PARASITES
ON
PARADE!!
(Updated September 30,
2009)
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Dr.
Stan Eisen
Biology Department
Christian Brothers University
650
To the course schedule: http://www.cbu.edu/~seisen/BIOL413LcLbDesc.htm
TABLE
OF CONTENTS
Articles You May Not Want to Read Before Lunch
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:
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
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
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
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Symbiont 2 |
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+ |
0 |
- |
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+ |
Mutualism, which may be either obligate or facultative, e.g.
clownfish and sea anemones |
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Symbiont 1 |
0 |
Commensalism, e.g. barnacles on the
skin of whales. |
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- |
Predation, if symbiont 1, as prey,
gets eaten by symbiont 2, as predator; Parasitism, if symbiont 2 lives in or
on symbiont 1. |
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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://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
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
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.
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Close-up of malformed frogs. Deformations are associated with infestations of Ribeiroia ondotrae. |
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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. |
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Although there was no positive
diagnosis, the following image appeared in:
Scott, A.F. (1999). Malformed Southern Leopard Frogs (Rana
sphenocephala utricularius) Discovered in
Parasitology-Related Websites and
Resources
Professional Societies:
American
Society of Parasitologists
c/o Daniel 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
(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 -
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
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)
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INTESTINAL NEMATODES |
Human Infections |
Deaths per year |
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All Helminths |
3.5 Billion |
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Ascaris lumbricoides |
1 Billion |
20,000 |
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Hookworm (Necator sp., Ancylostoma spp.) |
900 million |
50,000-60,000 |
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Trichuris trichiura |
700 million |
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Enterobius vermicularis |
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Strongyloides stercoralis |
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Human Infections |
Deaths per Year |
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Wuchereria bancrofti |
350 million |
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Dracunculus medinensis |
80 million |
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Trichinella spiralis |
50 million |
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Onchocerca volvulus |
40 million |
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Loa loa |
20 million |
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Human Infections |
Deaths per year |
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Schistosoma spp. |
300 million |
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Clonorchis sinensis |
40 million |
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Fasciolopsis buski |
15 million |
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Paragonimus westermanni |
5 million |
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Human Infections |
Deaths per year |
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Taenia spp. |
80 million |
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Hymenolepis spp. |
40 million |
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Diphyllobothrium latum |
15 million |
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PROTOZOAN INFECTIONS IN HUMANS (From Markell & Voge: Medical Parasitology and Schmidt & Roberts, Foundations of
Parasitology, ed.5, 1996)
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SPECIES |
Human Infections |
Deaths per year |
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Entamoeba histolytica |
600 million |
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Plasmodium spp. |
489 million |
1-2 million |
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African trypanosomiasis |
35 million |
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American trypanosomiasis |
10 million |
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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
- Active: Host produces either chemical, thermal or light signals
to which the infective stage is sensitive.
- Passive:
Infective stages are dispersed passively through environment, such as
waves or water currents.
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 |
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FECAL EXAMINATION |
Intestinal Helminths,
e.g.: Hookworm ova
Intestinal Protozoa, Giardia lamblia cysts
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BLOOD SMEAR |
Plasmodium sp. (Malaria)
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URINALYSIS |
Schistosoma haematobium
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IMMUNOASSAY |
Pneumocystis carinii, Cysticercosis (Taenia solium), Echinococcus granulosus Cysts, Giardia lamblia |
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OCULAR EXAMINATION |
Toxoplasma gondii,
Toxocara spp.
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BIOPSY |
Onchocerca volvulus, Trichinella spiralis |
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VAGINAL SMEAR |
Trichomonas vaginalis
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IMMUNOBLOT |
Plasmodium falciparum |
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XENODIAGNOSIS |
Trichinella spiralis |
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ADHESIVE TAPE ACROSS PERIANAL FOLDS |
Enterobius vermicularis
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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,
PARASITIC PROTISTS
Entamoeba
histolytica (amebic dysentery)
Images:
http://www.k-state.edu/parasitology/625tutorials/Ehistolytica.html
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
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
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
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
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
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,
Organs
affected:
Brain tissue
Symptoms
and clinical signs:
Meningoencephalitis, involving convulsions leading to death.
Treatment:
None are available. Infection with Naegleria is always fatal.
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Giardia lamblia (intestinalis)
Images:
Cysts: http://www.k-state.edu/parasitology/625tutorials/Protozoa04.html
Trophozoites: http://www.k-state.edu/parasitology/625tutorials/Protozoa02.html
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
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
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.
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This
is what the book means by a copious white (frothy) discharge, swarming with
trichomonads.
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Treatment:
Metronidazole
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NOTE: To view the article with Web enhancements, go to:
Trichomoniasis Increases Risk of HIV
Infection
Reuters
Health Information 2007. © 2007 Reuters Ltd. 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 According to Dr. R. Scott
McClelland of the 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.
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Images: http://www.k-state.edu/parasitology/625tutorials/Kinetoplastids01.html
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:
Phylogeny:
Order Kinetoplastida
Preferred
definitive host:
Humans
Reservoir
hosts:
Dogs, jackals, foxes
Intermediate/vector
hosts:
Phlebotomus spp. sandflies
Geographical
location:
Southern Russia,
Organs
affected:
Reticuloendothelial system
Symptoms:
Fever, anemia, edema, difficulty breathing,
diarrhea, emaciation, hepatosplenomegaly as compensation for anemia
Treatment:
Antimony sodium gluconate, Pentamidine
Images:
Skin lesions:
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,
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
December
8, 2003, 7:37 AM EST
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
"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
The
disease is known as "Baghdad Boil" to
Cate said
the
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
About 150
Copyright
© 2003, The Associated Press
Images:
Phylogeny:
Order Kinetoplastida
Preferred
definitive host:
Humans
Reservoir
hosts:
Dogs, rodents, cats, kinkajou
Intermediate/vector
hosts:
Lutzomyia spp. sandflies
Geographical
location:
Central and
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:
Winterbottom’s
sign: Enlargement of lymph nodes in the
neck, a sign of early trypanosomiasis infection:
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
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
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:
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
|
NOTE: To view the article with Web enhancements, go to: 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
ContentChagas disease, a zoonotic
disease caused by the bloodborne parasite Trypanosoma cruzi, affects
an estimated 11 million persons throughout much of 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 ( 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 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 Reported by: SL Stramer, PhD, American Red Cross, Editorial NoteFindings 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 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 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 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
|
Phylogeny:
Order Kinetoplastida
Preferred
definitive hosts:
Humans
Reservoir
hosts:
Dogs, cast, opossums, armadillos, wood rat
Intermediate/vector
hosts:
Triatoma bugs in
Geographical
location:
Central and
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.
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 |
|
1638 |
Juan
del Vego uses a tincture from bark of a tree to treat the Countess of
Chinchon in |
|
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 |
|
1934 |
Chemist
Hans Andersag at Bayer laboratories in |
|
1939 |
Paul
Muller in |
|
1947-1951 |
National
Malaria Eradication Program established by state and federal agencies
essentially eradicates malaria in the |
|
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 |
|
|
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,
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,
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
We are taking the issue of side effects very seriously and are committed to full and accurate reporting about the situation.
Sincerely,
Dan Olmsted
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
.
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
.
"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
.
"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
.
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
.
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
.
"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
"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
|
To
Print: Click your browser's PRINT button. NOTE: To view the article with Web enhancements, go to:
WHO Urges Free Distribution of Anti-Malaria Nets
Reuters
Health Information 2007. © 2007 Reuters Ltd. 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> |
'Happy' Malaria
Awareness Day!
Today on campuses around the country
students with the Student Campaign for Child Survival
are demanding concrete
·
Students from
·
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.
·
·
·
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 & |
Tropical: Accounts For 50% of cases |
Africa,
S.E. Asia, |
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 |
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
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,
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.
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
2,000 people have reported symptoms
From Debra Goldschmidt
CNN
Tuesday, August 23, 2005; Posted: 9:25
a.m. EDT (13:25 GMT)
|
|
|
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
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
To
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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.
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.
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
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
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:
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:
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
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
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:
Phylogeny:
Subclass Digenea, Order Echinostomata
Preferred
definitive host:
Humans
Reservoir
hosts:
Pigs
Vector/intermediate
host:
Snails, genera Segmentina or Hippeutis
Geographical
location:
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:
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:
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
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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,
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
"The pennies cannot be found," said Frank Richards, a doctor who
heads a program to study the disease at the Atlanta-based
Schistosomiasis, also known as snail fever or bilharzia, has become yet another
plague--like intestinal worms, lymphatic filariasis and trachoma--running
rampant in
"These are forgotten diseases and forgotten people," Richards said.
The tropical disease is the second-most common in
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
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
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.
The Carter Center launched a program in 1999 with the government of
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.
Ex-President Jimmy Carter, who founded the
"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
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
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,
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:
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:
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:
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:
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
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