIONS

 

          Several

 

          Only 1

 

          ?

 

 

Relapses Possible

AGE OF SUSCEP-

TIBLE RBC'S

 

 

          Only young

 

 

          Any age

 

 

          Aging

Any age, but low incidence

# MEROZOITES

 

          16

 

          16

 

          8

 

          8

MULTIPLE INFECTIONS OF RBC'S?

 

          Rare

 

          Frequent

 

          No

 

          No

PROTECTION BY SICKLE CELL TRAIT

 

          No

 

          Yes

 

          No

 

          No

NECESSITY OF DUFFY FACTORS

 

          Yes

 

          No

 

          No

 

          No

 

Toxoplasma gondii

Images:

Brain cyst:
http://www.k-state.edu/parasitology/625tutorials/Cysts01.html
Live brain cyst:  
http://www.k-state.edu/parasitology/625tutorials/Apicomplexa05.html

toxoplasma_lifecycle

Toxoplasma gondii is a risk factor for congenital defects, e.g. hydrocephaly.  Image from Moore and Persaud (2003.  The Developing Human:  Clinically Oriented Embryology.  Saunders, An Imprint of Elsevier Science, ISBN 0-7216-9412-8, Philadelphia, PA.

hydrocephaly

Phylogeny:
Subphylum Apicomplexa

Preferred definitive host:
Domestic cats, Puma, Ocelot, bobcat, Jaguarundi

Reservoir hosts:Technically none, but cockroaches, flies and leeches serve as transport hosts.

Vector/intermediate host: Humans, Domestic animals such as sheep, wild animals such as sheep, insectivores, rodents, pigs, herbivores.

 Geographical location:
Cosmopolitan

Organs affected:
Lymph glands, lung, liver, heart, brain, eyes. Toxoplasma can pass through the placental barrier and affect the developing fetus.

 Symptoms and clinical signs:
Among adult humans, it can cause fever, headache, muscle pain, anemia, spastic paralysis, blindness, myocarditis, permanent heart       damage. Infection among pregnant women may cause stillbirths or spontaneous abortions. Congenital conditions include hydrocephalus, microcephaly, cerebral calcification, chorioretinitis and psychomotor disturbances.

Treatment:
Pyrimethamine with trisulfapyrimidines.

Pneumocystis carinii

Images:

Phylogeny:
Uncertain (Ribosomal RNA analysis suggests affinity to Fungi)

Preferred definitive host:
Apparently none. It is a saprophyte found in the lungs of many species of animals.
 

Reservoir hosts:
None

Vector/intermediate host:
None

Geographical location:
Cosmopolitan

Organs affected:
Lungs

Symptoms and clinical signs:
This organism causes interstitial pneumonia among immunosuppressed individuals. Among children, it may cause sever dyspnea, tachypnea, cyanosis, and instant death. Among adults, it may cause a dry, hacking cough, cyanosis, and dyspnea. Mild cases may show minimal alveolar septal infiltration with lymphocytes and occasional plasma cells, but sever cases may show widespread interstitial and alveolar edema,. with lymphocytic and plasma cell infiltration, necrosis of alveolar walls, and masses of P. carinii in the alveoli.

Treatment:
Pentamidine isethionate, Trimethroprim and sulfamethoxazole.

 

Cryptosporidium spp.

Images:
Life cycle:
http://www.k-state.edu/parasitology/625tutorials/Crypto01.html
Stages: 
http://www.k-state.edu/parasitology/625tutorials/Apicomplexa07.html

Phylogeny:
Phylum Apicomplexa

Preferred definitive host:
Difficult to determine since there are 10 named species among humans, birds, and other mammals.

Reservoir hosts:
Oocysts taken from an immunodeficient person were used to infect kittens, puppies and goats.

Vector/intermediate host:
None

Geographical location:
Cosmopolitan

Organs affected:
Small intestine

Symptoms and clinical signs:
Among immunocompetent individuals, it causes a self-limiting diarrhea and abdominal cramps lasting 1 to 10 days. However, it causes a profuse, watery diarrhea among immunosuppressed (AIDS) which can persist for months and be life-threatening.

Treatment:
No effective drug treatment has been found yet.

From CNN.com, August 23, 2005:

Illness traced to New York waterpark

2,000 people have reported symptoms

From Debra Goldschmidt
CNN

Tuesday, August 23, 2005; Posted: 9:25 a.m. EDT (13:25 GMT)

 

NEW YORK (CNN) -- More than 2,000 people in 24 New York counties have shown symptoms of a gastrointestinal illness traced to a water attraction at the Seneca Lake State Park in upstate New York, state health officials said Monday.

State and private laboratories have confirmed 39 cases of cryptosporidiosis, a diarrheal disease caused by the parasite cryptosporidium, said Robert Kenny, spokesman for the New York State Department of Health. Reports were still coming in, and health officials are focusing on trying to stop the outbreak from spreading, he said.  Health investigators have linked the cases to the park's sprayground -- an 11,000 square-foot play area with water jets that visitors can walk or run through to get relief from the summer heat.  The state parks department closed the sprayground August 15 after the health department notified managers that they had linked reports of illness to the attraction.

Cryptosporidium is one of the most common causes of waterborne disease in humans in the United States, according to the CDC. The state health department found the organism in two storage tanks that supply water to the attraction.  Tests of the lake area of the park determined that the water there is not contaminated.

Cryptosporidiosis symptoms typically begin two to 10 days after exposure and usually last for two weeks, according to the Centers for Disease Control and Prevention.  The most common symptom is diarrhea, but other symptoms may include dehydration, stomach cramps, weight loss, fever, nausea and vomiting.

Some of those reporting symptoms to the health department said their symptoms dated as far back as June, but there were no known cases reported in other states. Many of those sickened have recovered, according to the health department.

Authorities urged anyone who has visited the park since late July and is having symptoms to contact their local health department or their physician. Family members and close contacts of people who have been ill and are experiencing symptoms should do the same.  People who have had symptoms are advised not to swim in recreational water -- including swimming pools, hot tubs and lakes -- while they are ill and for two weeks after their symptoms have ended in an effort to prevent spreading of the disease.  Health care workers, day care staff and food workers with symptoms are urged to stay home from work until they feel better.

From Reuters.com, July 31, 2007

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Contaminated Recreational Water a Growing Cause of Cryptosporidiosis Outbreaks



Reuters Health Information 2007. © 2007 Reuters Ltd.
Republication or redistribution of Reuters content, including by framing or similar means, is expressly prohibited without the prior written consent of Reuters. Reuters shall not be liable for any errors or delays in the content, or for any actions taken in reliance thereon. Reuters and the Reuters sphere logo are registered trademarks and trademarks of the Reuters group of companies around the world.

NEW YORK (Reuters Health) Jul 26 - Outbreaks of gastrointestinal illness caused by the parasitic protozoa Cryptosporidium are associated with recreational water use, according to the Centers for Disease Control and Prevention. Eighteen cryptosporidiosis outbreaks have been reported to the CDC in 2006, up from five outbreaks reported in 2003.

Cryptosporidium is the leading cause of gastroenteritis outbreaks associated with treated recreational water venues - including swimming pools and "aquatic entertainment facilities typically containing water slides, wave pools, 'lazy rivers,' or interactive fountains."

Five of the 2006 outbreaks are described in the July 27th issue of the Morbidity and Mortality Weekly Report. The venues were a community water park, a day camp with a swimming pool, a water spray park, a local reservoir, and multiple similar locations.

Public health officials requested that owners of implicated sources use hyperchlorination to remove the protozoa and its oocysts. Cryptosporidium protozoa and their oocysts are resistant to normal recommended levels of chlorine disinfection.

Public health officials at the CDC advise that "a multifaceted approach for prevention of cryptosporidiosis in treated water venues must address operational, technological, and behavioral factors related to recreational water use."

Risk reduction will require enhanced disinfection practices, which may include in-line ultraviolet radiation or ozone systems, as well as "increased circulation flow rates, flocculents, remedial biocidal shock treatments (e.g., routine hyperchlorination: 20 ppm for 8 hours or equivalent), and occupancy-dependent water replacement."

Public education may be even more important in preventing outbreaks. The CDC recommends refraining from swimming when experiencing a diarrheal illness and for the following 2 weeks, not swallowing pool water, and practicing proper hygiene.

More information can be accessed at www.cdc.gov/healthyswimming

Mor Mortal Wkly Rep CDC Surveill Summ 2007;56:729-732.

 

 

  

Balantidium coli

Images:

Trophozoites: 
http://www.k-state.edu/parasitology/625tutorials/Balantidium.html
Cysts: 
http://www.k-state.edu/parasitology/625tutorials/Ciliates.html

Phylogeny:
Phylum Ciliophora

Preferred definitive host:
Humans

Reservoir hosts:
Pigs, guinea pigs, rats, other mammals.

Intermediate/vector hosts:
None

Geographical location:
Most common in Philippines, but is cosmopolitan

Organs affected:
Cecum and colon

Symptoms:
Proteolytic enzymes digest the intestinal epithelium of the host. Ulcer is flask-shaped, and causes lymphocytic infiltration, hemorrhage, secondary bacterial infection. Large intestine and appendix may be perforated.

 Treatment:
Carbarsone, diiodohydroxyquin, tetracycline. Epidemiological control and treatment are similar to those of E. histolytica.

  

 

PARASITIC PLAYTHELMINTHES

Clonorchis sinensis (Chinese liver fluke)

 Images:
Adult:
http://www.k-state.edu/parasitology/625tutorials/Clonor01.html
Eggs:
http://www.k-state.edu/parasitology/625tutorials/Clonor02.html
Comparison of preserved specimen and line drawing:
http://www.k-state.edu/parasitology/625tutorials/Trematodes08.html  

Clonorchis_LifeCycle

 PHYLOGENY:
Subclass Digenea, Order Opisthorchiata

Preferred definitive host:
Humans

Reservoir hosts:
Dogs and cats are probably most important. Others may include pigs, rats, and camels.

Vector/intermediate host:
#1. Snail-Genus Parafossarulus manchouricus: #2. Fish-mostly cyprinids.

Geographical location:
Japan, Korea, Taiwan, Vietnam

Organs affected:
Bile duct and liver

Symptoms and clinical signs:
Erosion of epithelial lining and fibrosis of the liver occur. Symptoms include ascites, bile retention, gallstone formation, indigestion, diarrhea, and hepatomegaly.

Treatment:
Praziquantel.

 

Fasciola hepatica (Sheep liver fluke)

Images:

Adult: 
http://www.k-state.edu/parasitology/625tutorials/Fasciola01.html
More adults: 
http://www.k-state.edu/parasitology/625tutorials/Hepatica.html
Eggs: 
http://www.k-state.edu/parasitology/625tutorials/Platys01.html
More eggs: 
http://www.k-state.edu/parasitology/625tutorials/Fasciola02.html

Life cycle:

Fasciola_LifeCycle

Phylogeny:
Subclass Digenea, Order Echinostomata

Preferred definitive host:
Sheep and cattle, rarely among humans

Reservoir hosts:
Sheep, cattle, rabbits

Vector/intermediate hosts:
#1. Snails – Fossaria modicella or Stagnicola bulimoides; #2. Metacercariae encyst on vegetation.

Geographical location:
Cosmopolitan. Human cases documented in Central & South America, Africa, Asia and Europe

Organs affected:
Biliary ducts, liver.

Symptoms:
Necrosis of liver occurs because of migration through the liver. Anemia can result in heavy infections. Worms in bile ducts cause inflammation and edema, leading to fibrous tissue forming in walls of the ducts. Back pressure causes atrophy of liver parenchyma, thus leading to cirrhosis and jaundice. Ectopic infections occur in eye, brain, skin and lungs.

Treatment:
Rafoxanide, praziquantel

 

Fasciolopsis buski

Images:

 Adults: 
http://www.k-state.edu/parasitology/625tutorials/Buski.html
Comparison of preserved specimen with line drawing: 
http://www.k-state.edu/parasitology/625tutorials/Trematodes09.html

Life cycle:

Fasciolopsis_LifeCycle

Phylogeny:
Subclass Digenea, Order Echinostomata

Preferred definitive host:
Humans

Reservoir hosts:
Pigs

Vector/intermediate host:
Snails, genera Segmentina or Hippeutis

Geographical location:
China and Southeast Asia

Organs affected:
Small intestine

Symptoms and clinical signs:
Blockage of passageway will cause ulceration, hemorrhage, abscesses, hepatic fibrosis, and verminous intoxication.

Treatment:
Praziquantel

 

Paragonimus westermani (Chinese lung fluke)

Images:

Adult Paragonimus kellicotti
http://www.k-state.edu/parasitology/625tutorials/Paragon01.html
Eggs: 
http://www.k-state.edu/parasitology/625tutorials/Paragon02.html

Life cycle:

Paragonimus_LifeCycle

ParagonimusWestermaniAdult

Phylogeny:
Subclass Digenea, Order Plagiorchiata

Preferred definitive host:
Carnivores (e.g. felids, canids, viverids, and mustelids), rodents, and pigs.

Reservoir hosts:
Humans

Vector/intermediate hosts:
1. Snail of Family Thieridae; 2. Crab-Eriocheir japonicus.

Geographical location:
Japan, Korea, Taiwan, Western Africa, South America

Organs affected:
Mainly the bronchioles of the lungs, but the worms may wander into the brain or mesentery.

Symptoms and clinical signs:
Victim suffers from breathing difficulties and chronic cough. Worm is often fatal due to penetration of the brain, spinal cord, or heart.

Treatment:
Bithionol, Praziquantel

Regarding Schistosoma spp.:

chicagotribune.com

 


http://www.chicagotribune.com/news/nationworld/chi-0703140248mar14,1,5656740.story?ctrack=1&cset=true

River parasite eats at children

Neglected scourge in Africa is cheap and easy to treat, but the `pennies cannot be found'

By Colleen Mastony
Tribune staff reporter

March 14, 2007

NASARAWA, Nigeria -- Flowing through the shantytowns and yam fields of this dust-choked region, the River Uke glimmers like a mirage, tiny white diamonds of sunlight dancing on its surface. As the temperature rises to 100 degrees, wiry boys run to the river and leap into its waters.

Ask the people of Nasarawa, and they say the river is the center of their lives. But the water hides a debilitating scourge: schistosomiasis, a disease spread by microscopic parasites that live in the river, burrow through skin and slowly infect organs, stunting children's growth and sometimes causing death.

The solution, experts say, lies with just one dose, once a year, of about three white pills called praziquantel. Studies show that a single dose--at a cost of 20 cents--can reverse up to 90 percent of the damaging health effects of schistosomiasis within six months of treatment.

But while Nigeria profits handsomely from its oil industry and giant pharmaceutical corporations donate millions every year to treat more prominent diseases in developing countries, no one has stepped forward to help mass-produce and distribute praziquantel, which costs 7 cents per pill to manufacture.

"The pennies cannot be found," said Frank Richards, a doctor who heads a program to study the disease at the Atlanta-based Carter Center.

Schistosomiasis, also known as snail fever or bilharzia, has become yet another plague--like intestinal worms, lymphatic filariasis and trachoma--running rampant in Africa, despite an inexpensive and readily available medicine. It is estimated that 200 million people suffer from the malady worldwide, a majority without treatment.

"These are forgotten diseases and forgotten people," Richards said.

The tropical disease is the second-most common in Africa behind malaria, and experts believe its numbers are rising. Development projects such as hydroelectric and irrigation dams provide the ideal environment, and increased construction has sparked outbreaks from sub-Saharan Africa to China.

Schistosomiasis rips through internal organs and leaves victims in misery. But because it usually isn't fatal, the disease remains largely untreated as governments fight killers such as malaria, tuberculosis and AIDS, which experts call "the big three."

The Carter Center, instrumental in battling the horrific Guinea worm and other neglected diseases across the globe, has launched a small but aggressive campaign against schistosomiasis. Armed with a grant of just $40,000 a year, a small band of doctors and workers has fanned out to distribute medicine to the remotest corners of Nigeria, a country with the highest numbers of "schisto" in the world.

Schistosomiasis plagues the poorest communities, places where people live without running water, latrines or basic sanitation. The parasite is carried and spread by snails that live in rivers and dams.

When mature, the parasite leaves the snail and enters the water, where it can penetrate the skin of people who are washing or swimming. Within several weeks, the parasite grows inside the blood vessels and produces thousands of eggs. The eggs travel to the bladder, lungs, liver and intestines, where they release an enzyme that eats through tissues.

The eggs eventually are discharged through urine or feces. When passed into water, the eggs hatch and infect the snails to restart the cycle.

In Nasarawa, a trash-strewn slum of densely packed concrete houses with rusting tin roofs, 63 percent of the children have blood in their urine, a sure sign that the worms' eggs are digging into the bladder. Children are most likely to become infected because they typically spend the most time playing in contaminated water.

Parents take children to local clinics. But doctors often have no way to treat the disease.

"The drugs are not available," said Dr. Emmanuel Miri, who runs health programs in Nigeria for the Carter Center. "You are faced with children urinating blood and there is nothing you can do."

Most of the 7,000 residents in Nasarawa eke out an existence, tilling fields of cassava, corn and rice. Few people have access to latrines or running water. Fewer can afford praziquantel, which costs 20 cents per dose to produce but is sold in local pharmacies for about $2.

The lack of treatment means the town's children are small and frail. Those who say they are 10 years old frequently look no more than 6.

Other ways to fight the disease have proven expensive or ineffective. A pesticide used to kill snails could be put in the water, but that chemical is more costly than praziquantel. A program to help the village build latrines might help, but experts don't believe that would stop the spread of the disease because, as Richards said, "it's hard to keep kids from peeing when they swim."

Though many know the river is contaminated, it is nearly impossible to avoid contact with its waters. On a recent day, women washed clothing on the rocky bank as men bathed nearby. Dozens of boys splashed in a deep pool.

Ishaya Emmanuel, 15, has seen blood in his urine, but he won't stop swimming in the river. "There is not enough water to wash and bathe," he said. After swimming, he often feels itchy, a sign that the worms likely are digging into his skin.

Acknowledging the shortage of praziquantel, the World Health Organization, or WHO, recommends that doctors ration the drugs. According to WHO guidelines, if testing finds that more than 50 percent of children have the disease, an entire village should be given praziquantel. If 50 percent to 20 percent have the disease, only children should receive the pills. If less than 20 percent have the disease, the village will not be treated.

Carter Center takes leading role

The Carter Center launched a program in 1999 with the government of Nigeria to treat the disease in three states. The program could afford to purchase 200,000 doses a year. So health officials devised a plan to rotate treatment, delivering pills to the most endemic towns, bringing down disease rates and then moving the drugs to other heavily infected areas.

In places where more than 50 percent of the population once suffered from the disease, rationing drugs brings infection rates to under 20 percent of the population in most communities. But when drugs are removed, rates of infection inevitably climb.

In Nasarawa, after the pills were withdrawn for two years, the rate of disease spiked to 63 percent.

On the riverbank or in classrooms, village children were hesitant to talk about the scourge. But when coaxed in private, they acknowledged having the symptoms.

`It was a stinging pain,' boy says

Ramalan Haruna, 13, a small boy in a dirty yellow T-shirt, saw blood and felt pain while urinating. "It was a stinging pain. I was worried when I saw the blood," Haruna said.

Adam Sulaiman, 12, has seen blood in his urine too. He complained to his parents, but a medicine they got for him did not work. "We will be happy when they give us drugs," Sulaiman said.

In February, government health workers returned to Nasarawa to distribute praziquantel. At a village health clinic, children held glass vials of urine samples--red with blood. The next day they were to receive the pills to treat the infection.

"When you treat a kid with praziquantel, they do better on their tests, they are more alert in the classroom. They grow taller and they gain weight. They do all the sorts of things that children like this are supposed to," Richards said.

Carter Center officials are searching for donors to expand the program. A Japanese foundation gives $40,000 per year, but it goes only so far.

Nigeria needs more praziquantel than any other country in the world. But while it works in cooperation with the Carter Center in the villages, the government of Africa's largest oil-producing country has yet to fulfill promises to provide more money.

Ex-President Jimmy Carter, who founded the Carter Center in part to treat neglected diseases, has twice asked the Nigerian government to help pay for pills. In a 2005 meeting, top government officials promised $2 million but never followed through, Carter Center officials said. Carter traveled again to Nigeria in February and received another pledge for $2 million-- half of what is needed.

"Each one of these children would require a 20-cent investment once a year," Richards said on the riverbank. "We should be able to afford that."

----------

cmastony@tribune.com

- - -

READER CONNECTION

To find out more about the global fight against diseases, including snail fever, go to the Carter Center's Web site at cartercenter.org and the World Health Organization site at who.int

Copyright © 2007, Chicago Tribune

 

 

Schistosoma haematobium

 Images:

Comparison of ova from 3 species infecting humans: 
http://www.k-state.edu/parasitology/625tutorials/Trematodes01.html
Ova of Schistosoma haematobium
http://www.k-state.edu/parasitology/625tutorials/Schistosoma02.html
Ova of Schistosoma japonicum
http://www.k-state.edu/parasitology/625tutorials/Schistosoma03.html
Ova of Schistosoma mansoni
http://www.k-state.edu/parasitology/625tutorials/Trematodes04.html
Schistosoma mansoni mating pair
http://www.k-state.edu/parasitology/625tutorials/Schistosoma01.html

Schistomes_LifeCycle

Phylogeny:
Subclass Digenea, Order Strigeata

Preferred definitive host:
Humans

Reservoir hosts:
None

Vector/intermediate host:
Snails-Genus Bulinus or Genus Physopsis

Geographical location:
Africa and the Middle East

Organs affected:
Adults reside in the venules of the urinary bladder.

Symptoms and clinical signs:
Initial phase involves abdominal pain, bronchitis, enlargement of the spleen and liver, and diarrhea. Hematuria and pain on urination follow. Because of cellular damage to urinary bladder, malignant tumors may form. Kidneys themselves are sometimes damaged.

 

Treatment:
Metrifonate, Preziquantel, Niridazole.

 

Schistosoma mansoni

Images:

Comparison of ova from 3 species infecting humans: 
http://www.k-state.edu/parasitology/625tutorials/Trematodes01.html
Ova of Schistosoma haematobium
http://www.k-state.edu/parasitology/625tutorials/Schistosoma02.html
Ova of Schistosoma japonicum
http://www.k-state.edu/parasitology/625tutorials/Schistosoma03.html
Ova of Schistosoma mansoni
http://www.k-state.edu/parasitology/625tutorials/Trematodes04.html
Schistosoma mansoni mating pair
http://www.k-state.edu/parasitology/625tutorials/Schistosoma01.html

Phylogeny:
Subclass Digenea, Order Strigeata

Preferred definitive host:
Humans

Reservoir hosts:
Certain monkeys and rodents

Vector/intermediate host:
Snails-Genus Biomphalaria

Geographical location:
Northern Africa, Middle East, S. America

Organs affected:
Adults reside in the portal veins of the large intestine

 

Symptoms and clinical signs:
Initial phase involves abdominal pain, bronchitis, enlargement of the spleen and liver, and diarrhea. Egg deposition in venules of large intestine induces pseudotubercle formation, resulting in necrosis and ulceration. Cirrhosis and portal hypertension develop as liver becomes damaged. Splenomegaly occurs. Pseudotubercles may develop in the lungs or nervous system.

Treatment:
Oxamniquine, Praziquantel, Niridazole.

 

Schistosoma japonicum

Images:

Comparison of ova from 3 species infecting humans: 
http://www.k-state.edu/parasitology/625tutorials/Trematodes01.html
Ova of Schistosoma haematobium
http://www.k-state.edu/parasitology/625tutorials/Schistosoma02.html
Ova of Schistosoma japonicum
http://www.k-state.edu/parasitology/625tutorials/Schistosoma03.html
Ova of Schistosoma mansoni
http://www.k-state.edu/parasitology/625tutorials/Trematodes04.html
Schistosoma mansoni mating pair
http://www.k-state.edu/parasitology/625tutorials/Schistosoma01.html

 

Phylogeny:
Subclass Digenea, Order Strigeata

Preferred definitive host:
Humans

Reservoir hosts:
Rats, dogs, cats, horses, swine, and deer.

Vector/intermediate host:
Snails-Genus Onchomelania

Geographical location:
Japan, China, Taiwan, Philippines, Indonesia.

Organs affected:
Adults reside in veins of the small intestine.

Symptoms and clinical signs:
Initial phase involves abdominal pain, bronchitis, enlargement of the spleen and liver, and diarrhea. Fibrous nodules containing eggs accumulate on serosal and peritoneal surfaces of the small intestine. Splenomegaly occurs. Cirrhosis and portal hypertension due to live damage follow. Neurological disorders, such as coma or paralysis, may occur due to egg deposition in the brain.

Treatment:
Praziquantel

 

 

 

 

          GENERALIZED LIFE CYCLES: CESTODES

          (Inner loop = cyclophyllidean pathway)

          (Outer loop = pseudophyllidean pathway)

Hermaphroditic Adults in Small Intestine

 
 

 

 

Intermediate host is ingested by definitive host

 

Eggs passed in feces

 
         

 

 

 

 

 


         

 

                                     

 

 

 

Eggs are ingested by invertebrate 1st intermediate host, larva develops into procercoid form.

 

1st intermediate host is ingested by vertebrate 2nd intermediate host, larva develops into plerocercoid form, as in Diphyllobothrium latum.

 
                    

 

 

 


Diphyllbothrium latum (broad tapeworm)

Images:

Egg:
http://www.k-state.edu/parasitology/625tutorials/Platys01.html
Proglottids and eggs:
http://www.k-state.edu/parasitology/625tutorials/Tapeworm05.html
Scolex: 
http://www.k-state.edu/parasitology/625tutorials/Tapeworm02.html

Life cycle:

D_latum_LifeCycle

Phylogeny:
Class Cestoda, Order Pseudophyllidea

Preferred definitive host:
Humans

Reservoir hosts:
Piscivorous mammals such as bears

Vector/intermediate host:
1. Diaptomus copepods; 2. Fish, particularly whitefish

Geographical location:
Scandinavia, Russia, Arctic, United States

Organs affected:
Small intestine

Symptoms and clinical signs:
Vague abdominal discomfort. Sometimes pernicious anemia due to vitamin B12 requirement of the parasite. Nausea and diarrhea sometimes occur, but these symptoms are rare.

 

Treatment:
Niclosamide, Quinacrine, Paromomycin


Taenia solium
(pork tapeworm)

Images:

Comparison of Taenia solium and Taeniarhynchus saginata scolecesL 
http://www.k-state.edu/parasitology/625tutorials/Tapeworm13.html

Cysticercosis:

cysticercosis01

Phylogeny:
Class Cestoda, Order Cyclophyllidea

Preferred definitive host:
Humans

Reservoir hosts:
None

Vector/intermediate host:
Pigs

Geographical location:
Cosmopolitan

Organs affected:
Adults reside in the small intestine. Cysticerci can reside in heart muscle, brain tissue, or inside the eye.

Symptoms and clinical signs:
Usually none among adults. Abdominal pain, dizziness, nausea, and diarrhea occur, but are relatively rare. Cysticerci, however, may cause irreparable damage to the eye or heart, may cause necrosis of heart tissue, and may cause severe damage to the central nervous system, leading to epilepsy and hydrocephalus.

Treatment:
For adults, niclosamide, quinacrine, or paromomycin. For cysticerci larvae, surgery is required. 

From

 

Medscape from WebMD

www.medscape.com

 

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