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Biodefense Reference Library
Foreign Animal and Zoonotic Disease Center
One Medicine: One Health (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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