81 Enteric Coccidiosis

8/11/2019 81 Enteric Coccidiosis

1/21

Infectious Diseases of the Dog and Cat, 3rd Edition

CHAPTER 81 Enteric Coccidiosis

J.P. Dubey

Craig E. Greene

Coccidia are obligate intracellular parasites normally found in the intestinal tract. They belong to the phylum

Apicomplexa, class Sporozoasida, order Eucoccidiorida, and depending on the species, familyEimeriidae,

Cryptosporidiidae, or Sarcocystidae. Coccidian genera that infect cats and dogs areIsospora(also called

Cystoisospora),Hammondia, Besnoitia, Sarcocystis, Toxoplasma, andNeosporaspecies (see Chapter 80), as well as

Cryptosporidiumand Cyclosporaspecies (see Chapter 82).5Caryosporainfections are also discussed in this chapter.

Another coccidian genus,Eimeria, found commonly in herbivores, birds, lagomorphs, and rodents, is found only in

feces of dogs and cats after they ingest intestinal contents or feces from these animals. The oocysts pass unchanged

through the feline or canine intestine. Some coccidians of dogs remain unclassified.

Intestinal coccidia discussed in this chapter are host specific. Infections of definitive or intermediate hosts generallyonly occur in cycles established by evolution. Some aberrant cycles exist, such as with Sarcocystis neurona

infections in horses. Human health risks from these parasites are considered minimal to nonexistent, even in

immunosuppressed humans.

INTESTINAL COCCIDIOSIS

All coccidians have an asexual and a sexual cycle. In some genera, such as Sarcocystis, the asexual and sexual

cycles occur in different hosts, whereas inIsosporaboth cycles may occur in the same host (Table 81-1and Fig.

81-1). The oocyst is the environmentally resistant stage in the life cycle of all coccidia and is excreted in feces of

the definitive host.

A representative coccidian life cycle is best described as follows. Oocysts are passed unsporulated in feces and

contain a single nucleated mass called a sporont, which almost fills the oocyst (Fig. 81-2). After exposure to warm(20 C to 37C [68 F to 98.6 F]) environmental temperatures and moisture, oocysts sporulate, forming two

sporocysts. Within each sporocyst are four sporozoites (Fig. 81-3). The sporozoites have a banana shape and are

the infective stage (Fig. 81-4). They can survive environmental exposure, protected inside the oocysts for many

months. After the ingestion of sporulated oocysts by cats or dogs, sporozoites excyst in the intestinal lumen, and

the sporozoites initiate the formation of schizonts or meronts. During schizogony or merogony, the sporozoite

nucleus divides into two, three, or more nuclei, depending on the parasite and the stage of the cycle. After nuclear

division, each nucleus is surrounded by cytoplasm, forming a merozoite. The number of merozoites within a

schizont varies from two to several hundred, depending on the stage of the cycle and the species of coccidia.

Merozoites are released from the schizont when the host cell ruptures. The number of schizogonic cycles varies

with the parasitic species. First-generation merozoites repeat the asexual cycle and form second-generation

schizonts or transform into microgamonts (males) and macrogamonts (females). The microgamont divides into

many tiny microgametes. A microgamete fertilizes a macrogamete, and an oocyst wall is formed around the

zygote. The life cycle is completed when unsporulated oocysts are excreted in feces.

81

81.1

CHAPTER 81 Enteric Coccidiosis Page 1 of 21


2/21


IsosporaSpecies

Members of the genusIsospora, the most commonly recognized coccidians infecting dogs or cats, are species

specific for the definitive host. At least four speciesIsospora canis,Isospora ohioensis, Isospora burrowsi,

andIsospora neorivoltainfect dogs, and two speciesIsospora felisandIsospora rivoltainfect cats.

Epidemiology

The life cycle ofIsosporainfecting dogs and cats is similar to the basic coccidian intestinal cycle, except an

asexual cycle can also occur in the definitive or intermediate host. On ingestion by definitive or suitable

paratenic (intermediate) hosts, oocysts excyst in the presence of bile, and free sporozoites invade the

intestine. Some sporozoites penetrate the intestinal wall and enter mesenteric lymph nodes or other

extraintestinal tissues, where they form enlarging unicellular cysts (Fig. 81-5). If no replication occurs, the

host is called aparatenic hostrather than an intermediate host. Monozoic cysts ofIsosporamay remain in

extraintestinal tissues of definitive and paratenic hosts for the life of the host. In dogs and cats, these cysts

may serve as a source of intestinal reinfection and relapse of enteric coccidiosis. Ingestion of monozoic cystsin paratenic hosts leads to intestinal infection in the definitive dog and cat host. The life cycle after the

ingestion of paratenic host is the same as after the ingestion of sporulated oocysts from feces.

777

81.1.1

81.1.1.1



3/21


Fig 81-1 Life cycle of I. felis, which is typical of the Isosporaspp. The mode of

transmission may be direct, via ingestion of sporulated oocysts from

the environment, or indirect via ingestion of cysts in prey animals. A,Either sporulated oocysts or monozoic tissue cysts are ingested. B,

These excyst in the intestine. C, They undergo asexual

(endodyogeny) and (D)sexual (merogony and gametogony)

reproduction with the formation of a zygote. E, The zygote becomes

an (F)unsporulated oocyst that is shed in the stool (G). This matures

into the infectious sporulated oocyst which can be ingested by the

definitive or intermediate host. H, In the intermediate host, the

excysted sporozoites migrate to tissues and form cysts. (Courtesy

University of Georgia, Athens, Ga.)



4/21


Table 81-1 Comparison of Selected Coccidial Genera That Infect Dogs and

Cats

GENUS DIRECT

TRANSMISSION

POSSIBLE?

SEXUAL CYCLE: INTESTINAL

REPLICATION

ASEXUAL CYCLE: EXTRAINTESTINAL

REPLICATION

DEFINITIVE

HOST

FORM OF

OOCYST PASSED

INTERMEDIATE OR

PARATENIC HOSTS

LOCATION OF TISSUE

CYSTS

Isospora Yes Dog and cat U Dog, cat, many other

mammals

Extraintestinal or

lymphoid tissues

(monozoic)

Besnoitia No Cat U Many vertebrates Fibroblasts

Hammondia No Dog and cat U Herbivores, rodents Skeletal muscle

Sarcocystis No Dog and cat Sa Many vertebrates Cardiac and skeletal

muscle

Cryptosporidium Yes Dog and cat Sb None None

Toxoplasma Yes Cat U Many vertebrates Many tissues

U,Unsporulated;S,sporulated.

a Free sporocysts.

b Naked sporozoites.

Fig 81-2 Unsporulated oocysts of Isospora canis (C), Isospora ohioensis (O),

and Hammondia heydorni (H)and sporulated sporocyst of

Sarcocystisspecies (S)from canine feces (unstained, 1700). (From

Dubey JP. 1976. A review ofSarcocystisof domestic animals and of

other coccidia of cats and dogs, J Am Vet Med Assoc169:1061-1078.)



5/21


Clinical Findings

Diarrhea with coccidiosis in immunocompetent animals probably represents incidental or concurrent

infections with coccidia and other infectious agents because coccidial infection can be present in the absence

of clinical illness. Enzootic infections are frequently found in catteries or kennels where animals congregate.

Clinical signs are most apparent in neonates. Experimental studies have shown that clinical signs of intestinal

disease are uncommon unless large numbers of oocysts are fed to very young (younger than 1 month) or

immunosuppressed animals. Clinically, severe diarrhea has been associated with naturally occurring

coccidiosis in immunosuppressed dogs and cats. German shepherd dogs may have an increased susceptibility

to clinical infection.27,41

Diarrhea with weight loss and dehydration and, although rare, hemorrhage is the

primary sign attributed to coccidiosis in dogs and cats. Anorexia, vomiting, mental depression, and

ultimately death may be seen in severely affected animals. Severely immunosuppressed dogs and cats may

have extraintestinal stages in macrophages of the lymphocyte-depleted mesenteric lymph nodes or

extraintestinal tissues.

Fig 81-3 Sporulated oocysts of I. canis (C), I. ohioensis (O), and H. heydorni (H)

(unstained, 1700). Compare with Fig. 81-2. (From Dubey JP. 1976. A

review ofSarcocystisof domestic animals and of other coccidia of

cats and dogs,J Am Vet Med Assoc169:1061-1078.)

Intestinal coccidiosis may be manifest clinically when dogs or cats are shipped or weaned or experience a

change in ownership. Diarrhea might result from the extraintestinal stages ofIsosporareturning to theintestines. Monozoic cysts do not cause clinical disease in paratenic hosts.

81.1.1.2



6/21


Fig 81-4 I. canissporulated oocyst treated with 5.25% sodium hypochlorite

solution to dissolve part of oocyst wall (OW). Two sporocysts occupy

most of oocyst. Each sporocyst has a thin sporocyst wall (SW), fourbanana-shape sporozoites (S), and a sporocystic residual body (SR).

SR may be compact or dispersed (unstained, 1600). (From

Kirkpatrick CE, Dubey JP. 1987. Enteric coccidial infections. Isapora,

Sarcocystis, Cryptosporidium, Besnoitia, and Hammondia, Vet Clin

North Am Small Anim Pract 17:1405-1420.)



7/21


Fig 81-5 Tissue cyst of I. ohioensisin smear of mesenteric lymph node of an

experimentally infected mouse. The sporozoite (S)is surrounded by

a thick cyst wall (CW). Vacuole around cyst wall is fixation artifact(PAS stain, 1250).

Diagnosis

Intestinal coccidial infection in dogs and cats is diagnosed by identification of the oocysts with any of the

fecal flotation methods commonly used to diagnose parasitic infections (see Fecal Examination, Chapter 70).

Shedding of oocysts by some animals may be erratic, therefore repeated examinations are recommended. In

dogs, onlyI. caniscan be identified with certainty by oocyst size and shape (see Fig. 81-2). The two species

ofIsosporafound in cats can be readily distinguished by oocyst size (see Fig. 80-9). Oocysts ofI. felisin

cats andI. canisin dogs are large and easily distinguished from small oocysts, whereas it is almost

impossible to distinguishI. rivolta, I. burrowsi, andI. ohioensismorphologically (Fig. 81-6; see also Fig.

80-9). AlthoughI. felis-, I. rivolta-, I. canis-, andI. ohioensis-like oocysts are passed unsporulated in freshly

excreted feces, they sporulate partially by the time a fecal examination is made. Partially sporulated oocysts

contain two sporocysts without sporozoites.Isosporaspp. may sporulate within 8 hours of excretion, and

theseIsosporaare highly infectious.

777

77881.1.1.3



8/21


Fig 81-6 Unsporulated oocysts of I. ohioensis (O)and H. heydorni (H)

compared with eggs of nematodes Toxocara canis (C)and

Ancylostoma caninum (A)in flotation of canine feces (unstained,385). (From Dubey JP. 1976. A review ofSarcocystisof domestic

animals and of other coccidia of cats and dogs,J Am Vet Med Assoc

169:1061-1078.)

Therapy

The presence of underlying disease or host immunosuppression should be suspected when coccidial

infections persist for extended periods in older animals or when associated with chronic diarrhea. Treatment

is often indicated in bitches and their newborn puppies because of the severity of clinical signs at this age. If

diarrhea or dehydration is severe, parenteral fluid therapy must be considered as a supportive measure. Blood

transfusion may be required when severe intestinal hemorrhage results in anemia.

Specific therapy involves the use of drugs that are coccidiostatic rather than curative (Table 81-2). However,

as with many protozoal diseases, the presence of low-level infection may lead to premunition. The drugs

shorten the prepatent period and may shorten the course of the disease.

Sulfonamides have long been the drugs of choice for the treatment of coccidiosis. Rapid-acting

sulfonamides, such as sulfadimethoxine or sulfaguanidine, can be given alone or in combination with otherantifolate drugs such as trimethoprim. Trimethoprim-sulfonamide offers the advantages of being readily

available and being less toxic than other drugs. It should be considered a drug of first choice. Nitrofurazone

can be administered alone or in combination with sulfonamides. Nitrofurazone is also available as a 4.59%

soluble powder that can be added to drinking water (up to 1 g/2 L) for 7 days.

81.1.1.4



9/21


Amprolium is considered an effective preventive and treatment for coccidiosis in kenneled puppies.

Although it is not currently approved for use in dogs, it can be administered as an undiluted liquid and a

paste, but it is unpalatable in these forms (see Drug Formulary, Appendix 8).

Table 81-2 Anticoccidial Drugs for Dogs and Cats

DRUGa SPECIES DOSE (mg/kg)

b ROUTE INTERVAL

(HOURS)

DURATION

(DAYS)

Sulfamethoxinec B 5060 PO 24 520

Sulfaguanidine B 100200 PO 8 5

Trimethoprim- D 3060d PO, SC 24 5

sulfonamide B 1530e PO, SC 1224 5

Ormetoprim-sulfadimethoxineD 66f PO 24 723

Furazolidoneg B 820 PO 1224 5

Amprolium D 300400 (total)h PO 24 5

D110200 (total)

i PO 24 712

C 60100 (total) PO 24 7

Quinacrine B 10 PO 24 5

Spiramycin H 50100 (total)j PO 24 5

Toltrazuril D 15 PO 24 36k

Ponazuril B 7.515l PO 24 28

Roxithromycin H 2.5 PO 12 15

B,Dog and cat; D,dog; C,cat; H,human; PO,by mouth;SC,subcutaneous.

a See Appendix 8, Drug Formulary, for additional information.

b Dose per administration at specified interval.

c Other sulfonamides, such as sulfadimidine and sulfaguanadine, can be used, but sulfaquinoxaline

should not be used because it interferes with ditamin K synthesis and may result in hemorrhagic

complications.

d Greater than 4kg body weight.

e Less than 4kg body weight.

f 11 mg ormetoprim and 55 mg of sulfadimethoxine.

g When furazolidone is combined with sulfonamides, 50% of this dose is used.

h Total dose per day. Lower dose recommended for puppies, with a maximum of 300 mg total per

day (see Drug Formulary,Appendix 8).

i Total dose per day. Combine 150 mg amprolium and 25 mg sulfadimethoxine per kilogram per

day for 14 days (see Drug Formulary, Appendix 8).

j Total dose per day. Dose on a mg/kg basis is listed in Drug Formulary,Appendix 8.

k Doses of 30 mg/kg have been used for 1 day; however treatment at half that dose for at least 3

days with repeating if needed, has been more effective in treatment of pups and kittens with

coccidiosis without relapses.

l Dose extrapolated from use in horses and mice for treatment of Sarcocystis neuronainfections.

778

779



10/21


Quinacrine, spiramycin, toltrazuril, tetracycline, and roxithromycin have been used on a limited basis to treat

canine and feline coccidiosis.4Their use might be considered if more established treatment regimens fail or

protozoal resistance develops.

Prevention

Coccidiosis tends to be a problem in unsanitary environments. The fecal shedding of large numbers of

environmentally resistant oocysts makes infection likely under such conditions. Animals should be housed in

a way that does not allow contamination of food and water bowls by oocyst-laden soil or infected feces.

Feces should be removed daily and incinerated. Oocysts survive freezing temperatures. Runs, cages, food

utensils, and other implements should be disinfected by steam cleaning or immersion in boiling water or by a

10% ammonia solution. Animals should have limited access to intermediate hosts and should not be fed

uncooked meat. Insect control is essential in animal quarters and food storage areas because cockroaches and

flies may serve as mechanical vectors of oocysts. Coccidiostatic drugs can be given to infected bitches before

or soon after whelping to control the spread of infection to puppies.

HammondiaSpecies

Two species ofHammondiaexist in domestic animals:Hammondia hammondi, with cats as definitive hosts,

andHammondia heydorni, with dogs and other canids as definitive hosts.5,25

UnlikeIsosporaspecies,H.

hammondiandH. heydornihave obligatory two-host life cycles (see Chapter 80and Table 81-1). Goats and

rodents are natural intermediate hosts forH. hammondi, and the domestic cat (Felis catus)and the European

wild cat (Felis sylvestris)are the definitive hosts.H. hammondidoes not invade extraintestinal tissues of the

cat, and cats are infected only by eating tissue cysts. Experimentally, many warm-blooded animals, including

monkeys, sheep, goats, pigs, rabbits, guinea pigs, and mice, can serve as intermediate hosts. Intermediate hosts

become infected by ingesting sporulated oocysts, which resemble those of T. gondii. Sporozoites excyst in the

intestinal lumen, invade the intestinal wall, and multiply as tachyzoites in the intestines, mesenteric lymph

nodes, and other tissues. The parasite eventually encysts principally in muscles (Fig. 81-7).

H. heydorni'slife cycle is not fully known but seems to be similar to that ofH. hammondi. Dogs and other

canids are definitive hosts, and cattle, sheep, goats, buffaloes, camels, moose, and deer serve as intermediate

hosts.14,26a

The structure of the parasite in the intermediate hosts is not known.H. hammondiandH. heydorni

are nonpathogenic, therefore no treatment is necessary.

BesnoitiaSpecies

Cats, not dogs, are definitive hosts for three species ofBesnoitia:Besnoitia wallaceiof rats and mice,Besnoitia

darlingiof opossums and possibly lizards, andBesnoitia oryctofelisiof rabbits.18,26

The life cycle ofBesnoitiais similar to that of T. gondii(see Table 81-1). Cats become infected by ingesting

tissue cysts, and schizonts (Fig. 81-8) and gamonts are formed in intestinal goblet cells or lamina propria.

Schizonts may be found in extraintestinal organs.26

Unsporulated oocysts are shed in feces, and they are

difficult to distinguish from those of T. gondii. Intermediate hosts become infected by ingesting sporulated

oocysts. The parasite develops in connective tissue, and cysts may become macroscopic.Besnoitiais

considered nonpathogenic in cats, and no treatment is necessary.

779

780

81.1.1.5

81.1.2

81.1.3



11/21


Fig 81-7 H. hammonditissue cyst in skeletal muscle of mouse. Note thin cyst

wall enclosing hundreds of periodic acidSchiff-positive bradyzoites

(PAS stain, 750).

Fig 81-8 B. oryctofelisischizonts in the lamina propria of jejunum of an

experimentally infected cat (H and E stain, 750).



12/21


IntestinalSarcocystisSpecies

Infections resulting from Sarcocystisspp. are ubiquitous in reptiles, birds, and warm-blooded animals.

5

Virtually all cattle and sheep are infected with this parasite. More than 90 species of Sarcocystishave been

identified, and they have an obligatory two-host life cycle (see Table 81-1). Carnivores (predators) are

definitive hosts, and herbivores (prey) are intermediate hosts. As the name implies, the parasite forms tissue

cysts (sarcocysts) in muscles and neural tissues of these intermediate hosts (Fig. 81-9). Sarcocysts are thin or

thick walled, and the zoites are usually separated from each other by septa. Cats and dogs become infected by

ingesting sarcocysts. The life cycle of Sarcocystisis distinct from other coccidians of domestic animals in that

oocysts sporulate within the definitive host and are excreted in the feces in an infective form (Fig. 81-10). The

intermediate hosts become infected by ingesting sporocysts or oocysts. One to three generations of schizogony

occur in blood vessels or hepatocytes (depending on the species of intermediate hosts). Merozoites then invade

skeletal muscles and nerve cells, where they form sarcocysts (see Figs. 81-10and 81-11). Certain species of

Sarcocystis, transmissible via dogs, are pathogenic in cattle, sheep, goats, pigs, and mule deer, whereas species

transmissible via cats are generally nonpathogenic.

Fig 81-9 Esophageal muscle with thick-walled sarcocyst ofSarcocystis hirsute(H

and E stain, 630). (From Gardiner CH, Fayer R, Dubey JP. 1988.An

atlas of protozoan parasites in animal tissues, Beltsville, Md, USDA

Agricultural Handbook No 651.)

More than 20 species of Sarcocystisinfect cats and dogs. It is not possible to differentiate species on the basis

of measurement of sporocysts. Sarcocystisis excreted in feces fully sporulated, often as free sporocysts when

examined microscopically (Fig. 81-12). They are small and not very dense, so they lie at a different plane of

focus than other parasites.

81.1.4



13/21


Sarcocystisspecies are not pathogenic for the intestinal tract of dogs or cats, so no treatment is necessary.

Infections can be prevented by cooking all meat fed to animals. Occasionally, sarcocysts are found in skeletal

muscles of immunosuppressed or wild cats and dogs, but their life cycle is unknown.8,12

ExtraintestinalSarcocystisspp.

Sarcocystis canis Infection

One of the extraintestinal Sarcocystis-like parasites (S. canis)has been found in Rottweiler dogs in the

United States.0a,21-23,48a

Only asexual stages (schizonts) were seen in various cells, including neurons,

hepatocytes, and dermal cells (Figs. 81-13and 81-14). Affected dogs ranged from 2 days old to adult dogs

and had neurologic and hepatic signs and dermatitis. Schizonts were 5 to 25 4 to 20 m and contained 6 to

40 merozoites. Occasionally, merozoites were arranged around a residual body. The parasite was named S.

canisbecause it differed from other species of Sarcocystis. Its life cycle is unknown. An unidentified

Sarcocystissp. caused granulomatous myositis in a dog.2a

FelineSarcocystis Infection

Sarcocysts have been identified in the skeletal and cardiac muscles of 11 free-ranging Florida panthers and

cougars,30

3 domestic cats32

and in hind-limb muscle biopsy specimens of 2 domestic cats.28

The sarcocysts

found in these studies were not specifically identified, and the immune status of the host may have been

compromised. Some of these infections might have been caused by Sarcocystis neurona, which is discussed

in the following section.

780

782

81.1.5

81.1.5.1

81.1.5.2



14/21


Fig 81-10 Life cycle ofS. cruzi, which is typical ofSarcocystisspp. A, Muscle

cyst is ingested by definitive carnivore host. B, These excyst in the

small intestine and penetrate epithelial cells. C, Gametes develop inthe intestinal epithelium and these (D)fuse to form a zygote which

matures into an unsporulated and then a sporulated oocyst. E,

Sporulated oocysts are shed in the feces. F, Oocysts, ingested by

herbivores, excyst in the small intestine to release sporozoites. G,

These penetrate the epithelium and migrate in the blood

vasculature where they replicate in two phases of schizogony. H, In

the final stages, mature schizonts rupture releasing merozoites

which enter the muscles to form sarcocysts which contain many

organisms. (Courtesy University of Georgia, Athens, Ga.)



15/21


16/21


Sarcocystis neurona Infection

S. neuronais the principal parasite associated with equine protozoal encephalomyelitis, although a species of

Neosporahas also been incriminated (see Chapter 80). Opossums (Didelphis virginiana)are the definitive

hosts for S. neurona(Fig. 81-15). Animals that ingest oocysts from opossums and serve as intermediate hosts

by developing muscle sarcocysts are the nine-banded armadillo (Dasypus novemcinctus), striped skunk

(Mephitis mephitis), raccoon (Procyon lotor), sea otter (Enhydra lutris), and brown-headed cowbird

(Molothrus ater).19,36

Experimentally and naturally, cats have been shown to be intermediate hosts of S.

neurona, although results have varied with individual isolates.1,19,49

Cats experimentally fed sporocysts shed

by opossums develop schizonts in their tissues and sarcocysts in their muscles, and infected cats develop

high antibody titers (1:4000) as measured by a serum agglutination test.17

Opossums were shown to shed S.

neuronasporocysts after ingesting feline tissues containing sarcocysts.16

Horses are considered incidental or

aberrant dead-end hosts because they only develop lesions within the central nervous system, and muscle

sarcocysts have not been documented. This organism can cause fatal encephalomyelitis in dogs, raccoons,

mink, and cats.

Fig 81-13 S. canisschizonts in section of dermal ulcer from dog. Note

distended macrophages (arrows)with parasites in inflammatory

exudate, mainly neutrophils (H and E stain, 750).

81.1.5.3



17/21


Fig 81-14 An intactS. canisschizont (arrow)and several merozoites

(arrowheads)released from ruptured schizont in smear of exudate

from dermal ulcer of dog (Giemsa stain, 750).

Sarcocystis-associated meningoencephalomyelitis was described in a 13-week-old Burmese kitten with

lethargy, depression and crying, and progressive upper motor neuron hemiparesis.13

Another 12-week-old

kitten developed progressive neurologic dysfunction 3 days after a routine castration.6Encephalomyelitis

was associated with numerous S. neuronaschizonts and merozoites in the brain and spinal cord. S. neurona

infection was also documented in a 13-year-old captive Canadian lynx (Felis lynx Canadensis).29

Serum

antibodies to S. neuronawere detected in 13% of 310 farm cats from Ohio48

and in 5% of 196 domestic cats

from Michigan whose sera were submitted for T. gondiiantibody testing.43

Diagnosis in horses has involved

immunoblot testing for specific antibodies to S. neuronain cerebrospinal fluid not contaminated with blood.

Use of feline antibody conjugates would be needed to apply this method for use in cats. Treatment of

affected cats has not been attempted because diagnosis of clinically affected cats was made after death.

Effective treatment of horses has involved the use of ponazuril. (See Table 81-2and Drug Formulary,

Appendix 8, for dosage information that has been extrapolated from dosages used to treat horses and mice.)

Other anticoccidial drugs such as clindamycin, tetracyclines, or antifolate inhibitors might also be considered.

782

784



18/21


Fig 81-15 Life cycle ofS. neurona. Opossums (Didelphis virginiana, D.

albiventris) are its definitive hosts. They ingest organisms from the

tissues of intermediate hosts. A, These excyst in the small intestineand enter the gut epithelium. B, Gametogony occurs followed by

fertilization producing a zygote which eventual forms an oocyst. C,

Sporulated oocysts shed in the feces are ingested by natural

intermediate hosts such as cats, armadillos, raccoons, sea otters,

skunks and possibly other mammals. D, Ingested sporocysts excyst

in the small intestine and (E)replicate to a limited extent within the

vascular endothelium and leukocytes within viscera and then

spread, probably by leukocytes, to other tissues. F, There,

sarcocysts, composed of bradyzoites, develop in the muscle and

neural tissues. Equids are considered aberrant intermediate hosts asdevelopment does not occur beyond schizont and merozoite

stages. (Courtesy University of Georgia, Athens, Ga.)



19/21


Fig 81-16 Section from skin of dog with Caryosporadermatitis. Note

numerous Caryosporastages in dermal cells, including gamonts and

schizonts (H and E stain, 750; bar = 10 m). (From Dubey JP, BlackSS, Sangster LT, et al. 1990a. Caryospora-associated dermatitis in

dogs, Parasitol76:552-556.)

VISCERAL AND CUTANEOUS CARYOSPOROSIS

A Caryospora bigeneticalike organism was isolated from cutaneous nodules in five dogs ranging in age from 2

to 6 months. The dogs were thought to be concurrently affected with a distemper virus-like infection.7The skin

nodules were up to 2 cm in diameter, and some had a central ulcerated area through which serohemorrhagic

exudate could be expressed. Microscopically, the dermatitis was characterized by edema and infiltrations by

polymorphonuclear cells, eosinophils, and macrophages (Fig. 81-16). Schizonts, male and female gamonts,

unsporulated and sporulated oocysts, and caryocysts were seen in macrophages. In one dog, infection had spread

to the lymph nodes.

Members of the genus Caryosporahave an oocyst with one sporocyst that contains eight sporozoites, and they

typically parasitize reptiles and raptors. At least two species, C. bigeneticaand Caryospora simplex, parasitize

rodents and snakes. Caryosporaspp. have a complicated life cycle involving asexual and sexual multiplication in

the prey (rodent) and the predator (snake). In addition to usual schizonts and gamonts, sporulated oocysts and

monozoic cysts (caryocysts) are formed in connective tissue cells of the prey. The caryocysts (unlike sporocysts

and oocysts) have a thin cyst wall enclosing the host cell nucleus. Two unusual features of Caryosporastages are

noted in histologic sections of dog tissue: (1) the small size (less than 15 m) of all developmental stages and (2)

the presence of gamonts, schizonts, and oocysts in a single macrophage.

81.2



20/21


Fig 81-17 Mesenteric artery with multinucleated first-generation meront ofS.

hirsute(synonymS. bovifelis) protruding into lumen (H and E stain,

630). (From Gardiner CH, Fayer R, Dubey JP. 1988.An atlas ofprotozoan parasites in animal tissues, Beltsville, Md, USDA Agricultural

Handbook No 651.)

INTRAHEPATIC BILIARY COCCIDIOSIS IN DOGS

Intrahepatic biliary coccidiosis is a rare condition in dogs.34

Clinical signs associated with hepatic disease include

icterus, weight loss, and vomiting. Small and large bile ducts are enlarged because of inflammation and

desquamation of epithelial cells. Lesions may extend into hepatic parenchyma. Asexual stages (schizonts) of an

unidentified coccidium are found in biliary epithelial cells (Fig. 81-17). These coccida are different from

Toxoplasma, Sarcocystis,Hammondia, and Cryptosporidiumspecies and any other known coccidium found in the

dog.

INTRAPULMONARY COCCIDIOSIS IN DOGS

An adult dog with clinical signs of weakness, fever, diarrhea, dehydration, weight loss, and harsh lung sounds was

found to have canine distemper complicated by pulmonary infection with coccidia-like organisms.38

Asexual

stages of coccidia were observed in cytoplasmic vacuoles of many bronchiolar epithelial cells.

Suggested Readings*

* See the CD-ROM for a complete list of references.

1. Butcher, M, Lakritz, J, Halaney, A, et al.: Experimental inoculation of domestic cats (Felis domesticus)

with Sarcocystis neuronaor S. neurona-like merozoites. Vet Parasitol. 107, 2002, 1142.

81.3

81.4

81.5



21/21


4. Daugschies, A, Mundt, HC, Letkova, V: Toltrazuril treatment of cystoisosporosis in dogs under

experimental and field conditions.Parasitol Res. 86, 2000, 797799.

6. Dubey, JP, Benson, J, Larson, MA: Clinical Sarcocystis neuronaencephalomyelitis in a domestic cat

following routine surgery. Vet Parasitol. 112, 2003, 261267.

Uncited references

45. Schares, G, Heydorn, AO, Cppers, A, et al.:Hammondia heydorni-like oocysts shed by a naturally

infected dog andNeospora caninumNC-1 cannot be distinguished.Parasitol Res. 87, 2001, 808816.

81.6


Documents

81 Enteric Coccidiosis