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
Print: Click your browser's PRINT button.
NOTE: To view the article with Web enhancements, go to:
http://www.medscape.com/viewarticle/560550
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
|
|
|
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
|
NOTE: To view the article with Web enhancements, go to: Deaths From Frank
J. Sorvillo; Christopher DeGiorgio; Stephen H. Waterman Emerg
Infect Dis. 2007;13(2):230-235. ©2007 Centers for Disease
Control and Prevention (CDC) Posted
02/23/2007
Abstract and IntroductionAbstractCysticercosis has emerged as a
cause of severe neurologic disease in the IntroductionCysticercosis, a parasitic
infection caused by the larval form of the pork tapeworm, Taenia solium,
has been increasingly recognized as a cause of severe but preventable
neurologic disease in the United States.[1-5]
Reports documenting hundreds of cases, mainly of neurocysticercosis, have
drawn attention to this previously underrecognized disease.[6,7] Cysticercosis has a complex
life cycle. The larval infection, cysticercosis, is transmitted through the
fecal-oral route. Eggs from the adult tapeworm T. solium, which are
directly infectious, are shed in the feces of a human tapeworm carrier and
subsequently ingested by pigs, the usual intermediate host.[8] The oncosphere embryos emerge from the eggs, penetrate the
intestinal wall, and are disseminated by the bloodstream to various tissues
where the larval stage, or cysticercus, develops. The cycle is completed when
humans, the only naturally infected definitive host, consume raw or
undercooked pork containing cysticerci, which attach to the small bowel and
develop into the adult tapeworm. However, humans may also become infected
with the larval stage when eggs are ingested, typically in contaminated food
or water. Neurocysticercosis, the most severe form of the disease, occurs
when larvae invade tissue of the central nervous system. Cysticercosis in the MethodsData SourceMortality data were obtained
from the Data AnalysisCysticercosis mortality rates
per million population were calculated. Population data were obtained from the
US Census Bureau. Crude cysticercosis mortality rates and 95% confidence
intervals (CIs) were computed by age group (<1, 1-4, 5-14, 15-24, 25-34,
35-44, 45-54, 55-64, 65-74, 75-84, ≥85 years), sex, race/ethnicity
(white, black, Latino, Asian, Native American), and state of residence.
Age-adjusted rates were calculated for race/ethnicity, sex, and state. The ResultsOver the 13-year study period,
221 cysticercosis deaths were identified, representing an annual age-adjusted
mortality rate of 0.06 per million population (95% CI, 0.05-0.07). Most
persons who died from cysticercosis (187 [84.6%]) were Latino; 15 (6.8%) were
white, 13 (5.9%) were black, 5 (2.3%) were Asian, and 1 (0.5%) was Native
American ( Table
1 ). By sex, 137 (62.0%) were male, and 84 (38.0%) were female.
Mean age at death was 40.5 years (range 2-88 years). Most persons who died
(187 [84.6%]) were foreign born, and 137 (62%) of all persons who died had
emigrated from
Figure. Frequency and percentage of
fatal cysticercosis cases by state, United States, 1990-2002. Shaded areas
indicate states with deaths from cysticercosis.
Age-adjusted cysticercosis mortality
rates were highest for Latinos (adjusted rate ratio [ARR] = 94.5, 95% CI
56.9-156.9, relative to whites) and men (ARR = 1.8, 95% CI 1.4-2.3) ( Table
2 ). The mean age at death was 40.5 years; >60% of deaths
occurred in persons <45 years of age. Most persons (61%) had <12 years
of education. Although no clear temporal trend was noted, cysticercosis
deaths varied by year; most deaths (23) occurred in 1992 and 1997. The 33 cysticercosis deaths in
US-born persons represented 15% of all cysticercosis deaths. Ten (30.3%) of
these 33 persons were Principal concurrent conditions
listed as contributing to death included hydrocephalus in 58 (26.2%) persons,
cerebral edema in 23 (10.4%), cerebral compression in 16 (7.2%), and
epilepsy/convulsions in 12 (5.4%). These conditions were significantly more
common in persons who died of cysticercosis than in matched controls
(p<0.001). Septicemia was recorded for 15 (6.8%) of persons with fatal
cysticercosis, but this figure was not significant. Reported place of death
included inpatient facility (64.7%), emergency room or outpatient clinic
(9.5%), nursing home (9.5%), and residence (11.3%). DiscussionOur findings indicate that in
the The elevated cysticercosis mortality
rates for Latinos reflect the substantial immigration from T. solium-endemic
areas of We noted several cysticercosis
deaths of persons who were born in the Alternatively, the occurrence
of cysticercosis among US-born persons may reflect travel-related exposure
and infection. Travel-associated cysticercosis, mainly in persons who have
visited Mexico and other Latin American countries, has been previously
documented; however the risk and frequency of such infections are unknown.[10,18] The Los Angeles County surveillance system identified 9
probable travel-related cases, which represented 6.5% of the total
cysticercosis cases. In a study of cysticercosis in Texas, de La Garza and
colleagues reported 6 cases in US-born persons, all of whom had a history of
frequent travel to rural Mexico or Central America.[19] Substantial numbers of US residents travel to
cysticercosis-endemic areas each year and may be exposed to food and water
contaminated with T. solium eggs. Therefore, many of the US-born
persons likely acquired infection during travel to endemic areas. Food and
water precautions for travelers to cysticercosis-endemic regions should be
reinforced. Although 21 states had at least
1 death from cysticercosis, mortality rates were highest in The sex disparity noted in this
study is consistent with data from our recent population study, which
demonstrated a significantly higher prevalence of cysticercosis in men[16] and likely reflects the greater immigration of young men in
search of employment. Such immigration patterns may also explain the
relatively young age observed; >60% of cysticercosis deaths in our study
were in persons <45 years of age, a heavy toll among young, highly
productive persons. Although we could not assess
whether problems with access to healthcare contributed to cysticercosis
deaths, >20% of deaths occurred at home, in an emergency room, or in an outpatient
setting. Reduced access may have an effect on cysticercosis deaths;
additional data on this issue would be useful. Several large facility-based
case series studies have reported that the number of deaths from
cysticercosis is relatively low and that the case-fatality rate is <1%.
However, such facility-based studies, although providing valuable
information, have substantial limitations and may underestimate cysticercosis
as a cause of death. Limited data from the pilot Los Angles County surveillance
system found a mortality rate of ~6% (8 of 138 incident cases), and the Dixon
study of British troops who had served in India reported mortality rates of
nearly 10%.[10,20] However, these case-fatality rates must be viewed with caution
because they may reflect underdiagnosis or underreporting of less severe
cases and therefore probably represent overestimates. Mortality rates have
been reported to be higher for surgically treated patients and those with
hydrocephalus, primarily because of increased intracranial pressure and
shunt-related infection.[21] We found that hydrocephalus, cerebral compression/edema, and
epilepsy/convulsions were common concurrent conditions recorded on the death
certificate. Fatal cysticercosis may also occur in persons who have ingested
large numbers of eggs, which may cause an overwhelming, fatal acute infection
with numerous larvae and severe central nervous system pathologic changes.
Racemose cysticercosis, a phenomenon in which cysticerci continue to grow and
proliferate through tissue, may also have a poor prognosis. Newer, less
invasive, endoscopic surgical techniques for removing intraventricular
cysticerci offer promise of reducing mortality rates.[22] Our data, although population
based, likely underestimate cysticercosis deaths for several reasons. To be
listed on the death certificate, cysticercosis must be recognized and
diagnosed, which requires confirmation of infection through biopsy, autopsy,
or specialized serologic testing.[23]
Consequently, some cases of fatal cysticercosis likely go undiagnosed and
unrecognized, which would result in the miscoding of cysticercosis-related
deaths as other conditions. For this reason, death records may be biased and
likely underestimate deaths from cysticercosis. The absence of fatal cases
reported from The use of death certificates
to assess the effect of disease has advantages and limitations. Because
submission of death certificates is required by state law, ascertainment and
registration of deaths are virtually complete. Use of mortality records
therefore provides population-based data and avoids the potential biases of
facility-based data or other data that are not population based. Mortality
data can also indicate disease severity and contribute to measures of disease
load. However, data from death certificates have several limitations,
including the possible coding of inaccurate information through careless
completion of cause of death, coding errors, and misclassification of
variables such as race/ethnicity.[25,26]
Reporting of country of birth may also be inaccurate, and persons with
cysticercosis who are recorded as having been born in the United States may,
in fact, be foreign born. Deaths from cysticercosis represent only a small
fraction of total disease burden. In addition, census data and intercensus
population estimates used for the calculation of rates may be uncertain. For
these reasons, our estimate of cysticercosis mortality rate must be
interpreted with caution. Cysticercosis can cause severe
neurologic disease and death and result in substantial cost to the healthcare
system, yet simple public health measures can reduce or eliminate this
parasitic disease. In fact, cysticercosis has been identified as 1 of 6
potentially eradicable diseases.[27] Because most cysticercosis cases in the
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Characteristic |
No. |
% |
|
Sex |
||
|
Male |
137 |
62.0 |
|
Female |
84 |
38.0 |
|
Race/ethnicity |
||
|
White |
15 |
6.8 |
|
Black |
13 |
5.9 |
|
Latino |
187 |
84.6 |
|
Asian/Pacific
Islander |
5 |
2.3 |
|
Native
American |
1 |
0.5 |
|
Age
group, y |
||
|
1-4 |
1 |
0.5 |
|
5-14 |
5 |
2.3 |
|
15-24 |
37 |
16.7 |
|
25-34 |
66 |
29.9 |
|
35-44 |
29 |
13.1 |
|
45-54 |
36 |
16.3 |
|
55-64 |
20 |
9.1 |
|
65-74 |
15 |
6.8 |
|
75-84 |
9 |
4.1 |
|
≥85 |
3 |
1.4 |
|
Education,
y* |
||
|
<12 |
135 |
61.1 |
|
12 |
43 |
19.5 |
|
>12 |
25 |
11.3 |
|
Country
of birth† |
||
|
|
33 |
14.9 |
|
|
137 |
62.0 |
|
Other |
50 |
22.6 |
*Unknown for 18 persons.
†Unknown for 1 person.
Table 2. Cysticercosis Mortality Rates, United States, 1990-2002
|
|
Rate/106 population (95% CI) |
ARR (95% CI)* |
|
Sex |
||
|
Male |
0.08 (0.07-0.1) |
1.8 (1.4-2.3) |
|
Female |
0.05 (0.04-0.06) |
Referent |
|
Race/ethnicity |
||
|
White |
0.006 (0.003-0.008) |
Referent |
|
Black |
0.03 (0.01-0.05) |
5.1 (3.1-8.6) |
|
Latino |
0.56 (0.47-0.65) |
94.5 (56.9-156.9) |
|
Asian/Pacific
Islander |
0.04 (0.0-0.07) |
6.7 (4.0-11.2) |
|
Native
American |
0.04 (0.0-0.12) |
6.2 (3.7-10.3) |
*CI, confidence interval; ARR,
age-adjusted rate ratio.
Table 3. Selected Characteristics of US-Born and Foreign-Born Persons With Fatal Cysticercosis, United States, 1990-2002
|
Characteristic |
US-born, n = 33, no. (%) |
Foreign-born, n = 187, no. (%) |
p value |
|
Sex |
|||
|
Male |
22 (66.7) |
114 (61.0) |
0.53 |
|
Female |
11 (33.3) |
73 (39.0) |
|
|
Race/ethnicity |
|||
|
White |
12 (36.4) |
3 (1.6) |
<0.001 |
|
Latino |
17 (51.5) |
169 (90.4) |
|
|
Black |
3 (9.1) |
10 (5.4) |
|
|
Asian/Pacific
Islander |
0 (0) |
5 (2.7) |
|
|
Native
American |
1 (3.0) |
0 (0) |
|
|
Mean
age, range |
50.1, 2-88 |
38.7, 7-86 |
<0.01 |
|
Education,
y |
|||
|
<12 |
12 (36.4) |
123 (65.8) |
<0.001 |
|
12 |
10 (30.3) |
33 (17.7) |
|
|
>12 |
8 (24.2) |
17 (9.1) |
|
|
Unknown |
3 (9.1) |
14 (7.5) |
|
References
|
1.
Schantz PM, Tsang VC. The US Centers for
Disease Control and Prevention (CDC) and research and control of
cysticercosis. Acta Trop. 2003;87:161-3. 2.
DeGiorgio CM, 3.
Schantz PM, Wikins PP, Tsang VCW.
Immigrants, imaging, and immunoblots: the emergence of neurocysticercosis
as a significant public health problem. In: Scheld WM, Craig WA, Hughes JM,
editors. Emerging infections. 4.
White AC Jr. Neurocysticercosis: updates
on epidemiology, pathogenesis, diagnosis, and management. Annu Rev Med.
2000;51:187-206. 5.
Ong S, Talan DA, Moran GJ, Mower W,
Newdow M, Tsang VC, et al. Neurocysticercosis in radiographically imaged
seizure patients in 6.
Richards FO, Schantz PM, Ruiz-Tiben E,
Sorvillo FJ. Cysticerosis in 7.
Shandera WX, White AC Jr, Chen JC, Diaz
P, Armstrong R. Neurocysticercosis in 8.
Beaver PC, Jung RC, Cupp EW. Clinical
parasitology, 9th ed. 9.
Schantz PM, Moore AC, Munoz JL, Hartman
BJ, Schaefer JA, Aron AM, et al. Neurocysticercosis in an Orthodox Jewish
community in New York City. N Engl J Med. 1992;327:692-5. 10.
Sorvillo FJ, Waterman SH, Richards FO,
Schantz PM. Cysticercosis surveillance: locally acquired and travel-related
infections and detection of intestinal tapeworm carriers in 11.
Centers for Disease Control and
Prevention. Locally acquired neurocysticercosis -- 12.
Roman G, Sotelo J, Del Brutto O, Flisser
A, Dumas M, Wadia N, et al. A proposal to declare neurocysticercosis an
international reportable disease. Bull World Health Organ. 2000;78:399-406.
13.
Sorvillo FJ, Portigal L, DeGiorgio C,
Smith L, Waterman SH, Berlin GW, et al. Cysticercosis-related deaths,
California. Emerg Infect Dis. 2004;10:465-9. 14.
15.
Garcia HH, Gilman RH, Gonzales AE, Tsang
VCW, Verastegui M. Epidemiology of Taenia solium infection in Peru.
In: Garcia HH, Martinez SM, editors. Taenia solium taeniasis/cysticercosis.
2nd ed. 16.
DeGiorgio C, Pietsch-Escueta S, Tsang V,
Corral-Leyva G, Ng L, Medina MT, et al. Seroprevalence of Taenia solium
cysticercosis and Taenia solium taeniasis in California, USA. Acta
Neurol Scand. 2005;111:84-8. 17.
Shandera WX, Schantz PM, White AC. Taenia
solium cysticercosis: the special case of the 18.
Schantz PM, Wilkins PP, Tsang VC. A case
of neurocysticercosis in a traveler to 19.
del la Garza Y, Graviss EA, Daver NG,
Gambarin KJ, Shandera WX, Schantz PM, et al. Epidemiology of
neurocysticercosis in Houston, Texas. Am J Trop Med Hyg. 2005;73:766-70. 20.
Dixon HBF, Lipscomb FM. Cysticercosis: an
analysis and follow up of 450 cases. Medical Research Council Special
Report series, vol. 299. 21.
DeGiorgio CM, Houston I, Oviedo S,
Sorvillo F. Deaths associated with cysticercosis. Report of three cases and
review of the literature. Neurosurg Focus. 2002;12:e2. 22.
Bergsneider M, Holly LT, Lee JH, 23.
Ash LR, Orihel T. Parasites: a guide to
laboratory procedures and identification. 24.
Daniels TL, 25.
Sorlie PD, Rogot E, 26.
Kircher T, Anderson RE. Cause of death.
Proper completion of the death certificate. JAMA. 1987;258:349-52. 27.
Centers for Disease Control and
Prevention. Update: International Task Force for Disease Eradication, 1992.
MMWR Morb Mortal Wkly Rep. 1992;41:691, 697-8. 28.
Wilkins PP, Allan JC, Verastegui M,
Acosta M, Eason AG, Garcia HH, et al. Development of a serologic assay to
detect Taenia solium taeniasis. Am J Trop Med Hyg. 1999;60:199-204. 29.
Flisser A, Sarti E, Lightowlers M,
Schantz P. Neurocysticercosis: regional status, epidemiology, impact and
control measures in the 30.
Weinberg M, Waterman S, Lucas CA, Falcon
VC, Morales PK, Lopez LA, et al. The U.S.-Mexico Border Infectious Disease
Surveillance Project: establishing bi-national border surveillance. Emerg
Infect Dis. 2003;9:97-102. |
Reprint
Address
Frank J. Sorvillo, Department
of Epidemiology, School of Public Health, UCLA, Box 951772, Los Angeles, CA
90095, USA; Email: fsorvill@ucla.edu
Frank
J. Sorvillo,*† Christopher DeGiorgio,* Stephen H. Waterman‡
*University of California, Los Angeles, California
†Department of Public Health, Los Angeles County, California
‡University of California, San Diego, California
Dr. Sorvillo is professor in-residence in the Department of
Epidemiology at the School of Public Health, University of California, Los
Angeles, California. His research interests include the epidemiology and
control of infectious diseases, particularly parasitic agents.
<hr size=1 width="100%" noshade color=gray align=center>
Taeniarhynchus saginata (beef tapeworm)
Images:
Comparison
of Taenia solium and Taeniarhynchus saginata scoleces:
http://www.k-state.edu/parasitology/625tutorials/Tapeworm13.html
Phylogeny:
Class Cestoda, Order Cyclophyllidea
Preferred
definitive host:
Humans
Reservoir
hosts:
None
Vector/intermediate
host:
Cattle
Geographical
location:
Worldwide, but common in Africa and
Organs
affected:
Small intestine
Symptoms
and clinical Signs:
Usually none, but abdominal pain, headache, diarrhea, and intestinal
obstruction may occur in heavy infection.
Treatment:
Niclosamide, quinacrine, paromomycin.
Hymenolepis diminuta (rat tapeworm)
Images:
Ova:
http://www.k-state.edu/parasitology/625tutorials/Hymenolepis.html
Phylogeny:
Class Cestoda, Order Cyclophyllidea
Preferred
definitive host:
Rats
Reservoir
hosts:
Humans, particularly children.
Vector/intermediate
host:
Tribolium and/or Tenebrio beetles
Geographical
location:
Cosmopolitan
Organs
affected:
Small intestine
Symptoms and clinical signs:
Usually none
Treatment:
Niclosamide or paromomycin
Vampirolepis nana (small rat tapeworm)
Images:
Scolex
and ova:
http://www.k-state.edu/parasitology/625tutorials/Vampirolepis.html
Phylogeny:
Class Cestoda, Order Cyclophyllidea
Preferred
definitive host:
Rats and mice
Reservoir hosts:
Humans, particularly children.
Vector/intermediate
host:
OPTIONAL - Grain beetles, such as Tribolium or Tenebrio
Geographical location:
Cosmopolitan
Organs
affected:
Small intestine
Symptoms
and clinical signs:
Usually none
Treatment:
Niclosamide or paromomycin
Dipylidium caninum (dog tapeworm)
Images:
Egg
packets:
http://www.k-state.edu/parasitology/625tutorials/Tapeworm06.html
Scolex and mature proglottid:
http://www.k-state.edu/parasitology/625tutorials/Tapeworm01.html
Composite:
Phylogeny:
Class Cestoda Order Cyclophyllidea
Preferred
definitive host:
Domestic dogs and cats
Reservoir
hosts:
Humans, particularly children
Vector/intermediate
host:
Fleas
Geographical
location:
Cosmopolitan
Organs
affected:
Small intestine
Symptoms
and clinical signs:
Usually none, although abdominal pain, headache, diarrhea, and verminous
intoxication may occur, particularly in patients with heavy infection.
Treatment:
Niclosamide, quinacrine, or praziquantel.
Images:
Entire
worm, scolex, protoscoleces:
http://www.k-state.edu/parasitology/625tutorials/Tapeworm03.html
Life
cycle:
|
Gross anatomy and histology of a hydatid cyst. |
|
|
Gross anatomy |
Histology |
|
|
|
Phylogeny:
Class Cestoda, Order Cyclophyllidea
Preferred
definitive host:
Carnivores, particularly dogs
Reservoir hosts:
Other mammals
Vector/intermediate
host:
Herbivores, particularly moose, reindeer, goats, camels and sheep. Humans are
'accidental' hosts.
Geographical
location:
Cosmopolitan
Organs
affected:
Cysts may develop in bone marrow, nervous system, liver, and lungs.
Symptoms
and clinical signs:
Specific symptoms depend on the site of cyst formation. In general, the
presence of the cyst will induce pressure in organs and cause necrosis. Hydatid
fluid can induce anaphylactic shock and death.
Treatment:
Surgical removal of the cyst is required.
PARASITIC
NEMATODA
http://www.cbu.edu/~seisen/Nematoda_files/frame.htm
Trichuris trichiura (whipworm)
Images:
Ova of Trichuris
vulpis:
http://www.k-state.edu/parasitology/625tutorials/Nematodes02.html
Phylogeny
Order Trichurata.
Preferred
Definitive host:
Humans
Reservoir
hosts:
Reported in monkeys and dogs.
Vector/intermediate
host:
None
Geographical
location:
Cosmopolitan, but most frequent in tropical countries
Organs
affected:
Human cecum, appendix, ileum.
Symptoms
and clinical signs:
In heavy infections, patients show small blood-streaked diarrheal stools,
abdominal pain and tenderness, nausea and vomiting, anemia and weight loss.
Prolapse of the rectum has occurred in some cases.
Treatment:
Mebendazole.
Images:
Adult
female:
http://www.k-state.edu/parasitology/625tutorials/Trichinella01.html
Larvae in muscle tissue:
http://www.k-state.edu/parasitology/625tutorials/Trichinella02.html
World distribution maps of species in genus:
http://www.k-state.edu/parasitology/625tutorials/Trichinella03.html
Life
cycle:
Phylogeny:
Order Trichurata
Preferred
definitive host:
Humans
Reservoir
hosts:
Carnivorous mammals, including rodents and pigs.
Vector/intermediate
host:
None
Geographical
location:
Cosmopolitan, but most frequently found in circumboreal countries.
Organs
affected:
1. Initial phase - Mucosa of small intestine
2. Penetration phase - larvae lodging in striated muscle, myocardium, brain and
meninges.
Symptoms
and clinical signs:
1. Initial phase - Nausea, vomiting, diarrhea, headache
2. Penetration phase - Edema, conjunctivitis, fever, chills, dyspnea, muscle
paint. Other symptoms include EKG disorders, headache, mental apathy, delirium,
coma.
Treatment:
Symptoms are relieved with analgesics and corticosteroids. Thiabendazole is
effective among experimental animals.
Images:
L1
larva:
http://www.k-state.edu/parasitology/625tutorials/Miscellaneous02.html
Phylogeny:
Order Rhabditata
Preferred
definitive host:
Humans
Reservoir
hosts:
Other primates, dogs, cats, other mammals
Vector/intermediate
host:
None
Geographical
location:
Cosmopolitan
Organs
affected:
Adult worms are generally found in the small intestine. Occasionally, they will
also be found the respiratory, biliary, or pancreatic system.
Symptoms
and clinical signs:
I. Invasion phase - Penetration of the skin by larvae will cause slight
hemorrhage and swelling. The site of entry will show intense itching.
II.
Pulmonary phase - Damage to lung tissue causes massive-host cell reactions. Symptoms
include a burning sensation in the chest, nonproductive cough, bronchial
pneumonia.
III. Intestinal phase - Among immunocompetent
individuals, the infection is generally asymptomatic. Among immunosuppressed
individuals, the problems arising from hyperinfection can become
life-threatening. There is persistent diarrhea, and migrating worms are known
to transport coliform bacteria throughout the body, and thereby may cause a
gram-negative encephalitis by entry into the nervous system.
Treatment:
Thiabendazole, Cambendazole
Hookworms
.
Images:
Ancylostoma
caninum adults:
http://www.k-state.edu/parasitology/625tutorials/Ancylostoma.html
Necator americanus buccal armature and ova:
http://www.k-state.edu/parasitology/625tutorials/Nematodes09.html
Phylogeny:
Phylum Nematoda, Order Strongylata
Preferred
definitive host:
Humans
Reservoir
hosts:
None
Vector/intermediate
host:
None
Geographical
location:
Cosmopolitan
Organs
affected:
Larvae affect the skin and lungs, while the adults affect the small intestine.
Symptoms
and clinical signs:
1. Cutaneous phase: Itching of skin
2. Pulmonary phase: Bronchitis, pneumonitis
3. Intestinal phase: None in light infection. In heavy infections, anemia
leading to dyspnea on exertion, weakness and dizziness occur. Heart shows
atrophy, and children may show physical, mental, or sexual retardation.
Treatment:
Mebendazole, pyrantel pamoate and supplemental iron to offset anemia.
Images:
Ancylostoma
caninum adults:
http://www.k-state.edu/parasitology/625tutorials/Ancylostoma.html
Necator americanus buccal armature and ova:
http://www.k-state.edu/parasitology/625tutorials/Nematodes09.html
Phylogeny:
Phylum Nematoda, Order Strongylata
Preferred
definitive host:
Humans
Reservoir
hosts:
None
Vector/intermediate
host:
None
Geographical
location:
Cosmopolitan
Organs
Affected:
Larvae affect the skin and lungs, while the adults affect the small intestine
Symptoms
and clinical signs:
1. Cutaneous phase: Itching of skin
2. Pulmonary phase: Bronchitis, pneumonitis.
3. Intestinal phase: None in light infection. In heavy infections, anemia
leading to dyspnea on exertion, weakness and dizziness occur. Heart shows
atrophy, and children may show physical, mental or sexual retardation.
Treatment:
Mebendazole, pyrantel pamoate and supplemental iron to offset anemia.
Comparison
of Human Hookworms
|
|
ANCYLOSTOMA DUODENALE |
NECATOR AMERICANUS |
|
MOUTH PARTS |
TWO VENTRAL PLATES WITH TEETH |
VENTRAL & DORSAL CUTTING PLATES |
|
8-11 |
7-9 |
|
|
LENGTH OF FEMALE (mm) |
10-13 |
9-11 |
|
AVERAGE FEEDING RATE (ML BLOOD/DAY) |
.15 |
.03 |
|
DAILY EGG PRODUCTION |
25,000 to 30,000 |
9,000 |
Correlation between Necator worm
burden and patient status
|
WORM BURDEN |
LEVEL OF PATHOLOGY |
|
< 25 |
SYMPTOMLESS |
|
25 TO 100 |
LIGHT SYMPTOMS |
|
100 TO 500 |
MODERATE |
|
500 TO 1000 |
SEVERE WITH GRAVE DAMAGE |
|
> 1000 |
POSSIBLY FATAL |
ANCYLOSTOMA,
TAKING MORE BLOOD PER DAY, WILL REQUIRE FEWER
CHRONIC INFECTIONS
LEAD TO MENTAL DULLNESS, PHYSICAL RETARDATION, HEART FAILURE, DEATH.
Subject: From netscape.com news -- Hookworm treatment
Date: Sat, 11 Jun 2005 23:22:46 -0500
Offbeat News
Saturday, June 11, 2005
Bill Gates foundation funds hookworm vaccine effort
WASHINGTON (Reuters) - Efforts to develop a vaccine against
hookworm, a parasite that causes severe anemia in millions
of people in the developing world, got a boost on Wednesday
with a $21 million grant from the Bill & Melinda Gates
Foundation.
Researchers testing the vaccine, which would be the first to
work against a parasitic worm, said they can continue their
work thanks to the cash.
"Hookworm is an example of a disease for which a relatively
modest investment in research and development could, and we
expect will, affect tens of millions of lives," said Gates
Foundation official David Brandling-Bennett.
The contribution from the Microsoft founder will human
trials being done by the Human Hookworm Vaccine Initiative,
a collaboration between
Sabin Vaccine Institute.
Hookworm infects more than 740 million people, or about one
in eight people globally, according to the World Health
Organization. It is a leading cause of anemia in the
developing world and can cause mothers to die in childbirth.
The little nematode worms live in the dirt and their larvae
can burrow into human skin, said Dr. Peter Hotez, chairman
of George Washington's Department of Microbiology and
Tropical Medicine. Inside the body, they migrate to the
intestines, where they attach and suck blood.
The vaccine works by stimulating antibodies, proteins made
by the immune system, which attach to the larva and prevent
them from getting into the intestine.
Ancylostoma caninum (dermal larva migrans)
Images:
Ancylostoma
caninum adults:
http://www.k-state.edu/parasitology/625tutorials/Ancylostoma.html
Necator americanus buccal armature and ova:
http://www.k-state.edu/parasitology/625tutorials/Nematodes09.html
Phylogeny:
Phylum Nematoda, Order Strongylata
Preferred
definitive host:
Domestic dogs and cats
Reservoir
hosts:
None. Humans are 'accidental' hosts
Vector/intermediate
hosts:
None
Geographical
location:
Northern Hemisphere
Organs
affected:
Skin
Symptoms
and clinical signs:
Creeping eruption, characterized by inflammation and itching along migration
pathways of larvae
Treatment:
Thiabendazole ointment.
Ascaris lumbricoides (large roundworm)
Images:
Ova:
http://www.k-state.edu/parasitology/625tutorials/Ascaris01.html
Parasites,
like politics, make strange bedfellows:
http://www.cbu.edu/~seisen/worm.jpg
Adults:
Life cycle:
|
“Boys
who bring in a bucket with the largest number of expelled worms get a new
soccer ball, and girls get a new pair of shoes.” Ew. |
|
Phylogeny:
Phylum Nematoda, Order Ascaridata
Preferred
definitive host:
Humans
Reservoir
hosts:
None, but Ascaris suum in swine is very similar
Vector/intermediate host:
None
Geographical
location:
Cosmopolitan
Organs affected:
Adults reside in the lumen of the small intestine
Symptoms
and clinical signs:
1. Initial phase: Vague symptoms arising from inflammatory responses
2. Pulmonary phase: Edema, pneumonitis
3. Intestinal phase: Abdominal pain, asthma, insomnia. Use of ineffective drugs
will stimulate migration, leading to serious and sometimes fatal results. Worms
have been known to escape through the nares, and to penetrate the intestinal
wall and emerge from the body wall.
Treatment:
Piperazine citrate, mebendazole, pyrantel pamoate.
Toxocara cati and T. caninum (visceral
larva migrans)
Images:
Toxocara
cati ova:
http://www.k-state.edu/parasitology/625tutorials/Nematodes03.html
Phylogeny:
Phylum Nematoda, Order Ascaridata
Preferred
definitive host:
Cats and Dogs
Reservoir
hosts:
None. Humans are 'accidental' hosts
Vector/intermediate
host:
None
Geographical
location:
Cosmopolitan
Organs
affected:
Liver, lungs, eye, brain, cardiac muscle, kidney
Symptoms
and clinical signs:
Visceral larva migrans results in inflammation and eosinophilic granulomas in
organs. Pneumonitis, hepatomegaly, spleen enlargement, anemia, iritis and
hemorrhage of the eye are common symptoms.
Treatment:
Thiabendazole
Enterobius vermicularis (pinworm)
Images:
Ova:
http://www.k-state.edu/parasitology/625tutorials/Nematodes08.html
Phylogeny:
Phylum Nematoda, Order Oxyurata
Preferred
definitive host:
Humans
Reservoir
hosts:
None
Vector/intermediate
host:
None
Geographical
location:
Temperate zone, especially in Europe and
Organs
affected:
Ileocecal region of the intestine
Symptoms
and clinical signs:
Generally asymptomatic, but heavy infections will result in disturbed sleep.
This, in turn, will debilitate the patient. Itching and pruritis are observed.
Minute ulcerations of the intestinal mucosa and fatal subserosal penetration has
been reported.
Treatment:
Piperazine citrate, pyrvinium pamoate, mebendazole.
This might be a little intense to
watch…
http://blog.sciam.com/index.php?p=166&more=1&c=1&tb=1&pb=1#more166
"Do not look at this....
unless you are fascinated by all things parasitological..."
A video clip that accompanies an article in New England Journal of Medicine
http://content.nejm.org/cgi/content/full/354/13/e12
"A colonoscopy was ordered and revealed multiple mobile 1-cm worms, Enterobius
vermicularis, in the cecum "
From: The Scientist 22(3):22
Ana Vicente and her team at the Oswaldo Cruz Institute in
In 1994, Araujo stopped in at San Pedro's
Enterobius vermicularis,
or pinworm, is an itchy but harmless intestinal parasite that has been with
humans since before they were human. Pinworm eggs have been recovered from a
communal latrine near the ancient Dead Sea settlement of Qumran, from
fossilized feces in
"During the movement from North to
Of course, a couple thousand years of heat, humidity, and
bacterial activity wreaks havoc on long chains of nucleic acids. Add to that
the fact that most coprolites - fossilized feces - were collected by
archaeologists who hadn't guarded them from genetic contamination, leaving them
languishing on museum shelves for 10 years or more. PCR becomes a nightmare.
Geneticist Alena Ińiguez from Vicente's group was able to
piece together an SL1 RNA gene using a molecular magic trick developed in the
1990s and known as reconstructive polymerization. Essentially, the team let
these small fragments polymerize on their own before they ran their PCR.
Overlapping fragments tend to anneal themselves to each other and are then
extended by the action of DNA polymerase. What goes in is jumble and what comes
out is sequence.
Dispelling any misconceptions about the work, Araujo says
that working with ancient feces isn't much different from handling its modern
day counterpart. "Coprolites look like dried feces," he says. Back in
Their work paid off recently, a paper in the International Journal
of Parasitology (36:1419-25, 2006), confirms the presence of a pinworm
infection in 27 pre-Columbian coprolite samples from the San Pedro site along
with two others from
Ińiguez says the search has only just begun, and they're
widening their scope to look at other sites in
Though the group spends a good deal of time down in the
dumps, the results lift their spirits. When Ińiguez first sequenced pinworm RNA
from a reconstituted coprolite in 2003, "It was a big party," says
Vicente. In short order the scientists gathered ice, limes, sugar, and Cachaça
to mix
Wuchereria bancrofti (elephantiasis)
An
e-article on filariasis:
http://www.emedicine.com/MED/topic794.htm
Images:
Microfilariae in blood:
http://www.k-state.edu/parasitology/625tutorials/Nematodes07.html
Maybe you
shouldn't go here:
http://www.cbu.edu/~seisen/mammaryeleph.jpg
Maybe you
shouldn't go here either:
http://www.cbu.edu/~seisen/eleph-fijiEN.gif
http://elephantiasis.freeyellow.com/elephantiasis_clip.mpg
It’s a
form of immortality…sort of….
http://www.collegehumor.com/pictures/100384/
Biology
as art, or maybe it's art as biology:
http://www.cbu.edu/~seisen/doorknocker.jpg
Two very
disturbing images of elephantiasis, one authentic and the other clearly Photoshopped:
Not just
any old scrotal and penile elephantiasis, but massive scrotal and penile
elephantiasis, from:
http://tmcr.usuhs.mil/tmcr/chapter26/clinical1.htm
(The text states: “In this African
patient, the urethral orifice is at the level of the knees.”
Although
this image is clearly Photoshopped, it is still disturbing…
Life
cycle:
Phylogeny:
Phylum Nematoda, Order Filariata
Preferred
definitive host:
Humans
Reservoir
hosts:
None
Vector/intermediate
host:
Mosquitos, including the genera Anopheles, Aedes, Culex, and Mansonia
Geographical
location:
Central Africa,
Organs
affected:
Microfilariae are in the blood, and adults reside in major lymphatic ducts.
Symptoms
and Clinical signs:
Microfilariae are virtually symptomless. Inflammation caused by the presence of
adults leads to chills, fever, and toxemia. Lymph vessels become swollen,
leading to swelling of organs and the accumulation of lymph in urine.
Treatment:
Microfilariae and adults are killed by diethylcarbamazine. Mechanical damage is
treated with pressure bandages or surgical removal of elephantoid tissue.
Onchocercus volvulus (river blindness)
Images:
Phylogeny:
Phylum Nematoda, Order Filariata
Preferred
definitive host:
Humans
Reservoir
hosts:
None
Vector/intermediate
host:
Simulium blackflies
Geographical
location:
Africa, South and
Organs
affected:
Microfilariae are in skin, while adults reside in subcutaneous tissue.
Symptoms
and Clinical signs:
Adults cause relatively minor problems. their presence lead to formation of
subcutaneous nodules, but they are relatively benign and elicit no pain.
Microfilariae cause dermatitis, skin lesions, depletion of vitamin A, and
blindness due to corneal invasion.
Treatment:
Surgical removal of nodules, and administration of diethylcarbamazine and/or
suramin.
Dirofilaria immitis (heartworm)
Images:
Adults
extracted from dog heart:
http://www.k-state.edu/parasitology/625tutorials/Nematodes06.html
Dog heart
with heartworms:
Larvae:
Phylogeny:
Phylum Nematoda, Order Filariata
Preferred
definitive host:
Dogs
Reservoir
hosts:
None. Humans are rare 'accidental' hosts. Cats are rarely infected.
Vector/immediate
host:
Anopheline mosquitos
Geographical
location:
Cosmopolitan
Organs
affected:
Right heart and pulmonary artery
Symptoms
and Clinical signs:
Microfilariae are virtually symptomless. However, the presence of a large
number of adults will cause right heart failure and pulmonary complications in
dogs. In humans, the symptoms are vague and unpredictable. It takes
significantly less worms to elicit such symptoms in cats.
Treatment:
Adults are destroyed by thiacetarsamide sodium solution, and microfilariae are
destroyed by the oral administration of dithiazamine iodide. Heartworm disease
is prevented with diethylcarbamazine.
Dracunculus medinensis (Guinea worm)
Images:
Unruptured
blister, ruptured blister, adult female protruding from lesion
Phylogeny:
Phylum Nematoda, Order Camallanata
Preferred
definitive host:
Humans
Reservoir
hosts:
Other mammals
Vector/intermediate
host:
Copepods, genus Cyclops
Geographical
location:
Africa, Southwestern Asia, Northeastern South America,
Organs
affected:
Adults reside in subcutaneous tissues, especially in the legs, arms, shoulder
and trunk.
Symptoms
and Clinical signs:
Blister formation is accompanied by urticaria, erythema, dyspnea, vomiting,
pruritus, all of which are of allergic nature. Severe inflammation may occur if
worm is snapped.
Treatment:
Metronidazole, niridazole, thiabendazole.
FEATURE:
This article first appeared in the July 2005 issue of Baptists Today,
a national news journal based in
Closing in on the Guinea worm
By John Pierce
Executive Editor
Baptists Today
The debilitating Guinea worm disease has been around since biblical times
according to Dr. Donald Hopkins, who directs the health programs of The Carter
Center, founded in 1982 by President Jimmy and Rosalynn Carter. But the end of
the dreaded disease is in sight.
In the 1940s, tens of millions
of people mostly in Africa and
The larvae grow undetected
inside a persons abdomen for about a year, Dr. Hopkins explained in an interview
with Baptists Today. There is no treatment to cure the infection, he
said. The worm just has to come out.
SPECTACULAR DISEASE
The two- to three-foot-long
worm or in some cases multiple worms in the same person emerges slowly through
a large painful blister. The disease cycle is continued when a person with a
worm enters a water source and the worm releases new larvae.
This disease is so spectacular
when you see it, you cant get over it, said Dr. Hopkins, who served the Center
for Disease Control and Prevention, taught at Harvard School of Public Health
and directed the Smallpox eradication program in
More spectacular, however, will
be the complete eradication of the dreaded disease for which there is no
vaccine. It will be the first parasitic disease in human history to be
eradicated.
When The Carter Center turned
its attention to the disease in 1986 there were 3.5 million cases of Guinea
worm disease in 20 countries worldwide. Last year the number was down to
16,222 cases in limited parts of
Like the old saying about
horseshoes and hand grenades, however, close is not good enough for those
vigilantly working to make Guinea worm disease a thing of the past.
This is an eradication program,
said Dr. Hopkins. Weve got to get the last one-half of 1 percent.
FACING CHALLENGES
Prevention of Guinea worm
disease is done in four ways, Dr. Hopkins explained. The first and most
expensive solution is to provide drinking water from underground wells rather
than contaminated water sources.
Approximately $100 million in
cash and in-kind gifts have supported the project, he said, including a recent
$25 million matching grant from the Bill and Melinda Gates Foundation.
The second is an educational
effort to keep infected persons out of drinking water and to teach the value of
filtering water. This practical approach to prevention of a disease once
attributed to witchcraft has had astounding results.
One important thing this
project has taught us, said Dr. Hopkins, is that it is possible to persuade
people in large numbers to change their behavior.
A third measure of prevention
is the use of nylon cloths manufactured and donated by DuPont as water filters.
The fourth preventive step is use of the chemical Abate provided by BASF that
kills the larvae-bearing water fleas without harming the water.
Political unrest has been a
major obstacle to reaching the last stage of disease eradication. However, Dr.
Hopkins said the final affected areas in Northern Ghana and, most
significantly, in
COMMUNITY HEALTH
Individuals (infected with
Guinea worm disease) are generally incapacitated for two to three months, said
Dr. Hopkins. In a given village, a third or half of a village could be infected
at the same time.
The diseases impact extends
beyond the physical health of the village causing significant economic
repercussions. Often the disease is more prevalent in poorer, agrarian areas
responsible for food production.
Dr. Hopkins pointed to a UNICEF
study in 1987 that showed the diseases impact on rice production in one part of
Sometimes non-health arguments
are your best motivations, he said of taking the eradication plan to various
international leaders. Its more expensive not to do something about this
(disease) than to do something about it.
However, the ripple effect of
Guinea worm disease goes beyond economics. Ill parents cannot take their
children to be immunized against other diseases and infected children are
slowed in their education. Traditionally, the long thin worm is slowly and
painfully removed over a period of weeks.
This disease affects poor
people without political clout, said Dr. Hopkins, whose interest in preventing
tropical diseases goes back to before his college years. It kept farmers from
farming and kids from walking to school.
The disease, he added, is
impossible to cure but easy to prevent with proper funds, access to the people
and behavioral changes.
THE LAST WORM
President Carter said
dedication, compassion and action have resulted in the soon-to-be-realized goal
of making Guinea worm a thing of the past. He sees the elimination of human
suffering as an important expression of faith.
To me, faith is not just a noun
but also a verb, said Carter. Too often we think about evangelism only as
preaching the Gospel, but there is also powerful ministry in the alleviation of
suffering, reaching out in harmony, respect and partnerships to others, and
sharing life.
Carter said he and his wife,
Rosalynn, active members of Maranatha Baptist Church in Plains, Ga., continue
to put our faith into action through the non-profit centers programs to advance
peace and health worldwide.
The Carter Centers Guinea worm
eradication effort took a major step forward in 2004 with a 50 percent
reduction in the disease. Overall, since 1986, the eradication program has
reduced the disease by 99.5 percent. The final stage is set.
However, nothing short of
complete eradication is the Centers goal. The Guinea worm must pass through a
human once a year for survival
As long as there is one case,
its possible for it to bounce back, said Dr. Hopkins.
PARASITIC
ANNELIDA (HIRUDINEA)
Characteristics:
|
System |
Type/remarks |
|
1. Circulatory |
Some oligochaetes have an open system. Most have a closed system. Earthworms have five pairs of contractile esophageal vessels = hearts. Hemoglobin present. |
|
2. Respiratory |
Most show diffusion through the body wall. Some polychaetes have parapodia or gills. |
|
3. Excretory |
Protonephridial or metanephridial type. Aquatic groups excrete ammonia. Earthworms secrete urea. |
|
4. Digestive |
Complete |
|
5. Skeletal |
Generally hydrostatic |
|
6. Nervous |
Cerebral ganglia, two closely fused ventral nerve cords, various other ganglia. |
|
7. Type of coelom |
True |
|
8. Muscular |
Circular, longitudinal, oblique |
|
9. Reproductive |
Polychaetes are diecious, oligochaetes and leeches are hermaphroditic. |
It
conjures up SUCH a lovely image:
From the
April 1854 issue of Scientific American:
"Dr.
Hooker, in his 'Himalayan Journals,' just published, gives the following sketch
of a pleasant excursion on the Nepaulese Himalaya: 'Leeches swarmed in
incredible profusion in the streams and damp grass, and among the bushes; they
got into my hair, hung on my eyelids, and crawled up my legs and down by my
back. I repeatedly took upwards of a hundred from my legs where they collected
in clusters on the instep; the sores which they produced were not healed for
five months, and I retain the scars to the present day.'"
:)
Dr. Eisen
Limnatis SPP. (AQUATIC LEECHES)
Phylogeny:
Phylum Annelida, Class Hirudinea
Preferred
definitive host:
Humans
Reservoir
hosts:
None
Vector/intermediate
host:
None
Geographical
location:
Organs
affected:
Primarily skin, but the worm is small enough that the respiratory and digestive
systems will be affected. Bathers frequently have infections in the vagina,
urethra or eyes.
Symptoms
and clinical signs: Pain, hemorrhage
Treatment:
Removal of worms
Haemadipsa SPP. (terrestrial
leech)
Phylogeny:
Phylum Annelida, Class Hirudinea
Preferred
definitive host:
Humans
Reservoir
hosts:
None
Vector/intermediate host:
None
Geographical
location:
Organs
affected:
Skin
Symptoms
and clinical signs: Painless, unnoticed wounds on skin take a considerable time
to clot due to anticoagulant used by leech to suck its blood meal.
Treatment:
Removal of worm by use of either a local anesthetic, a strong salt solution, or
a lighted match. Repellents such as dimethyl phthalate are used on clothing.
Hirudo
medicinalis (Medicinal leech)
Phylogeny:
Phylum Annelida, Class Hirudinea
Preferred
definitive host:
Human
Reservoir
hosts:
None
Vector/intermediate host:
None
Geographical location:
Cosmopolitan, but they are cultivated in numerous areas.
Organs
affected:
Skin
Symptoms
and clinical signs:
Painless, unnoticed wounds on skin take a considerable length of time to clot
due to anticoagulant used by leech to suck its blood meal.
NOTE: The
medicinal leech was extensively used in medieval medicine to remove excess
blood from "feverish" or "sanguine" people. More recently,
the medicinal leeches have been used as an integral part of microsurgery, where
severed limbs and structures are resutured back into place. Leech saliva
contains anticoagulants, and antibacterial proteins which are extremely useful
in promoting blood flow and vein formation.
Here's a
reply from Dr. Rudy Buntic, MD, a microsurgeon, regarding the use of leeches in
microsurgery:
From:
"Rudy Buntic" <rbuntic@microsurgeon.org>
To: "Dr. Stan Eisen" <seisen@cbu.edu>
Subject: Re: Do you use medicinal leeches in any of your microsurgery cases?
Date: Mon, 5 Nov 2001 19:49:26 -0800
Dear Dr.
Eisen :
Thank you
for your note. We do use leeches clinically, and fairly routinely. The most
common indication is in finger replantation, when venous circulation is suggish
or not present. Essentially, we examine the blood flow in a finger with two
things in mind: arterial and venous circulation. If a replanted finger is nice
and pink, then it has good arterial flow (inflow) and good venous flow (outflow).
If a finger is white and therefore without good arterial inflow, then we don't
usually find leeches helpful because there is no blood for the leeches to latch
onto. In this case they cannot aid in the circulation of the finger. If the
finger is bluish, dark and full of deoxygenated blood, then venous outflow is
poor or non-existent and the finger will die. When venous circulation is
compromised, a leech placed on the tip of the finger will cause a bleeding
point that will allow blood to exit the finger, and therefore new oxygenated
pink blood can nourish the finger. Often, within 7 to 10 days the finger will
neovascularize with small capillaries, and then leeching will not be necessary
because the capillaries will allow outflow of deoxygenated blood.
Another
indication is microvascular transplants with a skin component. In these
procedures, skin and subcutaneous tissue with muscle or bone is transplanted
from one part of the body to another for reconstructive purposes. This is
typically done with one artery and vein - similar to the situation in a
replant. If venous circulation is problematic, we may use leeches.
I hope
this is of some use to you. Let me know if you need any other information.
-Rudy
Buntic, MD
Division of Microsurgery
And
here's fantastic news, from the 9 July 2004 issue of Science
License
to Leech
"The
Food and Drug Administration (FDA) has approved the sale of leeches as a
medical device. The French company that received FDA's thumbs up, Ricarimpex
SAS, has been breeding leeches for 150 years. Although this is the first time
FDA has explicitly granted permission for a company to sell them, there are
plenty of homegrown leech vendors; several were grandfathered in under a 1976
law requiring the licensing of medical-device sellers.
Medical
leeches, Hirudo medicinalis, are already used in plastic surgery to
remove pooled blood from damaged areas, says Carl Krasniak of the
Slocum-Dickson Medical Group of New Hartford, New York. The animals use a
combination of chemicals in their saliva to prevent clotting and suck blood.
FDA deemed them "devices" because their sucking action is considered
more medically important than their anti-clotting saliva."
The following article appeared in the Commercial Appeal. The important paragraph states “Sterile
medicinal leeches were placed on the ear and scalp to suck away blood until
veins can heal and begin pumping naturally.”
ACANTHOCEPHALA
CHARACTERISTICS OF MAJOR ANIMAL PHYLA
PHYLUM ACANTHOCEPHALA
|
SYSTEM |
TYPE/REMARKS |
|
1. Circulatory |
None. Exchange by Diffusion |
|
2. Respiratory |
None. Exchange by Diffusion |
|
3. Excretory |
Protonephridia With Flame Cells That Unite To Form A Common Tube That Opens Into Sperm Duct Or Uterus |
|
4. Digestive |
None. Absorption Is Through Tegument |
|
5. Skeletal |
None. |
|
6. Nervous |
Central Ganglion Within The Proboscis Receptacle |
|
7. Type of Coelom |
Pseudocoelomate |
|
8. Muscular |
Body Wall With Circular And Longitudinal Muscles |
|
9. Reproductive |
Egg layers, Dioecious |
Macracanthorhynchus hirudinaceus
Images:
Ova:
http://www.k-state.edu/parasitology/625tutorials/Miscellaneous01.html
Phylogeny:
Phylum Acanthocephala
Preferred
definitive host:
Hogs, wild boas, peccaries.
Reservoir
hosts:
To a limited degree, cats and dogs serve as hosts. Humans are accidental hosts.
Vector/intermediate
host:
Larval beetles
Geographical
location:
Cosmopolitan. Human cases have been documented in
Organs
affected:
Intestine
Symptoms
and clinical signs:
Abdominal pain
Treatment:
None indicated
Moniliformis
moniliformis
Images:
Egg,
acanthella, cystacanth, adult
http://www.biosci.ohio-state.edu/~parasite/moniliformis.html
Phylogeny:
Phylum Acanthocephala
Preferred
definitive host:
Rats, mice, hamsters, dogs and cats
Reservoir
hosts:
Humans are incidental hosts
Vector/intermediate
host:
Beetles and cockroaches
Geographical
location:
Cosmopolitan. Human cases have been reported from
Organ
affected:
Small intestine
Symptoms
and clinical signs: Abdominal pain, diarrhea, and exhaustion.
Treatment:
None indicated.
Polymorphus
paradoxus
Images:
Egg,
acanthella, cystacanth, adult
http://www.nhc.ed.ac.uk/index.php?page=24.25.333.372
Phylogeny:
Phylum Acanthocephala
Preferred
definitive host:
ducks
Reservoir
hosts:
None
Vector/intermediate
host:
Gammarus spp. amphipods
Geographical
location:
Cosmopolitan
Organ
affected:
Small intestine
Symptoms
and clinical signs:
Generally none detectable: It may be fatal among ducklings.
Treatment:
None indicated
NOTE: A
considerable amount of research has been conducted on the behavioral
alternations on the intermediate hosts. Infected intermediate hosts are
considerably more likely to be found by their predator, which is also the
definitive host of the parasite.
Comparative
vulnerability of uninfected Gammarus lacustris and ones infected with Polymorphus
paradoxus. (Adapted from Table 1 of Bethel and Holmes [1977], Increased
vulnerability of amphipods to predation owing to altered behavior induced by
larval acanthocephalans. Canadian Journal of Zoology 55(1):110-115.
|
|
|
|
Gammarids eaten/No. available |
|
|
|
Test No. |
Duration (min) |
No. predators |
Uninfected |
Infected with Polymorphus paradoxus |
P* |
|
1 |
7 |
2 |
6/25 |
16/25 |
<0.01 |
|
2 |
5 |
2 |
13/50 |
35/50 |
<0.001 |
|
3 |
5 |
2 |
12/50 |
42/50 |
<0.001 |
|
4 |
5 |
1 |
8/50 |
18/50 |
<0.05 |
|
5 |
10 |
1 |
0/75 |
48/75 |
<0.001 |
|
6 |
15 |
1 |
24/75 |
63/75 |
<0.001 |
|
TOTAL |
|
|
63/325 |
222/325 |
<0.001 |
*P = probability,
by chi-square contingency tests
MOLLUSCA
CHARACTERISTICS
|
SYSTEM |
TYPE/REMARKS |
|
1. Circulatory |
Cephalopods Have A Closed System With A Chambered Heart. Hemocyanin and Hemoglobin Are Blood Pigments. Others have An Open System. |
|
2. Respiratory |
Aquatic Forms have Gills, Terrestrial Forms Have A Mantle Modified To Form A Lung |
|
3. Excretory |
Metanephridial Form. Principal Nitrogenous Waste Among Aquatic Forms Is Ammonia And Uric Acid Among Terrestrial Forms |
|
4. Digestive |
Complete |
|
5. Skeletal |
Shell May Be External, Internal Or Absent |
|
6. Nervous |
Ganglia Are Consolidated Around Esophagus -- Cerebral Ganglia |
|
7. Type of Coelom |
True, Reduced In Size |
|
8. Muscular |
Many Have Muscular Foot Or 'Pad' For Locomotion |
|
9. Reproductive |
Egg layers -- Most Are Dioecious |
N.B. The larvae of unionid clams
(called glochidia) are parasitic on the gills and skin of freshwater fish.
Female clams attract fish and then "spray" larvae out of excurrent siphon.
Valves clamp down on tissue, and a cyst of host-derived tissue forms around the
larva. After the larvae reaches a certain size, it emerges from cyst and falls
to bottom.
PARASITIC
ARTHROPODS
CHARACTERISTICS
|
SYSTEM |
TYPE/REMARKS |
|
1. CIRCULATORY |
OPEN HEMOLYMPH FOUND IN MOST GROUPS HEMOGLOBIN FOUND IN LARVAE ADAPTED TO OXYGEN-POOR WATER |
|
2. RESPIRATORY |
SPIRACLES CHARACTERISTIC OF TERRESTRIAL FORMS, GILLS CHARACTERISTIC OF AQUATIC FORMS |
|
3. EXCRETORY |
MALPIGHIAN TUBULES AMONG TERRESTRIAL FORMS |
|
4. DIGESTIVE |
COMPLETE |
|
5. SKELETAL |
EXOSKELETON COMPOSED OF CHITIN |
|
6. NERVOUS |
ANTERIOR GANGLIA |
|
7. TYPE OF COELOM |
REDUCED IN SIZE, CALLED HEMOCOEL |
|
8. MUSCULAR |
STRIATED MUSCLE, JOINTED APPENDAGES |
|
9. REPRODUCTIVE |
MOST ARE DIOECIOUS. ISOLATED, SPECIFIC GROUPS SHOW PARTHENOGENESIS, POLYEMBRYONY |
MAJOR GROUPS
CLASS MEROSTOMATA: HORSESHOE CRABS
CLASS ARACHNIDA: SPIDERS, TICKS, MITES, SCORPIONS
CLASS CRUSTACEA: LOBSTER, CRABS, CRAYFISH, SHRIMP
CLASS DIPLOPODA: MILLIPEDES
CLASS CHILOPODA: CENTIPEDES
CLASS INSECTA: INSECTS
PHYLUM ARTHROPODA
I. CLASS
INSECTA
A.
ANOPLURA: SUCKING LICE
B.
DIPTERA: FLIES, MOSQUITOS, MIDGES
C.
HOMOPTERA: CICADAS, APHIDS
D.
HEMIPTERA: TRUE BUGS
E.
LEPIDOPTERA: MOTH AND BUTTERFLIES
F.
COLEOPTERA: BEETLES
G.
ORTHOPTERA: GRASSHOPPERS, COCKROACHES
H.
HYMENOPTERA: ANTS, BEES, WASPS
I.
ODONATA: DRAGONFLIES, DAMSELFLIES
J.
ISOPTERA: TERMITES
II. CLASS
CRUSTACEA
A. SUBCLASS BRANCHIOPODA: FAIRY
SHRIMP, OR
B.
SUBCLASS OSTRACODA: SEED SHRIMP
C.
SUBCLASS COPEPODA:
D.
SUBCLASS BRANCHIURA: FISH LICE
E.
SUBCLASS CIRRIPEDIA: BARNACLES
F.
SUBCLASS MALACOSTRACA: WOOD LICE, PILL BUGS, SAND
HOPPERS, CRABS, LOBSTER, CRAYFISH
III.
CLASS ARACHNIDA
A.
ORDER SCORPIONIDAE: SCORPIONS
B.
ORDER ARANEAE: SPIDERS
C.
ORDER PHALANGIDA: DADDY-LONG-LEGS
D.
ORDER ACARINA: MITES AND TICKS
E. SUBCLASS
XIPHOSURA: HORSESHOE CRABS
IV. CLASS
MYRIAPODA INCLUDES
A.
SUBCLASS CHILOPODA: CENTIPEDES
B.
SUBCLASS DIPLOPODA: MILLIPEDE
IMPORTANCE
OF ARTHROPODS IN PARASITOLOGY
- Lernaea cyprinacea among
freshwater fish
- Argulus among
freshwater fish
- Unicola mites among
freshwater clams.
II. As parasitoids: (bloodsucking insects
which then fly off the host.
- Mosquitos
- Horseflies
- Assasin bugs.
III.
As Intermediate hosts.
- 1st. : Dipylidium caninum.
- 1st. : Diphyllobothrium latum
- 2nd. : Paragonimus westermani
IV.
As vectors for disease.
- Mechanical transmission -
Cockroaches carry bacteria, feces on legs, mechanically carried to food.
- Biological transmission
V.
As hyperparasites
Types
of Biological Transmission
Propagative
biological transmission, in which the disease-causing organism reproduces in
the arthropod, but undergoes no further developmental changes.
- Plague
bacillus in flea
- yellow fever virus
Cyclopropagative
biological transmission, in which the disease-producing organism undergoes
cylical changes and reproduces in the arthropod.
- Plasmodium in mosquitos
- Trypanosoma in tsetse
flies
Cyclodevelopmental
biological transmission, in which the disease-producing organism must undergo
development in the arthropod but does not multiply there.
- Microfilarie in mosquitos
Transovarian
transmission, in which disease-causing organisms are transmitted
from the infected parent arthropod to their offspring.
|
And you thought your family was strange
-- meet the wasp's
Bugs - Most larvae grow up feasting
on caterpillar blood, then things get really weird Wednesday, August
15, 2007 CARL ZIMMER The Oregonian
To
understand the rules that govern life, biologists often seek out the weird
extremes. When it comes to family life, it's hard to find a stranger example
than that of a common wasp, Copidosoma floridanum. "You
couldn't dream up a more surreal life cycle than these guys have," said
Mike Strand, a Copidosoma
floridanum, native throughout the Each
grapelike mass of cells develops into a wasp embryo. A single egg can give
rise to more than 3,000 genetically identical siblings, each about a fifth of
an inch long. "The caterpillar is about 2 to 3 inches long, so you can
stuff a lot of wasps in there," Most
of the larvae are maggotlike creatures that drink the caterpillar's blood.
But up to a quarter of the wasps take on an entirely different form. They
develop slender, snakelike bodies and rasping jaws. Instead of slurping
blood, these hundreds of soldiers attack other wasp larvae. "They just
latch on and suck away," The
bloodsuckers that are not killed by the soldiers eventually begin to devour
the organs of their host, become pupae, and then develop into adults that fly
away. The soldiers, on the other hand, cannot escape. Biologists
have known about Copidosoma floridanum's strange soldiers for more than a
century, but they're enjoying a new surge of interest as a model that
scientists can study to learn about the evolution of families. "The
big debate about these soldiers is what they're doing in their host,"
said Andrew Gardner, an evolutionary biologist at the Some
of the evidence scientists have gathered suggests that soldiers exist to wipe
out the competition. A cabbage looper often plays host to larvae from several
wasp mothers. It can even carry larvae from other species of wasps. Soldiers
kill off unrelated wasps, thus allowing their siblings to enjoy a bigger
meal. The
soldiers themselves cannot reproduce. Yet natural selection might favor genes
for these dead-end creatures. By killing off competitors, they increase the
odds that their genetically identical siblings will survive and have
offspring. When
a Copidosoma mother lays two eggs in a host, one egg produces thousands of
males, the other thousands of females. The female soldiers will kill off many
of their brothers. Gardner
and his colleagues recently built a mathematical model of Copidosoma
floridanum's soldiers and blood-feeders to understand how this kind of
fratricide might have evolved. While the soldiers are genetically identical
to the sisters, they share only some of their genes with the males, which
come from a separate egg. That
means the soldiers get a bigger evolutionary benefit from the success of
their sisters than from that of their brothers. A few males are more than
enough to fertilize thousands of female wasps. Any more males inside a host
are just competition for the sisters.
©2007 The
Oregonian |
Photo of Copidosoma floridanum:
FAMILY CULICIDAE (MOSQUITOS),
INCLUDING GENERA Anopheles, Culex, Mansonia, Aedes
Images:
Adult Culex emerging
from pupal case:
http://www.k-state.edu/parasitology/625tutorials/Arthropods09.html
Life cycle:
Phylogeny:
Order Diptera
Metamorphosis:
Complete. Larvae are aquatic.
Geographical
location:
Cosmopolitan
Organs
affected:
Skin
Symptoms
and clinical signs: Bite is followed by erythema, swelling and itching.
Diseases
transmitted:
Yellow fever, dengue, viral encephalitis, filariasis, malaria.
Treatment/control:
Residual spraying, drainage of marsh or swamp areas, covering of cisterns with
diesel oil or covers. Biological control of larvae is accomplished with
predaceous fish such as Gambusia (mosquitofish).
Malaysia's dengue deaths mount – from
cnn.com, August 3, 2007
KUALA LUMPUR, Malaysia (Reuters) -- Deaths from dengue fever in Malaysia have risen by a
third so far this year, and health authorities said on Friday that the worst is
yet to come.
The mosquito-borne virus has killed hundreds in
"There is a rising trend of dengue cases across the country," he
said in a statement.
He said the bulk of the cases were in the states of Selangor, Kelantan,
Johor and the capital, Kuala Lumpur.
The dengue virus has also spread rapidly in
The virus, which is transmitted by the Aedes aegypti mosquito, causes
severe fever, headaches, rashes and muscle and joint pain. Severe forms can
cause haemorrhagic fever. There is no vaccine.
Malaysia's health minister blamed the people for not getting their act together.
"These selfish people like to blame others whenever there are dengue
cases in their areas," Chua Soi Lek was quoted by the New Straits Times as
saying. "They blame the authorities for failing to collect rubbish on time
and for stagnant drains." 
Copyright 2007 Reuters. All
rights reserved.This material may
Mutation
Found in Resistant Mosquitoes
By RICK CALLAHAN, Associated Press Writer
May 12, 2003, 12:01 PM EDT
http://www.newsday.com/news/science/wire/sns-ap-exp-resistant-mosquitoes,0,6480575.story?coll=sns%2Dap%2Dscience%2Dheadlines
Scientists
have discovered the same genetic mutation in 11 types of
The
findings could give chemical companies a molecular target for new insecticides
to combat mosquitoes no longer kept in check by existing chemicals.
French
scientists who discovered the mutation in the ace-1 gene said it appears to
endow the mosquitoes with an immunity to two potent chemicals that cause a
fatal paralysis in other mosquitoes.
Researchers
from the
They also
found it in resistant populations of the Anopheles gambiae mosquito -- which
transmits the malaria parasite -- that were collected in the
The
scientists said the mutation in the ace-1 gene, which normally encodes a key
enzyme targeted by some insecticides, makes the mosquitoes resistant to those
chemicals.
The
findings appear in the May 8 issue of the journal Nature.
Molecular
biologist Mylene Weill led the
Normally,
insecticides containing either of two families of chemicals, organophosphates
and carbamates, paralyzes and kills
mosquitoes by blocking an enzyme that regulates nerve signals.
In the
case of A. gambiae, its insecticide resistance has allowed malaria's deadly
scourge to rebound in African nations where the parasite's courier was once
controlled by spraying.
Since
finding the mutation in 10 populations of insecticide-resistant C. pipiens, the
researchers have found it in additional strains of that species, and expect to
find it in others.
"We
have looked at something like 15 resistant populations of C. pipiens and every
time we've tested them we find the same mutation," Weill said.
While the
findings are intriguing, much work remains to determine the precise genetic
basis of mosquitoes' insecticide resistance, said Dyann Wirth, a microbiologist
who directs the Harvard Malaria Initiative.
She said
there may well be other genes that play a role in making the mosquitoes immune
to many insecticides. "I think it's a very good lead but there clearly
needs to be more work done," Wirth said.
Dr.
Joseph Vinetz of the
Weill
said she and her colleagues, whose discovery was aided by the recently mapped
genome of the A. gambiae mosquito, are now collecting other resistant
populations of the same species from
She
believes the same mutation may also be present in other insect pests, including
those that eat crops.
Although
malaria is primarily a problem in Africa and the developing world, a wild
reservoir of the parasite was found last year in
Weill
said she hopes concern about malaria and West Nile -- which killed 284 people
in the
"Malaria
is seen as an African problem, but with
National
Copyright
© 2003, The Associated Press
From
cnn.com:
High
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Find this article
at: |
Irradiation
as a control method for mosquitos:
Birth control to combat
malaria
By
Bethany Bell
BBC News, Vienna
Mosquito bites can be deadly.
Anopheles mosquitoes carry the parasite that causes malaria, a disease which kills around a million people every year.
Traditionally mosquito populations have been controlled by pesticides.
But scientists at the International Atomic Energy Agency (IAEA) are working on another method - using radiation to sterilize male mosquitoes.
“ The idea is to
produce large numbers of male mosquitoes that are sexually sterile ”
Mark Benedict International Atomic Energy Agency
The sterile insect technique (SIT) has worked well in reducing tsetse flies and some other insect pests, such as fruit flies.
The IAEA scientists are now trying to adapt the technique to the anopheles mosquito.
Birth control
Mark Benedict, a medical entomologist at the IAEA, says SIT is "birth control" for insects.
"The idea is to produce large numbers of male mosquitoes that are sexually sterile," he said.
"Those males will be released into the wild and find virgin female mosquitoes and they will mate with them."
A female usually only mates once in her life so if her partner has been sterilized none of the hundreds of eggs she lays will hatch.
Sterilization takes just a couple of minutes.
Mosquito pupae are gathered into a metal pot and are lowered into a machine, where they are exposed to radiation.
When they come out they are sexually sterile.
In the hot and humid laboratories at the IAEA, the team is trying to develop methods of raising male mosquitoes that are strong enough to survive the irradiation - and sexy enough to attract females out in the wild.
They are also working on ways to transport and release them in the wild.
Field project
Preparations for a pilot field project in Northern Sudan are underway to test the feasibility of SIT for mosquitoes.
The area is marked by extreme desert, but humans, livestock and wild mosquitoes live along the edge of the Nile River.
Despite a relatively small number of mosquitoes, there are high levels of malaria transmission there.
Mark Benedict says the sterilized pupae will be released along the river banks where the wild mosquitoes breed.
"That will give us a good idea of over what area we can release and what population densities we can see controlled" he says.
It is early days but Mark Benedict is optimistic about the prospects of SIT.
It is hoped that along with other tactics such as insecticide treated bed-nets, the technique can work as a tool in the fight against malaria.
The technique is "very well suited to elimination and eradication programmes."
"What we need to do now is get one or two projects off the ground, measure the potential and see where we can take it from there," he said.
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/8074259.stm
Published: 2009/06/15 09:56:00 GMT
© BBC MMIX
Print Sponsor
Simulium spp. (BLACKFLIES)
Phylogeny:
Order Diptera
Metamorphosis:
Complete
Geographical
location:
Cosmopolitan
Organs
affected:
Skin
Symptoms
and clinical signs:
Bites, which are painless at first, bleed profusely. Swelling, pruritis, and
pain develop later.
Diseases
transmitted:
Onchocerciasis
Treatment/control:
Residual insecticide
Phlebotomus spp. (SANDFLIES)
Phylogeny:
Order Diptera
Metamorphosis:
Complete
Geographical
location:
Tropical and Subtropical Countries of the
Organs
affected:
Skin
Symptoms
and clinical signs:
Rose-colored papules and stinging pain at site of bites.
Diseases
transmitted:
Leishmania donovani, Leishmania braziliensis, sandfly fever (viral), and
Bartonellosis (bacteria).
Treatment/control:
Residual insecticides.
Lutzomyia
spp. (NEW WORLD SANDFLIES)
Phylogeny:
Order Diptera
Metamorphosis:
Complete
Geographical
location:
Tropical and subtropical areas of the
Organs
affected:
Skin
Symptoms
and clinical signs:
Rose-colored papules and stinging pain at site of bites.
Diseases
transmitted:
Leishmania donovani, Leishmania braziliensis, sandfly fever (viral), and
Bartonellosis (bacterial).
Treatment/control:
Residual insecticides.
Glossina
spp. (TSETSE FLIES)
Images:
Adult
wing structure:
http://www.k-state.edu/parasitology/625tutorials/Wings02.html
Phylogeny:
Order Diptera
Metamorphosis:
Complete
Geographical
location:
Organs
affected:
Skin
Symptoms
and clinical signs:
Dermal irritation
Diseases
transmitted:
Nagana and African sleeping sickness.
Treatment/control:
Residual insecticides, destruction of brush used for breeding.
Chrysops
spp. (DEERFLY)
Images:
Adult
horsefly (Tabanus sp.)
http://www.biosci.ohio-state.edu/~parasite/tabanus.html
Phylogeny:
Order Diptera
Metamorphosis:
Complete
Geographical
location:
Cosmopolitan, but abundant in
Organs
affected:
Skin
Symptoms
and clinical signs:
Dermal irritation and hemorrhage of blood through wound.
Diseases
transmitted:
Loa loa
Treatment/control:
Soothing lotion to treat symptoms, residual insecticide, larvicides.
Order Hemiptera:
from
http://insects.about.com/od/truebugs/p/char_hemiptera.htm
Characteristics
of Order Hemiptera, the True Bugs
By Debbie Hadley,
About.com
Milkweed
bugs
Photo:
© Debbie Hadley, WILD Jersey
More Images (3)
When is a bug really
a bug? When it belongs to the order Hemiptera – the true bugs. Hemiptera comes
from the Greek words hemi, meaning half, and pteron, meaning
wing. The name refers to their fore wings, which are hardened near the base and
membranous near the ends, giving the appearance of a half wing. This diverse
group of insects includes cicadas, aphids, hoppers, and water bugs.
Description
Though members of this
order may look quite different from one another, Hemipterans share common
characteristics. They are best defined by their mouthparts, which are modified
for piercing and sucking. Many members of Hemiptera feed on plant fluids like
sap, and require the ability to penetrate plant tissues. Some Hemipterans, like
aphids, can do considerable damage to plants by feeding in this way.
While the fore wings
of Hemipterans are only half membranous, the hind wings are entirely so. When
at rest, the insect folds all four wings over each other, usually flat. Some
members of Hemiptera lack hind wings. Hemipterans have compound eyes, and may
have as many as three ocelli.
The order Hemiptera is
usually subdivided into four suborders:
1. Auchenorrhyncha – the
hoppers
2. Coleorrhyncha – a
single family of insects that live among mosses and liverworts
3. Heteroptera - the true
bugs
4. Sternorrhyncha –
aphids, scale, and mealy bugs
Habitat and Distribution
Because this order is
so diverse, the habitats are widely varied, Hemiptera includes terrestrial and
aquatic insects, and members of the order may be found on plants and animals.
They are abundant worldwide.
Major Infraorders or Superfamilies in the Order
·
Aphidoidea - aphids
·
Pentatomoidea – shield bugs
·
Gerromorpha – water striders, water crickets
·
Cicadoidea - cicadas
·
Tingoidae – lacebugs
·
Coccoidea – scale insects
Families and Genera of Interest
·
Marine skaters in the genus Halobates live their entire
lives on the surface of the ocean. They lay eggs on floating objects.
·
The family Pentatomidae, stink bugs, have
glands in the thorax that emit a
foul-smelling compound. This defense helps them repel potential predators.
·
Cicadas of the genus Magicicada are famous for their
odd life cycles. Cicada nymphs stay underground for 13 or 17 years, when they
emerge in large numbers and with a deafening song.
·
Females of the genus Belostoma, giant water bugs, lay
their eggs on the back of a male. The male cares for the eggs, bringing them to
the surface for proper aeration.
Hemipteran life cycle:
Images:
Phylogeny:
Order Hemiptera
Metamorphosis:
Incomplete
Geographical
location:
Organs
affected:
Skin
Symptoms
and clinical signs:
Bites are often symptomless
Diseases
transmitted:
Trypanosoma cruzi
Treatment/control:
Insecticides and replacement of thatched roofs with sheet metal.
Youtube.com clip: Assassin Bug of Malaysia: http://www.youtube.com/watch?v=WG56RZ3TDcY&feature=fvw
Phylogeny:
Order Hemiptera
Metamorphosis:
Incomplete
Geographical
location:
Organs
affected:
Skin
Symptoms
and clinical signs:
Bites are frequently symptomless. occasionally, victims will have pruritic skin
reactions
Diseases
transmitted:
Trypanosoma cruzi
Treatment/control:
Lindane, dieldrin. Spraying of juvenile hormone appears promising as a means of
control.
Cimex spp. INCLUDING C. lectularis
and C. hemipterus (bedbugs)
Youtube.com
clip:
Bed Bugs! Attack! *EMMY WINNING
DOCUMENTARY*: http://www.youtube.com/watch?v=4qx751dNw7Q
Adult:
http://www.k-state.edu/parasitology/625tutorials/Arthropods02.html
Phylogeny:
Order Hemiptera
Metamorphosis:
Incomplete
Geographical
location:
C. lectularis is cosmopolitan, whereas C. hemipterus is found in
Organs
affected:
Skin
Symptoms
and clinical signs:
Bites are frequently symptomless, but they may disturb sleep, reduce
hemoglobin, or induce inflammation.
Diseases
transmitted:
None
Treatment/control:
Residual insecticides. itching is relieved with calamine lotion.
Order Siphonaptera - Characteristics of Fleas
From: http://insects.about.com/od/fleas/p/char_siphonapte.htm
By Debbie Hadley,
About.com
A
female oriental rat flea, vector of plague.
Photo:
World Health Organization
Sponsored
Links
Ground Beetles Get Rid of Fleas Cat Fleas Condition Candy Insects Kill Fleas in House
Only a true insect
lover will appreciate the remarkable traits of fleas. Fleas entertained people
in the 19th century, when flea circuses were popular sideshow attractions.
Today, they're considered a pest to pet owners, and a persistent one at that.
Siphonaptera, which is Greek in origin, means tube (siphon) without
wings (aptera).
Description
All adult fleas suck
blood from host animals, usually mammals. These ectoparasites are well-equipped for
life on a furry food source. A hungry flea in search of a bloodmeal uses its
maxillary blades to puncture the skin of its host. A bit of flea spit keeps the
blood from clotting while the parasite assembles its siphon, using modified
mouthparts which form a tube.
Flea bodies are
flattened laterally, giving them a thin profile for moving between hairs. Tiny
bristles project backwards from the head so they don't get tangled when the
flea moves forward. These projections, called ctenidae, help the flea hang on
to Fido when he starts scratching. Fleas lack compound eyes, but may have two
small ocelli.
Siphonapterans undergo
complete
metamorphosis. The female flea lays up to two dozen eggs per day. Eggs fall
from the host animal, and hatch into larvae within a few days. Larvae have no
legs, and feed on whatever waste falls their way, usually excrement from adult
fleas. Within weeks, the larvae spin their silken cocoons, and pupate. Adult
fleas emerge in weeks or months, depending on species and temperature.
Though descended from
flying insects, fleas have evolved into wingless arthropods. Their only need
for locomotion is to land on a host, and for that they've developed superior
jumping abilities. Fleas can launch themselves quite high in the air, up to 80
times their own height. In addition to strong rear legs designed for jumping,
fleas have a substance called resilin above the hind legs. This rubbery
substance compresses as the flea prepares to jump, storing potential energy. When
the flea thrusts upward, this energy is converted to kinetic energy, the energy
of motion.
Habitat and Distribution
Fleas live wherever
you find mammals, throughout the world. Most of the nearly 2,400 described
species of fleas live in temperate zones.
Major Families in the Order
·
Pulicidae – common fleas
·
Ceratophyllidae – bird and rodent fleas
·
Ischnopsyllidae – bat fleas
·
Rhopalopsyllidae – marsupial fleas
Families and Genera of Interest
·
Cat fleas, Ctenocephalides felis, are the most common
fleas found on dogs (and cats, of course).
·
Rodent fleas are best known as vectors of the Black Death, aka
Bubonic Plague, which wiped out much of the world's population during the
Middle Ages.
·
Female sand fleas (Tunga penetrans) take up residence
under people's toenails.
Sources
·
Insects - Their Natural History and Diversity by Stephen A. Marshall
·
Siphonaptera.(Accessed April 30,
2008).
·
Gordon's
Flea Page (Accessed April 30, 2008).
Images:
Phylogeny:
Order Siphonoptera
Metamorphosis:
Complete
Geographical
location:
Europe and
Organs
affected:
Skin
Symptoms
and clinical signs:
Itching dermatitis
Diseases
transmitted:
None
Treatment/control:
Environmental control with insecticides
Ctenocephalides spp. including C. canis and C.
felis
Youtube
clips:
Diagnosing flea
infestation: http://www.youtube.com/watch?v=DMlRYhtsnx4&feature=related
Worst Case Of Fleas: http://www.youtube.com/watch?v=OIkPljV3jbU&feature=related
Adult:
http://www.k-state.edu/parasitology/625tutorials/Arthropods02.html
Line drawing of adult:
http://www.k-state.edu/parasitology/625tutorials/Arthropods07.html
Phylogeny:
Order Siphonoptera
Metamorphosis:
Complete
Geographical
location:
Cosmopolitan
Organs
affected:
Skin
Symptoms
and clinical signs:
Itching dermatitis
Diseases
transmitted:
Dipylidium caninum, Dirofilaria immitis, Dipetalonema reconditum
Treatment/control:
Residual insecticides and maintenance of a clean environment.
Youtube
clip:
NewSpring Foot-washing/Jigger Removal: http://www.youtube.com/watch?v=ajdVs3s2k3U
Images:
Adult,
infected foot
http://www.biosci.ohio-state.edu/~parasite/tunga.html
Phylogeny:
Order Siphonoptera
Metamorphosis:
Complete
Geographical
location:
Tropical
Organs
affected:
Skin
Symptoms
and clinical signs:
Fertilized female burrows into the skin of mammals or humans. Lesions can
become a festering, painful sore. Secondary bacterial infections are common.
Diseases
transmitted:
None
Treatment/control:
Tropical DDT treatment. Burrowing females are surgically removed.
Xenopsylla cheopis (RAT FLEA)
Youtube.com
clip:
The Black Death and its social consequences.
[English]: http://www.youtube.com/watch?v=9NX8TvfoJDk&feature=related
Image:
Adults:
http://www.k-state.edu/parasitology/625tutorials/Arthropods03.html
An
anthology of essays on the effect of Bubonic Plague on Medieval
http://jefferson.village.virginia.edu/osheim/intro.html
Phylogeny:
Order Siphonoptera
Metamorphosis:
Complete
Geographical
location:
Cosmopolitan on Rattus spp. rats except in cold climates.
Organs
affected:
Skin
Symptoms
and clinical signs: Dermal irritation.
Diseases
transmitted:
Bubonic plague. Symptoms of plague include swollen lymph nodes, hemorrhage,
mental dullness. Within a relatively short time, patient shows anxiety,
delirium, coma and death.
Treatment/control:
Anti-rat campaigns must be preceded by a spraying program to eradicate fleas.
Antibiotics are effective against plague.
Pediculus humanus (body and head lice)
Images:
Adults:
http://www.k-state.edu/parasitology/625tutorials/Arthropods05.html
From: http://www.historyhouse.com/in_history/lousy/
During
the Russian revolution, there was an outbreak of typhus (transmitted by lice)
so severe that Lenin remarked, "Either socialism will defeat the louse,
or the louse will defeat socialism."
To get
an idea of how powerful a force disease is, and to remind the historian that it
should not be overlooked, allow us to quote Hans Zinssner's account of a famous
plague of ancient times -- the Plague of Justinian. It started in the year 540,
perhaps prompted by a series of earthquakes and floods which created refugee
conditions across much of Eastern Christendom.
From
Hans Zinsser’s Rats, Lice and History (copyright 1941)
|
|
Four months the plague remained in
Also From Hans Zinsser’s Rats, Lice and History
(copyright 1941)
...among the Aztecs before the advent of Cortez, is the
tale cited from Torquemada. 'During the abode of Montezuma among the Spaniards,
in the palace of his father, Alonzo de Ojeda one day espied... a number of
small bags, tied up. He imagined at first that they were filled with gold dust,
but on opening one of them what was his astonishment to find it quite full
of Lice!' Cortez... then asked... for an explanation. He was told that the
Mexicans had such a sense of duty to pay tribute to their ruler that the
poorest, if they possessed nothing else to offer, daily cleaned their bodies
and saved the lice. And when they had enough to fill a bag, they laid it at
the feet of their king.
MacArthur's story of Thomas a Becket's funeral illustrates
[this]: -- The archbishop was murdered in Canterbury Cathedral on the evening
of the twenty-ninth of December. The body lay in the Cathedral all night,
and was prepared for burial on the following day... He had on a large brown
mantle; under it, a white surplice; below that, a lamb's-wool coat; then
another woolen coat; and a third woolen coat below this; under this, there was
the black, cowled robe of the Benedictine Order; under this, a shirt; and next
to the body a curious hair-cloth, covered with linen. As the body grew cold,
the vermin that were living in this multiple covering started to crawl out,
and, as MacArthur quotes the chronicler: 'The vermin boiled over like water in
a simmering cauldron, and the onlookers burst into alternate weeping and
laughter.'
Robert Burns’ Ode to a Louse, appearing at http://forums.eslcafe.com/student/viewtopic.php?p=738
Robert Burns (1759-1796)
TO A LOUSE, ON SEEING ONE ON A LADY’S BONNET AT CHURCH
Ha! whare ye gaun, ye crowlan ferlie!
Your impudence protects you sairly;
I canna say but ye strunt rarely,
Owre gauze and lace;
Tho', faith! I fear ye dine but sparely
On sic a place.
Ye ugly, creepan, blastit wonner,
Detested, shunn'd by saunt an' sinner,
How daur ye set your fit upon her,
Sae fine a Lady!
Gae somewhere else and seek your dinner
On some poor body.
Swith! in some beggar's haffet squattle;
There ye may creep, and sprawl, and sprattle,
Wi' ither kindred, jumping cattle,
In shoals and nations;
Whare horn nor bane ne'er daur unsettle
Your thick plantations.
Now haud you there, ye're out o' sight,
Below the fatt'rels, snug and tight,
Na, faith ye yet! ye'll no be right,
Till ye've got on it,
The verra tapmost, towrin height
O' Miss's bonnet.
My sooth! right bauld ye set your nose out,
As plump an' grey as onie grozet:
O for some rank, mercurial rozet,
Or fell, red smeddum,
I'd gie you sic a hearty dose o't,
Wad dress your droddum!
I wad na been surpriz'd to spy
You on an auld wife's flainen toy;
Or aiblins some bit duddie boy,
On's wylecoat;
But Miss's fine Lunardi, fye!
How daur ye do't?
O Jenny, dinna toss your head,
An' set your beauties a' abread!
Ye little ken what cursed speed
The blastie's makin!
Thae winks and finger-ends, I dread,
Are notice takin!
O wad some Pow'r the giftie gie us
To see oursels as others see us!
It wad frae monie a blunder free us,
An' foolish notion:
What airs in dress an' gait wad lea'e us,
And ev'n Devotion!
Here is THE quote from Hans Zinsser's Rats, Lice and
History (copyright 1941):
"Weizl (an Austrian anthropologist) informs us that, when
sojourning for a short time among the natives of
An example of “Vagabond’s skin”, from http://dermatlas.med.jhmi.edu/derm/IndexDisplay.cfm?ImageID=1017889414
Case history: A
47 year old homeless man was evaluated for an itchy rash present for 3-4 months
on his extremities. Examination demonstrated widespread hyperpigmentation,
lichenification and excoriations particularly severe on his legs. His socks
were covered with multiple adult and immature lice and, in some areas, almost
confluent nits. He received a bath, a new set of clothes, and a total body
application of 5% permethrin cream with rapid elimination of the lice and nits.
Pruritus gradually improved over 3-4 weeks and he was continued on emollients.
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Youtube
clips:
Louse
walking along nit comb: http://www.youtube.com/watch?v=1N-wRQAL2XY&feature=related
Sprinting louse: http://www.youtube.com/watch?v=tGx1YAcIor0&NR=1
Phylogeny:
Order Anoplura (sucking lice)
Metamorphosis:
Incomplete
Geographical
location:
Cosmopolitan
Organs
affected:
Skin
Symptoms
and clinical signs:
Saliva induces roseate elevated papules. Severe infestation lead to scarring,
induration, ulceration.
Diseases
transmitted:
Epidemic typhus, trench fever, relapsing fever
Treatment/control:
Head lice: Shampoo with pyrethrins (0.2%), piperonyl butoxide and copper
oleate. If that doesn't work, use olive oil or mayonnaise, leave on head
overnight. Brush hair thoroughly.
Body
lice: Shampoo containing 0.2% or 0.3% allethrin synergized with piperonyl
butoxide.
Phthirus pubis (crab lice) (AKA "Le Papillon d'Amour", the
Butterfly of Love, in French.)
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Youtube
clips –
Phthiriasis: http://www.youtube.com/watch?v=TpKvYtLxvvI
Phthiriasis, one week follow-up: http://www.youtube.com/watch?v=EFhdFzJcs00&feature=related
Images:
Adult:
http://www.k-state.edu/parasitology/625tutorials/Arthropods04.html
Phylogeny:
Order Anoplura (sucking lice)
Metamorphosis:
Incomplete
Geographical
location:
Cosmopolitan
Organs
affected:
Skin, particularly of the pubic region.
Symptoms
and clinical signs:
Saliva induces roseate elevated papules. Severe infestations lead to scarring,
ulceration.
Diseases
transmitted:
None
Treatment/control:
On pubic area, treat as for head lice. Nits and lice may be removed from
eyelashes with forceps. Ophthalmic ointments of Eserine or of yellow oxides of
mercury are both effective.
Tick
and other Acarines
Tick Testing Centers
North American Laboratory
New Britain, CT
203-826-1140
800-866-NALG
203-223-6279-fax
New Jersey Laboratories
New Brunswick, NJ
732-249-0148
IgeneX
Palo Alto, California
http://www.igenex.com/
415-424-1191
800-832-3200
Tick Research Laboratory
Kingston, Rhode Island
401-874-2650
From cnn.com, August 11, 2005:
Dog tick found to
spread spotted fever
Wednesday,
August 10, 2005; Posted: 8:20 p.m. EDT (00:20 GMT)
(AP)
-- Scientists have discovered that a very common type of dog tick can spread
Rocky Mountain spotted fever, a serious and often fatal illness that reached
historic highs in the
Two types of ticks already were known to transmit the disease, but
they're not as common and are carried mostly by rodents and dogs that live near
wild or rural areas. This is the first
time that a tick that routinely plagues house pets has been implicated. The discovery was made through an
investigation of
"We may have been missing this in the past," said Linda
Demma, who led the study for the federal Centers for Disease Control and
Prevention. "It's almost certainly
occurring in other places and not diagnosed," agreed Dr. J. Stephen
Dumler, an expert on the disease at
Rocky Mountain spotted fever was first recognized a century ago in
The disease is caused by bacteria that infect ticks, which then
bite and infect animals and people.
Symptoms occur five to 10 days later and can include fever, nausea,
vomiting, muscle pain, lack of appetite and severe headache -- signs often
mistakenly attributed to common viral ailments.
Late symptoms include a spotted rash, abdominal pain, joint pain and
diarrhea. Antibiotics, particularly
doxycycline, are effective when given early.
Fatality rates as high as 20 percent have been reported when cases
are not recognized, and the disease is especially severe in children. From a low point of 365 cases in 1998, cases
have risen to 1,514 last year, but officials think that far more have gone
unreported. The CDC and Indian Health
Service officials from
Researchers found infected common brown dog ticks in all of the
victims' yards. Ticks turned up in the
cracks of stucco walls inside homes, in crawl spaces underneath them and on
furniture that children played on outside.
The investigators have since found another three people they believe had
the disease in 2001 from the same area of
Until now, the only ticks known to spread Rocky Mountain spotted
fever were the less common American dog tick and the
"No longer can we consider Rocky Mountain spotted fever a
disease of only rural and southern venues; it has emerged and re-emerged
again," Dumler wrote. "The
disease is in the midst of its third emergence since 1920, after peaks from
1939 to 1949 and again from 1974 to 1984," according to Dumler, who has
compiled numbers from published accounts and cases reported to CDC.
Officials recommend these steps to avoid ticks:
· Wear light-colored clothes
so ticks are more visible.
· Tuck pants legs into your
socks.
· Use insect repellents on
skin, clothes and boots.
· Use a mirror to carefully
check for ticks after being in tick-infested areas. Parents should check
children's hair for ticks.
· Use tweezers to remove
ticks and protect your fingers with a tissue or gloves. Grasp the tick as close
to the skin as possible and pull up with steady, even pressure, without
twisting or jerking the tick. Apply a disinfectant to the skin and wash your
hands.
· Save the tick so it can be
identified if you later become ill. Seal it in a plastic bag and put it in your
freezer, and note the date.
Copyright 2005 The Associated Press. All rights reserved.This
material may not be published, broadcast, rewritten, or redistributed.
Dermacentor
andersoni (wood tick)
Images:
Adult Dermacentor
variabilis:
http://www.k-state.edu/parasitology/625tutorials/Arthropods12.html
Phylogeny:
Class Arachnida
Metamorphosis:
'Incomplete'. Larvae and nymphs resemble adults.
Geographical
location:
Organs
affected:
Skin
Symptoms
and clinical signs:
Inflammation, edema, hemorrhage, secondary bacterial infection, tick paralysis.
Diseases
trasmitted:
American spotted fever (rickettsia), Q fever (rickettsia),
Treatment/control:
Topical insecticide and use of repellants on clothing.
Ixodes spp.,
Boophilus spp., Amblyomma spp. (HARD TICKS)
Images:
Ixodes
scapularis (black-legged tick) adults:
http://www.k-state.edu/parasitology/625tutorials/Arthropods22.html
Phylogeny:
Class Arachnida
Metamorphosis:
'Incomplete". Larvae and nymphs resemble adults.
Geographical location:
Cosmopolitan
Organs
affected:
Skin
Symptoms
and clinical signs:
Inflammatory responses, including local hyperemia, edema, hemorrhage.
Diseases
transmitted:
American spotted fever (rickettsia), Viral encephalitis, Tularemia (bacteria),
Babesia (protozoa).
Treatment/control:
Topical insecticide and use of repellents.
Trombicula alfreddugesi (CHIGGERS)
Images:
Phylogeny:
Class Arachnida
Metamorphosis:
'Incomplete'. larvae and nymphs resemble adults. larvae are parasitic.
Geographical
location:
North America and
Organs
affected:
Skin
Symptoms
and clinical signs:
Bite causes swelling and intense itching. Infection may be debilitating due to
loss of sleep.
Diseases
transmitted.
Tsutsugamushi disease.
Treatment/control:
Hot soap and water bath followed by the application of a 10% sulfur ointment
containing 1% phenol relieve itching. Residual insectides and repellents are
used.
Sarcoptes scabiei (SCABIES), Notoedres cati (FACIAL MANGE in
cats)
Images:
Adults:
http://www.k-state.edu/parasitology/625tutorials/Arthropods01.html
More adults:
http://www.k-state.edu/parasitology/625tutorials/Arthropods15.html
Phylogeny:
Class Arachnida
Metamorphosis:
'Incomplete'. Larvae and nymphs resemble adults.
Geographical
location:
Cosmopolitan
Organs
affected:
Skin
Symptoms
and clinical signs:
Lesions appear as reddish slightly elevated tracts in the skin. Intense itching
causes scratching, leading to secondary infections.
Diseases
transmitted:
None
Treatment/control:
Ointment containing 1% gamma benzene hexachloride. Pyrethrins are also used and
are less toxic.
Demodex
spp. including D. folliculorum and D. canis
Images:
Companion
animal Demodex spp.:
http://www.k-state.edu/parasitology/625tutorials/Arthropods17.html
More adults:
http://www.k-state.edu/parasitology/625tutorials/Arthropods08.html
"Eyelash
Creatures": http://www.geocities.com/thesciencefiles/eyelash/creatures.html
Phylogeny:
Class Arachnida
Metamorphosis:
'Incomplete'. Larvae and nymphs resemble adults.
Geographical
location:
Cosmopolitan
Organs
affected:
Hair follicles and sebaceous glands
Symptoms
and clinical signs:
Acne, blackheads, localized keratitis. Demodex induces mange among dogs.
Diseases transmitted:
None
Treatment/control:
Treatment is rarely required for human infections.
Vertebrates
Cuckoos and other brood
parasites:
From Nature's
Camouflage, by Edith Banks,
"An
interesting sort of mimicry is found in cuckoos: not in the birds themselves, but in their eggs. As is well known, many
cuckoos lay their eggs in the nests of other birds which then rear the baby
cuckoo as if it were their own. Not all cuckoo species do this. Some build a
nest and raise their own young, and these provide an interesting comparison
with the parasitic cuckoos.
The
non-parasitic species usually lay quite large, plain, white eggs. The parasitic
species almost all lay smaller eggs, and these are coloured and patterned to
mimic the eggs of the birds who unwittingly adopt them. Many different birds
are used as foster-parents by cuckoos, but generally, in any one region, a
cuckoo species parasitizes one particular bird, and the cuckoo's eggs
specifically imitate the eggs of that bird.
If the
nest belongs to a large, intelligent species, such as a Crow or a Magpie, the
egg mimicry is very good. Smaller birds are not so intelligent, and can be
duped just as easily by an egg which is only an approximate copy of their own.
Most can detect that an egg is an alien one if the pattern and colour are very
different, and will eject it from the next. But they do not seem perturbed by
an egg which is larger than their own. Often the pattern and colouring are the
same but the cuckoo's eggs are half as large again as those of the foster
parent.
It may
even be that birds prefer larger eggs. Experiements with Herring Gulls (which,
incidentally, are not parasitized by cuckoos) , have shown that this is so for
them. If a model of the Herring Gull's egg, correct in colour, shape and
pattern but three times larger than normal, is offered to a female gull, she
will brood it in preference to her own. The egg is acting as a
'super-stimulus'. The large, fake egg compels the gull to incubate it far more
strongly than one of her own, much smaller eggs.
The same
mechanism is at work when small birds which have hatched a cuckoo's egg continue
to feed the nestling even though it grows to twice their size. A tiny Reed
Warbler will persist in feeding even though it may have to perch on the back of
the grotesquely large cuckoo chick in order to reach its beak. Go to http://www.isle-of-wight.uk.com/jeffbrett/cuckoo.jpg to see what the possible difference in size between
the cuckoo chick and its much smaller foster parent.
So
powerful is the sight of the cuckoo chick's open beak that another small bird
passing by will respond to it, although it has never seen the chick before. The
passing bird will suddenly stop and push into the greedy mouth a morsel of food
which was destined for its own young ones.
A cuckoo
which is fostered by the more intelligent Crows and Magpies needs to be more
restrained. IT has to share the nest with the foster bird's own young (those
that parasitize small birds just push the other eggs out of the nest as soon as
they can). But since these larger birds are less gullible the cuckoo chick
needs to mimic one of their own nestlings in order to be fed. Such cuckoo
chicks have evolved colouring on the tops of their heads, on their backs and
inside their beaks which mimics that of the other young birds. Their undersides,
however, look quite different, but this does not matter since the parent bird
never sees them from below."
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A cuckoo's egg in the nest of a Meadow Pipit; the egg is only an approximate copy of the foster bird's own since small birds are easily duped. (NSP, T.D. Bonsah) |
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Brown-headed cowbirds, located in
the continental
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Figure 4. Brown-headed Cowbird nestlings grow rapidly, frequently outcompeting the host's nestlings for food and parental care. This adult Common Yellow-throat is feeding a cowbird fledgling that's more than twice its size. Photo by John Gavin, as it appears at http://birds.cornell.edu/conservation/tanager/images/cowbird.jpg . |
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SO, in
a nutshell --
I.
Cuckoos do not produce their own nests, but lay eggs in nests produced by other
species.
II. Eggs
laid by cuckoos resemble those of "foster" parents in size and coloration
pattern, but are generally larger. Larger size allows for earlier hatching.
Sometimes, foster parents can tell, in their own "birdy" way, that
something is not right with their nest, so they will toss out one egg. Because
of hyperstimulation by the cuckoo's egg, they are more likely to toss out one
of their own.
III.
Cuckoo nestlings show similar "begging" behavior for eliciting food
from foster parents. Cuckoos start getting fed even before the foster parents'
young are hatched.
IV.
Cuckoo nestlings push foster nestlings out of the nest, so the cuckoo nestling
is often the only remaining one in the nest. (This is not pleasant to watch.)
V.
Cuckoos are often found along borders of different communities, so native bird
populations, already reduced because of fragmentation of their habitats, are
getting clobbered.
References:
Payne, Robert B. and Laura L. Payne.
1997. Brood parasitism by cowbirds: risks and effects on reproductive success
and survival in indigo buntings. Behavioral Ecology 9(1):64-73.
Payne, Robert B. 1998. Brood
parasitism in birds: Strangers in the nest. Bioscience May 1998.
Petromyzon
marinus (sea lamprey)
Phylogeny:
Class Agnatha
Metamorphosis:
Complete - See illustration
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Geographical
location:
Over the past 100 years, populations have succeeded in bypassing the marine
stage, so that they can live their entire lives in freshwater. Adults live in
deep waters of the
|
|
Organs
affected:
Skin. Rows of numerous teeth cause severe damage to skin, thereby promoting
secondary bacterial & fungal infections which can be fatal.
|
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Numerous lamprey may be attached to the same host fish. |
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Treatment/control:
Larvicides are applied in small rivers and streams
Vandellia cirrhosa, AKA Candiru
Image:
http://www.k-state.edu/parasitology/625tutorials/Candiru.html
(Description
is from http://www.sciencenet.org.uk/database/Biology/0003/b00768d.html (Link is no longer active.)
I have
heard about a tropical fish which can detect traces of mammalian urine in the
water and will enter the urinary tract of the mammal. Is this true? What is
it's taxonomy etc.?
The fish
you are referring to is the Vandellia cirrhosa, common name candiru, a member
of the family Trichomycteridae the pencil or parasitic catfishes.
Vandellia
is about an inch (2.5 cm) in length and when it has not fed is slender and
almost transparent (except for the eyes). It lives in the rivers of tropical
South America.This small catfish is a vampire - it feeds on the blood of other
fish.
It has
been described as entering the gill chambers of larger fish to suck blood from
their gills. Once in the gill chamber it anchors itself there, so as not to be
flushed out as the fish pumps water over its gills, with spines on its gill
covers. As it feeds the body becomes engorged and distended with blood. Once it
has fed the candiru swims out of the gill chamber and burrows into the
river-bed to digest its blood meal.
You are
correct in believing that the candiru poses a hazard to humans (and other
mammals that might urinate in the water). It seems attracted to the flow of
urine (possibly as it resembles the stream of water from the gills of a large
fish). The candiru may swim up the stream of urine and enter the urethra of a
bather urinating into the river.
This, of course, not part of the fish's normal feeding behaviour - the fish has made a fatal mistake. Once up the urethra the fish can not turn nor can it move backwards because of the rear-pointing spines on its gill covers. It is locked in. The fish invariably dies and the dead fish and associated swelling o