Visceral larval migrans can occur in humans
following infection by Toxocara canis, Toxocara cati, or Baylisascaris
procyonis eggs. Following ingestion of infectious eggs, larvae penetrate
the intestinal wall and migrate through the tissues leading to eosinophilic
granulomatous reactions involving the skin, lungs, central nervous system,
and eyes. Ocular larva migrans most commonly involves the retina and can
cause reduced vision, strabismus, uveitis and endophthalmitis. Adult T.
cati have been detected in some infected children. Cutaneous larval migrans
can be induced with infection by three species of hookworms infecting dogs
and cats in the United States:
Ancylostoma caninum, Ancylostoma braziliense,
and Uncinaria stenocephala. Larvae are released from eggs passed into the
environment in feces; infectious larvae infect humans by skin penetration.
Larval migration results in the development of an erythematous, pruritic
cutaneous tunnel. Occasionally, larvae will reach the lungs and cornea.
Ancylostoma caninum has been linked with eosinophilic enteritis in humans.
Prevention revolves around control of animal
excrement in human environments. Since hookworm and roundworm infections
are sometimes occult, anthelmintics such as pyrantel pamoate should be
routinely administered to all puppies and kittens at least twice, 14 to
21 days apart. In high-risk puppies, pyrantel could be given every two
weeks from two to eight weeks of age. In high-risk kittens, pyrantel could
be given at 6, 8, and 10 weeks of age. Fecal flotation should be performed
as well to assess for other parasites. Fecal flotation should be performed
once or twice yearly on all dogs and cats, particularly if they go outdoors,
and even if they are on heartworm preventatives.
Dipylidium caninum, Echinococcus granulosa, and Echinococcus multilocularis are cestodes that can infect humans. Transmission to humans occurs following ingestion of the intermediate host (flea, Dipylidium) or by the ingestion of eggs (Echinococcus). Dogs and cats can be the definitive hosts of Echinococcus spp. Dipylidium infection is most common in children and can lead to diarrhea and pruritis ani. Following human ingestion of eggs, Echinococcus enters the portal circulation and spreads throughout the liver and other tissues. Prevention and/or control is primarily by use of taeniacides and sanitation procedures. Praziquantel has been shown to be effective for the treatment of echinococcosis in pets.
The enteric protozoans infecting dogs and cats that can be zoonotic include Entamoeba histolytica, Balantidium coli (dogs), Cryptosporidium parvum, C. felis, Giardia spp., and Pentatrichomonas hominus. Cysts do not form following infection of cats by Entamoeba or Pentatrichomonas and so these parasites are unlikely to lead to infection of humans following exposure to cats; both genera are rare in dogs as well. Metronidazole may be effective for the treatment of E. histolytica, B. coli (dogs), Giardia spp., and P. hominusin some animals. Some trichomonads are resistant to metronidazole but respond clinically to paromomycin (see cryptosporidiosis).
Giardia is a flagellate with worldwide distribution
that causes significant gastrointestinal disease in dogs, cats, and people.
The organism is felt to have a wide host range; mammalian isolates are
all currently classified as G. lamblia. Using DNA sequences from a number
of different genes, there appears to be two or three genotypes of Giardia
in people as well as two distinct genetic groups isolated exclusively from
dogs. However, whether these genotypes vary in biologic activity including
zoonotic potential is for the most part unknown. There have been varying
results concerning cross-infection potential of Giardia spp. isolates.
In one study, Giardia spp. from humans was inoculated into cats; the cats
were relatively resistant to infection. In contrast, evaluation of human
and feline Giardia spp. isolates by isoenzyme electrophoresis suggests
that cats couldserve as a reservoir for
human infections. Since it is impossible to determine zoonotic strains
of Giardia spp. by microscopic examination, it seems prudent to assume
feces from all dogs and cats infected with Giardia spp. to be a potential
human health risk.
Giardia is a common enteric pathogen in dog
and cat studies and can be detected in feces of animals with and without
diarrhea. These findings emphasize that fecal examination should be performed
on all dogs and cats, at least yearly, and treatment with anti-Giardia
drugs like praziquantel-pyrantel-febantel, fenbendazole, or metronidazole
should be administered if indicated. Albendazole is also effective for
the treatment ofgiardiasis but has been
associated with neutropenia. Vaccination against Giardia could be considered
in animals with recurrent infection; this practice is being evaluated as
a therapeutic.
Infection of people with the coccidian parasite Cryptosporidium parvum results in severe gastrointestinal tract disease; infection of immunosuppressed individuals may be life threatening. Infection is common in humans; approximately 300,000 people in Milwaukee developed cryptosporidiosis when a water purification system malfunctioned, approximately 10–20% of AIDS patients are infected with C. parvum at some timeduring their life, and the organism commonly causes diarrhea outbreaks in daycare centers. Many infected individuals require hospitalization for administration of intravenous fluid therapy; people with AIDS may never be cured. Cryptosporidiosis has been documented in people as well as cats or dogs in the same environment suggesting the potential for zoonotic transfer exists. Cryptosporidium parvum oocysts have been documented in feces of many domestic dogs and cats in the United States, Japan, Scotland, Australia, and Spain.
Presence of serum antibodies can be used to estimate numbers of individuals exposed to C. parvum. An enzyme-linked immunosorbent assay for detection of C. parvum IgG was developed and applied to serum of cats. Using this assay, the seroprevalences of C. parvum antibodies in serum of cats in Colorado and the United States are 15.3% and 8.3%, respectively. Oocysts or antigens of C. parvum were detected in feces of 5.4% of cats tested and 6.0% of dogs tested in north-central Colorado. These results suggest that C. parvum infection is common in dogs and cats. It is usually undetermined where people acquire C. parvum infection; contaminated water is the most likely source, but contact with infected dogs or cats is also possible. There have been limited cross-infection studies performed with C. parvum isolates from cats or dogs. In one study, a feline isolate failed to cross infect mice, rats, guinea pigs, or dogs. In another study, a C. parvum isolate from a cat cross-infected lambs. An alternative to cross-infection studies is comparison of isolates genetically. Canine and feline genotypes that vary considerably from human and cattle genotypes have been identified. The feline and canine genotypes were documented in an infected human and the feline genotype was documented in an infected cow suggesting the genotypes can infect other mammals.
As for Giardia, it is impossible to determine zoonotic strains of C. parvum by microscopic examination thus, it seems prudent to assume feces from all dogs and cats infected with C. parvum to be a potential human health risk. Techniques for the detection of C. parvum should be included in the diagnostic evaluation of dogs and cats with diarrhea and all dogs or cats in the homes of immunosuppressed individuals. Infected cats anddogs generally do not shed large numbers of Cryptosporidium oocysts and so acid-fast staining, immunofluorescent antibody staining of feces, or fecal antigen ELISA will aid in the identification of the extremely small oocysts (5 microns).
Paromomycin (Parke-Davis, Morris Plains, NJ) administered at 165 mg/kg q12h PO, for five days is the drug of choice for cryptosporidiosis and is an alternate drug for Pentatrichomonas and Giardia, but has been associated with acute renal failure and deafness in some cats with hemorrhagic diarrhea. Sequential administration of clindamycin (Antirobe, Upjohn Co.) followed by tylosin blocked oocyst shedding andresolved diarrhea in one cat with chronic, clinical cryptosporidiosis. Prevention of these parasites revolves around controlling exposure.
Toxoplasma gondii is one of the most common small animal zoonoses; approximately 30–40% of adult humans in the world are seropositive, suggesting previous or current infection by T. gondii. People are most commonly infected by T. gondii after ingestion of sporulated oocysts or ingestion of tissue cysts. Thus, prevention of toxoplasmosis in people can be achieved by avoiding those two life stages.
Fortunately, clinical disease is generally mild following primary infection of immunocompetent people. Self-limiting fever, malaise, and lymphadenopathy are the most common clinical abnormalities and the majority never realizes when their first T. gondii infection occurred. The disease is potentially confused with infectious mononucleosis. Clinical disease can be much more severe in immunosuppressed individuals. At particular risk: the fetus, people with AIDS, and people treated with immunosuppressive agents for the treatment of cancer and to prevent organ transplant rejection. Toxoplasma gondii is a common opportunistic CNS infection of people with AIDS; as T-helper cells counts decline, toxoplasmic encephalitis from activation of bradyzoites in tissue cysts can result. If a mother has her first T. gondii infection during gestation, stillbirth, CNS disease, and ocular disease are common clinical manifestations in the fetus. The importance of T. gondii as a zoonotic disease should not be underestimated. Cat owners with potentially immunosuppressive diseases are commonly counseled by human health care providers to adopt or euthanatize their pet cats due to risk of acquiring toxoplasmosis. However, it is very difficult to acquire toxoplasmosis from an individual cat; most people are infected by ingesting sporulated oocysts from theenvironment or by ingesting tissue cysts in undercooked meat.
Once passed into the environment, sporulated oocysts survive for months to years and so it is likely that many people acquire toxoplasmosis when working with soil or drinking contaminated water. Clinical toxoplasmosis developed in a group of people following a common exposure in a riding stable and in a group of soldiers drinking contaminated water in Panama. All water collected from the environment should be boiled or filtered prior to drinking. Care should be taken to wash hands carefully after working with soil;alternately gloves should be worn. Produce from the garden should be washed carefully prior to ingestion. The children’s sandbox should be covered when not in use. If cats are owned, a litter box liner should be used and the litter box should be cleaned daily; oocysts require 1–5 days to sporulate. Immunosuppressed or pregnant cat owners should not clean the litter box. Sporulated oocysts are extremely resistant to most disinfectants; it requires exposure to 10% ammonia for 10 minutes to inactivate this stage of the parasite. Thus, cleaning with scalding water or steam is most practical.
Veterinarians are commonly consulted concerning
the risk of individual cats for the zoonotic transfer of T. gondii. While
it cannot be stated definitively that a person will not acquire toxoplasmosis
from their personal cat, it is probably unlikely. It is true that cats
are the only definitive host for toxoplasmosis but oocysts are only shed
for days to several weeks following primary inoculation. Thus, an individual
cat will be passingoocysts into the human
environment for only a small fraction of its entire life span.Following
primary inoculation of cats, it is difficult to induce repeat oocyst shedding.
Prednisolone administered at 10–80 mg/kg
PO or methylprednisolone administered at 10-80 mg/kg IM will induce repeat
oocyst shedding in some cats with toxoplasmosis. However, these doses are
not routinely used in clinical practice. Administration of methyprednisolone
acetate administered at 5 mg/kg, weekly for four to six weeks to cats infected
with T. gondii for 14 weeks or 14 months failed to induce oocyst shedding.
Cats infected with T. gondii were given FIV
followed by FeLV and shown to develop immunodeficiency associated syndromes
(unpublished data), however, repeat T. gondii oocysts shedding could not
be demonstrated. Cats with FIV or FeLV infections have been inoculated
with T. gondii; oocyst shedding periods and number of oocysts shed were
similar to those for cats without FIV or FeLV infections. It has been shown
that gut immunity to T. gondii in cats is not permanent; four of nine cats
inoculated six years after primary inoculation shed oocysts even though
each had high serum antibody titers.
However, T. gondii infected cats with and
without FIV infection failed to repeat oocyst shedding when reinfected
with T. gondii 16 months after primary inoculation. Thus, cats that are
exposed to T. gondii frequently probably do not shed large numbers of oocysts
after the first infection.
Toxoplasma gondii oocysts are not infectious
when passed by cats; sporulation requires one to five days in the environment.
Most cats are fastidious and do not leave faeces on their fur for this
period. Bioassay failed to detect oocysts on the fur of cats seven days
after they were shedding millions of oocysts in feces. These findings suggest
that touching individual cats is an unlikely way to acquire toxoplasmosis;
this hypothesis issupported by epidemiologic
studies as well. In general, veterinary health care providers are no more
likely than the general population to be seropositive for T. gondii infection.
Since oocysts are passed unsporulated and
non-infectious, working with fresh feline feces (< 1 day old) is not
a risk for veterinary health care personnel. People with HIV infection
that owned cats were not more likely to acquire toxoplasmosis during their
illness than people with HIV infection that did not have cat contact.
Oocysts measuring 10 X 12 µ in a cat fecal sample could be T. gondii. Hammondia hammondi and Besnoitia darlingi are morphologically similar coccidians passed by cats but are not human pathogens. The faeces should be collected daily until the oocyst-shedding period is complete; administration of clindamycin (25-50 mg/kg q24h PO), sulfonamides (100 mg/kg q24h PO), or pyrimethamine (2.0 mg/kg q24h PO) can reduce levels of oocyst shedding.
There is no serologic assay that accurately predicts when a cat shed T. gondii oocysts in the past and most cats that are shedding oocysts are seronegative. Most seropositive cats have completed the oocyst-shedding period and are unlikely to repeat shedding; most seronegative cats would shed the organism if infected. But since humans are not probably not commonly infected with T. gondii from contact with individual cats andsince serologic test results cannot accurately predict the oocyst shedding status of seropositive cats, testing healthy cats for toxoplasmosis is of little clinical use. Fæcal examination is an adequate procedure to determine when cats are actively shedding oocysts but cannot predict when a cat has shed oocysts in the past. If an owner is concerned that they may have toxoplasmosis, they should see their doctor for testing.
Ingestion of T. gondii in tissues can result
in human toxoplasmosis. Meats (particularly pork in the United States)
should be cooked to medium-well to inactivate tissue cysts.
Gloves should be worn when handling raw meats
(including field dressing) for cooking, or hands should be cleansed thoroughly
afterwards. Freezing meat at -12° C for several days will kill most
tissue cysts. Ingestion of raw goat’s milk can also result in human toxoplasmosis.
Salmonella spp., Campylobacter jejuni, E. coli, and Yersinia enterocolitica each infect dogs and cats and can cause disease in humans. Gastroenteritis can occur in both species following infection by these agents; Yersinia enterocolitica is probably a commensal agent in animals but induces fever, abdominal pain, and bacteremia following infection of humans. Dogs are occasionally subclinically infected by Shigella. Helicobacter pylori causes ulcers in people and has been isolated from a colony of cats; the zoonotic risks are currently undetermined. Infected pets and people in the same family have been found to be infected with Helicobacter spp. However, it is possible the human led to the infection of the animal. Salmonella infection in cats and dogs is often subclinical. Approximately 50% of clinically affected cats have gastroenteritis; many are presented with abortion, stillbirth, neonatal death, or signs of bacteremia. If neutrophils are noted on rectal cytology, culture for Salmonella and Campylobacter is indicated. Infection occurs after faecal-oral or fomite exposure and prevention is based on sanitation and control of exposure to faeces. Antibiotic therapy can control clinical signs of disease but should not be administered to subclinical Salmonella carriers due to risk of antibiotic resistance. In bacteremic animals, parenterally administered quinolones are usually effective atcontrolling clinical signs of disease. Salmonella spp. and Campylobacter spp. infections were uncommon in client-owned dogs and cats with and without diarrhoea in north-central Colorado; less than 2% of the animals in any group were infected.