Article #1

CE Canine Protothecosis
Erik Strunck, DVM*
Oberlin Animal Hospital
Raleigh, North Carolina

Leonard Billups, DVM, DACVP

Tuskegee University

Sophia Avgeris, DVM*

Sound Technologies, Inc.
Carlsbad, California

ABSTRACT:
Canine protothecosis is a rare disease that has the ability to cause severe gastrointesti-
nal (GI) pathology as well as ocular, cutaneous, and disseminated disease. Successful ther-
apy for protothecosis has not been previously reported. The case study included in this
article involves a dog diagnosed with GI protothecosis in which a novel therapeutic
approach was used. This treatment was successful in halting progression and dissemina-
tion of the disease. Unfortunately, the long-term benefits of this therapy could not be
determined in this patient. Dissemination of disease was not observed in this patient for
12 months following the onset of clinical signs.

P
rototheca spp are colorless algae related to canine cases previously reported, the collie and
the green algae of the genus Chlorella.1–4 spayed females appear to be overrepresented.1–3
There are three recognized species of Pro- The age range of infected animals is wide: 1.5
totheca organisms: Prototheca zopfii, Prototheca to 10 years of age.3
wickerhamii, and Prototheca stagnora. 1,3,5,6 A
fourth species has also been proposed: Pro- CLINICAL SIGNS
totheca salmonis.7 Of these species, only P. zopfii Despite their abundance in nature, Prototheca
and P. wickerhamii have been found to be path- organisms very rarely cause disease in domestic
ogenic.1–3,8 Prototheca organisms can be found in animals. 1,2,4,43 The most commonly affected
abundance in nature in sources such as raw or domestic animals are dogs, cats, and cows.3 In
treated sewage, the slime flux of trees, animal cows, manifestation of the disease is usually
waste, soil, food, and flowing or standing in the form of mastitis caused by P. zop-
water. 1,3,6,9 These organisms have a nearly fii. 2,3,27,35,41,42,44,45 Cats are most commonly
worldwide distribution, having been reported affected with the cutaneous form of protothe-
on five of the seven continents: North cosis and present with large, firm nodules on
America, 3,10–26 Europe, 3,27–32 Asia, 3,33–35 Afri- the limbs and feet.1,14,18,33,38,40,46–49 Other areas
ca,3,36,37 and Australia.2,3,38–42 Because Prototheca that may be affected are the nose, pinnae, fore-
infections are rare in domestic animals, it is dif- head, and tailbase.1 P. wickerhamii is most com-
ficult to establish breed, age, monly isolated from these cutaneous lesions in
Email comments/questions to and sex predilections. In the cats.3,14,40
[email protected],
fax 800-556-3288, or log on to *Drs. Strunck and Avgeris were affiliated with Tuskegee University when this article was
www.VetLearn.com prepared.

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 Canine Protothecosis CE 97

Dogs often show a wide range of clinical signs with white to tan nodules identical to those seen in the colon
protothecal infections. The most common clinical pre- or on the retina were discovered.1,4 The kidneys tend to
sentation is protracted hemorrhagic enteritis. The colon show larger lesions because these clumps of organisms
is the most commonly affected portion of the gastroin- can grow to several centimeters.1
testinal (GI) tract.1,2,4 Lesions within the colon include The differential diagnosis for dogs infected with pro-
diffuse reddening and multiple raised white nodules as tothecosis depends greatly on which organ systems are
well as ulcerations and may be accompanied by hemor- affected. Protothecosis is not a common disease in
rhage. Necrosis is rarely observed.1,3 Disseminated dis- domestic animals and should be considered only after
ease involving the eyes, ears, skin, skeletal muscles, kid- diagnostic testing has ruled out more common condi-
neys, liver, heart, spinal cord, and brain has been tions. However, one presentation that should arouse clin-
reported.1,2,4,50 It is believed that infection occurs via ical suspicion of protothecosis is a dog that presents with
ingestion, where organisms grow within the GI tract hemorrhagic enteritis concurrent with acute blindness.1,3,4
and eventually disseminate via lymphatics and
blood.1–4,6,13,25 DIAGNOSIS
Ocular involvement is one of the most common man- Diagnosis of Prototheca infections can be confirmed
ifestations of dissemination.1,2,35 A recent review revealed with cytology of rectal scrapings when the GI tract
that of the 26 reported cases of protothecosis, 20 cases is involved.1–3 Positive cytology results include typical
showed ocular involvement (77%).2,3,10,11,13,15,16,19–22,24,26,37,50 Prototheca cells (i.e., 3 to 20 µm in diameter with a thin,

The most common clinical presentation of protothecosis

in dogs is protracted hemorrhagic enteritis.

These retinal lesions are most commonly described as refractile cell wall).1,2 The cells have a granular, basophilic
white to tan, raised clusters 1 to 2 mm in diameter.3 cytoplasm with a small, central nucleus.1,2 Some cells can
Further progression of the disease can lead to granulo- be seen undergoing endosporulation, with as many as
matous chorioretinitis, severe retinal degeneration, or 20 daughter cells being released from the parent
exudative retinal detachment and acute blindness. 1,3 cell1–4,8,9,15 (see figure on p. 98). P. zopfii and P. wicker-
Leukocoria resulting from vitreous clouding has been hamii cannot be differentiated via microscopy; an alcohol
reported as a clinical finding on initial examination.1,3 or sugar assimilation test is accurate in determining the
Usually, both eyes are affected, although the progression species, but indirect fluorescent antibody tests are much
is often asymmetric.3 more rapid.1,3,9,15,20,22,51,52 Culture and sensitivity tests can
In dogs, cutaneous lesions are characterized as nod- also be conducted on Sabouraud’s glucose media with
ules, draining ulcers, and crusty exudates of the trunk, clotrimazole-impregnated disks for differentiating
extremities, and mucosal surfaces as well as scrotal gran- between the two species.1,2,53 P. wickerhamii is inhibited
ulomas.1 Hyperkeratosis frequently accompanies these by clotrimazole, but P. zopfii is not.1,2,53 Laboratory evalu-
lesions, and necrosis and secondary bacterial infections ation, including a complete blood cell count (CBC),
may complicate the condition.1 chemistry panel, and urinalysis, is often unremarkable.1,3
Six of the 26 cases previously reviewed showed neuro- Other diagnostic methods include biopsy specimens of
logic signs other than blindness. Among the signs the colon or regional lymph nodes, but any other affected
exhibited were incoordination,21,24 cervical pain,30 head tissue may be sampled.1,3,4 Urine can also reveal the pres-
tilt, 2,24,26 circling, 2 ataxia, 21,24 paresis, 24,26,37 and deaf- ence of these organisms if dissemination to the kidneys has
ness.13,37 These signs were caused by dissemination of occurred. Microscopic examination of urine sediment can
Prototheca organisms to the brain and spinal cord.1,2,24 be an excellent means of detecting dissemination to the
Other organs that have been found to have pathology kidneys.2–4,21 Cerebrospinal fluid tap or vitreous aspiration
associated with protothecosis include the heart, liver, may also yield the presence of disseminated organisms
kidneys, and skeletal muscles. 1,2,4,50 In these tissues, when neurologic or ocular infection is present.3,4,10,19,20,22,26

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98 CE Canine Protothecosis

Case Study
Signalment and History
A 2-year-old neutered male cocker spaniel was
referred to the clinic with an owner complaint of chronic,
intermittent, bloody diarrhea for 4 to 5 months. The
referring veterinarian had treated the patient with
pyrantel pamoate (Strongid T, Pfizer), metronidazole
(Flagyl, Searle), and sulfamethoxazole–trimethoprim
(Tribrissen, Schering-Plough), none of which reduced
the clinical signs. In addition, fecal flotation test results
were repeatedly negative. Therefore, the patient was
referred for further evaluation and diagnostics.

Physical Examination and Diagnostics

Physical examination findings revealed no significant
abnormalities. The patient was overweight at 36 lb (16.4
kg), with an adequate hydration status and no pain on
rectal palpation. The stool was dark brown and liquid. A section of colon from the patient. Numerous
Tenesmus and frank blood were present throughout organisms, some of which contain daughter cells, are
defecation. A complete ocular examination revealed no noted within the mucosa.
evidence of lesions. CBC, chemistry panel, and urinalysis
results as well as chest and abdominal radiographs were
normal. A cytology sample from a rectal scraping revealed
the presence of many spherical to ovoid cells identified were cause for canceling the scheduled therapy. Repeat
as Prototheca spp (see figure at right). A subsequent rectal scrapings for colonic cytologic samples were taken
colonoscopy revealed markedly hyperemic mucosa in the at 2 weeks and 4 weeks postinitiation of therapy.
colon and duodenum. One focal area of necrosis in the Decreasing numbers of Prototheca organisms were noted
intestinal mucosa was also observed in the proximal colon. with each progressive sample. Although this could have
Biopsy samples were taken and again revealed the presence been reflective of the sample taken and not definitive for
of Prototheca spp. Immunoglobulin levels were checked to success of therapy, the marked decrease in numbers seen
ascertain the patient’s immune status. IgG and IgA levels combined with improvement of clinical signs were
were elevated. The IgM level was within the normal range, considered positive prognostic factors. The rectal
as would be expected for the chronicity of the condition. scrapings were always taken by the same person and
were evaluated by one pathologist.
Treatment A repeat colonoscopy was conducted at 6 weeks,
Following diagnosis, the patient was started on a revealing that the mucosa was still hyperemic, but no
treatment regimen of amphotericin B lipid-based areas of necrosis were visible. Biopsy samples were also
(Abelcet, Liposome Co.; 1 mg/kg IV every other day) taken at this time, and Prototheca organisms were still
and clotrimazole (Monistat 1% ointment enema twice found within the colonic mucosa. An amphotericin B
weekly). Amphotericin B was scheduled to be given three enema (3% amphotericin B cream [Fungizone,
times a week, preceded and followed by 2 L of 0.9% Apothecon]) was administered. It was believed that
sodium chloride (saline) IV to decrease the nephrotoxicity direct contact with the intestinal mucosa would bring the
of amphotericin B. Renal function was closely monitored drug into contact with organisms that had been
by blood urea nitrogen level, creatinine level, and unreachable via the bloodstream because of damaged or
urinalysis on the mornings of amphotericin B treatments. necrotic areas of epithelium. To our knowledge, this
Amphotericin B treatments were scheduled to continue procedure had not been performed previously. Ideally,
until a cumulative dose of 12 mg/kg was reached. After amphotericin B blood levels could have been checked to
the amphotericin therapy, the patient was to receive ensure the safety of this procedure. Chemistry panels and
itraconazole (Sporanox, Ortho Biotech) therapy (100 mg urinalyses were continuously conducted to monitor for
PO bid) at home for 2 months beyond the resolution of signs of renal toxicity. Clinically, the patient showed
clinical signs. gradual improvement. Following initiation of treatment
Rather than three amphotericin B treatments per with amphotericin B, the patient’s stools progressed from
week for 4 weeks (12 doses total) as planned, the patient being thin and liquid to becoming more formed but still
received two doses per week for 5 weeks (10 doses total) containing small amounts of frank blood. The frequency
because of renal toxicity. A low urine specific gravity or of defecation decreased, and tenesmus was no longer
elevation of serum blood urea nitrogen and creatinine observed. Although the stools became progressively

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Case Study (Continued)

firmer after the first week of therapy, small amounts of protothecal cells within the colonic sample. A repeat
frank blood were often observed. Mild clinical colonoscopy was conducted. The appearance of the
improvement continued; at discharge, the patient’s stools mucosa was a mixture of healthy tissue and patches of
were well formed, with only a small amount of frank inflamed, hyperemic mucosa. No areas of necrosis were
blood at the end of defecation. noted. An amphotericin B enema was performed after
Repeat cytology results from this time also revealed a the colonoscopy. Repeat radiography, ultrasonography,
marked decrease in the number of Prototheca cells and ocular examination showed no evidence of
compared with the first cytology sample submitted. These dissemination.
biopsy samples were unlikely to be from the same areas as The owners were unwilling to pursue another IV
those previously obtained; however, these findings were amphotericin B protocol. A total of six amphotericin B
consistent with cytology of the rectal scrapings and the enemas were given by the referring veterinarian over the
clinical improvement seen in this patient. The patient was next 2 weeks followed by oral ketoconazole (Nizoral,
discharged with itraconazole and the owner instructed to Janssen) therapy. However, the owners did not heed the
return with the patient for a recheck in 30 days. At that recommended advice of continuing the oral medications
time, the patient would be given another 30 days of for 2 months beyond the resolution of clinical signs and
itraconazole, which would be administered until at least did not refill the prescription once the patient was free of
2 months beyond clinical resolution. signs. The dog presented again 6 weeks after therapy and
died the next day. A necropsy was not performed.
Follow-Up
Follow-up telephone conversations with the owner Conclusion
indicated that the patient was doing very well and had no This case demonstrates the frustration in treating
blood in its stool. The patient did not return for a protothecosis. Despite initial improvement, the clinical
recheck until 2 months after discharge. The itraconazole signs returned when medications were discontinued. It is
prescription had not been refilled after the first 30-day unknown whether long-term resolution of the disease
supply because the dog was showing no clinical signs. could have been achieved if the owners had continued
However, the patient presented after 2 months because therapy as directed. This dog did survive for
of reemergence of bloody diarrhea. The physical approximately 12 months without evidence of
examination indicated that the patient’s condition and dissemination. The combination of IV amphotericin B,
demeanor were good, but blood was noted on rectal oral itraconazole, and amphotericin enemas may hold
palpation, and feces were again very loose with frank promise as an effective treatment for protothecosis if
blood. A repeat rectal scraping revealed a large number of early diagnosis precedes widespread dissemination.

It is also important to consider how the infection was tory response.1,4,21,39 Therefore, leukocyte function tests
acquired. Prototheca spp are abundant in the environment cannot be used because it is impossible to distinguish
but very rarely cause disease in domestic animals.1,3 This between decreased function caused by an underlying
suggests that animals are immunocompromised at the immune problem or that caused by the infection itself.
time of infection.1,3,12,39 Immunoglobulin levels should be
checked to determine whether an animal has a sufficient TREATMENT
immune response to warrant treatment.3,12,39 The IgG Twenty-six cases have been reported in dogs from
level should be elevated to indicate an immune response 1969 to 2000.3 Successful treatment regimens have not
by the host. The IgM level is generally normal because yet been discovered for disseminated protothecal infec-
the acute phase of infection will have passed when these tions. All dogs were reported to have died within a short
patients present for clinical evaluation. period of time after diagnosis.3 Some treatments have
Despite advances in the ability to analyze the func- been able to slow progression of the disease, but because
tional capacity of leukocytes, such tests are of limited all of these cases involved disseminated forms of the dis-
value in forming a diagnosis or prognosis associated with ease, there were no survivors.3,20,22 The longest survival
protothecosis. Protothecal organisms decrease the func- time of any dog in this study was 11 months.3,20,22 Cuta-
tional capacity of neutrophils, either by deactivating them neous infections with P. wickerhamii have been success-
or by decreasing their chemotactic abilities.1,3,4,12,21,39 One fully treated, but therapy for P. zopfii has thus far been
of the features of protothecal infections is that the organ- unsuccessful.3,12,39
isms themselves are surrounded by a very mild inflamma- In treating human protothecosis, many drugs (e.g.,

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100 CE Canine Protothecosis

griseofulvin, potassium iodide, pentamidine isethionate, copper sulfate, gen-

tian violet, brilliant green, chlorinated lime) have been tried.1 Because of
their in-vitro efficacy, aminoglycosides have also been tried but have been
found to have little effect clinically.3,54 Amphotericin B has been used in
combination with tetracycline, ketoconazole, fluconazole, or clotrimazole to
successfully combat P. wickerhamii.1,2 However, treatment is more difficult in
dogs because P. zopfii is the most common species. Amphotericin B has
been successful in slowing progression of the disease, but it is not curative.1
One dog with cutaneous and systemic infection survived nearly 1 year after
treatment with amphotericin B alone.1 However, amphotericin B alone was
not effective in another case with ocular lesions.1 Ketoconazole has been
used successfully twice but only in cutaneous P. wickerhamii infections.1
Two canine cases had some short-term treatment success. In one patient,
protothecal chorioretinitis abated during treatment with IV amphotericin
B.3,20 However, the treatment was discontinued because of nephrotoxicity,
and clinical signs of chorioretinitis returned 12 days later.3,20 In the other
case, a dog presented with ophthalmic lesions only and was treated with
itraconazole (5 mg/kg bid for 1 month, then once daily for 10 months).3,22
The lesions in this dog were not reversed, but progression of the disease was
slowed, and the dog survived for 11 months.3,22
Although the success of these two therapies was limited, they became the
basis for our treatment protocol. Amphotericin B (1 mg/kg IV three times
weekly until attaining a cumulative dose of 12 mg/kg) used in combination
with ketoconazole, fluconazole, or itraconazole (5 to 10 mg/kg/day PO)
appeared to be the best option for long-term use against P. zopfii. Using
amphotericin B for a short time followed by an azole drug can minimize
nephrotoxicity without compromising the strength of treatment needed to
kill the organism. Amphotericin B enemas (3% amphotericin B cream) were
also introduced to place the drug into direct contact with organisms that
may not have been reachable via the bloodstream. Surgical resection of any
involved tissue augments medical therapy, but this is not always possible,
especially in disseminated cases.1–3,46,55
Cost must also be considered in these cases. Antifungal therapies
(amphotericin B and azole drugs) are very expensive, and a lengthy hospital
stay is likely. Based on previous reports, owners must be given a grave prog-
nosis for their pets and an expensive estimate.3,20,22

SUMMARY
Twenty-six cases of canine protothecosis have been reported since 1969.
Successful therapy has yet to be discovered for this disease.
In the case study presented in this article, a 2-year-old castrated male
cocker spaniel was referred for evaluation of chronic diarrhea that had been
unresponsive to antibiotics or deworming. An unusual pathogen, Prototheca
zopfii, was discovered from a colonic scrape and subsequent colonoscopy. A
novel therapeutic regimen was attempted: IV amphotericin B and oral itra-
conazole were used as has been traditionally reported, but amphotericin B
enemas were also given. These enemas allow the drug to directly contact the
colonic mucosa and pathogenic organism. Poor owner compliance made
complete evaluation of this therapy impossible. However, a good clinical

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response and no dissemination of disease were seen. 29. Gibb AP, Aggarwal R, Swainson CP: Successful treatment of Prototheca peri-
tonitis complicating continuous ambulatory peritoneal dialysis. J Infect 22:
Numerous additional cases will be needed to determine 183–185, 1991.
whether this therapy offers a better prognosis than what 30. Macartney L, Rycroft AN, Hammil J: Cutaneous protothecosis in a dog:
First confirmed case in Britain. Vet Rec 123:494–496, 1988.
has been previously reported for canine protothecosis. 31. Mettler F: Generalisierte protothecose bei einem flughund (Pteropus lylei). Vet
Pathol 12:118–124, 1975.
32. Povey RC, Austwick PKC, Pearson H, et al: A case of protothecosis in a dog.
ACKNOWLEDGMENT Pathol Vet 6:396–402, 1969.
The authors thank the referring veterinarian, Dr. T. C. Branch of Oporto Animal 33. Matsuda T, Matsumoto T: Protothecosis: A report of two cases in Japan and
Clinic in Birmingham, Alabama. a review of the literature. Eur J Epidemiol 8:397–406, 1992.
34. Takaki K, Okada K, Umeno M, et al: Chronic Prototheca meningitis. Scand J
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WB Saunders, 1998, pp 430–435. caused by Prototheca zopfii in a cow. Vet Pathol 31:123–125, 1994.
2. Hollingswotrh SR: Canine protothecosis. Vet Clin North Am Small Anim 36. Davies RR, Spencer H, Wakelin PO: A case of human protothecosis. Trans
Pract 30(5):1091–1101, 2000. R Soc Trop Med Hyg 58:448–451, 1964.
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67:25–27, 1990. Onderstepoort J Vet Res 44:1–6, 1977.
4. Blogg JR, Sykes JE: Sudden blindness associated with protothecosis in a dog. 38. Coloe PJ: Protothecosis in a cat. JAVMA 180:78–79, 1982.
Aust Vet J 72(4):1995, pp 147–149. 39. Cox EG, Wilson JD, Brown P: Protothecosis: A case of disseminated algal
5. Chandler FW, Kaplan W, Callaway CS: Differentiation between Prototheca infection. Lancet 2:379–382, 1974.
and morphologically similar green algae in tissue. Arch Pathol Lab Med 102: 40. Finnie JW, Coloe PJ: Cutaneous protothecosis in a cat. Aust Vet J 57:307–
353–356, 1978. 308, 1981.
6. Pore RS, Barnett EA, Barnes WC, et al: Prototheca ecology. Mycopathologia 41. Hodges RT, Holland JTS, Neilson FJA, et al: Prototheca zopfii mastitis in a
81:49–62, 1983. herd of dairy cows. N Z Vet J 33:108–111, 1985.
7. Smith C: Ultrastructural study of Prototheca salmonis and comparison with 42. Rogers RJ: Protothecal lymphadenitis in an ox. Aust Vet J 50:281–282, 1974.
known isolates of Prototheca. Mycopathologia 71:95–101, 1980. 43. Wilkenson GT, Leong G: Protothecosis in a dog. Aust Vet Pract 18:47–49, 1988.
8. Sudman MS: Protothecosis: A critical review. Am J Clin Pathol 61:10–19, 1974. 44. Dion WM: Bovine mastitis due to Prototheca zopfii. Can Vet J 20:221–222,
9. Migaki G, Font RL, Sauer RM, et al: Canine protothecosis: Review of the 1979.
literature and report of an additional case. JAVMA 181:794–797, 1982. 45. Frank N, Ferguson LC, Cross RF, et al: Prototheca, a cause of bovine mastitis.
10. Buyukmihci N, Rubin LF, DePaoli A: Protothecosis with ocular involvement Am J Vet Res 30:1785–1794, 1969.
in a dog. JAVMA 167:158–161, 1975. 46. Mayhall CG, Miller CW, Eisen AZ, et al: Cutaneous protothecosis. Arch
11. Carlton WW, Austin L: Ocular protothecosis in a dog. Vet Pathol 10:274– Dermatol 112:1749–1752, 1976.
280, 1973. 47. Pegram PS, Kerns FT, Wasilauskaus BL, et al: Successful ketoconazole treat-
12. Chan JC, Jeffers LJ, Gould EW, et al: Visceral protothecosis mimicking scle- ment of protothecosis with ketoconazole-associated hepatotoxicity. Arch
rosing cholangitis in an immunocompetent host: Successful antifungal ther- Intern Med 143:1802–1805, 1983.
apy. Rev Infect Dis 12:802–807, 1990. 48. Venezio FR, Lavoo E, Williams JE, et al: Progressive cutaneous prototheco-
13. Cook JR, Tyler DE, Coulter DB, et al: Disseminated protothecosis causing sis. Am J Clin Pathol 77:485–493, 1982.
acute blindness and deafness in a dog. JAVMA 184:1266–1272, 1984. 49. Woolrich A, Koestenblatt E, Don P, et al: Cutaneous protothecosis and
14. Dillberger JE, Homer B, Daubert D, et al: Protothecosis in two cats. JAVMA AIDS. J Am Acad Dermatol 31:920–924, 1994.
192:1557–1559, 1988. 50. Van Kruiningen HJ, Garner FM, Schiefer B: Protothecosis in a dog. Pathol
15. Font RL, Hook SR: Metastatic protothecal retinitis in a dog: Electronic Vet 6:348–354, 1969.
microscopic observations. Vet Pathol 21:61–66, 1984. 51. Sudman MS, Kaplan W: Identification of the Prototheca species by immuno-
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JAVMA 185:906–907, 1984. 52. Wolf AM: Opportunistic fungal and algal infections, in Bonagura JD (ed):
17. Holscher MA, Shasteen WJ, Powell HS, et al: Disseminated canine pro- Current Veterinary Therapy XII. Philadelphia, WB Saunders, 1995, pp 326–
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18. Kaplan W, Chandler FW, Holzinger EA, et al: Protothecosis in a cat: First 53. Arnold P, Ahearn DG: The systematics of the genus Prototheca. Mycologia 64:
recorded case. Sabouraudia 14:281–286, 1976. 265, 1972.
19. Meredith RE, Gwin RM, Samuelson DA, et al: Systemic protothecosis with 54. Shahan TA, Pore RS: In vitro susceptibility of Prototheca spp to gentamicin.
ocular manifestations in a dog. JAAHA 20:153–156, 1984. Antimicrob Agents Chemother 35:2434–2435, 1991.
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ARTICLE #1 CE TEST
22. Schultze AE, Ring RD, Morgan RV, et al: Clinical, cytologic, and histo-
pathologic manifestations of protothecosis in two dogs. Vet Ophthal 1:239– This article qualifies for 1.5 contact hours of continuing CE
243, 1998. education credit from the Auburn University College of
23. Sudman MS, Majka JA, Kaplan W: Primary mucocutaneous protothecosis in
a dog. JAVMA 163:1372–1374, 1973. Veterinary Medicine. Subscribers who wish to apply this
24. Tyler DE, Lorenz MD, Blue JL, et al: Disseminated protothecosis with cen- credit to fulfill state relicensure requirements should consult
tral nervous system involvement in a dog. JAVMA 176:987–993, 1980.
25. Van Kruiningen HJ: Protothecal enterocolitis in a dog. JAVMA 157:56–63,
their respective state authorities regarding the applicability
1970. of this program.To participate, fill out the test form inserted
26. Ward DA: Canine protothecosis: A retrospective study of 7 cases. Proc Am at the end of this issue.
Coll Vet Ophthalmol:26–27, 1996.
27. Bodenhoff J, Schmidt Madsen P: Bovine protothecosis. Acta Pathol Microbiol 1. Prototheca is classified as a(n)
Scand 86(B):51–52, 1978.
28. Gentels JC, Bond PM: Protothecosis of Atlantic salmon. Sabouraudia 15: a. fungus. c. algae.
133–139, 1977. b. bacteria. d. virus.

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2. Which of the following is not a species of c. congestion of the mucosa and the presence of raised,
Prototheca? white foci in the small intestine
a. zopfii c. wickerhamii d. congestion of the mucosa and the presence of raised,
b. mirabilis d. stagnora white foci in the colon

3. Which breed appears to be overrepresented in 7. Clinical presentation of a dog with GI protothe-

protothecosis? cosis includes all of the following except
a. collie c. Labrador retriever a. vomiting. c. frank blood in the stool.
b. boxer d. German shepherd b. diarrhea. d. tenesmus.

4. Which canine body system is most commonly 8. Diagnosis of Prototheca infections can be
affected by protothecosis? confirmed with which of the following tests?
a. ocular c. GI a. CBC/chemistry panel c. cerebrospinal fluid tap
b. central nervous d. cutaneous b. cytology d. culture and sensitivity

5. Lesions of the ocular system do not include 9. Which of the following has shown no clinical
a. raised, white clusters on the retina. effectiveness against Prototheca spp?
b. hyperpigmentation of the retina. a. aminoglycosides c. itraconazole
c. granulomatous chorioretinitis. b. amphotericin B d. ketoconazole
d. retinal detachment.
10. ________________ signs should immediately put
6. Which of the following most accurately describes protothecosis at the top of the differential
the GI lesions associated with protothecosis? diagnosis.
a. widespread necrosis throughout the small intestine a. GI c. Cutaneous
b. widespread necrosis throughout the colon b. Ocular d. Concurrent GI and ocular

February 2004 COMPENDIUM