.
|
|
Click
here for additional
information
|
.
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
NEMATODE
ANISAKIASIS
Centers
for Disease Control and Prevention: Division of Parasitic Diseases
Anisakiasis
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(Herring
worm disease) A common parasitic infection from fish. The parasites are
widely distributed. Human disease occurs where people eat raw or
lightly
smoked or salted saltwater fish or squid (e.g., in Japan, the
Netherlands,
Scandinavia and Central America). The causative agents are Anisakis,
Phocanema
and Contracaecum (Nematoda). There is no vaccine.
RESERVOIR
AND MODE OF
TRANSMISSION:
Definitive
hosts are marine mammals such as dolphins or seals. These pass the
parasite's
eggs in their feces. The eggs hatch and produce larvae which infect the
first intermediate host, usually a crustacean. A fish may be the second
intermediate host. Humans are aberrant hosts infected by eating
fish.
INCUBATION
PERIOD:
Humans
and animals. A few hours to a few weeks.
CLINICAL
FEATURES:
Humans.
There may be fever, abdominal pain, vomiting, hematemesis, coughing,
pseudoappendicitis,
and possibly symptoms associated with intestinal perforation. Animals.
Fish fail to thrive if heavily infected.
PATHOLOGY:
Humans.The
larvae usually remain in the intestine causing few lesions. However,
they
sometimes invade the stomach wall causing hematemesis and may lodge in
the mesenteric veins or in the viscera where they induce eosinophilic
granulomas
and abscesses. Larvae may migrate up the esophagus to the oropharynx.
There
is a low grade eosinophilia. Animals. In fish, atrophy of the liver
occurs
and sometimes fatal infection of the heart. Visceral adhesions and
muscle
damage can be severe.
DIAGNOSIS:
Humans.
Stools may show occult blood. Mild leukocytosis and eosinophilia may be
present. ELISA and RAST serologic tests may be tried but are not
reliable
in chronic disease. In acute infection, the larvae sometimes can be
seen
and removed endoscopically from the stomach. X-rays of the stomach may
show a localized edematous, ulcerated area with an irregularly
thickened
wall, decreased peristalsis, and rigidity. Double contrast technique
may
show the threadlike larvae. Small bowel x-rays may show thickened
mucosa
and segments of stenosis with proximal dilation. Ultrasound examination
of gastric and intestinal lesions may also be useful. In the chronic
stage,
x-rays and endoscopy of the stomach-but not of the bowels-may be
helpful.
The diagnosis is often made only at laparotomy with surgical removal of
the parasite. Animals. Demonstrate the parasite in tissues of
fish.
PROGNOSIS:
Humans.
The condition is rarely fatal. Animals. Wide distribution of the
parasites
and consequent disease results in difficulty in maintaining marine
vertebrates
in laboratories.
PREVENTION:
Humans.
Avoid raw or undercooked fish. Freezing fish kills larvae. Eviscerate
fish
immediately after catching. Animals. Impractical.
TREATMENT:
Humans.
Physical removal of larvae by gastroscopy or surgery. Animals. Not
appropriate.
Legislation Humans and animals. None.
TRICHINOSIS
Centers
for Disease Control and Prevention: Division of Parasitic Diseases
Trichinosis
Office
International des Epizooties
Trichinellosis:
Manual of standards Diagnostic Tests and Vaccines 2000
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
AGENT:
Trichinella
spiralis, an intestinal nematode.
RESERVOIR
AND INCIDENCE
Swine,
dogs, cats, rats and many wild animals. Worldwide. In the U.S., there
has
been a marked reduction in the prevalence of trichinosis both in humans
and pigs; prevalence in commercial pork now ranges from nil to 0.7%.
Fewer
than 100 human cases are reported annually and usually have been as a
result
of eating homemade sausage and other meat products using pork, horse
meat,
or arctic mammals.
TRANSMISSION:
In the
natural cycle, larvae develop into adult worms in the intestines when a
carnivore ingests parasitized muscle. Pigs generally become infected by
feeding on uncooked scraps or, less often, by eating infected rats. In
humans, infection occurs by eating insufficiently cooked meat. In the
epithelium
of the small intestine, larvae develop into adults. Gravid female worms
then produce larvae, which penetrate the lymphatics or venules and are
disseminated via the bloodstream throughout the body. The larvae become
encapsulated in skeletal muscle.
DISEASE
IN ANIMALS:
Usually
subclinical.
DISEASE
IN HUMANS:
Clinical
disease in humans is highly variable and can range from inapparent
infection
to a fulminating, fatal disease depending on the number of larvae
ingested.
Sudden appearance of muscle soreness and pain, together with edema of
upper
eyelids are common early and characteristic signs. These are sometimes
followed by subconjunctival, subungual and retinal hemorrhages, pain
and
photophobia. Thirst, profuse sweating, chills, weakness, prostration
and
rapidly increasing eosinophilia may follow. GI symptoms may also occur.
Remittent fever, cardiac and neurologic complications may appear.
Lastly,
death due to myocardial failure may occur.
DIAGNOSIS:
Serologic
testing and muscle biopsy.
TREATMENT:
Treatment
is principally supportive, since in most cases recovery is spontaneous.
Mebendazole, thiabendazole, or albendazole can be given.
PREVENTION/CONTROL:
Cooking
(at 77oC [171oF] or above) destroys the parasite. Freezing meat up to
15
cm at 5oF for 30 days or -13oF for 10 days will destroy the parasite.
Thicker
pieces need to be frozen at the lower temperature for at least 20 days.
These temperatures will not kill the cold-resistant Arctic strains,
however.
Gamma irradiation will kill the parasite. Prevent pigs from gaining
access
to rats or uncooked offal.
ANGIOSTRONGYLIASIS
Centers
for Disease Control and Prevention: Division of Parasitic Diseases
Angiostrongyliasis
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
SYNONYMS:
Angiostrongylosis,
eosinophilic meningitis or meningoencephalitis (A. cantonensis),
abdominal
angiostrongylosis (A. costaricensis).
ETIOLOGY:
Two metastrongylids,
Angiostrongylus (Morerastrongylus) costaricensis and A. cantonensis,
are
the etiologic agents. The first species is responsible for abdominal
angiostrongyliasis,
and the second one for eosinophilic meningitis or
meningoencephalitis.The
definitive hosts of both species are rodents; man is an accidental
host.
Both species require mollusks as intermediate hosts for the completion
of their life cycle. The main definitive host of A. costaricensis is
the
cotton rat, Sigmondon hispidus, in which the adult nematode lodges in
the
mesenteric arteries and their branches on the intestinal wall. The
first-stage
larva emerges from eggs laid in the arteries, penetrates the intestinal
wall, and is then carried with the fecal matter to the exterior. In
order
to continue their development, the first-stage larvae have to be
ingested
by a slug. Vaginulus ameghini, in which they change successively into
second-
and third-stage larvae. When the infective third-stage larva is
ingested
by a rodent, it seeks the ileocecal region, where it penetrates the
intestinal
wall and locates in the lymphatic vessels (both inside and outside the
abdominal lymph nodes). In this location the larvae undergo two molts
before
migrating to their final habitat, the mesenteric arteries of the cecal
region. Oviposition begins after about 18 days. and the first-stage
larvae
appear in the feces 24 days after infection (prepatent period). In man,
an accidental host. the parasite can reach sexual maturity and produce
eggs, but the eggs usually degenerate, causing a granulomatous tissue
reaction.
The development cycle of A. cantonensis is similar to that of A.
costaricensis.
The intermediate hosts are various species of land snails, slugs, and
freshwater
snails. The definitive hosts can become infected by ingesting infected
snails, or plants and water contaminated by them with the third larvae.
In addition, infection can occur as a result of consuming transfer
hosts
(paratenic hosts), such as crustaceans, fish, amphibians, and reptiles,
which in turn have eaten infected mollusks (primary intermediate
hosts).
The definitive hosts of A. cantonensis are primarily various species of
the genus Rattus. When they enter a rat's body, the third-stage larvae
(which developed in a mollusk) penetrate the intestine and are carried
by the circulatory system to the brain, where they undergo two more
molts
and become young adult parasites. From the cerebral parenchyma they
migrate
to the surface of the brain. They remain for a time in the subarachnoid
space and later migrate to the pulmonary arteries, where they reach
sexual
maturity and begin oviposition. The eggs hatch in the pulmonary
arterioles,
releasing the first larva, which migrates up the trachea, is swallowed,
and is eliminated with the feces. Mollusks are infected by ingesting
fecal
matter of infected rodents. In man, who is an accidental host, the
larvae
and young adults of A. cantonensis generally die in the brain,
meninges,
or medulla oblongata. The nematode can occasionally be found in the
lungs.
GEOGRAPHIC
DISTRIBUTION
AND OCCURRENCE:
Abdominal
angiostrongyliasis, caused by A. costaricensis, is a parasitosis
described
a few years ago in Costa Rica; it is one of the most recently
recognized
zoonoses. Human disease has also been confirmed in Honduras, El
Salvador,
and Brazil. Suspected clinical cases have occurred in Nicaragua and
Venezuela.
In Panama, the adult parasite was found in five species of rodents
belonging
to three different families. In the past few years, the parasite has
been
found in several specimens of Sigmodon hispidus in Texas, USA. Ozyomys
caliginosus in Colombia; and slugs in Guayaquil, Ecuador. The
parasitosis
is probably much more widespread than is currently recognized. A.
costaricensis
has not been recorded outside the Americas. Human cases of parasitism
by
A. cantonensis have occurred in Thailand, Vietnam, Kampuchea, the
Philippines,
Indonesia, Taiwan, Japan, Australia, and several Pacific islands. The
parasite
is much more widely distributed, and its existence in rats has been
confirmed
in southern China, India, Malaysia, Sri Lanka, Madagascar, Mauritius,
and
Egypt. Until recently, the geographic distribution of A. cantonensis
was
thought to be limited to Asia, Australia, the Pacific islands, and
Africa.
However, in recent years its presence has been confirmed in Cuba, where
infected rats (Rattus norvegicus) and mollusks have been found;
likewise,
five human cases of meningoencephalitis have been attributed to A.
cantonensis
in that country. It is believed that the parasite was introduced to the
island some years ago by rats from a ship from Asia. In a study carried
out on rat species (R. norvegicus, R. rattus, and R. exulans) on the
Hawaiian
and Society Islands, the parasite was found in more than 40% of the
specimens
captured. In Egypt, 32.7% of 55 specimens of R. norvegicus harbored the
parasite. In the province of Havana, Cuba, 12 out of 30 captured R.
norvegicus
were infected. In view of the worldwide distribution of R. norvegicus
and
R. rattus, these rodents were examined for the parasite in Puerto Rico,
London, and New Orleans, but the results were negative. Eosinophilic
meningitis
associated with infection by A. cantonensis has been recorded in
several
hundred patients in endemic areas.
THE
DISEASE IN MAN:
The clinical
manifestations of abdominal angiostrongyliasis caused by A. cantonensis
are moderate but prolonged fever, abdominal pain on the right side.
and,
frequently, anorexia, diarrhea, and vomiting. Leukocytosis is
characteristic
(20,000 to 50,000 per mm3), with marked eosinophilia (11 to 82%).
Palpation
sometimes reveals tumoral masses or abscesses. Rectal examination is
painful,
and a tumor can occasionally be palpated. Lesions are located primarily
in the ileocecal region, the ascending colon. appendix, and regional
lymph
nodes, but they are also found in the small intestine. Granulomatous
inflammation
of the intestinal wall can cause partial or complete obstruction.
Appendicitis
was the preoperative.
DIAGNOSIS:
In 34
cases, all but two of the children survived and recovered. The highest
prevalence (53%) was found in children 6 to 13 years old, and twice as
many boys as girls were affected. Ectopic localizations may occur; when
the liver was affected in some Costa Rican patients, the syndrome
resembled
visceral larva migrans. Serologic studies carried out in Australia, in
human populations living in localities where the infection occurs in
rats
and those living in other places where it does not, indicate that many
human infections are asymptomatic.
THE
DISEASE IN ANIMALS:
In rodents,
A. costaricensis produces lesions that are located primarily in the
cecum,
as well as focal or diffuse edema of the subserosa, a reduction in
mesenteric
fat, and swelling of the regional lymph nodes. In highly parasitized
animals,
eggs and larvae may be found in various viscera of the body. No
significant
difference in weight between parasitized and nonparasitized animals has
been confirmed. Rats infected by A. cantonensis may show consolidation
and fibrosis in the lungs. However, the physical appearance of the
animals
does not reflect the degree of pathologic changes. For both parasites,
the prevalence of the infection is greater in adult than in young
rodents.
SOURCE
OF INFECTION
AND MODE OF TRANSMISSION:
Several
species of rodents are known to serve as definitive hosts of A.
costaricensis:
Sigmodon hispidus, Rattus rattus, Zygodontomys microtinus, Liomys
adspersus,
0ryzomys fulvescens, and 0. caliginosus; also, natural infection has
been
found in a coati (Nasua narica) and marmosets (Saguinus mystax). In a
study
carried out in Panama, the highest prevalence of the infection was
found
in the cotton rat S. hispidus, which was also the most abundant rodent
in the six localities studied. The cotton rat inhabits areas close to
dwellings
in both tropical and temperate America. it is omnivorous, feeding on
both
plants and small vertebrate and invertebrate animals, including slugs
(V.
ameghini). All these facts indicate that the cotton rat is a prime
reservoir
and that it plays an important role in the epidemiology of the
parasitosis.
Rodents are infected by ingesting infected mollusks. Another probable
source
of infection is plants contaminated with mollusk secretions "slime")
containing
third-stage infective larvae of the parasite. The manner in which man
contracts
the infection is not well known. Infection probably occurs by ingestion
of poorly washed vegetables containing small slugs or their secretions.
It is believed that children can become infected while playing in areas
where slugs are abundant by transferring snail secretions found on
vegetation
to their mouths. An increase in cases in children occurs in Costa Rica
during the rainy season, when slugs are most plentiful. Humidity is an
important factor in the survival of both the first- and third-stage
larvae
in the environment, since they are susceptible to desiccation. The
parasite
species in the Far East (A. cantonensis) has been found in at least ten
different species of the genus Rattus and in Bandicota indica and
Melomys
littoralis. These rodents, natural definitive hosts, are infected by
consuming
mollusks or paratenic hosts that harbor third-stage larvae. The
infection
rate of the mollusks is usually high; both the prevalence and the
number
of larvae an individual mollusk can harbor vary according to the
species.
Man, who is an accidental host, is infected by consuming raw mollusks
and
also paratenic hosts such as crustaceans or fish. The ecology of
angiostrongyliasis
is closely related to the plant community, since it ultimately supports
the appropriate mollusks and rodents. The frequency of the human
parasitosis
depends on the abundance of these hosts and the degree to which they
are
infected, and, also, in the case of A. cantonensis, on eating habits
(consumption
of raw mollusks, crustaceans, and fish).
DIAGNOSIS:
The spinal
fluid characteristically shows elevated protein and an eosinophilic
pleocytosis.
Occasionally, the parasite can be recovered from spinal fluid.
Peripheral
eosinophilia with a low-grade leukocytosis is common. A serologic test
is available from the Centers for Disease Control and Prevention; its
sensitivity
and specificity are not established. CT and MRI may show a central
nervous
system lesion.
TREATMENT:
No specific
treatment is available; however, levamisole, albendazole, thiabendazole
(25 mg/kg three times daily for 3 days), or ivermectin can be tried.
Symptomatic
treatment with analgesics or corticosteroids may be necessary. The
illness
usually persists for weeks to months, the parasite dies, and the
patient
then recovers spontaneously, usually without sequelae. However,
fatalities
have been recorded.
CONTROL:
At least
theoretically, angiostrongyliasis could be controlled by reducing
rodent
and mollusk populations. Preventive measures at the individual level
consist
of washing vegetables thoroughly, washing hands after garden or field
work,
not eating raw or undercooked mollusks and crustaceans, and not
drinking
water that may be unhygienic.
ANCYLOSTOMIASIS
Centers
for Disease Control and Prevention: National Center for Infectious
Diseases
Ancylostoma
infection
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(Uncinariasis,
Necatoriasis, Hookworm Disease)
AGENT:
The causative
agents are mainly Necator americanus and Ancylostoma duodenale;
occasionally
A. ceylanicum and A. caninum.
RESERVOIR
AND INCIDENCE
A common
worm infection of humans and domestic dogs and cats in various tropical
and subtropical countries where disposal of human feces is inadequate.
The reservoirs are humans, dogs, and cats.
TRANSMISSION:
Adult
worms, living in the small intestines of humans, produce eggs which
pass
on to the ground in feces. The eggs hatch and go through three larval
stages.
Human infection results from the third-stage larvae which survive in
soil
for several weeks in moist and warm conditions. Animals and man become
infected by contact with infected soil, the larvae penetrating through
skin or mucosa of the digestive tract. The parasites then migrate
through
the blood capillaries to the lung, eventually to be coughed up and
swallowed.
They reach maturity and complete their cycle in the intestines.
DISEASE
IN ANIMALS:
Factors
such as the weight of infection and nutritional state of the animal are
important. Loss of blood together with malnutrition produce anemia.
Severe
enteritis causes hemorrhagic diarrhea and weight loss from intestinal
malabsorption.
Prenatal infection of the dog causes death of the fetal pups. Mild
infections
generally cause no clinical signs.
DISEASE
IN MAN:
The condition
is often asymptomatic. Self-limiting vesicular/pustular skin eruptions
may appear at the site of larval entry. A. caninum does not penetrate
human
skin beyond the epidermis. With other species chronic symptoms due to
iron
deficiency anemia may occur. Rarely there is tracheitis and coughing
due
to lung infiltration with parasites.
DIAGNOSIS:
Fecal
flotation
TREATMENT:
Pyrantel
pamoate, mebendazole, albendazole, levamisole, or
tetrachloroethylene.
PREVENTION/CONTROL:
Educate
the public to the dangers of soil contamination by feces. Wear shoes!
Screen
feces from persons and animals from endemic areas. Keep kennel floors
dry
and avoid feeding animals on the ground.
CAPILLARIASIS
Centers
for Disease Control and Prevention: Division of Parasitic Diseases
capillariasis
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
AGENT:
The causative
agents are Capillaria hepatica (hepatic form), C. philippinensis
(intestinal
form) and C. aerophila (respiratory form).
RESERVOIR
AND INCIDENCE
C. hepatica
and C. aerophila are very rare infections with isolated cases reported
from North, Central and South America, Asia, and Europe. C.
philippinensis
is endemic in certain areas of the Philippines and cases have been
reported
from Thailand and Japan. Humans are the reservoir for C.
philippinensis.
With C. hepatica, rodents are the reservoirs. Cats and dogs are the
reservoir
for C. aerophila. Peromyscus maniculatus and Cletheronomys gapperi are
the major hosts in North America.
TRANSMISSION:
Humans
are infected by eating raw fish containing infective larvae. The worm
parasite
lives in the intestines of humans and autoinfection occurs. Human feces
contain large numbers of ova which contaminate watercourses and infect
freshwater fish. Humans may be infected by the ingestion of ova in the
soil also.
DISEASE
IN ANIMALS:
Infection
with C. aerophila causes coughing, sneezing, and nasal discharge in
dogs,
cats, and foxes. Worms of C. hepatica mature and deposit eggs in liver
tissue causing a local chronic inflammatory response in mice and
rats.
DISEASE
IN MAN:
C. hepatica:
acute and subacute hepatitis. The liver lesions consist of enlargements
with foci of granulation tissue containing worms and ova. C.
philippinensis:
progressive weight and protein loss due to diarrhea and malabsorption.
The jejunal villi are obliterated with massive accumulations of worms
and
ova. C. aerophila: fever and coughing. Worms present in epithelial
lining
of respiratory tract causing pneumonitis.
DIAGNOSIS:
Liver
or intestinal biopsy, necropsy, clinical signs & symptoms. Fecal
exam
for ova, larva, or adults.
TREATMENT:
Albendazole,
Thiabendazole, Mebendazole.
PREVENTION/CONTROL:
Do not
eat uncooked fish and other aquatic animal life in endemic areas.
Control
rodents and improve hygiene. Prevent pica. Sanitary disposal of
feces.
FILARIASIS
Centers
for Disease Control and Prevention: National Center for Infectious
Diseases
filariasis
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(Brugiasis)
AGENT:
The commonest
causative agent is Wuchereria bancrofti, which is not zoonotic. Brugia
malayi is zoonotic. Dirofilaria immitis may occasionally infect
humans.
RESERVOIR
AND INCIDENCE
B. malayi
has been identified in Malaya and the Philippines. D. immitis occurs in
dogs in North and South America, Australia, India, the Far East and
Europe.
Wild monkeys and felines are the reservoir for B. malayi.
TRANSMISSION:
Transmission
to humans is via the bite of a mosquito vector (Mansonia and
Anopheles).
These, on biting humans, release microfilariae on to skin which enter
the
body through the puncture wound and pass via the lymphatics to lymph
nodes.
The worms are viviparous, producing microfilaria. These appear in the
blood
and reinfect the biting insect.
DISEASE
IN ANIMALS:
D. immitis
is found in the right ventricle of dogs and in the pulmonary artery.
Mild
infection causes no signs, but long continued infection leads to
cardiac
insufficiency with ascites and passive congestion.
DISEASE
IN MAN:
B. malayi:
Repeated bouts of fever, lymphadenopathy, lymphangitis and abscesses
occur.
This leads to lymphatic obstruction and massive lymphedema followed by
fibrosis (so-called elephantiasis) especially in the legs. D. immitis:
Initial symptoms include cough, chest pain, or hemoptysis. However, the
filariae die in the human pulmonary vasculature and consequently
nodules
have been found in the skin or as solitary 1-2 cm "coin" lesions in the
periphery of the lungs.
DIAGNOSIS:
Diagnosis
is established by finding microfilariae in the blood. Serologic testing
is available but false-positive and false-negative reactions
occur.
TREATMENT:
Diethylcarbamazine.
PREVENTION/CONTROL:
Diethylcarbamazine
or Ivermectin can be given as a prophylaxis. Control vectors and avoid
their bites. Prophylactic treatment of dogs.
VISCERAL
LARVAL MIGRANS
Centers
for Disease Control and Prevention: National Center for Infectious
Diseases
toxocariasis
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(Toxocariasis)
AGENT:
Most cases
of visceral larval migrans (VLM) are due to Toxocara canis, an ascarid
of dogs and other canids, but in a few cases Toxocara cati in domestic
cats has been implicated and rarely Baylisascaris procyonis of
raccoons.
RESERVOIR
AND INCIDENCE
The reservoir
mechanism for T. canis is latent infections in female dogs which are
reactivated
during pregnancy. Transmission from mother to puppies is via the
placenta
and milk. The life cycle of T. cati is similar, but transplacental
transmission
does not occur. Human infections are sporadic and occur worldwide.
TRANSMISSION:
Infection
is generally in dirt-eating young children who ingest T. canis or T.
cati
eggs from soil or sand contaminated with animal feces, most often from
puppies. Direct contact with infected animals does not produce
infection,
as the eggs require a 3 to 4 week extrinsic incubation period to become
infective; thereafter, eggs in soil remain infective for months to
years.
In humans, hatched larvae are unable to mature and continue to migrate
through the tissues for up to 6 months. Eventually they lodge in
various
organs, particularly the lungs and liver and less often the brain,
eyes,
and other tissues, where they produce eosinophilic granulomas up to 1
cm
in diameter.
DISEASE
IN ANIMALS:
The first
indication of infection in young animals is lack of growth and loss of
condition. Infected animals have a dull coat and often are
"potbellied".
Worms may be vomited and are often voided in the feces. In the early
stages,
pulmonary damage due to migrating larvae may occur; this may be
complicated
by bacterial pneumonitis, so that respiratory distress of variable
severity
may supervene. Diarrhea with mucus may be evident. In severe infections
of puppies, verminous pneumonia, ascites, fatty degeneration of the
liver,
and mucoid enteritis are common. Cortical kidney granulomas containing
larvae are frequent in young dogs.
DISEASE
IN MAN:
Migrating
larvae induce fever, cough, wheezing; hepatomegaly, and sometimes
splenomegaly
and lymphadenopathy are present. The acute phase may last 2-3 weeks,
but
resolution of all physical and laboratory findings may take up to 18
months.
Leukocytosis is marked due to eosinophils. Hyperglobulinemia occurs
when
the liver is extensively invaded. Ocular toxocariasis results in a
eosinophilic
granuloma of the retina that may be mistaken for retinoblastoma.
DIAGNOSIS:
ELISA,
no parasitic forms can be found by fecal exam.
TREATMENT:
Thiabendazole,
Mebendazole, or Ivermectin. Corticosteroids, antibiotics,
antihistamines,
and analgesics are given for symptomatic relief. Treatment for Ocular
Toxocariasis
includes the above plus vitrectomy and laser photocoagulation.
PREVENTION/CONTROL:
Disease
in humans is best prevented by periodic treatment of puppies, kittens,
and nursing dogs and cats. Children should be supervised to prevent
pica;
their hands should be washed after playing in soil and sand; and play
areas
should be protected from animal feces.
CUTANEOUS
LARVAL MIGRANS
Centers
for Disease Control and Prevention: National Center for Infectious
Diseases
cutaneous
larva migrans
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(Creeping
Eruption)
AGENT:
Caused
by the larvae of the dog and cat hookworms, Ancylostoma braziliense and
Ancylostoma caninum. A number of other animal hookworms,
gnathostomiasis,
and strongyloidiasis are rarely also causative agents.
RESERVOIR
AND INCIDENCE
Cutaneous
Larval Migrans is prevalent throughout the tropic and subtropics. Human
infection is common in SE U.S., particularly where people come in
contact
with moist sandy soil (e.g., beaches, children's sand piles)
contaminated
by dog or cat feces.
TRANSMISSION:
direct
skin contact with larvae. soil to skin contact. contamination with
animal
feces.
DISEASE
IN ANIMALS:
Same as
Ancylostomiasis.
DISEASE
IN MAN:
At the
site of larval entry, particularly on the hands or feet, up to several
hundred minute, intensely pruritic erythematous papules appear. Two to
3 days later, serpiginous eruptions appear as the larvae migrate at a
rate
of several millimeters a day; the parasite lies slightly ahead of the
advancing
border. The process continues for weeks or up to a year, and the
lesions
may remain severely pruritic, vesiculate, and become encrusted and
secondarily
infected. Without treatment, the larvae eventually die and are
absorbed.
DIAGNOSIS:
Presumptive
- Characteristic clinical manifestations. Etiologic - ID of agent by
biopsy
in skin section but this is usually very difficult to achieve. Most
cases
are really not confirmed. No valid serodiagnostic tests currently
available.
TREATMENT:
Simple
transient cases require no treatment. Albendazole or thiabendazole.
Antihistamines
and antibiotic ointments.
PREVENTION/CONTROL:
Minimize
contact (e.g., wear shoes!). Decontaminate environment: 10 lbs/ 100 sq
ft. sodium borate - gravel/clay dog run; 1% sodium hypochlorite
solution
- cement dog run. Prevent environmental contamination. Public health
education.
OESOPHAGOSTOMIASIS
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(Nodular
Intestinal Worm Infection)
AGENT:
The causative
agents are Oesophagostomum stephanostomum, bifurcum, and
aculeatum.
RESERVOIR
AND INCIDENCE
The parasite
lives in the intestines of various primates and sometimes humans. These
definitive hosts can sometimes serve as intermediate hosts. It occurs
mainly
in Africa, but occasionally in South America and Asia.
TRANSMISSION:
Eggs passed
in feces release larvae which infect the definitive host on ingestion.
The parasite invades the intestinal wall to form nodules. The fourth
stage
larvae which develop in these nodules migrate to the lumen of the large
intestine to form the adult worm and complete the life cycle.
DISEASE
IN ANIMALS:
Mild infection
is subclinical. Abdominal pain follows more severe infection with
diarrhea
or even dysentery. Death in the NHP may ensue from perforation of the
intestine
and peritonitis.
DISEASE
IN HUMANS:
Mild infection
goes unnoticed but sometimes abdominal pain, and GI bleeding and even
peritonitis
occur. Granulomatous nodules in the intestinal wall contain larvae and
parasites. These may be secondarily infected and lead to
abscesses.
DIAGNOSIS:
Fecal
flotation. Culture to obtain larvae for species ID.
TREATMENT:
Anthelmintic
therapy.
PREVENTION/CONTROL:
Fecal
screening of NHP's Wearing of protective clothing and gloves. Ensure
good
personal hygiene. Sanitary disposal of feces is important.
STRONGYLOIDIASIS
Centers
for Disease Control and Prevention: Division of Parasitic Diseases
strongyloidiasis
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
AGENT:
Strongyloidiasis
is caused by infection with Strongyloides stercoralis.
RESERVOIR
AND INCIDENCE
The condition
is an infection of humans, but dogs, cats, and primates have been found
naturally infected. The disease is endemic in tropical and subtropical
regions; although the prevalence is generally low, in some areas
disease
rates exceed 25%. In the USA, the disease is endemic in southern wet
areas.
TRANSMISSION:
The parasite
is uniquely capable of maintaining its life cycle both within the human
host and in soil. Infection occurs when filariform larvae in soil
penetrate
the skin, enter the bloodstream, and are carried to the lungs, where
they
escape from capillaries into alveoli and ascend the bronchial tree to
the
glottis. The larvae are then swallowed and carried to the duodenum and
upper jejunum, where maturation to the adult stage takes place. The
parasitic
female, generally held to be parthenogenetic, matures and lives
embedded
in the mucosa, where its eggs are laid and hatch. Rhabditiform larvae,
which are noninfective, emerge, and most migrate into the intestinal
lumen
to leave the host via the feces. The life span of the adult worm may be
as long as 5 years. In the soil, the rhabditiform larva metamorphose
into
the infective (filariform) larvae. However, the parasite also has a
free-living
cycle in soil, in which some rhabditiform larvae develop into adults
that
produce eggs from which rhabditiform larvae emerge to continue the life
cycle. Internal autoinfection takes place in the lower bowel when some
rhabditiform larvae, instead of passing with the feces, develop into
filariform
larvae that penetrate the intestinal mucosa, enter the intestinal
lymphatic
and portal circulation, are carried to the lungs, and return to the
small
bowel to complete the cycle.
DISEASE
IN ANIMALS:
Young
dogs and cats have thin skins which allow massive infection to
penetrate,
giving severe dermatitis, inappetence, coughing and even
bronchopneumonia.
Vomiting occurs, as does severe dermatitis during the period of larval
penetration.
DISEASE
IN MAN:
Pruritic
dermatitis is seen at sites of larval penetration. Diarrhea, epigastric
pain, nausea, malaise, weight loss, coughing, rales, transient
pulmonary
infiltrates are also seen. In the hyperinfection syndrome,
autoinfection
is greatly increased, resulting in a marked increase in the intestinal
worm burden and in massive dissemination of filariform larvae to the
lungs
and most other tissues, where they can cause local inflammatory
reactions
and granuloma formation. Severe diarrhea, bronchopneumonia, and ileus
can
result.
DIAGNOSIS:
Diagnosis
requires finding the larval stages in feces or duodenal fluid. ELISA
and
IFA serologic tests are being developed.
TREATMENT:
Thiabendazole,
albendazole, mebendazole, cambendazole, ivermectin, or levamisole.
PREVENTION/CONTROL:
Rigid
attention to hygienic habits, including use of footwear in endemic
areas.
Sanitary disposal of feces. Fecal exams of monkeys, dogs, and cats in
quarantine.
TRICHOSTRONGYLOSIS
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(Trichostrongyliasis,
Trichostrongylosis)
AGENT:
Several
species of Trichostrongylus including Trichostrongylus axei, T.
affinis,
T. colubriformis, and many others. RESERVOIRS AND INCIDENCE: The
reservoirs
of most of the species of Trichostrongylus are domestic and wild
herbivores.
Trichostrongylids are very common parasites in domestic ruminants and
their
distribution is worldwide.
TRANSMISSION:
The sources
of infection are soil and vegetation, in which the eggs deposited with
the animal host's feces develop in a few days to the infective larval
stage.
Man and animals are infected orally. Man acquires the infection mainly
by consuming raw vegetables contaminated with the infective larvae.
Another
important factor in transmission is the preparation and use of animal
manure
as fuel.
DISEASE
IN ANIMALS:
In horses,
these worms produce a chronic catarrhal gastritis and may result in
weight
loss. The lesions comprise nodular areas of thickened mucosa surrounded
by a zone of congestion and covered with a variable amount of mucus.
The
lesions may be rather small and irregularly circumscribed, or may
coalesce
and involve most or all of the glandular portion of the stomach, and
erosions
and ulcerations may be seen. In ruminants, gastritis with superficial
erosion
of the mucosa, hyperemia, and diarrhea may result. Protein loss from
the
damaged mucosa and anorexia cause hypoproteinemia and weight loss.
DISEASE
IN MAN:
Most cases
asymptomatic. Severe infections - diarrhea, blood in stool, abdominal
cramps,
and emaciation.
DIAGNOSIS:
:Flotation
and fecal culture (identification of larvae used to distinguish between
species).
TREATMENT:
Pyrantel
pamoate, mebendazole, or levamisole.
PREVENTION/CONTROL:
Regular
deworming of animals. Preventive measures for humans consist of
improved
food, environmental, and personal hygiene. In endemic areas, raw
vegetables
or other foods should not be eaten. Pasture management is important.
Most
of the larvae die in a field left ungrazed for a month.
ASCARIASIS
Centers
for Disease Control and Prevention: Division of Parasitic Diseases
ascariasis
Disease
Overview:
Institutional
Animal Care and Use Committee, University of California, Santa
Barbara.
(Roundworm
infection, ascaridiasis) A common, but usually mild, roundworm
infection
of both humans and animals, occurring worldwide. There is doubt whether
the worms cross between species. The causative agent in humans is
usually
Ascaris lumbricoides. Ascaris suum in pigs is considered occasionally a
zoonotic infection (Nematoda). There is no vaccine.
RESERVOIR
AND MODE OF
TRANSMISSION:
A. lumbricoides
has its reservoir in humans and in contaminated soil. A. suum occurs in
pigs. Eggs are passed in feces and become infective after two weeks.
Infection
is by the ingestion of eggs in soil or undercooked food. Eggs hatch in
the gut, penetrate its wall and reach the lungs via the bloodstream.
Larvae
develop in the lungs, ascend the trachea and are swallowed and mature
in
the gut. Egg-laying begins 45-60 days after initial infection.
INCUBATION
PERIOD:
Humans.
About two months. Animals. Development of A. suum in the pig is said to
be quicker than in the human.
CLINICAL
FEATURES:
Humans.
The condition is usually asymptomatic but there may be fever with
asthma,
spasmodic coughing and possibly pneumonitis. Abdominal pain, and even
bowel
or bile duct obstruction, is possible. Occasionally migrating larvae
cause
symptoms referable to the brain, eyes, kidneys and liver. Animals.
Migrating
larvae cause irregular breathing and coughing. Heavy infection gives
abdominal
pain with diarrhoea. Suckling pigs are most affected.
PATHOLOGY:
Humans.
Eosinophilia and pulmonary eosinophilic infiltration occur. Liver
abscesses
and cholangitis are sometimes seen. Animals. Larvae migrating through
the
lung cause pneumonia. Worms in the intestine give enteritis.
DIAGNOSIS:
Humans.
Identify eggs or adult worms in feces. Larvae in sputum or gastric
washings
are diagnostic. Animals. Examine feces for eggs, or monitor worms
passed
rectally or via mouth and nose. An egg count of more than 1OOO/g of
feces
indicates clinical disease.
PROGNOSIS:
: Humans.
The condition is rarely fatal. Aberrant larvae in brain, eyes and
kidney
can give severe symptoms. Animals.Rarely fatal.
PREVENTION:
Humans.
Sanitary disposal of feces coupled with good personal and food hygiene
are essential. Animals. Worm and wash sows before farrowing. Rear pigs
on concrete or avoid close confinement on soil.
TREATMENT:
Humans
and animals. Pyrantel pamoate is the treatment of choice. Stools should
be rechecked at 2 weeks and patients retreated until all ascarids are
removed.
LEGISLATION:
Humans
and animals. None.
. |
