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Biodefense
Reference Library
Foreign
Animal and Zoonotic Disease Center
Zoonotic
Disease Online Course
Presented
by
Stephen M.
Apatow, Director
of Research and Development
Humanitarian
Resource Institute
Biodefense Reference Library
Foreign
Animal and Zoonotic Disease Center
[Vitae][Email]
ZOONOTIC
DISEASES
PROTOZOAN
BABESIOSIS
Centers
for Disease Control and Prevention: Division of Parasitic Diseases
babesiosis
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(Piroplasmosis)
AGENT:
Babesiosis
in humans is a rare intraerythrocytic infection caused by Babesia
divergens
and microti.
RESERVOIR
AND INCIDENCE
Natural
hosts for B. microti are various wild and domestic animals,
particularly
the white-footed mouse and white-tailed deer. With extensions of the
deer's
habitat, the range of human infection appears to be increasing. In the
USA, the parasite has been found in coastal and island areas of the
northeast
and mid-Atlantic states as well as Wisconsin, Minnesota, and
California.
B. divergens occurs in Europe.
TRANSMISSION:
Humans
are infected as a result of Ixodes tick bites, but transmission from
blood
transfusion has also been reported. Splenectomized, elderly, or
immunosuppressed
persons are the most likely to have severe manifestations.
DISEASE
IN ANIMALS:
Many animals
show only mild fever and recover spontaneously. Deaths, which occur
commonly
in cattle, are due to either anemic anoxia or pulmonary thrombosis.
Other
lesions stem from the hemolysis and include enlarged spleen, liver, and
hemoglobinuric nephrosis.
DISEASE
IN HUMANS:
B. microti
infection lasts a few weeks to a month; the illness is characterized by
irregular fever, chills, headache, diaphoresis, myalgia, and fatigue
but
is without malaria-like periodicity of symptoms. Most patients have a
moderate
hemolytic anemia, and some have hepatosplenomegaly. The disease is
self-limited
and most patents recover without sequelae. Infection with B. divergens
has only been reported in splenectomized patients and progresses
rapidly
with high fever, severe hemolytic anemia, jaundice, hemoglobinuria, and
renal failure; death usually follows.
DIAGNOSIS:
ID of
the intraerythrocytic parasite on Giemsa-stained blood smears or
serology.
TREATMENT:
B. divergens:
blood transfusions, renal dialysis, pentamidine plus
trimethoprim-sulfa.
B. microti: Treat symptomatically since most case are self-limiting. In
splenectomized patients, quinine plus clindamycin and
transfusions.
PREVENTION/CONTROL:
Control
rodents and ticks. Vaccinate livestock.
TOXOPLASMOSIS
Centers
for Disease Control and Prevention: National Center for Infectious
Diseases
toxoplasmosis
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
AGENT:
Toxoplasma
gondii - 4 to 7 microns long. 2-4 wide - Subphylum Apicomplexa, Family
Eimeriidae.
RESERVOIR
AND INCIDENCE
Infection
in humans and lower animals is widespread. An estimated 500 million
humans
have been infected with the organism. Serologic surveys in the United
States
using the SABIN-FELDMAN DYE TEST have demonstrated T. gondii infection
in 30-80% of cats. Significance - Presumably all serologically positive
cats have shed toxoplasma oocysts and could re-shed organisms during
reinfection
or reactivation. Life cycle consists of: 1. Definitive host (felids:
intestinal
infection with shedding of oocysts; only host in which sexual form
develops.)
- Domestic cat predominates as reservoir for zoonotic transmission in
the
home and laboratory environment. 2. Intermediate hosts - *Mice, rats,
hamsters,
G. pigs, rodents, rabbits, dogs, sheep, cattle, & NHP's. - These
have
not proved to be important in zoonotic infection in the laboratory
animal
environment (organism replicates asexually in extraintestinal sites
only).
TRANSMISSION:
Fecal-Oral:
Ingestion of meat containing cysts or tachyzoites or ingestion of
oocysts
Oocysts become infective after sporulation - occurs in 2 to 3 days.
Transmission
to man occurs via a. Eating raw or undercooked meat containing cysts.
b.
Ingesting sporulated oocysts from cat feces. c. Transplacentally. 1/3
of
US human population has serologic evidence of past infection.
DISEASE
IN CATS:
Most postnatally
acquired infections in cats are ASYMPTOMATIC. Prepatent period variable
- 3 days to several weeks. Shedding occurs for 1-2 weeks - PUBLIC
HEALTH
HAZARD. Oocyst shedding reactivated by induction of hypercorticism or
superinfection
with other feline microorganisms.
DISEASE
IN MAN:
The infection
is very common in humans, but clinical disease is of low incidence and
occurs only sporadically. Postnatal infection - Less severe disease and
commonly presents as a generalized lymphadenopathy that may resolve
without
treatment in a few weeks. Congenital infection results in systemic
disease
often with severe neuropathological changes. Rarely, serious ocular or
systemic toxoplasmosis can be acquired by older individuals or
reactivated
in immunocompromised individuals. Clinical Signs include fever, skin
eruption,
malaise, myalgia, arthralgia, cervical lymphadenopathy, pneumonia,
myocarditis,
meningoencephalitis, and chorioretinitis.
DIAGNOSIS:
Serology,
isolation, microscopic demonstration of organisms in smear or section.
Paired serum samples taken one or more weeks apart. a. IFA: serial
titers
of suspected infections. b. Sabin- Feldman Dye Test: most sensitive
test,
but rarely used. c. ELISA. The demonstration of cysts does not
establish
a causal relationship to clinical illness, since cysts may be found in
both acute and chronic infections. However, only finding tachyzoites in
blood or body fluids confirms active infection.
TREATMENT
IN MAN:
The treatment
of choice is pyrimethamine plus either trisulfapyrimidines or
sulfadiazine.
Folinic acid is given to avoid the hematologic effects of
pyrimethamine-induced
folate deficiency.
PREVENTION/CONTROL:
Freezing
of meat to -20oC (-4oF) for 2 days or heating to 60oC (140oF) kills
cysts.
Under appropriate environmental conditions, oocysts passed in cat feces
can remain infective for a year or more. Thus, children's play areas
should
be protected from cat and dog feces. Cats a. Daily cleaning of litter
pans
(since oocysts not infective for 2 to 3 days) b. Wear gloves c. Wash
hands
before eating d. Should only be fed dry, canned, or cooked meats
Pregnant
women should have their serum examined for Toxoplasma antibody. If the
IgM test is negative but an IgG titer is present and less than 1:1000,
no further evaluation is necessary. Those with negative titers should
take
measures to prevent infection by avoiding contact with cat feces and
avoid
working in soil or gardens that could be contaminated by cats, etc. and
by thoroughly cooking meat. Hands should be washed after handling raw
meat
and before eating or touching the face.
PLASMODIUM
spp.
Centers
for Disease Control and Prevention: National Center for Infectious
Diseases
Plasmodium
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
Cause
of malaria. Both quartan and tertian types occur in NHP. There is a
high
incidence in newly imported animals. Requires anopheline mosquitoes for
transmission. Therefore zoonotic potential exists anywhere mosquitoes
have
access to infected animals. Generally thought that these conditions
prevail
only in Southern climates where monkeys are housed outdoors, but
mosquitoes
are found in Northern as well as Southern U.S. In general, human
malaria
caused by plasmodia of simian origin resembles a mild and benign
infection
caused by human plasmodia. The disease is of short duration,
parasitemias
are low, and relapses are rare. Must control flying insects in all
primate
facilities.
AFRICAN
TRYPANOSOMIASIS
Centers
for Disease Control and Prevention: National Center for Infectious
Diseases
trypanosomiasis
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(African
Sleeping Sickness, Gambian Trypanosomiasis, Rhodesian
Trypanosomiasis)
AGENT:
Trypanosoma
brucei gambiense and rhodesiense.
RESERVOIR
AND INCIDENCE
Many wild
and domestic animals harbor infection. In Gambian trypanosomiasis,
humans
are the main reservoir and source of infection for the vector tsetse
fly
(Glossina palpalis, tachinoides, or fuscipes). In Rhodesian
trypanosomiasis,
animals, especially domestic cattle and pigs, play an important role as
reservoirs.
TRANSMISSION:
The tsetse
fly is infected when it bites during the parasitemic phases and the
trypanosome
develops in the vector, culminating in infection of its saliva.
Transmission
is by the tsetse fly bite. In humans, intrauterine infection has been
recorded.
DISEASE
IN ANIMALS:
Occasionally
mild disease occurs in domestic animals with chronic nervous sequela in
T. gambiense infection.
DISEASE
IN HUMANS:
The trypanosomal
chancre: This a local pruritic, painful inflammatory reaction with
regional
lymphadenopathy that appears about 48 hours after the tsetse bite and
lasts
2-4 weeks. The hemolymphatic stage: Usually absent or unnoticed in T.
b.
gambiense infections. Irregular fevers, headaches, joint pains,
malaise,
pruritus, papular skin rash, edemas. Patients may succumb to
myocarditis
before signs of central nervous system invasion appear. The
meningoencephalitic
stage: Insomnia, motor and sensory disorders, abnormal reflexes,
somnolence
to coma. Trypanosomes and increased white cells and protein in
cerebrospinal
fluid.
DIAGNOSIS:
Definitive
diagnosis requires identifying the organism in the bite lesion, blood,
lymph node aspirate, or CSF. Serologic tests become positive after 12
days.
TREATMENT:
Hemolymphatic
stage: Suramin, eflornithine or pentamidine. Late disease: melarsoprol
or eflornithine or tryparsamide plus suramin.
PREVENTION/CONTROL:
Wear long
sleeves and trousers in endemic areas. Avoid wearing dark-colored
clothing,
and use mosquito nets while sleeping. Repellents do not work on tsetse
flies. Pentamidine is used as a chemoprophylaxis against the Gambian
type.
AMERICAN
TRYPANOSOMIASIS
Centers
for Disease Control and Prevention: National Center for Infectious
Diseases
Trypanosoma
cruzi
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(Chagas's
Disease, Chagas-Mazza Disease, South American Trypanosomiasis)
AGENT:
Trypanosoma
cruzi
RESERVOIR
AND INCIDENCE
Dogs,
cats, and guinea pigs are the main reservoirs for human infection. T.
cruzi
occurs only in the Americas; it is found from southern South America to
northern Mexico, Texas, and the southwestern U.S. An estimated 12
million
people are infected, mostly in rural areas, resulting in about 60,000
deaths
yearly.
TRANSMISSION:
Humans
are infected when the insect's feces become rubbed into the wound
caused
by the bite of an infected bloodsucking insect (triatomid) or when the
conjunctiva, mucous membranes or abrasions become contaminated. After
invading
local reticuloendothelial cells, the trypanosome multiplies in the
blood.
Adaption of triatomid vector to the human domestic environment allows
transfer
of infection between animals, from animals to humans or from human to
human.
Transmission by blood transfusions from infected persons, congenital
infection,
breast milk and laboratory accidents are possible.
DISEASE
IN ANIMALS:
Acute
and inapparent infection occur in wild animals and chronic disease is
seen
in dogs. The acute form, which includes fever, enlarged liver and lymph
nodes and heart irregularities, lasts 10-30 days before becoming
chronic
without further clinical signs, though sometimes myocarditis occurs.
Lesions
in dogs resemble those in humans.
DISEASE
IN HUMANS:
Acute
illness usually occurs in children with a furuncle at the site of
infection.
Signs include fever, malaise, enlarged lymph nodes, liver and spleen.
If
the primary site of infection is the eye there is unilateral edema of
eyelids
and conjunctivitis. Rarely myocarditis and meningoencephalitis occur.
Chronic
symptoms in adults result from arrhythmias and dilation of the heart,
esophagus
and colon. Furuncles (chagoma) appear at the point of entry of the
infection.
Enlarged liver and spleen, myocarditis, grossly dilated heart,
intestines,
esophagus, ureter and bladder and meningoencephalitis occur.
DIAGNOSIS:
Several
serologic tests are available and are of presumptive value; when
possible,
more than one test should be used. In the acute stage, trypanosomes
should
be looked for by examination of anticoagulated fresh blood for motile
organisms.
In the chronic stage, the parasite can only be detected by culture or
xenodiagnosis.
TREATMENT:
Therapy
is unsatisfactory; the drugs are toxic and often ineffective. In the
acute
phase, however, cure is usually possible. In the chronic phase,
although
parasitemia and xenodiagnosis become negative, treatment does not alter
the serologic reaction, cardiac function, or progression of the
disease.
Nifurtimox or benznidazole is used. Ketoconazole shows promise
also.
PREVENTION/CONTROL:
Destroy
the vector by insecticides. Use insect nets to prevent bites. Screen
blood
donors.
AMEBIASIS
Centers
for Disease Control and Prevention: National Center for Infectious
Diseases
amebiasis
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(Amebic
Dysentery, Amebiosis)
AGENT:
Entamoeba
histolytica.
RESERVOIR
AND INCIDENCE
The reservoir
of E. histolytica is man. The infections is present worldwide but is
most
prevalent and severe in tropical areas, where rates may exceed 40%
under
conditions of crowding, poor sanitation, and poor nutrition. It is
estimated
that there are about 50 million case of invasive amebiasis and
40,000-100,000
deaths annually worldwide. In temperate areas, however, amebiasis tends
to be asymptomatic or a mild, chronic infection that often remains
undiagnosed.
In the USA, seropositive rates up to 2-5% have been reported in some
populations.
Reported incidence of 0-31% in the feces of clinically normal Rhesus
monkeys,
2-67% in Chimps, and up to 30% in other NHP.
TRANSMISSION:
Transmission
may be by ingestion of infective cysts, contaminated water or food, by
flies, or fomites. Exists as resistant cysts or more fragile
trophozoites
CYSTS are the INFECTIOUS form found in the stool of asymptomatic
carriers
or patients with mild disease. The cysts remain viable, if moist and
cool
for 12 days. Remain viable for 30 days in water. Laboratory animal
personnel
are usually infected from fecal matter transferred to the skin or
clothing.
DISEASE
IN ANIMALS:
In dogs,
infection by E. histolytica is generally asymptomatic and frequently
localized
in the cecum. Occasionally, it can invade tissues and cause acute or
chronic
amebiasis. Rhesus monkeys are generally resistant and usually
experience
asymptomatic infection, but chronic, mild colitis can occur. In
chimpanzees,
the infection can persist for a long time, in most cases subclinically,
but sometimes it invades the tissues causing ulcerative colitis and
hepatic
abscesses. New World monkeys are considered more susceptible to the
disease
than Asian or African monkeys. Wild rats can also harbor E.
histolytica;
the protozoan can be found in the large intestine as a commensal or it
can invade the mucosa and cause amebic dysentery.
DISEASE
IN HUMANS:
Mild to
moderate colitis: recurrent diarrhea and abdominal cramps, sometimes
alternating
with constipation; mucus may be present; blood is usually absent.
Severe
colitis: semiformed to liquid stools streaked with blood and mucus,
fever,
colic, prostration. In fulminant cases, ileus, perforation,
peritonitis,
and hemorrhage occur. Hepatic amebiasis: fever, hepatomegaly, pain,
localized
tenderness.
DIAGNOSIS:
Use fresh
fecal specimen to identify cysts or trophozoites. Sedimentation. Must
measure
to distinguish from other nonpathogenic amoebae. Indirect HI For
hepatic
amebiasis, ultrasonography can locate the cyst and fine needle
aspiration
is performed to find the organism.
TREATMENT:
May require
the concurrent or sequential use of several drugs. The tissue
amebicides
dehydroemetine and emetine act on organisms in the bowel wall and in
other
tissue but not in gut lumen. Chloroquine is active principally against
amebas in the liver. The luminal amebicides diloxanide furoate,
iodoquinol,
and paromomycin act on organisms in the bowel lumen but are ineffective
against amebas in the bowel wall or other tissue. Metronidazole is
unique
in that it is effective both in the lumen and in the wall and in other
tissue. However, when used alone, it only cures 50% of the cases.
PREVENTION/CONTROL:
Strict
sanitation & personal hygiene, protective clothing and gloves.
Fecal
screening of NHP. Protect water supply from fecal contamination. Usual
chlorine levels don't destroy cysts. *10ppm chlorine residual necessary
to destroy cysts Heat to 50oC (122oF) kills cysts. Adequate cooking to
destroy cysts. Protect food from fly contamination.
BALANTIDIASIS
Centers
for Disease Control and Prevention: Division of Parasitic Diseases
Balantidium
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(Balantidial
dysentery)
AGENT:
large
ciliated protozoan, Balantidium coli. Trophozoite 50-70 microns by
40-50
microns.
RESERVOIR
AND INCIDENCE
Distributed
worldwide especially in the tropics. Swine and possibly rats and NHP's
are the reservoir hosts. Humans, great apes, & several monkey
species
may carry it. Incidence in NHP colonies - 0 to 63% Usually
asymptomatic,
but may see diarrhea.
TRANSMISSION:
Ingestion
of cysts or trophozoites from infected animal or human feces. Cyst is
the
infectious form. Contaminated water or food.
DISEASE
IN ANIMALS AND
MAN:
Many infections
are asymptomatic and probably need not be treated. Chronic recurrent
diarrhea,
alternating with constipation, is most common, but severe dysentery
with
bloody mucoid stools, tenesmus, and colic may occur
intermittently.
DIAGNOSIS:
Use fresh
fecal samples to identify trophozoites or cysts Trophozoites in
scrapings
or biopsy of ulcers of the large bowel.
TREATMENT:
Tetracycline
or iodoquinol.
PREVENTION/CONTROL:
Good sanitation
& personal hygiene practices in NHP & Swine colonies. Protect
water
& food from fecal contamination Identify positive lab animals and
treat.
CRYPTOSPORIDIOSIS
Centers
for Disease Control and Prevention: National Center for Infectious
Diseases
cryptosporidiosis
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
AGENT:
Extracellular
protozoal organisms - similar to coccidia. Genus: Cryptosporidium, it
remains
unsettled whether more than one species exists. Taxonomy of species
somewhat
controversial but considered to be infective across species lines.
RESERVOIR
AND INCIDENCE
Rodents,
birds (particularly turkeys and chickens), ruminants, fish, reptiles,
cats,
dogs, rabbits, NHP's. Children over 2 years of age, animal handlers,
travelers,
homosexual men, and close personal contacts of infected individuals
(families,
health care and day-care workers) may be particularly likely to be
infected.
More than a dozen outbreaks have been reported in day-care centers
around
the world. Two major waterborne outbreaks have been documented.
Cryptosporidium
antibodies were detected in the serum of 20 of 23 cats (87%) suggesting
that the exposure rate may be high.
TRANSMISSION:
Fecal-oral
transmission is from animals to humans or humans to humans; waterborne
transmission is also important. Oocysts passed in stool are fully
sporulated
and infectious; infection occurs as a result of their ingestion. In
humans
and animals, the full life cycle occurs within a single host. The
organisms
attach to the microvillous borders of enterocytes of the small bowel
and
also are found free in mucosal crypts. The host cell membrane
deteriorates,
leaving the parasitic membrane in direct contact with epithelial cell
cytoplasm.
The organisms do not, however, invade the tissues.
DISEASE
IN ANIMALS:
Severe
watery diarrhea in neonatal calves and lambs. In turkeys and chickens,
the parasites are reported to occur in the sinuses, trachea, bronchi,
cloaca,
and bursa of Fabricius. The respiratory disease causes coughing,
gasping,
and airsacculitis. In reptiles, cryptosporidiosis is frequently
reported
in association with postprandial regurgitation. The organism affects
the
GI mucosa, resulting in marked thickening of the rugae and loss of
segmented
motility.
DISEASE
IN MAN:
In immunocompetent
persons, infection varies from no symptoms to mild enteritis to marked
watery diarrhea (up to 10 stools daily) without mucus or gross or
microscopic
blood. Low-grade fever, malaise, nausea, vomiting, abdominal cramps,
anorexia
and weight loss may occur. The infection is generally self-limited and
lasts a few days to about 2 weeks. In immunologically deficient
patients,
the illness is characterized by profuse (up to 15L daily), cholera-like
diarrhea and by fever, severe malabsorption, marked weight loss, and
lymphadenopathy.
In AIDS, infection may involve any part of the GI tract, and
multisystemic
involvement has been described, especially involving the respiratory
tract.
DIAGNOSIS:
Diagnosis
is by detection of oocysts in stool by a variety of flotation or
concentration
methods or by mucosal biopsy, followed by special staining methods that
use modifications of an acid-fast stain (routine fecal staining methods
do not detect the organisms). Three stools should be examined over 5
days.
A fluorescein-labeled IgG monoclonal antibody test has recently become
available to detect oocysts.
TREATMENT:
No successful
treatment has been developed so far. Generally, no treatment other than
supportive is needed in immunocompetent persons since it is
self-limiting.
In immunoincompetent persons, spiramycin, zidovudine (AZT),
paromomycin,
octreotide, and eflornithine have been reported of value.
PREVENTION/CONTROL:
Personal
hygiene. Careful handwashing by those in contact with any animals with
scours.
GIARDIASIS
Centers
for Disease Control and Prevention: National Center for Infectious
Diseases
giardiasis
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
Most
common intestinal protozoan parasite of people in the U.S.
AGENT:
Giardia
lamblia Has both a cyst (infective) and trophozoite form
RESERVOIR
AND INCIDENCE
The parasite
occurs worldwide and is nearly universal in children in developing
countries.
Humans are the reservoir for Giardia, but dogs and beavers have been
implicated
as a zoonotic source of infection. In psittacines, the disease is
commonly
found in cockatiels and budgerigars. Giardiasis is a well-recognized
problem
in special groups including travelers, campers, male homosexuals, and
persons
with impaired immune states. However, Giardiasis does not appear to be
an opportunistic infection in AIDS.
TRANSMISSION:
Only the
cyst form is infectious by the oral route; trophozoites are destroyed
by
gastric acidity. Most infections are sporadic, resulting from cysts
transmitted
as a result of fecal contamination of water or food, by
person-to-person
contact, or by anal-oral sexual contact. After the cysts are ingested,
trophozoites emerge in the duodenum and jejunum. They can cause
epithelial
damage, atrophy of villi, hypertrophic crypts, and extensive cellular
infiltration
of the lamina propria by lymphocytes, plasma cells, and
neutrophils.
DISEASE
IN ANIMALS:
Giardia
infections in dogs and cats may be inapparent or produce weight loss
and
chronic diarrhea or steatorrhea, which can be continuous or
intermittent,
particularly in puppies and kittens. Calves with clinical giardiasis
have
been reported. Feces are usually soft, poorly formed, pale, and contain
mucus. Gross intestinal lesions are seldom evident, although
microscopic
lesions, consisting of villous atrophy and cuboidal enterocytes, may be
present.
DISEASE
IN MAN:
Most infections
are asymptomatic. In some cases, acute or chronic diarrhea, mild to
severe,
with bulky, greasy, frothy, malodorous stools, free of pus and blood.
Upper
abdominal discomfort, cramps, distention, excessive flatus, and
lassitude.
DIAGNOSIS:
Diagnosis
is by identifying cysts or trophozoites in feces or duodenal fluid.
Unless
they can be examined with an hour, specimens should be preserved
immediately
in a fixative. Three stool specimens should be examined at intervals of
2 days or longer. A stool ELISA test or IgM serology are
available.
TREATMENT:
Tinidazole,
Metronidazole (FLAGYL), quinacrine, or furazolidone. Alternative drugs
are Tinidazole or albendazole.
PREVENTION/CONTROL:
Fecals
to screen dogs and NHP's. Hygiene, protective clothing, when handling
animals.
Prevention requires safe water supplies, sanitary disposal of human
feces,
adequate cooking of foods to destroy cysts, protection of foods from
fly
contamination, washing hands after defecation and before preparing or
eating
foods, and, in endemic areas, avoidance of foods that cannot be cooked
or peeled.
LEISHMANIASIS
Centers
for Disease Control and Prevention: National Center for Infectious
Diseases
leishmaniasis
Office
International des Epizooties
Leishmaniosis:
Manual of standards Diagnostic Tests and Vaccines 2000
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
[Cutaneous
leishmaniasis: Chiclero ulcer, espundia, pianbols, uta, and buba (in
the
Americas); oriental sore, Aleppo boil (in the Old World); Bagdad boil,
Delhi boil, Bauru ulcer (in the Middle East). Visceral leishmaniasis:
kala-azar]
AGENT:
The causative
agents of cutaneous leishmaniasis are Leishmania mexicana and L.
brasiliensis
in the Americas, and L. tropica in the Old World; and of visceral
leishmaniasis,
L. donovani, L. infantum, and L. chagasi.
RESERVOIRS
AND INCIDENCE:
The geographic
distribution of the cutaneous disease is Texas, Mexico, Central and
South
America, India, Pakistan, the Middle East, southern Russia, the
Mediterranean
coast and Africa. The distribution of visceral leishmaniasis is poorly
reported, but foci probably occur in the Mediterranean basin, the
Middle
East, India, China, Mexico, Central and South America, and Africa. Wild
animals, dogs and humans serve as reservoirs. Domestic dogs may be an
important
reservoir for humans. Humans are the only known reservoir in
India.
TRANSMISSION:
Sandfly
vectors transmit cutaneous leishmaniasis. Person-to-person, congenital,
and blood-borne transmission of visceral leishmaniasis are
possible.
DISEASE
IN ANIMALS:
L. mexicana
causes ulcers of the skin in rodents and other wild animals, usually at
the base of the tail. L. braziliensis causes a systemic infection with
few skin lesions in wild animals. No skin lesions have been found in
dogs.
Dogs infected by L. tropica may suffer form cutaneous lesions similar
to
those found in humans. L. donovani produces visceral lesions in dogs,
with
enlarged lymph nodes, liver and spleen.
DISEASE
IN HUMANS:
In the
cutaneous disease, the primary lesion is a painful ulcer or nodule at
the
site of infection persisting for several months, with residual
scarring.
Further lesions may develop in skin and mucous membranes. Infiltration
by inflammatory cells at the inoculation site supports the growth of
the
parasite. This progresses into a large area of chronically inflamed
granulation
tissue. The overlying skin undergoes hyperplasia and then necrosis with
spreading ulceration. Metastatic lesions occur with a similar
inflammatory
reaction. The lesions may heal, become fibrosed or extend indefinitely
to produce considerable disfigurement. In the visceral disease,
intermittent
irregular fever occurs with sweats, enlarged spleen, weight loss and
anemia
leading to ascites, edema, diarrhea and secondary infections. Dark
pigmentation
of the skin may occur. There is gross enlargement of liver and spleen.
Without treatment, the case fatality rate is 90%.
DIAGNOSIS:
Definitive
diagnosis is achieved by finding the parasite-either the amastigote in
stained smears or biopsies, or the motile promastigote in culture.
Serologic
and skin tests provide only indirect evidence of infection.
TREATMENT:
Treatment
remains inadequate because of drug toxicity, long courses required, and
frequent need for hospitalization. The drug of choice is sodium
antimony
gluconate. Alternative drugs for some forms of infection are
amphotericin
B and pentamidine.
PREVENTION/CONTROL:
Use insecticides
in house and buildings to control the vector. Eliminate rubbish heaps
which
are breeding areas for sandflies. Avoid sandfly bites by using insect
repellents
and protective clothing. Keep dogs indoors after sundown and remove
infected
dogs.
MICROSPORIDIOSIS
Centers
for Disease Control and Prevention: Division of Parasitic Diseases
microsporidiosis
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
Protozoa
of the order Microsporidia (Phylum: Microspora) are represented by
about
700 species parasitic in hosts of many invertebrate and vertebrate
groups.
These protozoa have only recently been recognized as "opportunistic"
parasites
in patients with AIDS. In veterinary medicine, Microsporidia are well
known
as causative agents of certain animal infections, such as nosemosis in
bees, encephalitozoonosis in rabbits and of numerous fish diseases.
Microsporidia
are obligatory intracellular parasites (macrophages, histiocytes,
endothelial
cells, kidney tubular cells, etc.) with a characteristic spore stage
and
a unique mode of infecting host cells. Spores of Microsporidia species
infecting mammals are ovoid or piriform, 1.5-5.0 þm long with
mostly
a thick wall consisting of 2 main layers (exospore, endospore). The
spore
contains a coiled, minute tube (polar tube or polar filament) connected
with a complex extrusion apparatus and a nucleated, infective
sporoplasm.
After ingestion by a suitable host, the physiological conditions of the
digestive tract stimulate the spores to evert with force the coiled
polar
filament. The tip of the filament penetrates the host cell membrane,
the
sporoplasm migrates through the tube and enters the cytoplasm where
asexual
multiplication (merogony) and spore formation (sporogony) occur.
Sporoplasms
usually infect the gut epithelium either to develop there or to be
transferred,
probably by the action of phagocytic cells, to the circulation and
their
preferred site of development in various organs. The spores, released
to
the environment from the intestinal or urinary tract, are ingested by a
new host. All Microsporidia examined so far have a direct developmental
cycle. Up to now 5 genera of Microsporidia have been identified as
causative
agents of human infections. ENCEPHALITOZOON CUNICULI has a worldwide
distribution
and is a common parasite of wild and domesticated rabbits, laboratory
rodents
and a wide spectrum of other mammals such as carnivores, ruminants,
pigs,
monkeys and man. Encephalitozoon parasites found in birds may belong to
other species. E. cuniculi, widespread in conventional rabbit colonies
in up to 76% of the stock, mostly causes latent infections and only
rarely
disease. Focal granulomatous encephalitis and nephritis are the main
pathological
changes. Natural transmission in rabbits is possible by the oral,
tracheal
and transplacental routes, but oral infection appears to be the most
important
way. In rabbits, spores of E. cuniculi are excreted in the urine in
concentrations
up to 106 spores/ml. The human cases of E. cuniculi infections include
two cases of encephalitis with a favorable evolution in two
immunocompetent
children. In a 35-year old man with AIDS the E. cuniculi infection
resulted
in a granulomatous hepatitis. Recently, another case in a 45-year old
patient
with AIDS (Greek nationality) was described in Switzerland. An unusual
peritonitis with a large granulomatous mass, containing developmental
stages
of E. cuniculi, were found at autopsy. In Sweden (S) and Great Britain
(GB) high prevalences of serum antibodies against E. cuniculi antigen
have
been detected in persons with malaria (S: 38%, GB: 7%), Chagas disease
(S: 15%), schistosomiasis (GB: 12%), filariases (S: 9%), neurological
disorders
(GB: 6%) and in travellers after a stay in the tropics (S: 12%) while
non-exposed
persons, animal dealers and some other groups were seronegative. The
question
is open whether E. cuniculi is more common in the tropics or whether
tropical
parasites cause immunodepression which supports microsporidian
infections.
Besides a systemic infection in a immunodefective child with Nosema
conori
and two cases of keratitis caused by Microsporidian species, the recent
description of a myositis in an AIDS patient due to Pleistophora sp. is
of special interest as parasite transmission from fish was suspected.
Another
species of this group is Enterocytozoon bieneusi. This parasite was
first
described in 1984 in France in a 29-year old AIDS patient who had
suffered
from heavy diarrhea. Microsporidia were found in enterocytes of the
duodenum,
jejunum and ileum. This parasite or similar forms were subsequently
detected
in at least 9 other patients with AIDS in the USA, Uganda and the
Netherlands.
The origin of this parasite is unknown. An infection similar to E.
bieneusi
in the enterocytes of a Callicebus monkey has been described.
DIAGNOSIS:
Diagnosis
is based on the direct detection of Microsporidia by histology after
hematoxylin-eosin,
Giemsa, Gram or other staining (spores are Gram-positive!) or by
electron
microscopy in autopsy or biopsy material. Serum antibody detection
provides
another tool for the in vivo diagnosis of encephalitozoonosis.
TREATMENT:
Information
on chemotherapy of microsporidian infections is scanty. In experimental
infections chloroquine and oxytetracycline reduced harvests of E.
cuniculi
spores only by 69% and 58%, respectively. Treatment of an AIDS patient
suggested that either metronidazole or ganciclovir may have inhibited
the
microsporidian infection.
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