Parasitos en Reptiles

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Topics in Medicine and SurgeryTopics in Medicine and Surgery

Gastrointestinal Protozoal Diseases in ReptilesFrancis T. Scullion, MVB, PhD, MRCVS,M. Geraldine Scullion, MVB, MRCVS

Abstract

This article outlines the principal gastrointestinal protozoal diseases that have beenrecorded as affecting reptiles. It covers 9 genera of flagellates/amoebae, 1 ciliategenus, and 5 genera of coccidia, describing their pertinent anatomy and what isknown about their epidemiology, including clinical presenting signs and intestinal

pathological changes. The agents are initially discussed individually and, to avoidrepetition, common information about diagnostics, treatment, and control is then

presented. 2009 Published by Elsevier Inc.

Key words:Amoebae; ciliates; coccidia; flagellates; gastrointestinal parasites; reptiles

Protozoa are commonly found in the gastroin-testinal tract of reptiles. Some are commensalorganisms, some are mutualistic, assisting in

digestion, and others may be transient organismsoriginating in prey species.1-3Although parasitism isthe single most common disorder of the digestive

system seen in pet reptiles, information on theprecise role of many protozoa is limited. 4 To im-prove our understanding, it is necessary to ascer-tain the exact role of individual protozoan speciesin disease. Morphological features of structuressuch as the locomotor apparatus taxonomicallydefine most major groups of protozoa. In the past,many reports of protozoa of reptiles gave only atentative identification to genus and species levelpartly because the distinguishing features of pro-tozoa are at the limits of what can be discernedsolely by light microscopy. More recent use of

other scientific parameters such as developmentalbiology, host specificity, histopathology, electronmicroscopy, and immunological and molecular bi-ology has shown characteristics that provide reli-able identification to genus and species level. Theability to further identify parasites with advancedscientific methods assists in further defining spe-cies, extending epidemiological information, andunderstanding the host/parasite relationships(see Cooper, this issue).

In the host/parasite/environment triad of diseasecausation, the prominent role of environment fur-ther complicates disease pathogenesis in ectother-mic animals because many captive reptiles are main-tained in suboptimal environmental conditions (seePerez, this issue). Multifactorial disease conditions

are a feature of reptile medicine, and, indeed, someresearchers believe that the stress induced by otherinfections is a prerequisite for parasitic disease.5

In many countries, there is an increase in thenumber of pet reptiles. With a concomitant in-creased interest in biodiversity, more informationhas become available about the veterinary aspects ofreptile health and disease. Any effort to improve anunderstanding of disease requires a review of theinformation that is currently available. This articleoutlines the principal gastrointestinal protozoal dis-

From the Royal (Dick) School of Veterinary Studies, University

of Edinburgh, Easter Bush, Midlothian, Scotland, and Veteri-nary Services, Ballygawley, Tyrone, Northern Ireland.

Address correspondence to: Francis T. Scullion, MVB, PhD,MRCVS, Veterinary Services, 16 Cranlome Rd, Ballygawley, Co.Tyrone, Northern Ireland, BT70 2HS, United Kingdom. [email protected].

2009 Published by Elsevier Inc.1557-5063/09/1804-$30.00doi:10.1053/j.jepm.2009.09.004

266 Journal of Exotic Pet Medicine, Vol 18, No 4 (October), 2009: pp 266-278
mailto:[email protected]:[email protected]:[email protected]


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eases that have been recorded as affecting reptiles. Itcovers flagellates/amoebae, ciliates, and coccidia,

outlining pertinent anatomy and what is known re-garding their epidemiology, and describes clinicalsigns and intestinal pathological changes. Each or-ganism is initially discussed individually, and, so as toavoid repetitive information diagnostics, treatmentand control that are common to that particular or-ganism are then presented. The classification in thistext follows that used by Barnard and Upton.6 Mi-crosporidia and myxozoans are not included, be-cause recent work classifies these organisms as fungiand metazoa, respectively.7 Protozoa from 3 of the 5recognized phyla are reported to cause gastrointes-

tinal disease in reptiles (Tables 1-3).

Phylum Sarcomastigophora

Flagellates and amoebae are unicellular organismsthat usually possess a single nucleus and use flagellaor pseudopodia to move.

Anatomy

Flagellates. Flagellate protozoan trophozoites move

with up to 8 whiplike flagella, each composed of a

central axoneme and an outer sheath that arisesfrom a kinetosome (basal body) in the cytoplasm.

The anatomy of the flagellar apparatus helps to de-fine taxonomic relationships. Sometimes the flagellaare free or can be attached to the body, either alongits entire length or at several points forming anundulating membrane. Different species of flagel-late are also defined by the length and width of thetrophozoite. Although traditionally classified bymeasurements using light microscopy, more precisedetermination has been reported for some genera byuse of the electron microscope.8

Amoebae. Amoebae move with 4 types of tempo-

rary pseudopods: lobopods, filopods, myxopods, andanopods. Amoeboid movement can be described assmooth, gliding, bending, snapping, jerky, or twist-ing when observed under the microscope. Both thetype of pseudopod and movement help with specificamoebae identification (see Cooper, this issue).

Amoebae sometimes have flagella during differentstages of development such as reproduction ordispersal.6

Epidemiology

Flagellates and amoebae have direct life cycles andreproduce asexually by binary fission. The motile

vegetative trophozoites thrive in damp, warm condi-tions, some forming infective cysts to resist desicca-tion. Infections are spread by fomites, mechanical

vectors including insects, and on ingestion of con-taminated food and water. When ingested, cysts re-lease invasive trophozoites, which can be detected infecal smears (see Cooper, this issue).

Many protozoan parasites seem to be associatedwith concurrent infection of the host by bacteria,viruses, or yeasts.7 Flagellates are found in low num-

Table 1. Flagellates and amoebae associated with gastrointestinal disease in reptiles

Phylum Sub phyla Order Genus

Sarcomastigophora Mastigophora

(Flagellates)

Trichomonadida

(Trichomonads)

Hexamastix

Hypotrichomonas

Monocercomonas

TetratrichomonasTritrichomonas

Diplomonadida

(Diplomonads)

Giardia

Spironucleus

Kinetoplastida

(Kinetoplasts)

Leptomonas

Sarcodina

(Amoebae)

Entamoeba

Table 2. Ciliates associated with

gastrointestinal disease in reptiles

Phylum Class Order Genus

Ciliophora

(Ciliates) Litostomatea

Vestibuliferida

Balantidium

Gastrointestinal Protozoal Diseases in Reptiles 267


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bers in the intestinal lumen of most clinically healthyreptiles, and it is therefore difficult to attribute dis-ease causation to flagellates that are found in fecalsamples of sick reptiles. Disease attributable to flagel-

lates usually depends on a combination of factors,including host resistance, immune status, socialstressors, incorrect environmental temperatures,parasite load (numbers), and the pathogenicity ofthe protozoa. Although several species of amoebaeare found in reptiles as commensals, pathogenicityin some cases depends on the hosts body tempera-ture.2

Diseases

Flagellates: Trichomonads. The evidence linkingtrichomonads with intestinal disease in reptiles isscant and based mainly on case reports.Table 1lists5 genera of trichomonads that have been associated

with large intestine enteritis in reptiles, one ofwhich, Monocercomonas, is discussed below. Table 4lists some anatomical features that differentiatethese pathogenic trichomonads. Trichomonads aregenerally pear shaped with a prominent supportingmicrotubule anteriorly (cranially) and 4 to 6 flagella.One flagellum is directed posteriorly (caudally), of-

ten with an associated undulating membrane.Trichomonads do not form cysts, but some speciesare capable of withstanding passage through thestomach.

Monocercomonasis found in lizards and snakes andcan cause gastrointestinal signs such as anorexia,lethargy, gastric swelling, gray soft to watery feces,occasional colic, and cloacal prolapse. Mononuclearcell inflammatory infiltrates are found in the laminapropria of the entire gastrointestinal tract associated

with hyperemia and edema. In animals exhibitingmucopurulent enteritis, monocercomonads havebeen found attached to intestinal epithelia or inmore severe cases undermining the mucosal surface.

A variety of other disease conditions, including oo-phoritis, cholecystitis, and pneumonia suggests that

further tissue invasion of this organism is possible.

9,10

One study illustrated a combined gastrointestinalinfection ofMonocercomonasspp. andEntamoebaspp.Focal invasion of intestinal mucosa by monocer-comonads was associated with invading entamoebae,tissue lesions, and inflammatory reactions.11

Flagellates: DiplomonadsHexamita parva.Many parasitic species ofHexamitaare often placed inthe genusSpironucleus.6 Infestation of reptiles is com-

Table 3. Coccidia associated with gastrointestinal disease in reptiles

Phylum Subclass Suborder Genus

Apicomplexa

Coccidiasina

Eimeriorina

(Eimeriids) CryptosporidiumCaryospora

Eimeria

Isospora

Sarcocystis

Table 4. Some anatomical features of pathogenic trichomonadsGenus Flagellar characteristics Undulating membrane

Hexamastix 5 anterior flagella and one trailing flagellum. Absent

Hypotrichomonas 3 anterior flagella and a recurved flagellum which

extends freely.

Shallow; shorter than the body

Monocercomonas 3 anterior flagella and a trailing flagellum usually larger

than the anterior flagella.

Absent

Tetratrichomonas 4 flagella and a posterior flagellum which extends freely. Extends nearly entire body length

Tritrichomonas 3 anterior flagella; the recurrent flagellum extends

beyond the body as a free flagellum.

Present

268 Scullion and Scullion


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mon, although pathogenicity appears to be less oftenobserved. Trophozoites move fast in straight lines,quickly changing direction. In more viscous mate-rial, they rotate around their long axis and appear

very flexible. Although pleomorphic, they are recog-nized as egg-shaped parasites in stained preparations(see Cooper, this issue). Six flagella originate from

the basal bodies. The nuclei are situated at the bluntanterior end and often slightly protrude. Caudal tothe nuclei, 2 microtubular skeletal structures, re-ferred to as rhizostyles, traverse the body and termi-nate before reaching the tapering posterior end andcontinue as 2 caudal flagella of unequal length. Tro-phozoites measure about 8 m long by 5 m wideand are excreted in feces and urine with exposure toother animals through ingestion. The organismsthen invade other tissues with direct access to theintestine such as the urinary tract or liver.

Clinical disease related to primary pathology inthe urinary tract is manifest as failure to thrive, pro-gressive lethargy, and weight loss in chelonians. Theseverity of lesions associated with infestation de-pends on the extent and duration of disease. Al-though no clinical signs of enteritis are evident, focalnecrosis of duodenal epithelium associated with par-asites has been seen, along with extensive epithelialerosion in the colon.12

Giardia spp. Their classic elliptical, symmetricalshape, with broad anterior and pointed posterior

ends and a falling-leaf motion, typifies the trophozo-ites ofGiardiaspp. The dorsal aspect is convex, andthe ventral face has a large, adhesive disc. There are4 pairs of flagella with 2 anteriorly placed nuclei,giving organisms a monkey-faced appearance. Cystsare roughly egg shaped with 2 or 4 nuclei in anoff-center position.13

There appears to be little information regardingGiardiaspp. in reptiles. Most consider the organismto be nonpathogenic in reptile species, but there wasa report ofGiardia spp. associated with enteritis insnakes (Causus spp. and Lampropeltis spp.) in the

early 1950s.2,14

Flagellates: Kinetoplasts. These flagellates have aconcentrated portion of DNA in a single mitochon-drial structure called the kinetoplast, located close tothe basal body. This mitochondrial DNA stains well

with Giemsa, and the position of the kinetoplast inrelation to the nucleus defines each genus (see Spe-cial Stains).

Leptomonas. These protozoa are generally re-garded as parasites of invertebrates. It is recognized

that misidentification has occurred because of diffi-culties in classification of this genus.6 One report ofcolitis in chameleons should be viewed with theabove statement in mind.15

Amoebae: Entamoeba invadens. The most signif-icant amoeboid parasite of reptiles is the highly

pathogenicEntamoeba invadens. In some snakes, dis-ease due toEntamoebahas been shown to be depen-dent on the temperature at which the hosts aremaintained.16 The clinical signs are variable and in-clude listlessness, prolonged anorexia, and wasting.

Affected reptiles often have smelly, mucoid dysen-tery. Vomiting and polydipsia may occur, anddehydration becomes a problem as the diseaseprogresses. In the later stages of the disease, thick-ened intestines and gas accumulation cause swellingof the abdomen and cloacal protrusion. The para-sites can invade the liver and cause abscesses and

necrosis. Amoebae have also been found in bloodvessels, lungs, spleen, pancreas, kidneys, and subder-mal tissues. Death may occur early in the course ofthe disease or after months of illness. On postmor-tem examination, ulcerative, hemorrhagic colitis isobserved, sometimes extending to the ileum. Theintestinal contents are purulent, fibrinous, andblood stained, and the intestinal wall is thickened,congested, and necrotic. In chronic cases, granulo-matous inflammation can result in colonic occlu-sion. Ulcerative gastritis may be a terminal event.7

Unspecified Amoebae. There are reports of un-specified amoebae causing enterohepatitis in chelo-nians, crocodiles, and a tuatara.7

Phylum Ciliophora

Unicellular organisms from the phylum Ciliophora,which move using cilia, are known as ciliates. Theyall possess micronuclei and macronuclei and mosthave contractile vacuoles. Ciliates measure morethan 40 m in length. Cilia are small flagella ar-

ranged in large numbers that beat synchronously inrows, tufts, or as undulating membranes. True fla-gella may be temporarily present during the devel-opment of specific ciliates. Ciliates use a form ofsexual reproduction termed conjugation in which2 individuals temporarily fuse and donate a haploidpronucleus. Most ciliates found in reptiles are com-mensals. In herbivorous reptiles, ciliates are believedto contribute to large intestine digestion. Balantid-ium coli is the only ciliate thought to be potentiallypathogenic, and it has been reported to cause coli-tis.6



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Phylum Apicomplexa

Coccidia belonging to the subclass Coccidiasina aresingle-celled, intracellular, eukaryotic parasites ofthe phylum Apicomplexa that are shed as oocysts inthe feces of their definitive host.

Life Cycles. Coccidia life cycles are complex andinclude asexual phases, which produce very high

numbers of progeny that help facilitate the contin-uance of the species, and sexual phases that allow forgenetic recombination. Some, such as species ofEi-meria, Isospora, and Cryptosporidium, are single-hostforms (homoxenous) and have a direct life cycle.Others, such as species ofSarcocystis, require 2 hosts(heteroxenous) and have indirect life cycles (Fig 1).

Epidemiology. Coccidia are found in all orders ofreptiles and usually feed, grow, and develop in gas-trointestinal epithelial cells, although some may livein other organs. There is still much to be learned

about the life cycles of coccidia species in reptiles,but it is accepted that most that have direct life cyclesonly infect one or a small number of reptile species,and are unlikely to be transmissible to other classesof vertebrates, at least not as definitive hosts. Coc-cidia with indirect life cycles may infect a number ofdifferent reptile species but are less common in cap-

tive populations when suitable intermediate hostsare not present. Despite the fact that their life cyclesinvolve the destruction of host cells, many coccidiaare not considered to be pathogens in their reptilehosts. However, if large numbers are ingested, thesubsequent tissue damage can result in disease,

which is more likely to occur in captive reptiles.17

Diseases

Table 3 lists the most clinically significant coccidiathat cause gastrointestinal disease in reptiles, includ-

ing the genera Cryptosporidium, Caryospora, Eimeria,Isospora, andSarcocystis.

Cryptosporidium. Cryptosporidia are small (4-8m) coccidian protozoa found in free-living andcaptive reptiles around the world, but they appear tobe much less prevalent in wild (free-living) popula-tions. These coccidia have a wide range of host spec-ificity; disease is recorded in snakes after transmis-sion from lizards and chelonians. There is a large

variation of tissue tropism recognized in lizards, withcryptosporidial oocysts being associated with lesions

in gastric, enteric, renal, salivary, and pharyngealtissue.7 Morphometric studies suggest at least 5 dis-tinct reptilian cryptosporidian parasites.18

Cryptosporidia have been found on routine fecalexamination of apparently healthy animals, whichsuggests a carrier state or subclinical disease. Thisoffers options other than euthanasia for valuablespecimens, although such conditions do require in-tensive screening of animals with examination offecal samples, using acid-fast techniques (see Coo-per, this issue), several times a year.19 However, as

with other coccidia, recent work shows that routine

examination of reptile feces can reveal a high prev-alence of cryptosporidia derived from mammalianprey species that are not infective for reptiles; thisshould be borne in mind with screening programs.3

Cryptosporidium serpentisis recognized as a cause ofgastritis and occasionally enteritis in reptiles. Al-though affecting many species of reptiles, the Viper-idae, especially rattlesnakes, as well as amelanoticsnakes, appear to be particularly susceptible to dis-ease. In those species, C. serpentis is frequentlychronic and, with no readily effective treatment, of-ten proves fatal.20 Cryptosporidium saurophilum has

Figure 1. General coccidian life cycle.



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been found predominantly in the small intestine oflizards and some snakes, but its association with dis-ease is equivocal.21,22 Cryptosporidiumspp. have beenimplicated as a cause of diarrhea, emaciation, an-orexia, weight loss, and death in juvenile and adultleopard geckos (Eublepharis macularius) associated

with hyperplasia and mononuclear cell inflamma-

tion of the small intestine.23 Details of the cryptospo-ridian life cycle in reptiles is scant, but it is believedto follow the general pattern of coccidia previouslydescribed. No prepatent period has been deter-mined in reptiles for this parasitic disease. Directdisease transmission occurs after ingestion of fecal-contaminated material. However, an interesting fea-ture of cryptosporidia, derived from studies in mam-mals, is that some oocysts release their sporozoites

within the hosts body, resulting in autoinfection.In snakes,Cryptosporidium serpentisdevelops on the

gastric mucosa, and clinical signs are consistent withgastritis (e.g., anorexia, weight loss, postprandial re-gurgitation, lethargy, death). Secondary bacterial in-fections may exacerbate clinical signs. Physical exam-ination often reveals a palpable thickening of thestomach.24 Ultrasonography and contrast gastric ra-diographs that show a thickened stomach wall anddelayed gastric emptying of 1 to 2 days are suggestiveof cryptosporidiosis. On endoscopic examination,the stomach appears enlarged with thickened rugae.

A stomach biopsy (see Cooper, this issue) can con-firm the diagnosis with identification of Cryptospo-

ridium spp. as intracellular stages in a parasitopho-rous vacuole confined to the microvillous region.The normal gastric mucosal morphology is lost be-cause of glandular hypertrophy and hyperplasia.This may be accompanied by edema and inflamma-tion of the lamina propria and submucosa.7,25 How-ever, the focal distribution ofCryptosporidiumlesionsmay give a false negative result and any diagnostictest should be considered in conjunction with clini-cal signs and history (see Cooper this issue). Al-though gastritis is the most common presentation insnakes with this parasitic disease, some cases of en-

teritis in snakes have also been reported.26

Caryospora. Several different species ofCaryosporahave been identified in reptiles, mostly from snakesand lizards. Oocysts sporulate in the environmentafter being excreted by the definitive host. Sporu-lated oocysts are spherical to ovoid and contain asingle sporocyst with 8 sporozoites. Although in gen-eral few lesions are reported, infestations in somecases have been associated with restlessness, an-orexia, and weight loss.6,7 Caryospora cheloniae hasbeen reported as the cause of enteritis in captive and

free-living green sea turtles (Chelonia mydas) whereimmunological naivety, overcrowding, and poor hy-giene were thought to be predisposing factors.27,28

The disease caused serious losses in 4- to 8-week-oldcaptive turtles and was responsible for deaths inabout 70 free-living subadults in Australia. Clinicalsigns associated with C. cheloniae infection included

weakness, lethargy, and dehydration, with diarrheabeing infrequently observed. Affected reptiles hadsevere exudative mucoid, fibrinous, or necrotizingenteritis. In captive turtles, the disease was limited tothe distal intestines, whereas in the wild turtles theentire intestine was affected. There was thinning anddilation of the intestinal wall, epithelial necrosis, andfocal epithelial erosion with resultant hemorrhageinto the lumen. Inflammatory cells infiltrated themucosa. Intact epithelium was hyperplastic and con-tained developmental stages ofC.cheloniae.Nervous

signs due to coccidial-associated meningoencephali-tis were reported in the free-living turtles, with asevere inflammatory response to merozoites de-tected around blood vessels. Oocysts detected in thefeces were allowed to sporulate to prove that theparasite was, indeed, C. cheloniae. Unfortunately, at-tempts to rehabilitate sick turtles were unsuccessful.

Eimeria. More than 120 species ofEimeriaoccur inreptiles. Sites of infection in host species are usuallyintestinal epithelium, but depending on the speciesof coccidia, epithelia in the bile duct, gallbladder,

and kidney can also be infected.6 Variable-sizedspherical or elongate oocysts contain 4 sporocysts,each with 2 sporozoites. Relatively fewEimeria spp.appear to have been associated with disease in rep-tiles. Eimeria cascabeli infection in snakes was associ-ated with epithelial erosion and connective tissueproliferation in the gallbladder and extra hepaticducts.29 Jacobson questions the accuracy of reportsby Fantham and Porter in the early 1950s of a singlespecies, E. bitis, infecting different genera of snakesand causing necrotizing cholecystitis, owing to thegeneral host specificity ofEimeriaspp.7

Genetic sequencing suggests there are 2 distinctEimeriaspp. associated with disseminated visceral coc-cidiosis in turtles. Oocysts in multiple organs were vari-ably associated with inflammation. Coccidian oocysts

were present throughout the lamina propria of theintestine and extended into the submucosa, accompa-nied by a moderate diffuse lymphoplasmacytic infil-trate. The inflammatory reaction was proportional tothe density of oocysts.5

Other unspecified Eimeria spp. have been re-ported to cause severe catarrhal and diphtheroid



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inflammation of the large and small intestine insnakes.30

Isospora. Isospora species are coccidian protozoathat have oocysts with 2 sporocysts, each with 4sporozoites (Fig 2). They are easily confused withSarcocystisspp., and many that were previously iden-tified in snakes have been reclassified as being in the

genusSarcocystis.31Isospora amphiboluri has been associated with de-

layed growth, diarrhea, and mortality in youngbearded dragons (Pogona vitticeps).7,17,32 As withother coccidia, there is discrepancy in the literatureas to the pathogenicity ofIsosporaspp. to reptiles.14

Miscellaneous Coccidians. There have been re-ports in the literature of significant but unclassifiedcoccidial disease in chelonians and crocodiles.7

Intranuclear Coccidiosis in Chelonians. Most

coccidia undergo intracytoplasmic development, buta small number of reptilian coccidia use intranucleardevelopment.33,34 Intranuclear coccidia have beenassociated with anorexia, lethargy, and mortality intortoises and turtles. At postmortem examination,lesions described in multiple organs include prolif-erative pneumonia, otitis interna, chronic active en-teritis, hepatic necrosis, pancreatitis, and nephritis.Lesions in the small intestine and colon were severe.Intranuclear coccidia in various stages of develop-ment were detected in the epithelium and cells inthe lamina propria or submucosa, and these were

associated with epithelial hyperplasia, necrosis, andinfiltrates of lymphocytes and plasma cells, with a fewgranulocytes and macrophages. In some cases, bac-terial overgrowth was evident in colonic ulcers, andothers had concurrent amoebic infection. Edema ofthe submucosa was prominent in all affected tor-toises. Coccidia were also found in glandular epithe-lium of the pancreas and in bile duct epithelium,hepatocytes, and melanomacrophages of the liver.Parasites were accompanied by inflammation, tissueatrophy, fibrosis, and moderate to severe degenera-tion and necrosis of infected cells.35,36 Genetic se-quencing of intranuclear coccidian samples from 6tortoise species revealed that they were identical andclosely related to a frog renal coccidium.37

Unclassified Coccidia in Crocodilian Species.

Coccidial infections in crocodiles appear to havebeen rarely recorded. However, visceral lesions asso-ciated with coccidiosis, including epithelial hyper-plasia, irregular, fused, and atrophic intestinal villi,and inflammatory infiltration of the lamina propriahave been described in farmed crocodiles.38,39

Sarcocystis. Sarcocystisspp. have fragile oocysts thatmay rupture spontaneously, releasing 2 sporocysts,each with 4 sporozoites. Identification is compli-cated by the similarity ofSarcocystisspp. oocysts andsporocysts to those of Isospora spp. Sarcocystis spp.

have an indirect life cycle, requiring 2 hosts withgametogony and sporogony occurring in the intesti-nal mucosa of the definitive host. In the intermedi-ate host, merogony and endopolygeny (an addi-tional type of asexual reproduction in which theprogeny form bradyzoite-filled sarcocysts) providean extra multiplicative phase in the life cycle. Nu-merous sarcocysts that occur in the muscle of theintermediate host (prey) are infective for the defin-itive host (predator) when eaten. Generally, the sar-cocyst is the stage causing damage that results inclinical disease. There are occasional reports of sar-cocysts causing pathology in muscle of lizard preyspecies, but clinical intestinal sarcocystosis in defin-itive reptilian hosts is rare. One pathological reportof intestinalSarcocystisin a snake describes anorexia,emaciation, and death. Histologically, there was dis-ruption of villi in the proximal intestine, with ne-crotic epithelium and bacterial overgrowth; the re-maining enterocytes contained oocysts. The laminapropria was thickened and packed with bisporocystidoocysts. There was congestion of the serosal vascula-ture with an infiltrate of granulated leukocytes.40

Figure 2. Sporulating Isosporaoocyst.



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Diagnostics

Gastrointestinal protozoa can be detected on exam-ination of fecal or regurgitated material, biopsies, orpostmortem samples. The use of these and othertechniques in the practice environment or underfield conditions is discussed elsewhere (see Cooper,this issue).

Sample Collection

Saline solution enemas are useful for obtaining fecalsamples because defecation may be infrequent inreptiles. Flush the colon with warm saline solutionadministered via soft tubing, and massage the abdo-men before recovering colon contents. These can becentrifuged before examining a fresh smear of thesediment. Gastric intubation can similarly be used to

sample the upper gastrointestinal tract. Touchsmears, suction biopsies, fine-needle aspirates, gutscrapes, and tissue lesions taken at necropsy alsoprovide samples for investigation (see Cooper, thisissue).

Initial Diagnostics

Definitive diagnosis of protozoa to species level canbe difficult (see Cooper, this issue). Some of thefollowing techniques will allow the veterinary practi-

tioner to identify protozoa to the generic level usinga light microscope with an ocular micrometer tomake measurements. Specialists may be required forfurther identification (see Cooper, this issue).41

Active protozoa can be recognized readily in un-stained fresh material by mixing the sample in weaksaline solution on a glass slide until the preparationis transparent on application of the coverslip. Thereis a range of other techniques available to assist indiagnostic testing for protozoal parasites.

Concentration TechniquesIn some instances, smaller protozoa and cysts needto be separated from extraneous sample material.One method is to concentrate the organisms byflotation. Saturated zinc sulfate flotation is useful toidentify cysts and oocysts. A viscous medium such asSheathers solution can be used to slow fast-movingprotozoa, thus aiding in their identification. It is alsosuitable for use with oil-immersion microscopy andallows for accurate measurements to be made (Table5). However, concentrated solutions may distort or

disrupt some protozoal cell walls and affect the mor-phometric analysis that is required for diagnostics.To avoid this, the sample can be strained through agauze filter and centrifuged at 1200 to 1500 rpm for10 minutes before making a smear of the sediment.Smears should immediately be examined.

Special Stains

Staining highlights features of diagnostic impor-tance in motile or cystic stages of protozoa and someoocysts. Some selected preparations appropriate fordifferent groups are listed inTable 6.

Postmortem Examination

During postmortem examination, the gut epithe-lium can be scraped, saline solution smears exam-ined, stained preparations made, and sections ofgastrointestinal organs submitted for histopatho-logy.47 These can all help determine whether a proto-zoal infection is associated with disease and will assistin study of the parasites natural history (see Perez,

Table 5. Solutions useful for flotation

and fixation of protozoa

Preparation of flotation solutions

Zinc sulphate (ZnSO4) solution

Add 386 g of ZnSO4to 1 litre of water. Check the

specific gravity of the mixture with a hydrometer

and adjust to 1.18. Store the solution in a

tightly-capped container to prevent evaporation

and a resultant change in the specific gravity.

Sheathers solution

Add 454 g of table sugar to 355 ml of hot water.

Stir until dissolved and allow to cool. Refrigerate

this solution and use within a few days to avoid

problems of mold growth. Some people add six

ml of formaldehyde to the solution to preserve it.

Preparation of fixation solution

Sodium acetate - acetic acid fixative (SAF)

Sodium acetate 1.5 g

Glacial acetic acid 2.0 ml

40% Formaldehyde solution 4.0 ml

Distilled water 92.5 ml

This preserves protozoan cysts and trophozoites

when used at a concentration of one part

sample to five parts fixative for making

permanent smears and is less hazardous than

preservatives that contain mercuric compounds.



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this issue). However, specific identification of proto-zoa in histological sections is limited because all ofthe distinguishing features may not be seen; in someinstances, special stains can help with preliminaryidentification (Table 6). Scanning and transmissionelectron microscopic studies have also allowed moreaccurate grouping of protozoan pathogens in reptilesamples.8

Fixation

Numerous fixatives have been described for preserv-ing protozoa in samples. Each has benefits and draw-backs, but sodium acetate-acetic acid fixative is agood all-around fixative that allows protozoan cystsand trophozoites to be preserved for further study atanother date or at a distant laboratory (Table 5) (seeCooper, this issue). Two to three percent of aqueous(w/v) potassium dichromate (K2Cr2O7) is useful forthe preservation of coccidia.48

Culture

There are many techniques for the culture of proto-zoa. Culture has the potential for use in diagnostics,immunological research, and development and ther-apeutic advances but requires a degree of specializa-tion.49 Coccidia are categorized by sporulated oocystmorphology and, because most coccidia are ex-creted unsporulated, a culture technique that artifi-cially stimulates sporulation is necessary. A simplemethod involves mixing the feces with 3% aqueous(w/v) potassium dichromate (K2Cr2O7) (1 part fecesto 5 parts medium) in a specimen cup. This mixture

is aerated, either by bubbling air through the mix-ture or by leaving the cap off the cup. Bacterialgrowth is inhibited by the medium, and the oocystssporulate in 4 to 5 days, allowing determination to ageneric level.17

Immunodiagnostics

Immunodiagnostics are potentially potent tools fordiagnosing pathogens of reptiles. Few tests are cur-

rently commercially available, although some areaccessible through universities and research labora-tories.50 For example, an immunofluorescentCrypto-sporidium/Giardia monoclonal antibody test, Merif-luor (Meridian Diagnostics, Inc., Cincinnati, OHUSA), has been used successfully to detect mildshedders and early cases of cryptosporidiosis in rep-tiles, and diagnostic immunohistochemistry, using apolyclonal antibody against Entamoeba invadens, hasbeen developed for use in snakes.51,52

Molecular DiagnosticsReptile protozoan disease diagnostics, epidemiolog-ical investigation, and taxonomy can benefit fromthe rapidly expanding field of molecular biologicalstudies such as polymerase chain reaction and se-quencing, blotting, and hybridization. Chromogenicin situ hybridization with probes has been designedfor the detection of 18S ribosomal RNA genes fromCryptosporidiumspp.,Entamoebaspp.,E. invadens, andMonocercomonasspp.53 Although, to date, the appli-cation is limited by the availability of gene sequence

Table 6. Some staining procedures that are useful in protozoal diagnostics

Stain Protozoal type Effect Reference

Protargol silver protein Flagellates Highlights nuclei, microtubules and fibrillar structures grey

to black

42

Lugols iodine/1%

aqueous eosin

Protozoal cysts Cysts stain dark while everything else stains pink 43

Lugols iodine Flagellates Stains trophozoites

Amoebae Stains trophozoites

Feulgen stain Flagellates On fixed sections DNA stains red on a green background 44

Kinyounss acid-fast

stain

Cryptosporidium

oocysts

Oocysts stain as pale to bright pink spheres against a

dark green or purple background on fresh smears.

45

Giemsa Kinetoplastid

flagellates

DNA stains well and its position in relation to the nucleus

defines kinetoplastid genera

46

Cytoplasm stains blue and the nuclear material stains red

to purple



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information, the scope for expansion in this field isenormous.54

Treatment

Flagellates/Amoebae

These protozoa are sensitive to imidazole therapy.Table 7 lists some treatment regimens reported inthe literature that are based on empirical dosagesand schedules. Sick individuals will benefit from sup-portive therapy, including providing optimal envi-ronmental conditions, assisted feeding, parenteralantibiotics, and vitamin supplementation. Rehydra-tion may be performed by oral, subcutaneous,and/or intraperitoneal/coelomic injections of flu-

ids, but treatment is often unsuccessful in protractedcases.

Coccidia

Many of the genera of coccidia reported to causedisease in reptiles have been diagnosed post mor-tem. However, the empirical use of coccidiostats inreptiles has also been documented. Table 7 liststreatment regimens from the literature, but it shouldbe noted that in some cases complete clinical reso-lution proves unsuccessful despite the use of recom-mended treatments.

Isosporaspp.

Failure to eliminate Isospora amphiboluri frombearded dragons is common despite clinical im-provement after the use of coccidiostats. Recent

work with ponazuril (Marquis; Bayer HealthCare,Shawnee Mission, KS USA), a coccidiocide, suggeststhat eliminating I. amphiboluri is possible.67 Thor-ough, daily cage cleaning is recommended along

with concurrent therapies. Follow-up fecal examina-tions including eggs per gram measurements can beuseful in determining when to discontinue medica-tion (Table 8).

Cryptosporidium

Cryptosporidiosis is difficult to treat successfully, and

separation of affected reptiles by permanent quaran-tine or euthanasia has been advocated. Supportivetherapy, including small meals via gavage tube, andreduction of predisposing stressors by optimizingenvironmental conditions can lead to spontaneousrecovery in some individuals. The success of chemo-therapeutics for cryptosporidiosis is variable. Al-though sulfa drugs and paromomycin have someeffect in improving clinical signs, only very highdoses of paromomycin have been reported to haltshedding of the organism for a prolonged period inGila monsters (Heloderma suspectum).65 Bovine hyper-

Table 7. Treatment of gastrointestinal protozoa

Organisms Therapy Doses References

Flagellates and

amoebae

Paromomycin 35-100 mg/kg PO q 24 h for up to 4 weeks 55

Metronidazole 100 mg/kg PO repeat in 2 wk 55,56,57,58

40-60 mg/kg PO q 7 days for 2-3 doses 59

Fenbendazole 25 mg/kg PO q 7 days for up to 4 treatments 55Coccidia Sulfadimethoxine 90 mg/kg (first day) PO followed by 45 mg/kg PO q 24 h

for 9 days.

59

Sulfadimethoxine 50 mg/kg daily for 5 days,then q 48 h until the coccidia

are eliminated

60

Trimethoprim-sulfa 30 mg/kg daily for 5 days,then q 48 h until the coccidia

are eliminated

60

30 mg/kg PO q 24 h for 7 d 61

15 mg/kg PO q 12 h for 7 d 61

30 mg/kg PO q 24 h for 2 d then q 48 h for 3 wk 62

Sulfamethoxine 90 mg/kg PO, IM, IV then 45 mg/kg q 24 h for 5-7 d 62,63

50 mg/kg PO q 24 h, tx 3 days on 3 days off then 3 days

on

64

Cryptosporidia Paromomycin 300-360 mg/kg q 48 h for two weeks then repeated in 6

months

65

Hyperimmune bovine

colostrum

10 ml/kg PO q 7days for 6 gavage treatments 66



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immune colostrum therapeutic trials in snakes, tor-toises, and geckos have also shown promise.66 Nita-zoxanide has been reported to eradicate cryptospo-ridia in humans, and it may be of use in reptiles. 68

Control

Control of gastrointestinal protozoan parasites is

best achieved by paying attention to the overallhealth of the reptile population. This includes me-ticulous observation of changes in behavior (seeRamnath, this issue).

Sick individuals should be isolated promptly,stressors reduced by providing optimal living condi-tions, and hygiene enhanced so as to remove resis-tant encysted stages and intermediate hosts. Theprepatent periods for most protozoan parasites ofreptiles are unknown. The advocated period forquarantine of incoming reptiles is debatable andrecommendations vary from between 1 and 3

months. During quarantine, reptiles should be sub-jected to repeated clinical and fecal examinations.

Acknowledgments

The authors thank Stephen Scullion for diagramdesign.

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Table 8. Determination of eggs per gram

in feces

This method of determining the eggs per gram (EPG),

first used by the University of Wisconsins

Parasitology Laboratory, is a modification of the

Stoll technique. It is a flotation method and results

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the EPG.



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