Companion Animal Zoonoses E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 982

Veröffentlichungsjahr: 2010

Beschreibung

Companion Animal Zoonoses is a comprehensive resource on diseases transmissible between animals and humans. Presenting detailed prevention and control strategies for zoonotic diseases, the book is an in-depth guide to practical information on the spread of disease between pet animals and humans. This relevant work provides up-to-date information on emerging issues, disease incidence and risk, and management measures. Covering the complete range of companion animal zoonoses, each topic begins with information on etiology, geographic distribution, epidemiology, and pathophysiology. The discussion then moves into clinical presentation, diagnosis, and management, alongside prevention information for both animals and humans. Companion Animal Zoonoses is an essential reference for practicing veterinarians, public health veterinarians, and veterinary students. It will also appeal to physicians who wish to better understand zoonotic diseases.

Leseprobe

Table of Contents

Cover

Table of Contents

Half title page

Title page

Copyright page

Preface

Contributors

1 Parasitic Diseases

Introduction

Ascaris lumbricoides

Baylisascaris procyonis

Cheyletiella spp.

Cryptosporidium spp.

Demodex spp.

Dipylidium caninum

Dirofilaria immitis

Echinococcus spp.

Eucoleus aerophilus

Fleas

Giardia spp.

Hookworms

Leishmania spp.

Notoedres cati

Ornithonyssus bacoti

Otodectes cynotis

Sarcoptes scabiei

Strongyloides stercoralis

Taenia spp.

Ticks

Toxocara and Toxascaris spp.

Toxoplasma gondii

Trichuris vulpis

Tritrichomonas foetus

Trypanosoma cruzi

2 Bacterial Diseases

Introduction

Anaerobiospirillum spp.

Anaplasma phagocytophilum

Arcobacter spp.

Bacillus anthracis

Bartonella species

Bartonella henselae

Bartonella clarridgeiae

Bartonella vinsonii subsp. berkhoffii

Bergeyella zoohelcum

Bordetella bronchiseptica

Brucella canis

Campylobacter spp.

Capnocytophaga spp.

Chlamydophila felis

Chlamydophila psittaci

Clostridium difficile

Clostridium perfringens

Corynebacterium ulcerans

Coxiella burnetii

Edwardsiella tarda

Ehrlichia canis

Ehrlichia chaffeensis

Ehrlichia ewingii

Eikenella corrodens

Enterococcus spp.

Escherichia coli

Francisella tularensis

Helicobacter spp.

Leptospira spp.

Listeria monocytogenes

Mycobacterium avium complex (MAC)

Mycobacterium bovis

Mycobacterium lepraemurium

Mycobacterium marinum, Mycobacterium fortuitum, and Mycobacterium chelonae

Mycobacterium tuberculosis

Pasteurella multocida

Plesiomonas shigelloides

Rat-bite fever

Rickettsia felis

Rickettsia rickettsii

Salmonella spp.

Staphylococcus aureus

Staphylococcus pseudintermedius/Staphylococcus intermedius

Staphylococcus schleiferi

Streptococcus canis

Group A Streptococcus (GAS)

Streptococcus equi subsp. equi

S. equi subsp. zooepidemicus

Yersinia enterocolitica

Yersinia pestis

Yersinia pseudotuberculosis

3 Viral Diseases

Introduction

Cowpox

European bat lyssavirus (EBLV)

Hantavirus

Herpes simplex virus (HSV)

Human immunodeficiency virus (HIV)

Influenza: avian

Influenza: pandemic H1N1 influenza

Lymphocytic choriomeningitis virus (LCMV)

Monkeypox virus

Nipah virus

Rabies

Severe acute respiratory syndrome (SARS)

4 Fungal Diseases

Introduction

Aspergillus spp.

Blastomycosis

Coccidioidomycosis

Cryptococcosis

Dermatophytosis (ringworm)

Encephalitozoon cuniculi

Encephalitozoon hellem

Enterocytozoon bieneusi

Histoplasmosis

Malassezia pachydermatis

Pneumocystis

Sporotrichosis

5 Pets and Immunocompromised Individuals

Introduction

The human–animal bond

Pet-associated zoonotic disease

Zoonotic disease knowledge, attitudes, and practices of immunocompromised individuals

Existing recommendations for reducing zoonotic pathogen transmission from pets to immunocompromised individuals

Conclusions

6 Pet Bites

Introduction

Dog bites

Cat bites

Rodent bites

Microbiology

Assessment and management

Antimicrobials

Bite prevention

Index

Companion Animal Zoonoses

Edition first published 2011

© 2011 Blackwell Publishing Ltd.

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Library of Congress Cataloging-in-Publication Data

Companion animal zoonoses [edited by] J. Scott Weese, Martha B. Fulford.

p. ; cm.

 Includes bibliographical references and index.

ISBN 978-0-8138-1964-8 (hardcover : alk. paper)

ISBN 978-0-4709-5890-2 (ebk)

1. Zoonoses. 2. Pet medicine. I. Weese, J. Scott. II. Fulford, Martha B.

 [DNLM: 1. Zoonoses–transmission. 2. Animals, Domestic. 3. Communicable Diseases–veterinary. 4. Disease Reservoirs–veterinary. 5. Disease Transmission, Infectious–prevention & control. WC 950]

 RA639.C66 2011

 614.5'6–dc22

2010042170

A catalog record for this book is available from the U.S. Library of Congress.

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Preface

The concept of zoonotic diseases, those that can be transmitted from animals to humans, has been understood for centuries. Some of the oldest recognized and most devastating infectious diseases have been zoonoses, such as the bubonic plague, and zoonoses have played an important role in human history and development. Traditionally, the main focus has involved food animals, food, water, and wildlife as sources of zoonotic infection. While certainly of importance, those areas do not encompass all zoonotic disease risks, particularly as people in developed countries distance themselves from food animals and nature, and increase their contact with pets.

Companion animals play an important role in the lives of many individuals and are often considered to be members of the family. The majority of households in many countries contain pets, and a large percentage of the population has periodic, if not regular, close contact with a variety of companion animal species. As with any contact between individuals, every animal–human contact carries an inherent risk of pathogen transmission. While the risk is low in most situations, companion–animal-associated zoonoses certainly occur and can range from mild to fatal. Despite the role of companion animals in peoples’ lives and the risk of disease transmission, the field of companion animal zoonoses is one that has only received limited attention in veterinary medicine, human medicine, and public health, with attention being focused on a limited range of pathogens such as rabies virus.

There is no standard definition of a companion animal, and one could successfully argue that some farm animal species, particularly horses, are also true companion animals. This book, however, is restricted to discussion of issues surrounding household pets, because of the vastly different issues involving species like horses. We had a more difficult time deciding on what household pets to include, as the proliferation of exotic animal species has resulted in diverse types of animals in households. We chose to restrict the focus of this book to common household pets, particularly dogs, cats, rabbits, “pocket pets” (mice, rats, hamsters, gerbils, and guinea pigs), and common reptiles (turtles, nonvenomous snakes, lizards). Other animal species are included periodically in reference to specific issues or past outbreaks, such as the monkeypox outbreak in the United States that was associated with prairie dogs. Purists may argue that “humans are animals too,” but for the purposes of this book, “animals” refers to animal species other than humans.

Some nonzoonotic diseases and some with minimal zoonotic disease risks have been included. Concerns are often raised regarding diseases with minimal zoonotic potential, and resources clarifying the lack of risk can be useful. Understanding which diseases are not zoonoses, and the reasons for the lack of risk, can be as important as understanding which diseases do have a zoonotic potential. A major emphasis of this book is on infection control measures to reduce the transmission of zoonotic pathogens in households and veterinary hospitals. An unfortunate reality of the state of science in this field is that evidence-based recommendations are difficult to make because of the paucity of research regarding infection control in companion animals and in households. Whenever possible, recommendations that have been made are based on available evidence. However, many recommendations are expert opinion based on knowledge of pathophysiology, epidemiology, and principles of infection control.

While raising the profile of companion animal zoonoses is important, it can be accompanied by unintended consequences, namely a backlash against pets or inappropriate fear of pet contact. This can lead to unnecessary decisions to remove pets from households or have them euthanized, even in the absence of evidence of the role of pets in a particular disease situation. As an example, increased awareness among physicians, veteri­narians, and pet owners of the potential role of pets in the transmission of methicillin-resistant Staphylococcus aureus (MRSA) sometimes led to a rapid progression from “pets can’t be involved in this disease” to “pets are the root of all evil and should be eliminated.” The authors have dealt with many unfortunate situations where removal or euthanasia of a pet was recommended based on little to no evidence suggesting the pet was a source of infection. This book will hopefully fill some of the information void that is currently a major contributor to such problems.

Achieving a balance between pointing out possible risks and benefits of pet ownership is difficult, particularly in the absence of detailed epidemiological data for many diseases. This book raises many issues with respect to the potential for transmission of zoonotic pathogens in households, but hopefully does so in a balanced manner. It is certainly not our intent to raise fears regarding pets and diseases. Rather, we wholeheartedly support the presence of pets in households and fully understand the positive aspects that pets may bring to peoples’ lives. Instead of highlighting infectious disease risks as an indication that pet ownership is inherently dangerous, we hope that this information will promote safe and appropriate pet ownership, with a reduction in human and animal illness and an improvement of the undeniable human–animal bond.

J. Scott Weese

Martha B. Fulford

Contributors

Maureen E.C. Anderson, DVM, DVSc, DipACVIM. Department of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, Ontario, N1G2W1, Canada.

Martha B. Fulford, BSc, BEd, MA, MD, FRCPC. Division of Infectious Diseases, McMaster University Medical Centre, Hamilton, Ontario, L8N3Z5, Canada.

Andrew S. Peregrine, BVMS, DVM, PhD, DipEVPC, MRCVS. Department of Pathobiol­ogy, Ontario Veterinary College, University of Guelph, Guelph, Ontario, N1G2W1, Canada.

Jason Stull, VMD, MVPM, DACVPM. Department of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, Ontario, N1G2W1, Canada.

J. Scott Weese, DVM, DVSc, DipACVIM. Department of Pathobiology and Centre for Public Health and Zoonoses, Ontario Veterinary College, Uni­versity of Guelph, Guelph, Ontario, N1G2W1, Canada.

1

Parasitic Diseases

J. Scott Weese, Andrew S. Peregrine, Maureen E.C. Anderson, and Martha B. Fulford

Introduction

Companion animals can harbor a wide range of parasites, some of which are transmissible to humans. The overall burden of human diseases attributable to companion animal-associated parasites is unknown and varies greatly between regions. The risks associated with some are often overstated while others are largely ignored, and the range of illness can extend from mild and self-limited to fatal.

Ascaris lumbricoides

Introduction

A. lumbricoides is a roundworm that has typically been considered host specific to humans; however, there is evidence of infection of dogs and the potential for dogs to be an uncommon source of human infection.

Etiology

As with other intestinal nematodes, A. lumbricoides is a nonsegmented, elongated, cylindrical parasite that undergoes sexual reproduction. Like other ascarids, as well as hookworms and Trichuris, A. lumbricoides undergoes a maturation stage in soil and is therefore sometimes referred to as a geohelminth.1 Female worms are larger than males and can reach 40 cm in length and 6 mm in diameter.2

Life cycle

Adult worms live within the small intestinal lumen of humans and excrete massive numbers of eggs per day. As with other ascarids, eggs are not immediately infective and must mature to infective third-stage larvae in the environment over a period of days. After embryonated eggs are ingested by a human, larvae hatch, penetrate the intestinal mucosa, and reach the liver via portal circulation. After migrating through the liver, the larvae eventually reach the lungs, penetrate the airways, ascend the tracheobronchial tree, and are coughed up and swallowed. They mature into adults in the small intestinal lumen and complete the life cycle. The time from ingestion of infective eggs to development of adults is approximately 8 weeks.2

Geographic distribution/epidemiology

A. lumbricoides is one of the most prevalent nematodes in humans and is most common in tropical and subtropical regions, infecting approximately 25% of the world’s population.3–5 Up to 80% of people can be infected in some areas.1,4,6–9 The regional prevalence varies depending on factors such as climate, sanitation, socioeconomic status, and human behavior. Areas with warm, humid climates facilitate maturation and survival of infective eggs. Poor sanitation leads to an increased risk of contamination of the environment with human feces. Outdoor defecation similarly results in increased likelihood of contamination, and outdoor activities in contaminated areas that are accompanied by suboptimal hand hygiene increase the risk of fecal–oral infection. A. lumbricoides eggs can be found in the soil in public places such as parks10,11 and can survive outdoors for years in favorable environmental conditions.1 Infections are more common in children.

Some older studies reported the presence of ascarid eggs that could have been A. lumbricoides in canine feces.12,13 More recently, convincing evidence of the presence of A. lumbricoides in dogs has been reported. A study of dogs in tea-growing communities in northern India identified A. lumbricoides eggs in 18–37% of dogs.7 In that study, dogs were at increased risk of shedding A. lumbricoides if one or more household members regularly defecated outdoors. Simply finding eggs in feces, particularly in an environment where dogs may ingest human feces, does not necessarily indicate that dogs are involved in the biological cycle of the organism. Indeed, there has been some thought that dogs only act as mechanical vectors and that eggs passed in feces simply moved passively through the intestinal tract. However, a recent study of dogs in an area in Egypt where outdoor defecation by humans is common reported detection of adult A. lumbricoides in 8% of dogs.14 Furthermore, viable eggs were detected, suggesting that dogs can truly be infected and could potentially play a role in the life cycle of this human parasite. It has also been suggested that the dog’s coat could be a source of exposure since the eggs are “sticky” and highly tolerant of environmental effects, and could potentially adhere and mature to the infective stage on the animal.14

A study of young Nigerian children indicated that children whose families owned dogs were 3.5 times as likely to be shedding A. lumbricoides compared with non-dog-owning families.15 In contrast, contact with dogs was not a risk factor in a study of adult humans in northern India.7 Whether there truly is a risk from dogs is unclear, but the limited data indicate that consideration of the role of pets, particularly dogs, in the transmission of this predominantly human-associated parasite is required.

Animals

Clinical presentation

Little is known about A. lumbricoides in dogs. While it was previously thought that dogs shedding the parasite represented a mechanical, not biological, vector, there is now evidence that adult worms can grow in the canine intestinal tract. It is not known whether this can result in disease.

Diagnosis

Diagnosis is based on the detection of eggs in feces using fecal flotation and subsequent speciation of the parasite by evaluation of micromorphological features14 or using molecular methods such as PCR-RFLP.7

Management

No specific data are present, but presumably, any prophylactic or therapeutic agent that is used for the treatment of Toxocara in dogs would be effective against A. lumbricoides. These include milbemycin oxime, moxidectin, fenbendazole, and pyrantel.

Humans

Clinical presentation

Various presentations can occur, but most infections are asymptomatic.1,2 Large worm burdens can result in malnutrition, nonspecific gastrointestinal signs, or, in rare cases, intestinal obstruction.2 Obstruction of the bile duct can result in cholangitis, biliary colic, or pancreatitis.2 Chronic infections can produce insidious disease, with growth retardation and negative effects on cognitive function in children.5 During larval migration, acute pulmonary signs (Loeffler’s syndrome), fever, and marked eosinophilia can occur.2 There is also increasing concern about the broad effects of ascarid infection on the immune system, something that may be particularly important with concurrent infections such as malaria or for the development of allergic diseases,16,17 though more research needs to be performed in this area.

Diagnosis

Eggs are usually easily detectable in stool because of the large numbers that are shed by adult worms. Rarely, adult worms will be passed in stool or vomitus.2 Adult worms may also be identified ultrasonographically as an incidental finding or during investigation of gastrointestinal complaints.

Management

A single dose of albendazole, mebendazole, or pyrantel pamoate has high cure rates (88–95%).18 Three days of mebendazole or a single dose of ivermectin has also been recommended in people over 2 years of age.2 Nitazoxanide is also effective.19 Retesting of stool 2 weeks after treatment has been recommended.2 Most drugs are only effective against adult parasites, so repeated treatment may be needed.

Prevention

Prevention of zoonotic transmission of A. lumbricoides, should it occur, involves basic measures to reduce the incidence of exposure of dogs, to reduce contamination of the environment by dog feces, and to prevent fecal–oral exposure in humans. Evidence-based data are not available for any of these areas, but reasonable recommendations can be made.

Reducing exposure involves decreasing the chance that dogs will ingest infective A. lumbri­coides eggs, which are predominantly found in human feces. Reducing “promiscuous defecation” by humans, something that is common in some developing regions,14 is a means of achieving this and involves both education and improved infrastructure.

Reducing contamination of the environment by dogs is as discussed for similar organisms like Toxocara canis (e.g., reducing worm burdens, and therefore shedding levels, by routine antiparasitic chemoprophylaxis). Decreasing the numbers of free-roaming dogs and prompt removal of feces, particularly from public areas such as parks, would presumably help achieve that goal. General hygiene practices are the key to reducing inadvertent ingestion of infective larvae by humans, including good attention to hand hygiene and proper washing of food.

Prophylactic use of albendazole, mebendazole, or pyrantel pamoate in humans can be practical and affordable in endemic areas, particularly in school-age children.2,20 Based on the commonness of the parasite in humans in some regions and the very rare incidence of patent infections in dogs, prophylactic treatment of dogs directed specifically against A. lumbricoides is not indicated. However, routine deworming targeted against other roundworms will be effective against this parasite.

Baylisascaris procyonis

Introduction

B. procyonis is a large nematode that is highly prevalent in healthy raccoons in many regions.21 Human infections are very rare but can be devastating. Neural larva migrans is the most common form of this rare disease, but visceral (VLM) and ocular larva migrans (OLM) can also develop.

Dogs can shed B. procyonis in feces and can also theoretically be a source of human exposure through transporting infective eggs into the household on their hair coat. While objective evidence of a risk from pets is minimal, the severity of disease in humans indicates that basic measures should be taken to reduce the risk of exposure to this parasite.

Etiology

B. procyonis belongs to the order Ascaridida, along with Toxocora canis and T. cati.21 The North American raccoon (Procyon lotor) is the definitive host, and B. procyonis is often termed the “raccoon roundworm.” An unusual aspect of B. procyonis is its ability to infect a wide range of animal species, causing neural larva migrans in over 100 avian and mammalian species.21

Life cycle

Adult worms are found in the small intestine of raccoons. They are large, tan roundworms that can be up to 22 cm long. Female worms are prodigious egg layers, and infected raccoons can pass millions of eggs in feces per day, leading to heavy contamination of the environment. Eggs are not immediately infective, and second-stage larvae must develop in eggs in the environment before infection is possible. This usually requires 2–4 weeks, but may occur as quickly as 11 days in some situations.21 After ingestion, infective eggs hatch in the small intestine. In intermediate hosts, larvae can penetrate the intestinal mucosa and migrate via portal circulation to the liver, then to the lungs, where they are subsequently distributed throughout the body via the systemic circulation. Larvae that reach the central nervous system (CNS) continue to migrate and grow, causing neurological damage. Migration through other tissues may also occur, and extensive somatic migration is common.21

Young raccoons tend to be infected early in life by ingesting infective eggs off their mother’s hair coat or in the den environment. Adult raccoons are typically infected by ingestion of third-stage larvae in the tissues of infected intermediate hosts (i.e., rodents). Intermediate hosts (including humans) are infected by ingestion of infective eggs from the environment. Juvenile raccoons tend to have a higher parasite burden than adults.21

Geographic distribution/epidemiology

B. procyonis can be found in most places that raccoons can be found. Raccoons are indigenous to North America and B. procyonis can be found widely across the continent, although there appear to be regional variations in prevalence (e.g., this parasite is less common in the southeastern United States). Shedding rates of 13–92% have been reported in North American raccoons.22–27 During recent years, the parasite has been found, sometimes commonly, in North American regions where it was not previously thought to exist,21,22 suggesting that its range may be expanding. It is reasonable to assume that B. procyonis is present anywhere raccoons can be found. This includes other continents, since raccoons have been introduced into other regions of the world, and B. procyonis has been found in raccoons in some areas of Europe and Asia.28,29

Infected raccoons can shed massive numbers of eggs in feces and lead to marked environmental contamination. This is most pronounced in and around raccoon latrines, areas where raccoons tend to defecate. Raccoon latrines are thought to play a central role in B. procyonis transmission because they are so highly contaminated.30–32 Other environmental sites, including public parks and playgrounds, can also be contaminated.33 Infective eggs are highly resistant to environmental effects and can persist in the environment for years,21,34 long after obvious evidence of raccoon feces has disappeared. The surface of the egg is also rather “sticky,” and eggs tend to adhere to animal fur, hands, and other surfaces, which can contribute to exposure of pets and people.

Neural larva migrans and OLM are the main disease concerns associated with this parasite in humans. Neural larva migrans caused by B. procyonis is very rare but has been reported sporadically across North America. Most cases have involved children with developmental delays.21,35–37 Contact with infected raccoons, their feces, or a contaminated environment, and geophagia or pica are the main risk factors.21 Young children and developmentally delayed individuals are at increased risk because they are more likely to ingest raccoon feces and contaminated dirt. Children may also be more likely to play outside in or around raccoon latrines. Asymptomatic infections can occur, as evidenced by the presence of B. procyonis antibodies in some healthy individuals.21 While evidence is sparse, it is suspected that asymptomatic or subclinical infections are the most common form of infection.2 Asymptomatic infections probably represent infections caused by ingestion of small numbers of B. procyonis, which results in less damage through migration and inflammation. Since the likelihood of clinical infection and severity of neural larva migrans are thought to relate to the number of ingested larvae and the size of the brain (with damage to critical areas more likely in small brains), subclinical infections would be more likely in adults.21

The role of dogs in the epidemiology of B. procyonis is poorly understood. They likely play a minimal role in the propagation of this parasite. However, their close contact with humans raises concerns. There are reports of B. procyonis infection in dogs, both healthy dogs and dogs with neural larva migrans,21,38–40 though prevalence data are currently lacking. Even so, compared with raccoons, infections in dogs appear to be uncommon. Dogs can be infected by ingestion of infected small animals.41 They could also become infected by ingestion of eggs, particularly from raccoon latrines; however, infection following ingestion of eggs is much less likely than infection following ingestion of larvae. Given the ability of eggs to stick to surfaces, pets could theoretically be a source of infection as a mechanical vector, by bringing infective eggs from the environment into the household.

Infections have also been reported in other species, including wild rabbits,42 captive nonhuman primates,43 a cockatoo,44 and a pet guinea pig;45 however, patent infections have not been reported and the public health consequences are presumably minimal to nonexistent.

Animals

Clinical presentation

The implications of B. procyonis infection in dogs have not been well described, and it is likely that subclinical intestinal infection is most common. Neural larva migrans can occur and cause rapidly progressive encephalitis.38,39

Diagnosis

Eggs can be identified in feces using routine fecal flotation. Close examination is required to differentiate B. procyonis from Toxocara or Toxascaris spp.21 PCR may offer another means of directly detecting B. procyonis eggs in feces and differentiating them from other ascarids.46

Diagnosis of neural larva migrans is as described for humans below, involving clinical signs, peripheral and CSF eosinophilia and seropositivity, and exclusion of other possible causes of disease.38

Management

Fenbendazole, milbemycin oxime, moxidectin, and pyrantel are likely to be effective for the elimination of intestinal B. procyonis.47 Milbemycin oxime was effective at eliminating B. procyonis from a small group of naturally infected and experimentally infected dogs.48 No information is available regarding treatment of larva migrans. Presumably, anthelmintics and corticosteroids are indicated, as is the case in humans, but a grave prognosis would be expected.

Humans

Clinical presentation

Neural larva migrans produces severe and rapidly progressive eosinophilic meningoencephalitis. It is almost exclusively identified in young children or people with developmental delays that make them more likely to ingest dirt or feces. Weakness, lethargy, irritability, behavioral changes, difficulty speaking, headache, and ataxia may be observed, usually with rapid progression.37

OLM may occur with neural larva migrans or as a sole entity. Larval migration through the visual cortex or within the eye can lead to visual impairment or blindness.21 Chorioretinitis and optic neuritis or atrophy may be evident during oph­thalmoscopic examination.21 Occasionally, motile larvae may be observed within the eye. VLM tends to occur most often in the head, neck, and thorax.21

Diagnosis

Neural larva migrans is presumptively diagnosed through a combination of clinical signs, cerebrospinal fluid (CSF), and peripheral eosinophilia, and the presence of diffuse white matter disease on CT or MRI, ideally with a history of exposure to raccoons or raccoon feces.21 Demonstration of antibodies against B. procyonis in serum and CSF supports the diagnosis. Definitive diagnosis involves the identification of larvae on brain biopsy specimens.37 However, it is unlikely that a parasite would be obtained in a biopsy, and biopsy is not recommended if serological tests are available.21

Diagnosis of OLM is based on the detection of chorioretinal lesions or larvae on ophthalmoscopic examination.2 Differentiation of B. procyonis from other ocular parasites can be done by measurement of the larvae, with B. procyonis larvae being larger (1500–2000 × 60–70 µm) than Toxocara (350–445 × 20 µm).21

Management

Treatment is difficult because of a lack of objective information regarding different options and the typically advanced nature of disease by the time it is suspected or diagnosed. Currently, treatment involves anthelmintics, corticosteroids, and supportive care. Data regarding the efficacy of different anthelmintics in eliminating intestinal worms in raccoons must be used cautiously when considering the treatment of larva migrans, because drugs that are able to eliminate intestinal parasites in raccoons are typically much less effective in tissues of other hosts21 and adult worm stages may have different susceptibility to certain drugs compared with larval stages. Albendazole is the most commonly recommended treatment, along with high doses of corticosteroids.2

Regardless of treatment, the prognosis is poor. By the time the disease is suspected, patients are usually severely affected and there is little chance of effective treatment. Affected individuals typically die or are left with profound neurological deficits.37 There is only one report of recovery without residual neurological deficits––a 4-year-old child who had a relatively mild disease.35 Developmental disabilities, seizures, paralysis, and blindness are common sequelae.37

Prevention

Efforts at preventing B. procyonis infection in people are best directed against avoiding intentional or inadvertent ingestion of raccoon feces and soil from around raccoon latrines. Raccoons should not be kept as pets or encouraged to live around households. Contact with latrines and adjacent areas should be prevented, particularly by young children or other people at increased risk of geophagia or pica. Raccoon latrines should be cleaned, and contaminated areas should be disinfected.

The risk of human infection from dogs is probably very low, but measures should be taken to reduce the risk of dogs becoming exposed and potentially infected, or from having their hair coats become contaminated. Dogs should not be allowed to have contact with raccoon latrines. If a dog has been in a raccoon latrine or otherwise may have become contaminated with B. procyonis larvae, bathing it with soap and water to remove infective eggs is reasonable measure. Gloves and protective outerwear (i.e., lab coat) should be worn when bathing, and hands should be washed thoroughly in soap and water after contact with a potentially contaminated animal. Ideally, bathing should occur outside. If B. procyonis infection is identified during routine fecal examination, treatment is warranted, as described above.

If larva migrans is suspected in a dog or other household pet, the animal should be handled on the assumption that it may also be shedding eggs in feces. Since eggs are not immediately infective, contact with the animal is relatively low risk; however, contamination of the hair coat would be possible. Care should be taken around feces of potentially infected animals. Feces should be promptly removed so that infective eggs are not formed.

Preventive therapy with albendazole is indicated in children that have ingested soil or feces potentially contaminated with B. procyonis.2 Prophylactic treatment of dogs that have ingested raccoon feces could be similarly considered, but the need or usefulness of this is unclear. Routine deworming targeted solely against B. procyonis is not indicated because of the apparent rarity of the parasite in dogs. However, most drugs used for routine monthly deworming directed against other helminths should be effective against B. procyonis.

Cheyletiella spp.

Introduction

Often referred to as “walking dandruff,” cheyletiellosis is a dermatologic disease caused by mites. Different Cheyletiella species have different animal hosts, but they can also infest other species, including humans. Cheyletiellosis is a mild zoonotic infection that is most often linked to infested cats.

Etiology

Cheyletiella species are large (350 × 500 µm) mites belonging to the Arachnida class. There are three main species in companion animals: Cheyletiella yasguri, Cheyletiella blakei, and Cheyletiella parasitivorax. Dogs are the host of C. yasguri, while C. blakei is found on cats and C. parasitivorax is found on rabbits.49–52C. parasitivorax has also been reported in dogs and cats.53,54 A related genus, Lynxacarus radovskyi, can be found on cats in some regions.

Life cycle

Cheyletiella are hair-clasping mites that do not burrow. Rather, they live in the fur of animals and move around freely.49,50 Periodically, they attach to the epidermis and feed off the keratin layer. Eggs are laid on the host, attached to hairs by fine fibrillar strands.50 Prelarvae and larvae develop within the egg, and fully developed nymphs emerge.49 These nymphs develop through two stages and then become adults. The entire life cycle can be completed on a single host and takes approximately 35 days.50 Adult mites may live off the host for short periods of time, with conflicting data regarding how long this may be. Some authors state that survival is typically for a few days but can be up to 10 days, while others claim that survival for up to 1 month is possible.49,50 While Cheyletiella spp. can accidentally infect humans, they cannot complete their life cycle on human skin.50,55

Geographic distribution/epidemiology

Prevalence and incidence data for animals and humans are limited. C. parasitivorax was found on 57% of pet rabbits in a South Korean study,56 but little information has been reported about typical pet dog and cat populations. It has been variably suggested that the disease is uncommon or common but frequently undiagnosed. In dogs, infections appear to occur most often in puppies.50 No age, breed, or gender associations have been identified in cats. Infestations are most commonly found in animals in kennels or other confined systems.49 Introduction of new animals into the household may be associated with animal and human infections,57 although proper risk factor studies are lacking. Infested animals do not necessarily have signs of disease but can still act as a source of infection of people or other animals.58

Cheyletiella species appear to be well distributed internationally. Lynxacarus has been most commonly reported in Australia, New Zealand, Fiji, Texas, and Hawaii.59–64

Transmission is predominantly by direct contact between infected and susceptible individuals. Indirect transmission by the environment and fomites is also possible. Mites have also been found on fleas, lice, and flies, and these could be additional routes of transmission.50

Human infestation appears to be relatively com­mon, albeit mild and often undiagnosed.65,66 One author has reported human infestations associated with 30% of infected cats,50 but objective data on the incidence of infection are lacking. Infestations are most often associated with C. blakei and cats.67–69 It is unclear if this relates to a higher infectivity of C. blakei, greater risk of transmission from cats to humans because of the types of cat–human interaction, or other factors. Human infestations have been associated with C. yasguri from dogs,70–74 but this appears to be rare. Zoonotic Lynxacarus infestation has been reported on one occasion.

Animals

Clinical presentation

Infection results in a variably pruritic exfoliative dermatitis with scaling and crusting, most commonly over the dorsum and rump in dogs and around the trunk, face, and tailhead in cats.49,50 Mites are active, and the associated movement of mites and epidermal debris leads to the appearance of “walking dandruff.” The hair coat usually appears dull and dry, and may have a rust-colored tinge. Large numbers of mites and eggs may give the hair coat a granular appearance and feel. There may be excessive hair shedding,49 and miliary dermatitis may develop in cats.57

The distribution is usually different with L. radovskyic on cats. Mites are most commonly found on the tailhead, tip of the tail, and the perineum, but can be found over the entire body with severe infestations.

Diagnosis

The presence of dorsal seborrhea sicca (dry white scales) and corresponding “walking dandruff” is highly suggestive of cheyletiellosis.57 Mites are often visible to the naked eye over the dorsum. Use of magnification will assist in the identification of mites and eggs. Microscopic evaluation of mites allows for confirmation of infection and speciation. Mites may be observed with skin scrapings, not because they reside in the skin but because they are collected during the sampling process. They can also be identified with acetate tape preparations.50 Occasionally, mites are found in feces of cats after being ingested during grooming. Fecal examination for mites is, however, not a recommended diagnostic test.

Management

Ivermectin, selamectin, imidacloprid/moxidectin, or fipronil is effective.75–79 Ivermectin is also effective in rabbits.80 Pyrethrin- or pyrethroid-based shampoos, sprays, or spot-on formulations are effective for dogs,81 but pyrethroids should not be used on cats.49 Topical therapies are preferred by some authors because the mites do not live within the skin;58 however, there is good evidence of efficacy for various systemic treatments. Multiple treatments may be required depending on the potential for reinfection from other animals or the environment.82 All pets in the household should be treated at the same time. Bedding and grooming equipment should be disinfected or discarded.

Humans

Clinical presentation

Lesions may occur over any part of the body but are more common over the arms, legs, and torso.50,58,65,66,83,84 The face is rarely affected. Single or multiple macules may be observed initially, and pruritis may be intense. These progress to papules and frequently evolve into vesicles and pustules.50 There is often an area of central necrosis in older lesions, a finding that is quite suggestive of cheyletiellosis.65 Multiple people in the household may be affected.83,84 Systemic manifestations including myalgia, numbness in the fingertips, and poor general health have been reported in association with cheyletiellosis,65 but this is presumably very rare, if it is even associated with infestation.

Diagnosis

Diagnosis may be difficult if only the human patient is considered, and sometimes the diagnosis is only made after the pet has been diagnosed with cheyletiellosis.65 Mites may not be observed on the affected person and are rarely identified on skin scrapings.85 Usually, diagnosis is based on appropriate clinical signs and diagnosis of cheyletiellosis in a pet.50 Pet contact should be queried in all such cases, and the involvement of the veterinarian may be critical for diagnosis.70,86 The patient’s pet should be referred to his or her veterinarian if cheyletiellosis is suspected. Lack of history of contact with a pet with dermatologic disease does not rule out zoonotic cheyletiellosis as some animals can be infected without clinical signs.58 Resolution of skin lesions after treatment of the infected pet is further supportive of the diagnosis.

Management

Infection is self-limited since mites cannot complete their life cycle on human skin. Following elimination of infection in the pet, human skin lesions will resolve in approximately 3 weeks.50,57,83,84,87 Topical therapy with lindane has been used,65 but there is no evidence that it is required.

Prevention

Human infections are uncommon and mild, and the risk of transmission to other people is low. The mites are more likely to reside on parts of the body normally covered by clothing than on exposed skin. Frequent laundering of clothes and bedding will further help reduce the risk of transmission. The most important elements of prevention of zoonotic transmission from animals are prevention of infestation in pets and prompt diagnosis and treatment of any infestations that do occur.

If cheyletiellosis is diagnosed in a pet, owners should be made aware of the potential for acci­dental human infection. Pets should be promptly and appropriately treated. All pets should be treated at the same time to prevent cycling of infection in the household. The pet’s bedding, as well as other items with which the pet has frequent contact (e.g., bedsheets, sofa cushion covers) should be cleaned thoroughly. Laundering and hot-air drying should be highly effective for this and are likely the best means of decontaminating bedding and similar items. Carpets should be thoroughly vacuumed; steam cleaning may also help eliminate any eggs or mites deep within the carpet pile. Grooming items or other objects that come into regular contact with the pet should be disinfected, or discarded if disinfection is not possible. There is little information regarding optimal cleaning and disinfection techniques. Permethrin sprays can be used to eliminate environmental contamination.75

Animals receiving monthly antiparasitic prophylaxis are typically considered to be at low risk because of the high efficacy of most available products against Cheyletiella.

Cryptosporidium spp.

Introduction

Cryptosporidiosis is an important and well-recognized zoonotic disease, particularly in people who work with young cattle. It is capable of caus­ing severe diarrhea even in otherwise healthy, immunocompetent hosts, but it can cause life-threatening intestinal and extraintestinal infection in immunocompromised individuals. The relevance of cryptosporidiosis has increased because of its role in disease in HIV/AIDS and other immunosuppressed patients. The role of Cryptospo­ridium in disease in young cattle and humans is well established, but its clinical relevance in companion animals remains unclear. Similarly, the role of pets in human cryptosporidiosis is poorly understood.

Etiology

Cryptosporidium spp. are eukaryotic coccidian parasites of the suborder Eimeria in the phylum Apicomplexa. The taxonomy of the genus Cryptosporidium, like many protozoa, is controversial.88,89 Previously, two species were described, Cryptosporidium muris and Cryptosporidium parvum, but as many as 23 species have now been described based on various combinations of host predilection, geographic distribution, genotypic characteristics, and morphology.88 There is much debate as to which of these species should truly be called species with their own name versus genotypes or subgenotypes of C. parvum, of which there are also many.88 Currently, the more commonly accepted species (and primary hosts) include Cryptosporidium andersoni (cattle), Cryptosporidium baileyi (chickens and some other birds), Cryptosporidium canis (dogs), Cryptosporidium felis (cats), Cryptosporidium galli (birds), Cryptosporidium hominis (humans), Cryptosporidium meleagridis (birds and humans), Cryptosporidium molnari (fish), C. muris (rodents and some other mammals), C. parvum (ruminants and humans), Cryptosporidium wrairi (guinea pigs), Cryptosporidium saurophilum (lizards and snakes), Cryptosporidium serpentis (snakes and lizards), and Cryptosporidium suis (pigs).88–90

Most cryptosporidia that infect reptiles and birds do not appear to infect mammals, except for C. meleagridis, which is the third most common type found in humans after C. hominis and C. parvum. C. muris has a limited host range91 and is not considered a significant concern in humans or companion animals (beyond rodents), although it has been isolated from a cat.92C. felis can cause diarrhea in humans, although this is rare and may be of greatest concern in immunocompromised individuals. Infection is usually subclinical in cats. C. canis is found in dogs, with infection in both dogs and people being generally subclinical. C. parvum (also previously known as C. parvum genotype 2) has the widest host range, infecting primarily cattle (especially calves) as well as dogs, cats, sheep, goats, horses, laboratory rodents, and humans. C. hominis (also previously known as C. parvum genotype 1)89,93 is found primarily in humans and was previously thought to not cause natural infection in other species,88 but has since been found in a few isolated animal cases.94 Nonetheless, C. hominis is responsible for the majority of human cryptosporidial infections.88 These various species can only be definitively differentiated based on DNA/genetic testing. The question remains whether or not other strains/species of the parasite are a significant public health threat in general, a threat to only immunocompromised individuals, or not a threat at all,88 as host adaptation does not necessarily imply host specificity.88 The five most common species of Cryptosporidium (C. hominis, C. parvum, C. meleagridis, C. felis, and C. canis) have been found in both immunocompromised and immunocompetent individuals.88,95 Case reports of human infection with more uncommon species and genotypes have also been recently published.96–98

Geographic distribution/epidemiology

Cryptosporidium infection has a worldwide dis­tribution. The prevalence of oocysts in human feces in North America is thought to be between 0.6% and 4.3%.99 In the United States, 15–32% of the population may be seropositive for Cryptosporidium,100 while seropositivity in developing countries may be as high as 65%,99 indicating that exposure is common. Outbreaks of clinical disease in humans have been associated with contaminated food or water, but not household pets. From 1991 to 2000, Cryptosporidium was implicated in 40/106 outbreaks of recreational water-associated gastrointestinal disease and 11/130 outbreaks of drinking water-associated gastrointestinal disease.101–105 However, outbreaks account for less than 10% of diagnoses of Cryptosporidium in the United States,90 and large outbreaks would not be expected to occur from contact with pets. The limited information regarding the role of pets in human cryptosporidiosis must be tempered with an understanding that sporadic cases of cryptosporidiosis, the most likely form of pet-associated disease, would likely be undiagnosed or underreported, if they occur.

Risk factors for human infection include contact with infected farm animals, ingestion of contaminated recreational or drinking water, close contact with infected persons, and travel to high prevalence areas.93,99 Cryptosporidiosis is more common in immunocompromised individuals as well as in children under 2 years old, livestock handlers (particularly dairy farmers), and men that have sex with men.99 In most studies, contact with pets is either not associated or negatively associated with the risk of cryptosporidiosis, even among immunocompromised owners.90,106 Along with the negative association with pets, some studies have found a negative association with consumption of raw vegetables, and it has been hypothesized that these associations may be the result of repeated low-dose exposure to the parasite, producing better immunity and decreased dis­ease.90 In contrast, several studies have shown contact with calves or cows107–109 or farm visits110 to be significant risk factors for cryptosporidiosis for the general population. Cryptosporidial diarrhea is also common among children in daycare centers, making daycare workers at higher risk for infection.

Some studies have shown a predominance of C. parvum among isolates from sporadic cases of cryptosporidiosis, compared with outbreaks in which C. hominis is usually implicated.110,111 These studies and other reports90 cite this as evidence of zoonotic transmission from livestock (primarily cattle), although given that humans are capable of carrying both species, human-to-human transmission of C. parvum must also be considered. Better epidemiological evidence and demonstration of contamination of the water source with infectious effluent from cattle are required to determine the source of the C. parvum in these cases.

Exposure to Cryptosporidium appears to be common in animals. Reported seroprevalence rates in domestic and feral dogs and cats range from 1.3% to 74%, depending on the region and type of population studied.112,113 Cats that are allowed outdoors are more likely to be seropositive.113 Shedding of cryptosporidial oocysts (or the presence of cryptosporidal antigen in feces) is less common, typically ranging from 0% to 8%.114–119

In all affected domestic animal species, young unweaned animals are more susceptible to infection and disease from Cryptosporidium than adults.99 In general, kittens less than 6 months of age and cats living in households with more than one cat or with a dog are more likely to be infected.120

Cryptosporidium can also be commonly identified in ferrets,121 but most, if not all, belong to the ferret genotype of C. parvum. It is unknown if this genotype can cause disease in humans.122

Transmission of the infection occurs through ingestion of oocysts that are shed in the feces of infected humans or animals. As few as 30 oocysts of C. parvum can cause subclinical infection in an otherwise healthy person, and as few as 100 oocysts can cause clinical cryptosporidiosis,100 whereas as few as 10 oocysts of C. hominis can cause clinical disease in humans.123 There are three major routes of transmission in people: person to person, which is particularly important in daycare settings with young children; animal to person, which is sometimes implicated in outbreaks in rural areas although the relative importance of this route remains unclear; and transmission via contaminated water (or food) sources, which is a well-recognized route in outbreaks.88

Although owning a dog or a cat has not been identified as a risk factor for cryptosporidiosis in humans, transmission of the parasite from these animals to humans is possible. The most common species of Cryptosporidium in dogs, C. canis, has only been reported to cause subclinical infection in a few immunocompetent individuals. In contrast, C. felis has been reported to cause watery diarrhea in both immunocompetent and immunosuppressed individuals.124

Life cycle

Cryptosporidia can undergo their entire life cycle in a single host. Animals or humans are infected by ingesting oocysts from the feces of other infected individuals. In the small intestine, the oocysts release sporozoites that invade the brush border of the epithelium, forming intracellular but extracytoplasmic vacuoles containing trophozoites. The trophozoites replicate asexually to form type I meronts containing merozoites. The released merozoites go on to replicate in other intestinal epithelial cells to form more type I meronts as well as type II meronts. Type II meronts reproduce sexually, producing macrogamonts and microgamonts. Fusing of one of each type of gamont results in the formation of a zygote, which in turn forms an oocyst containing four sporozoites.125 The oocysts are either thin or thick walled. Thin-walled oocysts rupture within the intestine, and the entire life cycle is repeated (autogenous infection). Thick-walled oocysts are passed in the feces and are immediately infectious to the next host.125

Animals

Clinical presentation

Patent infections may be present in cats and dogs with no accompanying clinical signs. It is therefore debated whether or not the organism causes diarrhea in otherwise healthy, immunocompetent cats and dogs, or whether it may be a secondary finding in cases of other gastrointestinal disease. When clinical signs are associated with infection, the primary sign is diarrhea. In both dogs and cats, diarrhea is most severe in immunocompromised animals.

Clinically affected cats typically exhibit high-volume, low-frequency (small bowel type) diarrhea but can chronically develop tenesmus and hematochezia.126 In puppies experimentally infected with C. parvum from calves, the prepatent period was 3–5 days, peak shedding occurred at 7–9 days, and intermittent or low-level shedding continued for at least 80 days.126

The parasite may be a primary pathogen in birds in which it can infect both the gastrointestinal and respiratory tracts and bursa of Fabricius. Cryptosporidia tend to infect the stomach of reptiles and therefore cause gastritis and vomiting.126

Diagnosis

Although oocysts can be seen on direct fecal smears, concentration techniques using sugar solutions (e.g., Sheather’s solution, specific gravity 1.2–1.25) for fecal flotation are preferred.99,126 The use of phase-contrast or bright-field microscopy is recommended to detect oocysts on unstained preparations. Oocysts are typically slightly smaller than erythrocytes (approximately 2.5–5 µm in diameter) and are refractile (Figure 1.1).99 They appear as circular or possibly concave disks; dark shadows of four banana-shaped sporozoites can sometimes be seen within them. On wet mounts stained with crystal violet, the oocysts are apparent because they do not pick up stain.126 Of the various species that infect mammals, only C. muris and C. andersoni oocysts can be differentiated morphologically from the others.88

Figure 1.1Cryptosporidium parvum oocysts (4–5 µm) in a stool sample from a person with cryptosporidiosis

(public domain, Dr. Peter Drotman, Centers for Disease Control and Prevention).

Diagnostic laboratories may use formalin-ethyl acetate sedimentation followed by direct fluorescent antibody staining. The fluorescent antibody test has been used as the reference standard for comparison of other diagnostic tests.127 Enzyme-linked immunosorbent assays (ELISAs) designed for detection of parasitic antigen in human fecal samples are also available, although it is unknown if these tests can consistently identify certain species such as C. canis and C. felis. In a comparison of three antigen-based assays on feline fecal samples, the ProSpecT Microplate Assay had the highest sensitivity (71.4%) and specificity (96.7%) for detection of cryptosporidial antigen, compared with a direct fluorescent antibody test.127 Compared with fluorescent antibody testing of fecal samples from experimentally infected cats, PCR appeared to be more sensitive in another study.128 Further evaluation of these tests for use in veterinary medicine is warranted.

A serum ELISA for cats is available, but, as in humans, the test only indicates exposure and is not useful for predicting oocyst shedding in individual animals.129 Intestinal biopsy is an impractical means of diagnosis. Organisms can be found throughout the intestine in animals but are most numerous in the ileum.126

Management

Infection in otherwise healthy animals is self-limited. Supportive care including intravenous fluid therapy may be required to prevent or treat dehydration if diarrhea is severe and the animal’s fluid intake is inadequate. Specific treatment of coinfections, if possible, should be considered. If no coinfection exists and clinical signs are persistent or severe, specific therapy for Cryptosporidium could be considered, although objective information regarding treatment is limited. Currently, there are no drugs that have been shown to be consistently effective and safe for treatment of cryptosporidiosis in companion animals. Paromo­mycin or azithromycin are the most commonly recommended specific treatments in dogs and cats.126

Humans

Clinical presentation

Frequent, watery, and nonbloody diarrhea is the predominant clinical presentation.2 Nausea, abdominal cramps, low-grade fever, and anorexia may also be present.130 Fever and vomiting are more likely to occur in children.2 Diarrhea may be profuse and can result in dehydration, but illness is usually self-limited in immunocompetent individuals. However, cryptosporidiosis can be a serious disease in immunocompromised individuals, with severe diarrhea (over 70 evacuations per day, losing up to 25 L in fluids), dehydration, and a potentially fatal outcome.99 In HIV/AIDS, disease occurs more frequently and is more severe in patients with lower CD4+ lymphocyte counts, particularly those with CD4+ counts below 200 cells/µL.89 The incidence of symptomatic infection and severe disease in HIV/AIDS patients has declined with the widespread use of highly active antiretroviral therapy.90,93 Transplant patients and individuals with IgA deficiency are also at increased risk of severe disease.

Rarely, nonintestinal clinical signs of cryptosporidiosis may occur following acute diarrheal disease, including joint pain, eye pain, recurrent headache, dizzy spells, and fatigue. These signs and symptoms have only been associated with C. hominis.131 Infection of the respiratory and biliary tracts may also occur in immunocompromised individuals.132,133

Diagnosis

Infected persons have been reported to shed up to a billion oocysts per day, yet immunocompetent, symptomatic human patients do not always have positive stool samples, and conversely, oocyst shedding may persist for up to 15 days following resolution of clinical disease.93,134 Evaluation of at least three stool samples collected on different days is recommended.2 As described above for animals, oocysts can be detected by microscopic examination of stained or unstained fecal preparations. Several antigen-based fecal tests (e.g., fluorescent antibody, ELISA) are also available. PCR-based tests have been developed and appear to have a very low detection threshold (10–100 oocysts/mL compared with 10,000 oocyts/mL for the fluorescent antibody test).135,136 A nested multiplex PCR has been developed that can differentiate C. parvum, C. hominis, C. canis, and C. felis in human fecal samples,135 something that could be very useful for determining the potential source(s) of infection in sporadic cases and outbreaks.

Serological tests are available with acceptable sensitivity and specificity. However, antibodies usually appear too late to be of use in the diagnosis of acute disease, and may not appear at sufficient levels to be detected in immunocompromised individuals.99 In addition, they remain high after infection. Serology is most useful for epidemiological studies.

Management

Most infections in immunocompetent persons are self-limited, and individuals ultimately recover completely in 1–20 days (mean 10).2 In these cases, treatment, if necessary, is limited to supportive care, particularly fluid replacement (either oral or parenteral). A consistently effective anticryptosporidial drug has yet to be found, which leaves individuals with immature or weakened immune systems (including young children and the elderly) at risk of more severe disease.90,137 In the United States, the only drug approved for the treatment of cryptosporidiosis in people is nitazoxanide.138,139 Treatment with paromomycin may improve clinical signs and decrease oocyst shedding in people, and has been recommended for the treatment of immunocompromised patients.140,141 Azithromycin has also been used, but further study is required to determine its true efficacy.137

Immune reconstitution in HIV/AIDS patients through administration of highly active antiretroviral therapy will assist with the elimination of Cryptosporidium.2

Prevention

The key to preventing zoonotic cryptosporidiosis from pets is avoiding inadvertent ingestion of oocysts from the animal, or its environment. In households, diarrheic animals should be handled minimally in case there is fecal staining of the hair coat. Diarrheic animals should be taken outside frequently to reduce the risk of accidental defecation in the house. Ideally, affected dogs should not be walked in public areas. Feces should be promptly removed and hands should be thoroughly washed. If feces are passed in the house, contaminated areas should be promptly cleaned. Thorough cleaning to physically remove oocysts is the key because oocysts are resistant to most disinfectants. Care should be taken to avoid contamination of the environment or hands when cleaning litter boxes, and hands should be thoroughly washed after (even if gloves are used).

Immunocompromised individuals, especially people with HIV/AIDS, should take particular care, especially around diarrheic animals. Careful use of general infection control measures to reduce contact with fecal pathogens is important, regardless of whether the animal has diarrhea or not. Contact with diarrheic animals should be restricted. If possible, immunocompromised individuals should have someone else pick up feces or clean the litter box. If fecal staining of the pet’s hair coat occurs, this should be promptly and thoroughly cleaned, ideally not by the immunocompromised person. If contact with feces, litter boxes, or potentially contaminated hair coats is unavoidable, gloves should be used and hands should be washed immediately after glove removal. If there has been potential contamination of cloth­ing, clothes should be promptly removed and laundered, using hot water and a hot-air clothes dryer.

In veterinary clinics, diarrheic animals should be isolated and handled with appropriate contact precautions (e.g., gown, gloves, and designated footwear or shoe covers if there is potential fecal contamination of the floor). Currently, there is insufficient evidence to warrant full isolation of clinically normal pets in which low-level shedding of Cryptosporidium is diagnosed as an incidental finding. However, the animal should not be allowed to defecate in common animal areas, feces should be removed and disposed of promptly, and contact with immunocompromised individuals should be avoided.

Cryptosporidium oocysts are highly resistant to routine disinfectants. Oocysts are resistant to routine chlorination of drinking water and are very small (4.5 × 5.0 µm), making them difficult to filter from water.142 Prolonged contact with high concentrations of chemicals such as formalin (>10%) or ammonia (>50%) can be effective;141 however, this is typically impractical. Moist heat (e.g., steam, pasteurization), freezing and thawing, or thorough drying are more practical means of disinfection126 but may not be completely effective. Oocysts survive better in cool water: after 4 weeks in water at 8°C, 75% of oocysts survive, whereas only 50% survive after 4 weeks in water at 25°C.99 Because oocysts are so resistant to disinfectants, preventing environmental contamination through excellent sanitation (i.e., mechanical cleaning) is critical.

Demodex spp.

Demodex mites are part of the normal microflora of mammals and are not usually associated with disease. However, overgrowth of mites in certain situations can cause alopecia or mild to moderate dermatitis. Demodex canis is most common in dogs, although Demodex injai or other species may be found rarely.143–146 In cats, Demodex cati predominates, while Demodex gatoi can be found in some regions.147–149Demodex folliculorum and Demodex brevis are most commonly reported in humans.150,151

In animals, particularly dogs, demodectic mange can be localized or generalized. Either form is more likely to occur in purebred dogs, but any breed or sex can be affected. The localized form is most common in puppies from a few months to 1 year of age, causing alopecia and folliculitis on the head (often around the eyes) and extremities. The vast majority of infected dogs (90%) recover without treatment, but some will progress to the generalized form. Generalized demodecosis typically occurs in young dogs (6–18 months of age) but can also occur in geriatric or immunosuppressed animals. This form of infection is often complicated by secondary bacterial pyoderma, which can be life threatening. Demodecosis is rare in cats.

Demodecosis is not considered transmissible under normal conditions, even from a clinically affected animal to other animals of the same species. Furthermore, Demodex mites are host adapted, and there is no convincing evidence of cross-infectivity. There is one report of identification of D. folliculorum in a child and his pet dog;152 however, that is the only report of concurrent detection of the same Demodex species in humans and their pet and, being a human Demodex species, would possibly indicate human-to-pet transmission. Accordingly, Demodex should not be considered a zoonotic risk.

Dipylidium caninum

Introduction

D. caninum