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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
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.
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