Albendazole (Albenza, Valbazen)


Highlights Of Prescribing Information

Broad spectrum against a variety of nematodes, cestodes & protozoa; labeled for cattle & sheep (suspension only)

Contraindicated with hepatic failure, pregnancy, lactating dairy cattle

May cause GI effects (including hepatic dysfunction) & rarely blood dyscrasias (aplastic anemia)

Do not use in pigeons, doves or crias

What Is Albendazole Used For?

Albendazole is labeled for the following endoparasites of cattle (not lactating): Ostertagia ostertagi, Haemonchus spp., Trichostrongylus spp., Nematodius spp., Cooperia spp., Bunostomum phlebotomum, Oesphagostomum spp., Dictacaulus vivaparus (adult and 4th stage larva), Fasciola hepatica (adults), and Moniezia spp.

In sheep, albendazole is approved for treating the following endoparasites: Ostertagia circumcincta, Marshallagia marshalli, Haemonchus contortus, Trichostrongylus spp., Nematodius spp., Cooperia spp., Oesphagostomum spp., Chihertia ovina, Dictacaulus filaria, Fasciola hepatica, Fascioides magna, Moniezia expansa, and Thysanosoma actinoides.

Albendazole is also used (extra-label) in small mammals, goats and swine for endoparasite control.

In cats, albendazole has been used to treat Paragonimus kellicotti infections. In dogs and cats, albendazole has been used to treat capillariasis. In dogs, albendazole has been used to treat Filaroides infections. It has been used for treating giardia infections in small animals, but concerns about bone marrow toxicity have diminished enthusiasm for the drug’s use.


Benzimidazole antiparasitic agents have a broad spectrum of activity against a variety of pathogenic internal parasites. In susceptible parasites, their mechanism of action is believed due to disrupting intracellular microtubular transport systems by binding selectively and damaging tubulin, preventing tubulin polymerization, and inhibiting microtubule formation. Benzimidazoles also act at higher concentrations to disrupt metabolic pathways within the helminth, and inhibit metabolic enzymes, including malate dehydrogenase and fumarate reductase.


Pharmacokinetic data for albendazole in cattle, dogs and cats was not located. The drug is thought better absorbed orally than other benzimidazoles. Approximately 47% of an oral dose was recovered (as metabolites) in the urine over a 9-day period.

After oral dosing in sheep, the parent compound was either not detectable or only transiently detectable in plasma due to a very rapid first-pass effect. The active metabolites, albendazole sulphoxide and albendazole sulfone, reached peak plasma concentrations 20 hours after dosing.

Before you take Albendazole

Contraindications / Precautions / Warnings

The drug is not approved for use in lactating dairy cattle. The manufacturer recommends not administering to female cattle during the first 45 days of pregnancy or for 45 days after removal of bulls. In sheep, it should not be administered to ewes during the first 30 days of pregnancy or for 30 days after removal of rams.

Pigeons and doves may be susceptible to albendazole and fenbendazole toxicity (intestinal crypt epithelial necrosis and bone marrow hypoplasia).

Nine alpaca crias receiving albendazole at dosages from 33-100 mg/kg/day once daily for 4 consecutive days developed neutropenia and severe watery diarrhea. All required treatment and 7 of 9 animals treated died or were euthanized secondary to sepsis or multiple organ failure. ()

In humans, caution is recommended for use in patients with liver or hematologic diseases.

Albendazole was implicated as being an oncogen in 1984, but subsequent studies were unable to demonstrate any oncogenic or carcinogenic activity of the drug.

Adverse Effects

Albendazole is tolerated without significant adverse effects when dosed in cattle or sheep at recommended dosages.

Dogs treated at 50 mg/kg twice daily may develop anorexia. Cats may exhibit clinical signs of mild lethargy, depression, anorexia, and resistance to receiving the medication when albendazole is used to treat Paragonimus. Albendazole has been implicated in causing aplastic anemia in dogs, cats, and humans.

Reproductive / Nursing Safety

Albendazole has been associated with teratogenic and embryotoxic effects in rats, rabbits and sheep when given early in pregnancy. The manufacturer recommends not administering to female cattle during the first 45 days of pregnancy or for 45 days after removal of bulls. In sheep, it should not be administered to ewes during the first 30 days of pregnancy or for 30 days after removal of rams.

In humans, the FDA categorizes this drug as category C for use during pregnancy (Animal studies have shown an adverse effect on the fetus, hut there are no adequate studies in humans; or there are no animal reproduction studies and no adequate studies in humans.)

Safety during nursing has not been established.


Doses of 300 mg/kg (30X recommended) and 200 mg/kg (20X) have caused death in cattle and sheep, respectively. Doses of 45 mg/ kg (4.5X those recommended) did not cause any adverse effects in cattle tested. Cats receiving 100 mg/kg/day for 14-21 days showed signs of weight loss, neutropenia and mental dullness.

How to use Albendazole

Albendazole dosage for dogs:

For Filaroides hirthi infections:

a) 50 mg/kg q12h PO for 5 days; repeat in 21 days. Clinical signs may suddenly worsen during therapy, presumably due to a reaction to worm death. ()

b) 25 mg/kg PO q12h for 5 days; may repeat in 2 weeks (also for Oslerus osleri) ()

For Filaroides osleri (also known as Oslerus osleri) infections:

a) 9.5 mg/kg for 55 days or 25 mg/kg PO twice daily for 5 days.

Repeat therapy in 2 weeks. ()

For Capillaria plica:

a) 50 mg/kg q12h for 10-14 days. May cause anorexia. ()

For Paragonimus kellicotti:

a) 50 mg/kg PO per day for 21 days ()

b) 30 mg/kg once daily for 12 days ()

c) 25 mg/kg PO q12h for 14 days ()

For Giardia:

a) 25 mg/kg PO q12h for 4 doses ()

b) 25 mg/kg PO twice daily for 5 days ()

c) 25 mg/kg PO twice daily for 2- 5 days ()

For Leishmaniasis:

a) 10 mg/kg PO once daily for 30 days or 5 mg/kg PO q6h for 60 days ()

Albendazole dosage for cats:

For Paragonimus kellicotti:

a) 50 mg/kg PO per day for 21 days ()

b) 25 mg/kg PO q12h for 10-21 days ()

c) 30 mg/kg once a day for 6 days ()

d) 25 mg/kg PO q12h for 14 days ()

For Giardia:

a) 25 mg/kg PO twice daily for 5 days ()

b) 25 mg/kg PO q12h for 3-5 days; may cause bone marrow suppression in dogs and cats. ()

For treatment of liver flukes (Platynosum or Opisthorchiidae families):

a) 50 mg/kg PO once daily until ova are gone ()

Albendazole dosage for rabbits, rodents, and small mammals:

a) Rabbits: For Encephalitozoon phacoclastic uveitis: 30 mg/kg PO once daily for 30 days, then 15 mg/kg PO once daily for 30 days ()

b) Chinchillas: For Giardia: 50-100 mg/kg PO once a day for 3 days ()

Albendazole dosage for cattle:

For susceptible parasites:

a) 10 mg/kg PO (Labeled directions; Valbazen — Pfizer)

b) 7.5 mg/kg PO; 15 mg/kg PO for adult liver flukes ()

c) For adult liver flukes: 10 mg/kg PO; best used in fall when the majority are adults (little or no efficacy against immature forms). A second treatment in winter maybe beneficial. ()

d) For gastrointestinal cestodes: 10 mg/kg PO ()

Albendazole dosage for swine:

For susceptible parasites:

a) 5-10 mg/kg PO ()

Albendazole dosage for sheep and goats:

For susceptible parasites:

a) 7.5 mg/kg PO (0.75 mL of the suspension per 25 lb. body weight). (Labeled directions; Valbazen Suspension — Pfizer)

b) 7.5 mg/kg PO; 15 mg/kg PO for adult liver flukes ()

c) For adult liver flukes in sheep: 7.6 mg/kg ()

d) For treatment of nematodes in sheep: 3 mL of suspension per 100 lbs of body weight PO ()

Albendazole dosage for birds:

a) Ratites: Using the suspension: 1 mL/22 kg of body weight twice daily for 3 days; repeat in 2 weeks. Has efficacy against flagellate parasites and tapeworms. ()


■ Efficacy

■ Adverse effects if used in non-approved species or at dosages higher than recommended

■ Consider monitoring CBC’s and liver enzymes (q4-6 weeks) if treating long-term (>1 month)

Client Information

■ Shake well before administering

■ Contact veterinarian if adverse effects occur (e.g., vomiting, diarrhea, yellowish sclera/mucous membranes or skin)

Chemistry / Synonyms

A benzimidazole anthelmintic structurally related to mebendazole, albendazole has a molecular weight of 265. It is insoluble in water and soluble in alcohol.

Albendazole may also be known as. Albendazole may also be known by these synonyms: albendazolum, SKF-62979, Valbazen or Albenza; many other trade names are available.

Storage / Stability

Albendazole suspension should be stored at room temperature (15-30°C); protect from freezing. Shake well before using. Albendazole paste should be stored at controlled room temperature (15-30°C); protect from freezing.

Dosage Forms/ Regulatory Status

Veterinary-Labeled Products:

Albendazole Suspension: 113.6 mg/mL (11.36%) in 500 mL, 1 liter, 5 liters; Valbazen Suspension (Pfizer); (OTC). Approved for use in cattle (not female cattle during first 45 days of pregnancy or for 45 days after removal of bulls, or of breeding age) and sheep (do not administer to ewes during the first 30 days of pregnancy or for 30 days after removal of rams). Slaughter withdrawal for cattle = 27 days at labeled doses. Slaughter withdrawal for sheep = 7 days at labeled dose. Since milk withdrawal time has not been established, do not use in female dairy cattle of breeding age.)

Albendazole Paste: 30% in 205 g (7.2 oz); Valbazen (Pfizer); (OTC). Approved for use in cattle (not female cattle during first 45 days of pregnancy or for 45 days after removal of bulls or of breeding age). Slaughter withdrawal = 27 days at labeled doses. Since withdrawal time in milk has not been established, do not use in female dairy cattle of breeding age.

Human-Labeled Products:

Albendazole Tablets: 200 mg; Albenza (SmithKline Beecham); (Rx)

Practical Veterinarian

Parasites of the Liver



• Worldwide distribution in ruminants, pigs, and horses; occasionally in humans; distribution in North America centers on the Gulf Coast/southeastern states, Pacific Northwest (including Montana), and eastern Canada; highly significant to veterinary medicine; low significance to public health.

• Common name: liver fluke.

Life Cycle

• Indirect.

• Intermediate host: lymnaeid snails; require neutral, poorly drained soil.

• Eggs are passed with bile to intestine and out with the feces; miracidia develop in 10-12 days; require water to hatch; penetrate snail, undergo asexual development and produce cercariae in 1-2 months; one miracidium into a snail equals several hundred cercariae out of snail; leave and attach to vegetation where encyst becoming metacercariae; cercariae may also overwinter in snail.

• Definitive host acquires infection by ingesting metacercariae on vegetation; fluke penetrates the small intestine to abdominal cavity, migrates to and penetrates liver in 4 — 6 days; migrates throughout liver for 4 — 7 weeks and then enters bile ducts and matures.

• Prepatent period is 8-12 weeks; may live for several years.

• In temperate regions, carrier animals important in contaminating pastures in the spring; metacercariae appear during late summer into fall.

• In mild regions, infected snails may overwinter; metacercariae may appear during spring to early summer; spring occurrence depends on moisture and snail activity the preceding fall; carrier animals also important in maintaining pasture contamination.

Pathogenesis and Clinical Signs

• Migration of immature flukes causes traumatic hepatitis and hemorrhage; anemia may result; migratory tracts eventually heal by fibrosis.

• Adults ingest blood and may also cause anemia; presence of adults causes extensive proliferation of the bile duct epithelium, cholangitis, and necrosis of the ductal wall; fibrosis of the lamina propria of the bile duct occurs that may eventually calcify.

• Clinical disease occurs in four forms:

1. Acute — caused by short-term intake of massive numbers of metacercariae that invade the liver all at once; clinical signs include inappetence, weight loss, abdominal pain, anemia, ascites, depression, sudden death; course is only a few days; occurs primarily in sheep and goats.

2. Subacute — also caused by intake of massive numbers of metacercariae, but over a longer period of time; clinical signs include inappetence, decreased weight gain or weight loss, progressive hemorrhagic anemia, liver failure, and death; course is 4 — 8 weeks.

3. Chronic — caused by intake of moderate numbers of metacercariae over an extended period of time; clinical signs include decreased feed intake and weight gain, reduced milk yield, anemia, emaciation, submandibular edema, ascites; cattle tend to exhibit chronic disease.

4. Subclinical — caused by intake of low numbers of metacercariae over a long period of time; moderate cholangitis occurs without apparent clinical signs.



• May find eggs on fecal sedimentation during chronic and subclinical infections, possibly subacute infections also.

• Eggs are oval, operculate, yellow, 130-150 x 65-90 um.


• Mature flukes may be found within the bile ducts; flukes are leaf-shaped, greenish-brown, 2-4 x 1-1.5 cm; with conical anterior end and shoulders.

• Immature flukes (up to 7 mm in length) may be difficult to find within the liver parenchyma; requires sequential slicing of the liver and expressing flukes from cut surfaces.

Treatment and Control

• See Table 4-3 for treatment of cattle; albendazole at 7.5 mg per kg in sheep and 15 mg per kg in goats has been used.

• Strategic use of anthelmintics is cornerstone of control programs; purpose is to remove parasites before animal productivity is affected and to prevent egg shedding that subsequentiy contaminates pastures; the timing, frequency, and choice of anthelmintic vary based on the transmission patterns in each geographic region.

• Grazing management should avoid high-risk areas during periods of transmission; may need to fence off areas of snail habitat; control of snails themselves through draining of habitat or use of molluscicides is impractical in most cases.


• Distributed in North America, central Europe, Mexico, and South Africa; cervids are the usual definitive hosts; catde, sheep, and goats may be accidentally infected; low to moderate significance.

• Common name: large American liver fluke.

Life Cycle

• Indirect.

• Intermediate host: freshwater lymnaeid snails.

• In cervid definitive host, life cycle is essentially as for F. hepatica.

• Prepatent period is approximately 8 months.

• Patency is generally not achieved in catde or sheep (see Pathogenesis and Clinical Signs).

Pathogenesis and Clinical Signs

• Cervids: infections are inapparent; flukes are encapsulated by a thin-walled cyst with channels to the bile ducts; eggs leave the cysts via these channels.

• Cattle: infections tend to be inapparent; flukes reach the liver and are encapsulated in cysts that usually do not communicate with the bile ducts; eggs generally are not passed out of cysts.

• Sheep, goats: flukes tend to migrate continuously within the liver as well as to ectopic sites such as the lungs; traumatic hepatitis results, which is fatal before flukes mature.



• May find eggs on fecal sedimentation of deer feces; eggs are oval, operculate, yellow, 110-160 x ~ 75 um.


• Mature flukes may be found in cysts in liver of cervids and cattle or within the liver parenchyma or other organs of sheep and goats; flukes are leaf-shaped with no demarcated anterior cone, thick, up to 10 cm in length by 2.5 cm in width.

Treatment and Control

• Clorsulon at 20 mg per kg in both sheep and cattle has been used.

• Prevention is best achieved by not grazing sheep in endemic areas; avoid grazing cattle in high-risk areas during transmission.


• Worldwide distribution, except Australia, in cattle, sheep, and goats; sporadic occurrence, moderate significance.

Life Cycle

• Indirect.

• First intermediate host: terrestrial snails.

• Second intermediate host: ants.

• Embryonated eggs are passed with the feces and ingested by snails; cercariae develop in 3-4 months, are shed by the snail, and clump together in slime-balls; ants eat slime-balls and metacercariae form in 26-62 days; most develop in the hemocoel, but some lodge in the subesophageal ganglion; this causes tetanic spasms of the mouthparts as temperatures decrease, which locks the ant onto herbage overnight; ants are then available to grazing animals the following morning.

• Definitive host acquires infection by ingesting ant containing metacercariae; flukes enter the liver by migrating up the bile ducts from the small intestine.

• Prepatent period is 47-54 days; may live for 6 years or longer.

Pathogenesis and Clinical Signs

• Pathologic changes increase in severity as infection increases in age; advanced infections can cause hepatic cirrhosis and proliferation of bile duct epithelium.

• Clinical signs in young animals are usually not present; in sheep, may cause anemia, edema, decreased wool production, and lactation.



• Eggs may be found on fecal sedimentation.

• Eggs are brown, operculated, oval, 36-46 x 10-20 um, containing miracidia; operculum may be difficult to see.


• The flukes are flattened, leaf-like, 6-10 x 1.5-2.5 mm; found in bile ducts; because of their small size, they may be missed at necropsy.

Treatment and Control

• Generally do not treat domestic animals for infection; if heavy infections are present, can use albendazole at 15-20 mg per kg once or 7.5 mg per kg once and repeated 2-3 weeks later; fenbendazole at 100-150 mg per kg has also been used.


• Distributed in southern North America through Central and South America, West Africa, Malaysia, and Pacific Islands in cats; usually low significance except in highly endemic areas.

Life Cycle

• Indirect.

• First intermediate host: terrestrial snails.

• Second intermediate host: sowbugs, woodlice, lizards.

• Paratenic host: lizards, frogs.

• Embryonated eggs are passed with the feces and ingested by snails; sporocysts containing cercariae are shed by snail and ingested by second intermediate host in which metacercariae form.

• Cats acquire infection by ingesting infected lizards (hence the name “lizard poisoning disease”); flukes migrate from the small intestine up the common bile duct.

• Prepatent period is 2-3 months.

Pathogenesis and Clinical Signs

• Infections are usually inapparent with only a short-term inappetence occurring.

• Heavy infections can cause proliferative cholangitis and cirrhosis.

• Clinical signs may include anorexia, icterus, enlarged liver, diarrhea, vomiting, and death.



• Eggs may be found on fecal sedimentation; fecal flotation may be ineffective.

• Eggs are brown, operculated, oval, 35-50 x 20-35 um, containing miracidia.


• Adults live in bile ducts, gallbladder, and pancreas; worms are very small and generally not seen at necropsy; rather, may find them on histologic section.

Treatment and Control

• Praziquantel at 20 mg per kg has been used.

• Prevent predation and scavenging whenever possible.



• Worldwide distribution in gallinaceous birds; locally significant in free-ranging birds.

• Common name: blackhead.

Life Cycle

• Direct; indirect with Heterakis gallinarum or earthworm paratenic host.

• Trophozoites are passed in the feces or in the eggs of H. gallinarum (nematodes ingest trophozoites that infect oocytes); primary means of transmission is ingestion of trophozoites in eggs of H. gallinarum or in eggs of H. gallinarum in earthworms; trophozoites die quickly (within hours) but it is possible they can be ingested with contaminated food or water.

• Remains in flagellated form in cecal lumen approximately 1 week; penetrates subepithelial tissues appearing as a round form without flagellum; carried via circulation to liver 10-12 days postinfection.

• Chickens: nonpathogenic.

• Turkeys: causes inflammation and ulcers in the ceca; cores of necrotic tissue, exudate, and parasites plug ceca; in liver, causes characteristic circular, yellow-green areas of necrosis with a depressed center; clinical signs include depression, inappetence, sulfur-colored droppings, cyanosis of the head (hence the common name), death.



• None.


• Examination of fresh or fixed impression smears obtained from the edge of cecal or liver lesions for organisms; may also be able to find organisms in histological sections.

Treatment and Control

• Modern, intensive management has decreased the incidence of this parasite; separate turkeys from chickens and poults from adults; avoid contaminated ground and adhere to strict sanitation; reuse of litter may lead to build-up of H. meleagridis eggs; treat chickens for H. meleagridis.


Roundworms in Cattle, Sheep and Goats

1. Oesophagus and stomach

Gongylonema. Two species occur in ruminants and 1 in pigs. They are found just below the epithelium in the thoracic third of the oesophagus. The intermediate hosts are various species of dung-beetles.

Haemonchus contortus. This is the large stomach worm or ‘barber’s pole’ worm of ruminants, so-called because of the female’s spiral red and white stripes. The male is red. It is a trichostrongyle, with a length of about 30 mm and the thickness of a pin. It is a voracious blood-sucker, and inhabits the abomasum. It can cause serious anaemia and unthriftiness, especially in lambs.

Haemonchus placet is another of several species.

Ostertagia worms, which are of considerable economic importance, are peculiar in that while most infective larvae living in the abomasum moult twice to become adults, some — especially perhaps those ingested by the calf during late summer and autumn — moult only once and remain as 4th-stage larvae in a dormant state. These dormant larvae are unaffected by many anthelmintics but are usually, though not always, susceptible to ivermectin, fenbendazole and albendazole. Later they develop into adults causing a winter outbreak of gastroenteritis. Calves should therefore be dosed in September and moved to ‘clean’ pasture.

Also known as the small brown stomach worm, Ostertagia cause severe irritation of the mucous membrane by the formation of nodules. Infested animals may lose weight, scour, and become anaemic.

2. Small intestine

Ascaris vitulorum. This large round worm of cattle is generally of little importance, but it may be a frequent and fatal parasite of calves in certain localities.

Nematodirus. This is a common trichostrongyle genus found in large numbers in the small intestine of sheep. It is a very slender form under 2.5 cm long. In recent years nematodirus infestation has caused severe losses.

The infestation is a ‘lamb-to-lamb’ one, and can be avoided – where practicable – by confining lambs to pasture which carried no lambs in the previous 2 seasons. Nematodirus species found in Britain are Nematodirus filicollis, Nematodirus helvetianus, Nematodirus spathiges, and Nematodirus battus, Nematodirus helvetianus and Nematodirus battus are parasites of calves. (See PASTURE, CONTAMINATION OF.)

Cooperia species are important. They are usually present in association with other species of worms, e.g. Ostertagia, Trichostrongylus. They seldom cause anaemia, but are responsible for weight loss and scouring. Trichostrongylus worms are very small (only 2 to 7 mm long) and inhabit the abomasum and duodenum.

Bunestomum (hookworms) live in the small intestine. The larvae may either enter their host via the mouth or penetrate the skin. They suck blood and accordingly cause anaemia and sometimes oedema under the throat. (See HOOKWORMS.)

Oesophagostomum. This is a genus of strongyle worms related to the horse forms, and found in ruminants and pigs. They are about 2.5 cm long. They are the cause of nodular disease of the intestine (‘pimply gut’). If present in small numbers, the only result is to render the intestine unfit for sausage skins. If in large numbers, the symptoms are anaemia, emaciation, diarrhoea, and oedema. The disease in this case often has a fatal termination.

Trichuris. This genus of whip-worm occurs in the caecum of various animals, but is usually of little importance. The worms have very slender necks with stoutish bodies. The necks are threaded through the mucous membrane of their host.

They may cause inflammation at the point of insertion of the head and may admit bacteria.

Strongyloides worms are found in the small intestine, often deep in the mucosa. Scouring is caused in heavy infestations. The worm larvae can enter the body via the skin.

3. Lungs

Dictyocaulus. Three species are known in cattle, but only 1 is important – Dictyocaulus viviparus, which causes a form of bronchitis. The male is about 4 cm long and the female about 7 cm. Eggs hatch in the lung, and the larvae climbing up the trachea are swallowed, passing to the exterior with the faeces. After moulting twice, they reach the resistant infective stage, and can live thus on pasture through the winter. When swallowed, they continue their development.

The signs and treatment are described under PARASITIC BRONCHITIS.

Parasitic bronchitis (‘husk’) Several species of roundworm occur in sheep and goats.

Dictyocaulus filaria is the largest and most common species. The male is about 5 cm long and the female 8 cm. The infective stage is reached in about 10 days. Apparently lambs can be infected prenatally. This worm is cosmopolitan in its distribution. Its life-history is direct.

The symptoms are those of a verminous bronchitis, sometimes complicated by bacterial infection, but otherwise similar to those in cattle.

Protostrongylus (Synthetocaulus) rufescens is a red and much smaller form. The male is about 2 cm and the female 3 cm long. It is found mainly in Europe. These worms live in the bronchioles and in the pulmonary parenchyma, and cause a verminous lobular pneumonia. The eggs cause a diffuse nodular pneumonia. Cough is less prominent than in the above form, but breathing is difficult.

4. Connective tissues

Onchocerca. Several species occur in cattle in various parts of the world. They are the cause of ‘worm nodules’.

The nodules are found mainly in the brisket, but also occur in the flank and forequarters. They appear to cause little harm to their host, but as the capsule is a product of inflammation, beef containing worm nodules is condemned, and in Australia they have caused considerable loss in the export trade.

Dracunculus. Only 1 species of this worm is found in the domestic animals, Dracunculus medinensis, the guinea worm’. It is found in India, Africa, and South America. The female is of considerable length, but is generally recovered from the host in small pieces. It is milky white in colour, smooth and without markings. Nearly the whole of the worm is occupied by the uterus, packed with coiled-up embryos. The worm occupies a subcuticular site, as a rule in the extremities, with the head-end projecting to the exterior. The larvae are released by a prolapse of the uterus through the cuticle of the worm. They escape into the water, and are swallowed by a cyclops in which they develop. The cyclops is in due course swallowed in the drinking water by a suitable host – practically any of the domestic animals will do – and larvae are released by the digestive juices and proceed to their adult habitats. The worm may give rise to local abscesses, and sometimes affects the feet of dogs.

5. Eye

Thelazia. (See EYEWORMS.)



Balantidium coti

Balantidium coli is primarily a pathogen of sheep. Only one case report of natural infection in the dog has ever been published. In another report, a total of 375 fecal samples of 56 mammalian species belonging to 17 families of 4 orders were examined for the detection of Balantidium coli. B. coli organisms were detected in several animal species, but not in dogs or cats.

Entamoeba histolytica

Two isolated case reports of colitis in dogs and one in cats are associated with recovery of Entamoeba histolytica from the feces. E. histolytica can be recovered from the feces of healthy dogs and cats, but it appears to be of low pathogenicity in dogs and cats.


Giardia: Cause

Giardia spp. are protozoal parasites that primarily infect the small intestine of dogs and cats. The cecum and colon are only occasionally colonized by Giardia. All mammalian isolates are currently classified as Giardia lamblia, although some nomenclature systems use the name G. duodenalis or G. intestinalis. Recent DNA sequence technology suggests that one or two distinct Giardia genotypes can be isolated exclusively from dogs, and a distinct genetic group can be isolated from cats. It is not clear whether differences in pathogenicity exist between these genotypes. Giardia species have a worldwide distribution. Because Giardia is maintained in nature primarily by fecal-oral transmission, more cases are associated with crowded and unsanitary conditions. A recent study showed a prevalence in the dog of 7.2%.

Pathophysiology of Giardia

Giardia spp. are found on the surface of enterocytes, where the trophozoites attach to the brush border of the epithelium. Specific histologic changes have not been reported, but persistence of infection may promote apoptosis and inhibition of re-epithelialization.

Clinical examination

Although infected animals may remain asymptomatic, clinical signs such as acute or chronic diarrhea, weight loss, or even acute or chronic vomiting may develop. Although Giardia cysts and trophozoites have been found in the feces of dogs with both small bowel and large bowel diarrhea, Giardia infection is primarily a problem of the small intestine.

Diagnosis of Giardia

Giardia infections can be diagnosed by demonstrating motile trophozoites on fresh fecal smears or cysts by zinc sulfate sedimentation. Commercial enzyme-linked immunosorbent assay (ELISA) kits have also been used to detect Giardia antigen in fresh fecal samples. Enzyme-linked immunosorbent assay assays may be slightly more sensitive and specific than a single zinc sulfate concentrating technique in diagnosing Giardia infections in dogs. A direct immunofluorescent antibody test has been used in the diagnosis of Giardia infections in humans, but it has not yet been validated in the dog. Duodenal aspirates during gastrointestinal endoscopy appear to be ineffective in diagnosing Giardia infection.

Treatment of Giardia

Metronidazole, ipronidazole, fenbendazole, albendazole, and a praziquantel, pyrantel pamoate, febantel combination have all been used in the treatment of Giardia infections with varying levels of success. A Giardia vaccine has been shown to be effective in prevention and therapy in dogs, but efficacy has not yet been established in cats.

Prognosis of Giardia

The prognosis for long-term health and recovery is generally very favorable.

Isospora cants, Isospora ohioensis, Isospora felis, Isospora neorivoha

The Isospora species are the most common coccidial parasites of dogs (Isospora canis and Isospora ohioensis) and cats (Isospora felis and Isospora neorivoha). The coccidia are primarily parasites of the small intestine, but Isospora ohioensis may induce cecal and colonic pathology in puppies and young dogs. Sulfadimethoxine (50 mg / kg orally, once a day for 10 days) or sulfatrimethoprim (15 to 30 mg / kg orally, once a day for 5 days) may be used where clinical signs warrant treatment.

Tritrichomonas foetus

Tritrichomonas foetus: Cause

Tritrichomonas foetus is a flagellated protozoan parasite that is an important venereal pathogen in cattle. T. foetus has also been identified as an intestinal pathogen in domestic cats from which intraluminal infection of the colon leads to chronic large bowel diarrhea. Infected cats are usually young and frequently reside in densely populated housing such as catteries or animal shelters. Cats often have a history of infection with Giardia spp.; these infections are subsequently identified as trichomoniasis after failure to eradicate the organisms with standard antiprotozoal treatment (e. g., metronidazole or fenbendazole).


After experimental inoculation in cats, Tritrichomonas foetus organisms have been shown to colonize the ileum, cecum, and colon, reside in close contact with the epithelium, and are associated with transient diarrhea that is exacerbated by coexisting cryptosporidiosis.

Clinical examination

Infected animals have clinical signs that are consistent with chronic colitis-type diarrhea.

Diagnosis of Tritrichomonas foetus

Diagnosis of trichomonosis in cats is made by direct observation of trichomonads in samples of freshly voided feces that are suspended in physiologic saline (0.9% NaCl) solution and examined microscopically at x200 to x400 magnification. Tritrichomonas foetus can also be grown from feces via incubation at 37° C. in Diamond’s medium. The sensitivity of direct examination of a fecal smear for diagnosis of T. foetus in naturally infected cats is unknown but is suspected to be poor. A commercially available culture system that is sensitive and specific for culture of Tritrichomonas foetus will improve the diagnostic outcome. These kits are most useful when inoculated with less than or equal to 0.1 g of fresh feces at 25° C. More recently, a single-nested tube polymerase chain reaction technique has been developed that is ideally suited for diagnostic testing of feline lecal samples that are found negative by direct microscopy and by definitive identification of microscopically observable or cultivated organisms.

Treatment of Tritrichomonas foetus

At this time the origin of the infection in most cats is unknown, and no effective antimicrobial treatment exists for Tritrichomonas foetus infection. Metronidazole and fenbendazole may improve clinical signs but generally do not resolve infection. Nitazoxanide eliminates shedding of Tritrichomonas foetus and Gryptosporidium oocysts, but diarrhea and oocyst shedding recur with discontinuation of treatment. A series of cats that were treated with paromomycin for Tritrichomonas foetus infection subsequently developed kidney failure. Consequently, paromomycin should probably not be used in cats.

Prognosis of Tritrichomonas foetus

The prognosis for eradication of the organism is not encouraging at this time.



Cause of Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) may be defined using clinical, histologic, immunologic, pathophysiologic, and genetic criteria.

Clinical criteria Inflammatory bowel disease has been defined clinically as a spectrum of gastrointestinal disorders of an unknown cause that is associated with chronic inflammation of the stomach, intestine, or colon. A clinical diagnosis of inflammatory bowel disease is considered only if affected animals have: (1) persistent (> 3 weeks in duration) gastrointestinal signs (anorexia, vomiting, weight loss, diarrhea, hematochezia, mucosy feces), (2) failure to respond to symptomatic therapies (parasiticides, antibiotics, gastrointestinal protectants) alone, (3) failure to document other causes of gastroenterocolitis by thorough diagnostic evaluation, and (4) histologic diagnosis of benign intestinal inflammation. Small bowel and large bowel forms of inflammatory bowel disease have been reported in both dogs and cats, although large bowel inflammatory bowel disease appears to be more prevalent in the dog.

Histologic criteria Inflammatory bowel disease has been defined histologically by the type of inflammatory infiltrate (neutrophilic, eosinophilic, lymphocytic, plasmacytic, granulomatous), associated mucosal pathology (villus atrophy, fusion, crypt collapse), distribution of the lesion (focal or generalized, superficial or deep), severity (mild, moderate, severe), mucosal thickness (mild, moderate, severe), and topography (gastric fundus, gastric antrum, duodenum, jejunum, ileum, cecum, ascending colon, descending colon). As with small intestinal inflammatory bowel disease, subjective interpretation of large intestinal inflammatory bowel disease lesions has made it difficult to compare tissue findings between pathologists. Subjectivity in histologic assessments has led to the development of several inflammatory bowel disease grading systems.

Immunologic criteria Inflammatory bowel disease (IBD) has been denned immunologically by the innate and adaptive response of the mucosa to gastrointestinal antigens. Although the precise immunologic events of canine and feline inflammatory bowel disease remain to be determined, a prevailing hypothesis for the development of inflammatory bowel disease is the loss of immunologic tolerance to the normal bacterial flora or food antigens, leading to abnormal T cell immune reactivity in the gut microenvironment. Genetically engineered animal models (e. g., IL-2, IL-10, T cell receptor knockouts) that develop inflammatory bowel disease involve alterations in T cell development, function, or both, suggesting that T cell populations are responsible for the homeostatic regulation of mucosal immune responses. Immunohistochemical studies of canine inflammatory bowel disease have demonstrated an increase in the T cell population of the lamina propria, including CD3+ cells and CD4+ cells, macrophages, neutrophils, and IgA-containing plasma cells. Many of the immunologic features of canine inflammatory bowel disease can be explained as an indirect consequence of mucosal T cell activation. Enterocytes are also likely involved in the immunopathogenesis of inflammatory bowel disease. Enterocytes are capable of behaving as antigen-presenting cells, and interleukins (e. g., IL-7, IL-15) produced by enterocytes during acute inflammation activate mucosal lymphocytes. Up-regulation of Toll-like receptor 4 (TLR4) and Toll-like receptor 2 (TLR2) expression contribute to the innate immune response of the colon. Thus the pathogenesis and pathophysiology of inflammatory bowel disease appears to involve the activation of a subset of CD4+ T cells within the intestinal epithelium that overproduce inflammatory cytokines with concomitant loss of a subset of CD4+ T cells and their associated cytokines, which normally regulate the inflammatory response and protect the gut from injury. Enterocytes, behaving as antigen-presenting cells, contribute to the pathogenesis of this disease.

Pathophysiologic criteria Inflammatory bowel disease (IBD) may be defined patho-physiologically in terms of changes in transport, blood flow, and motility. The clinical signs of inflammatory bowel disease, whether small or large bowel, have long been attributed to the pathophysiology of malabsorption and hypersecretion, but experimental models of canine inflammatory bowel disease have instead related clinical signs to the emergence of abnormality motility patterns.

Genetic criteria Inflammatory bowel disease (IBD) may be defined by genetic criteria in several animal species. Crohn’s disease and ulcerative colitis are more common in certain human genotypes, and a mutation in the NOD2 gene (nucleotide-binding oligomerization domain2) has been found in a subgroup of patients with Crohn’s disease. Genetic influences have not yet been identified in canine or feline inflammatory bowel disease, but certain breeds (e. g., German shepherds, boxers) appear to be at increased risk for the dis-

Inflammatory Bowel Disease: Pathophysiology

The pathophysiology of large intestinal inflammatory bowel disease is explained by at least two interdependent mechanisms: (1) the mucosal immune response and (2) accompanying changes in motility.

Immune responses A generic inflammatory response involving cellular elements (B and T lymphocytes, plasma cells, macrophages, and dendritic cells), secretomotor neurons (e. g., vasoactive intestinal polypeptide, substance P, cholinergic neurons), cytokines and interleukins, and inflammatory mediators (e. g., leukotrienes, prostanoids, reactive oxygen metabolites, nitric oxide (NO], 5-HT, IFN-γ, TNF-α, platelet-activating factor) is typical of canine and feline inflammatory bowel disease. Many similarities exist between the inflammatory response of the small and large intestine, but recent immunologic studies suggest that inflammatory bowel disease of the canine small intestine is a mixed Th 1 and Th2 response, whereas inflammatory bowel disease of the canine colon may be more of a Th 1 type response with elaboration of IL-2, IL-12, INF-γ, and TNF-α. Other studies of canine colonic inflammatory bowel disease have demonstrated increased numbers of mucosal IgA- and IgG-containing cells, nitrate, CD3+ T cells, NO, and inducible nitric oxide synthase (iNOS) in the inflamed colonic mucosa (Table Immunologic and Motility Abnormalities in Canine Large Bowel Inflammatory Bowel Disease). Increases in the CD3+ positive T cell population of the inflamed colon are consistent with changes reported in the inflamed canine intestine. Thus important similarities exist, as do differences between small and large bowel inflammatory bowel disease.

Immunologic and Motility Abnormalities in Canine Large Bowel Inflammatory Bowel Disease

Histolocic Findings Immunologic Abnormalities
Lymphocytic-plasmacytic colitis Increased nitric oxide and IgG in colonic lavage fluid
Lymphocytic-plasmacytic colitis Increased expression of inducible nitric oxide synthase mRNA
Lymphocytic-plasmacytic colitis Increases in T cells and B cells in lamina propria
Lymphocytic-plasmacytic colitis Increases in CD3+ T cells and in lgA+ and lgC+ plasma cells
Lymphocytic-plasmacytic colitis Increased IL-2 and TNF-α mRNA expression
Tissue / Cell Type Motility Abnormalities
Colon Loss of spontaneous phasic contractions
Decreased frequency of migrating motor complexes (MMCs)
Increased frequency of giant migrating contractions (CMCs)
Colonic circular smooth muscle cells Decreased amplitude and duration of the slow wave plateau potential
Shift from the M3 to M2 muscarinic receptor subtype
Reduced calcium influx through L-type calcium channel
Reduced L-type calcium channel expression
Decreased open probability of KCa channels
Down-regulation of PKC α, β, ξ expression and activation
Reduced phospholipase A2 expression
Increased NF-κB expression and activation
Colonic enteric neurons Sensitization to substance P during colonic inflammation
Colonic interstitial cells of Cajal Reduced density of interstitial cells
Cytoplasmic vacuolation and damage to cellular processes

IgG, Immunoglobulin G; IgA, immunoglobulin A; IL-2, interleukin-2; TNF-α, tumor necrosis factor alpha; PKC, protein kinase C; M, muscarinic; NF-κB, nuclear factor-icB; KCa, calcium-activated potassium channel.

Motility changes Experimental studies of canine large intestinal inflammatory bowel disease have shown that many of the clinical signs (diarrhea, passage of mucus and blood, abdominal pain, tenesmus, and urgency of defecation) are related to motor abnormalities of the colon. Ethanol and acetic acid perfusion of the canine colon induces a large bowel form of inflammatory bowel disease syndrome indistinguishable from the natural condition. I Inflammation in this model suppresses the normal phasic contractions of the colon, including the migrating motility complex, and triggers the emergence of giant migrating contractions. The appearance of these giant migrating contractions in association with inflammation is a major factor in producing diarrhea, abdominal cramping, and urgency of defecation. Giant migrating contractions are powerful lumen-occluding contractions that rapidly propel pancreatic, biliary, and intestinal secretions in the fasting state (and undigested food in the fed state) to the colon to increase its osmotic load. Malabsorption results from direct injury to the epithelial cells and from ultrarapid propulsion of intestinal contents by giant migrating contractions so that sufficient mucosal contact time is not allowed for digestion and absorption to take place.

Inflammation impairs the regulation of the colonic motility patterns at several levels (i. e., enteric neurons, interstitial cells of Cajal, circular smooth muscle cells; summarized in Table Immunologic and Motility Abnormalities in Canine Large Bowel Inflammatory Bowel Disease). Inflammation-induced changes in the amplitude and duration of the smooth muscle slow wave plateau potentials contribute to the suppression of rhythmic phasic contractions. These alterations likely have their origin in structural and functional damage to the interstitial cells of Cajal. At the same time that inflammation suppresses the rhythmic phasic contractions, inflammation sensitizes the colon to the stimulation of giant migrating contractions by the neurotransmitter substance P. These findings suggest that SP increases the frequency of giant migrating contractions during inflammation and that selective inhibition of giant migrating contractions during inflammation may minimize the symptoms of diarrhea, abdominal discomfort, and urgency of defecation associated with these contractions.

Inflammation suppresses the generation of tone and phasic contractions in the circular smooth muscle cells through multiple molecular mechanisms (see Table Immunologic and Motility Abnormalities in Canine Large Bowel Inflammatory Bowel Disease). Inflammation shifts muscarinic receptor expression in circular smooth muscles from the M3 to the M2 subtype. This shift has the effect of reducing the overall contractility of the smooth muscle cell. Inflammation also impairs calcium influx” and down-regulates the expression of the L-type calcium channel, which may be important in suppressing phasic contractions and tone while concurrently stimulating giant migrating contractions in the inflamed colon. Changes in the open-state probability of the large conductance calcium-activated potassium channels (Kc) partially attenuate this effect. Inflammation also modifies the signal transduction pathways of circular smooth muscle cells. Phospholipase A2 and protein kinase C. (PKC) expression and activation are significantly altered by colonic inflammation, and this may partially account for the suppression of tone and phasic contractions. PKC α, β and ξ isoenzyme expression is down-regulated, PKC i and X isoenzyme expression is up-regulated, and the cytosol-to-membrane translocation of PKC is impaired. The L-type calcium channel, already reduced in its expression, is one of the molecular targets of PKC. Inflammation also activates the transcription factor NF-κB that further suppresses cell contractility.

Clinical Examination The clinical signs of large intestinal inflammatory bowel disease are those of a large bowel-type diarrhea (i. e., marked increased frequency, reduced fecal volume per defecation, blood pigments and mucous in feces, and tenesmus). Anorexia, weight loss, and vomiting are occasionally reported in animals with severe inflammatory bowel disease of the colon or concurrent inflammatory bowel disease of the stomach, small intestine, or both. Clinical signs usually wax and wane in their severity. A transient response to symptomatic therapy may occur during the initial stages of inflammatory bowel disease. As the condition progresses, diarrhea gradually increases in its frequency and intensity and may become continuous. In some cases the first bowel movement of the day may be normal or nearlv normal, whereas successive bowel movements are reduced in volume and progressively more urgent and painful. During severe episodes, mild fever, depression, and anorexia may occur.

There does not appear to be any sex predilection, but age may be a risk factor, with inflammatory bowel disease appearing more frequently in middle-aged animals (mean age approximately 6 years with a range of 6 months to 20 years). German shepherd and boxer dogs are at increased risk for inflammatory bowel disease, and pure-breed cats appear to be at greater risk. Cats more often have an upper gastrointestinal form of inflammatory bowel disease, whereas dogs are at risk for both small and large bowel inflammatory bowel disease.

Physical examination is unremarkable in most cases. Thickened bowel loops may be detected during abdominal palpation if the small bowel is concurrently involved. Digital examination of the anorectum may evoke pain or reveal irregular mucosa, and blood pigments and mucous may be evident on the examination glove.

Diagnosis of Inflammatory Bowel Disease

CBCs, serum chemistries, and urinalyses are often normal in mild cases of large bowel inflammatory bowel disease. Chronic cases may have one or more subtle abnormalities. One review of canine and feline inflammatory bowel disease reported several hematologic abnormalities including mild anemia, leukocytosis, neutrophilia with and without a left shift, eosinophilia, eosinopenia, lymphocytopenia, monocytosis, and basophilia. The same study reported several biochemical abnormalities including increased activities of serum alanine aminotransferase and alkaline phosphatase, hypoalbuminemia, hypoproteinemia, hyperamylasemia, hyperglobulinemia, hypokalemia, hypocholesterolemia, and hyperglvcemia. No consistent abnormality in the complete blood count or serum chemistry has been identified.

A scoring index for disease activity in canine inflammatory bowel disease was recently developed that relates severity of clinical signs to serum acute-phase protein (C-reactive protein (CRP], serum amyloid A) concentrations. The canine inflammatory bowel disease activity index (CIBDAI) assigns levels of severity to each of several gastroen-terologic signs (e. g., anorexia, vomiting, weight loss, diarrhea), and it appears to be a reliable index of mucosal inflammation in canine inflammatory bowel disease. Interestingly, both the activity index and serum concentrations of C-reactive protein improve with successful treatment, suggesting that serum C-reactive protein is suitable for the laboratory evaluation of therapy in canine inflammatory bowel disease. Other acute-phase proteins were less specific than C-reactive protein. One important caveat that should be emphasized is that altered CRP is not prima facie evidence of gastrointestinal inflammation. Concurrent infections or other inflammatory conditions could cause an acute-phase response, including C-reactive protein, in affected patients.

Treatment of Inflammatory Bowel Disease

Dietary therapy The precise immunologic mechanisms of canine and feline inflammatory bowel disease have not yet been determined, but a prevailing hypothesis for the development of inflammatory bowel disease is the loss of immunologic tolerance to the normal bacterial flora or food antigens. Accordingly, dietary modification may prove useful in the management of canine and feline inflammatory bowel disease. Several nutritional strategies have been proposed including novel proteins, hydrolyzed diets, antioxidant diets, medium chain triglyceride supplementation, low-fat diets, modifications in the omega-6 (ω-6) and omega-3 (ω-3) fatty acid ratio, and fiber supplementation. Of these strategies, some evidence-based medicine has emerged for the use of novel protein, hydrolyzed, and fiber-supplemented diets.

Food sensitivity reactions were suspected or documented in 49% of cats presented because of gastroenterologic problems (with or without concurrent dermatologic problems) in a prospective study of adverse food reactions in cats. Beef, wheat, and com gluten were the primary ingredients responsible for food sensitivity reactions in that study, and most of the cats responded to the feeding of a chicken- or venison-based selected protein diet for a minimum of 4 weeks. The authors concluded that adverse reactions to dietary staples are common in cats with chronic gastrointestinal problems and that they can be successfully managed by feeding selected protein diets. Further support for this concept comes from studies in which gastroenterologic or dermatologic clinical signs were significandy improved by the feeding of novel proteins.

Evidence is accruing that hydrolyzed diets may be useful in the nutritional management of canine inflammatory bowel disease. The conceptual basis of the hydrolyzed diet is that oligopeptides are of insufficient size and structure to induce antigen recognition or presentation. In one preliminary study, dogs with inflammatory bowel disease showed significant improvement after the feeding of a hydrolyzed diet, although they had failed to respond to the feeding of a novel protein. Clinical improvement could not be solely attributed to the hydrolyzed nature of the protein source because the test diet had other modified features (i. e., high digestibility, cornstarch rather than intact grains, medium-chain triglycerides, an altered ratio of ω-6 to ω-3 polyunsatu-rated fatty acids). Additional studies will be required to ascertain the efficacy of this nutritional strategy in the management of inflammatory bowel disease.

Fiber-supplemented diets may be useful in the management of irritable bowel syndrome (IBS) in the dog. IBS is a poorly defined syndrome in the dog that may or may not bear resemblance to IBS in humans. Canine irritable bowel syndrome has been defined as a chronic large bowel-type diarrhea without known cause and without evidence of colonic inflammation on colonoscopy or biopsy. Dogs fulfilling these criteria were successfully managed with soluble fiber (psyllium hydrophilic mucilloid) supplementation of a highly digestible diet.

Exercise Experimental inflammatory bowel disease (IBD) in the dog is accompanied by significant abnormalities in the normal colonic motility patterns. Physical exercise has been shown to disrupt the colonic MMCs and to increase the total duration of contractions that are organized as nonmigrating motor complexes during the fed state. Exercise also induces giant migrating contractions, defecation, and mass movement in both the fasted and fed states. The increased motor activity of the colon and extra giant migrating contractions that result from physical exercise may aid in normal colonic motor function.

Pharmacologic therapy Animals with mild to moderate forms of large bowel inflammatory bowel disease generally respond favorably to dietary modification alone, but pharmacologic therapy will be required with more severe forms of large bowel inflammatory bowel disease. Medical therapy includes anti-inflammatory (sulfasalazine and other 5-aminosalicylates, metronidazole, prednisone, budesonide), immunosuppressive (azathioprine, cyclosporine, chlorambucil), and motility-modifying (loperamide) drugs (Table Drug Index — Large Bowel Diarrhea).

Drug Index — Large Bowel Diarrhea

Drug Classification And Examples Dose Indication
Anthelmintic Drugs
Albendazole 25 mg / kg PO SID x 2 days Ciardia infection
Febantel 10 mg / kg PO SID x 3 days — adult dogs Trichuris infection
15 mg / kg PO SID x 3 days — puppies Trichuris infection
Fenbendazole 50 mg / kg PO SID x 3 days Trichuris, Ancylostoma, Ciardia infection
Ivermectin 200 μg / kg SQ once Larvicidal for Trichuris canis
Mebendazole 22 mg / kg PO SID x 3 days Trichuris infection
Metronidazole 25 mg / kg PO BID x 5 days Ciardia infection
Milbemycin oxime 0.5 mg / kg PO once per month Trichuris preventive
Praziquantel 44 mg / kg PO once Heterobilharzia
Pyrantel pamoate 5 mg / kg PO dog, 20 mg / kg cat Ancylostoma, Toxocara
Ampicillin 22mg / kg PO IV TID Salmonella, E. coli, Clostridium perfringens
Cefadroxil 22 mg / kg PO BID Salmonella, E. coli
Chloramphenicol 44 mg / kg PO TID — dogs Campylobacter
11 mg / kg PO BID — cats Campylobacter
Enrofloxacin 5 mg / kg PO IM SQ BID Salmonella, E. coli
Erythromycin 15-20 mg / kg PO TID Campylobacter, C. perfringens
Metronidazole 10-20 mg / kg PO BID-TID C. perfringens
Orbifloxacin 2.5-7.5 mg / kg PO SID Salmonella, E. coli
Trimethoprim sulfonamide 30 mg / kg PO IM SQ BID Salmonella
Tylosin 40-80 mg / kg PO SID Inflammatory bowel disease, C. perfringens
Antifungal Drugs
Amphotericin B 2-3 mg / kg IV QOD administered to a cumulative dose of 24-27 mg / kg Histoplasmosis, pythiosis, protothecosis
Itraconazole 5 mg / kg PO BID for several months Histoplasmosis, pythiosis, protothecosis
Ketoconazole 10-15 mg / kg PO BID several months Histoplasmosis, pythiosis. protothecosis
Anti-Inflammatory Drugs
Budesonide 1 mg / cat or 1 mg / dog PO SID Inflammatory bowel disease
Meselamine 10 mg / kg PO TID IBD
Metronidazole 10-20 mg / kg PO BID-TID for 4-6 weeks Inflammatory bowel disease
Olsalazine 5-10 mg / kg PO TID for 4-6 weeks IBD
Prednisolone 4.0-6.0 mg / kg PO SID for 4-6 weeks Feline eosinophilic colitis
Prednisone 1.0-2.0 mg / kg PO SID for 4-6 weeks IBD
Sulfasalazine 10-25 mg / kg PO TID for 4-6 weeks — dogs inflammatory bowel disease, ulcerative colitis
5-12.5 mg / kg PO TID for 2-4 weeks — cats Refractory IBD
Immunosuppressive Drugs
Azathioprine 2 mg / kg PO SID for 4-6 weeks — dogs Inflammatory bowel disease
Chlorambucil 2 mg / m PO every other day for 4-6 weeks IBD
Cyclosporine 3-7 mgAg PO BID for 4-6 weeks IBD
Motility-Modifying Drugs
Loperamide 0.08 mgAg PO TID-QID IBD, IBS
Propantheline 0.25 mg / kg PO BID-TID Irritable bowel syndrome
Aminopentamide 0.01-0.03 mg / kg PO BID-TID IBS
Enterococcus faecium (SF68) 5 x 10 colony-forming units / day IBD
Lactobacillus rhamnosus GC 1 x 10 to 5 x 10 colony-forming units / day Inflammatory bowel disease

PO, per os; SID, once per day; IV, intravenous; TID, three times per day; BID, twice per day; QOD, every other day.

Sulfasalazine Sulfasalazine is a highly effective prostaglandin synthetase inhibitor that has proven efficacy in the therapy of large bowel inflammatory bowel disease in the dog. Sulfasalazine is a compound molecule of 5-aminosalicylate (meselamine) and sulfapyridine linked in an azochemical bond. After oral dosing, most of the sulfasalazine is transported to the distal gastrointestinal tract where cecal and colonic bacteria metabolize the drug to its component parts. Sulfapyridine is largely absorbed by the colonic mucosa but much of the 5-aminosalicylate remains in the colonic lumen where it inhibits mucosal cyclooxygenase and the inflammatory cascade. Sulfasalazine has been recommended for the treatment of canine large bowel inflammatory bowel disease at doses of 10 to 25 mg / kg orally, three times a day for 4 to 6 weeks. With resolution of clinical signs, sulfasalazine doses are gradually decreased by 25% at 2-week intervals and eventually discontinued while maintaining dietary management. Salicylates are readily absorbed and induce toxicity in cats; therefore this drug classification should be used with great caution in cats. If used in cats, some authors have recommended using half of the recommended dog dose (i. e., 5 to 12.5 mg / kg orally, three times a day). Sulfasalazine use has been associated with the development of keratoconjunctivitis sicca in the dog, so tear production should be assessed subjectively (by the pet owner) and objectively (by the veterinarian) during use.

Other 5-aminosalicylates This drug classification was developed to reduce the toxicity of the sulfapyridine portion of the parent molecule (sulfasalazine) and to enhance the efficacy of the 5-aminosalicylate portion. Meselamine (Dipentum, Asachol) and dimeselamine (olsalazine) are available for use in the treatment of canine large bowel inflammatory bowel disease. Olsalazine has been used at a dose of 5 to 10 mg / kg orally, three times a day in the dog. Despite the formulation of sulfa-free 5-aminosalicylate preparations, instances of keratoconjunctivitis sicca have still been reported in the dog.

Metronidazole Metronidazole (10 to 20 mg / kg orally, twice a day to three times a day) has been used in the treatment of mild to moderate cases of large bowel inflammatory bowel disease in both dogs and cats. Metronidazole has been used either as a single agent or in conjunction with 5-aminosalicylates or glucocorti-coids. Metronidazole is believed to have several beneficial properties, including antibacterial, antiprotozoal, and immunomodulatory effects. Side effects include anorexia, hypersalivation, and vomiting at recommended doses and neurotoxicity (ataxia, nystagmus, head title, and seizures) at higher doses. Side effects usually resolve with discontinuation of therapy, but diazepam may accelerate recovery of individual patients.

Glucocorticoids Anti-inflammatory doses of prednisone or prednisolone (1 to 2 mg / kg orally, once a day) may be used to treat inflammatory bowel disease in dogs that have failed to respond to dietary management, sulfasalazine, or metronidazole, and as adjunctive therapy to dietary modification in feline inflammatory bowel disease. Prednisone or prednisolone are used most frequendy, because both have short durations of action, are cost-effective, and are widely available. Equipotent doses of dexamethasone are equally effective but may have more deleterious effects on brush border enzyme activity. Prednisone should be used for 2 to 4 weeks depending upon the severity of the clinical signs. Higher doses of prednisone (e. g., 2 to 4 mg / kg orally, once a day) may be needed to control severe forms of eosinophilic colitis or hypereosinophilic syndrome in cats.

Combination therapy with sulfasalazine, metronidazole, or azathioprine may reduce the overall dose of prednisone needed to achieve remission of clinical signs. As with sulfasalazine, the dose of glucocorticoid may be reduced by 25% at 1- to 2-week intervals while (it is hoped) maintaining remission with dietary modification.

Because of steroid side effects and suppression of the hypothalamic-pituitary-adrenal axis, several alternative glucocorticoids have been developed that have excellent topical (i. e., mucosal) anti-inflammatory activity but are significantly metabolized during first pass hepatic metabolism. Budesonide has been used for many years as an inhaled medication for asthma, and an enteric-coated form of the drug is now available for treatment of inflammatory bowel disease in humans (and animals). Little clinical evidence supports of the use of this medication in canine or feline inflammatory bowel disease, but doses of 1 mg / cat or 1 mg / dog per day have been used with some success in anecdotal cases.

Azathioprine Azathioprine is a purine analog that, after DNA incorporation, inhibits lymphocyte activation and proliferation. It is rarely effective as a single agent and should instead be used as adjunctive therapy with glucocorticoids. Azathioprine may have a significant steroid-sparing effect in inflammatory bowel disease. Doses of 2 mg / kg orally, every 24 hours in dogs and 0.3 mg / kg orally every 48 hours in cats have been used with some success in inflammatory bowel disease. It may take several weeks or months of therapy for azathioprine to become maximally effective. Cats particularly should be monitored for side effects, including myelosuppression, hepatic disease, and acute pancreatic necrosis.

Cyclosporine Cyclosporine has been used in the renal transplantation patient for its inhibitory effect on T cell function. In more recent times, cyclosporine has been used in a number of immune-mediated disorders, including keratoconjunctivitis sicca, perianal fistula (anal furunculosis), and IMHA. Evidence-based medicine studies will be needed to establish efficacy, but anecdotal experience would suggest that cyclosporine (3 to 7 mg / kg orally, twice a day) may be useful in some of the more difficult or refractory cases of inflammatory bowel disease.

Chlorambucil Chlorambucil (2 mg / m orally, every other day) has been used in place of azathioprine in some difficult or refractory cases of feline inflammatory bowel disease.

Motility-modifying drugs The mixed μ, δ-opioid agonist, loperamide, stimulates colonic fluid and electrolyte absorption while inhibiting-colonic propulsive motility. Loperamide (0.08 mg / kg orally, three times a day to four times a day) may be beneficial in the treatment of difficult or refractory cases of large bowel-type inflammatory bowel disease.

Probiotic therapy Probiotics (see Table Drug IndexLarge Bowel Diarrhea) are living organisms with low or no pathogenicity that exert beneficial effects (e. g., stimulation of innate and acquired immunity) on the health of the host. The gram-positive commensal lactic acid bacteria (e. g., Lactobacilli) have many beneficial health effects, including enhanced lymphocyte proliferation, innate and acquired immunity, and anti-inflammatory cytokine production Lactobacillus rhamnosus GG, a bacterium used in the production of yogurt, is effective in preventing and treating diarrhea, recurrent Clostridia difficile infection, primary rotavirus infection, and atopic dermatitis in humans. Lactobacillus rhamnous GG and Lactobacillus acidophilus (strain DSM13241) have been safely colonized in the canine gastrointestinal tract, although probiotic effects in the canine intestine have not been firmly established. The probiotic organism, Enterococcus faecium (SF68), has been safely colonized in the canine gastrointestinal tract, and it has been shown to increase fecal IgA content and circulating mature B (CD21+ / MHC class 11+) cells in young puppies. It has been suggested that this probiotic may be useful in the prevention or treatment of canine gastrointestinal disease. This organism may, however, enhance Campybbacter jejuni adhesion and colonization of the dog intestine, perhaps conferring carrier status on colonized dogs. Two recent studies have shown that many commercial veterinary probiotic preparations are not accurately represented by label claims. Quality control appears to be deficient for many of these formulations. Until these products are more tightly regulated, veterinarians should probably view product claims with some skepticism.

Behavioral modification Inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) very likely have underlying behavioral components. Abnormal personality traits and potential environmental stress factors were identified in 38% of dogs in one study. Multiple factors were present in affected households, including travel, relocation, house construction, separation anxiety, submissive urination, noise sensitivity, and aggression. The role of behavior in the pathogenesis and therapy of canine and feline gastrointestinal disorders remains largely unexplored.

Prognosis of Inflammatory Bowel Disease

Most reports indicate that the short-term prognosis for control of inflammatory bowel disease is good to excellent. After completion of drug therapy, many animals are able to maintain remission of signs with dietary management alone. Treatment failures are uncommon and are usually due to (1) incorrect diagnosis (it is especially important to rule out alimentary lymphosarcoma), (2) presence of severe disease such as histiocytic ulcerative colitis and protein-losing enteropathy or irreversible mucosa lesions such as fibrosis, (3) poor client compliance with appropriate drug and dietary recommendations, (4) use of inappropriate drugs or nutritional therapy, and (5) presence of concurrent disease such as small intestinal bacterial overgrowth or hepatobiliary disease. The prognosis for cure of inflammatory bowel disease is poor, and relapses should be anticipated.




Isospora spp.

hospora spp. are the most common coccidial parasites of dogs (Isospora canis, Isospora ohioensis) and cats (Isospora felis, Isospora rivolta). Transmission occurs by ingestion of ova or paratenic hosts. Sporozoites are liberated in the small intestine and enter cells to begin development. The prepatent period ranges from 4 to 11 days, depending on the species. Isospora organisms are rarely associated with clinical signs. Puppies and kittens kept in unhygienic conditions or immunosuppressed animals may develop heavy infestations, which occasionally are associated with diarrhea that is often mucoid but sometimes bloody. Isospora oocysts are found on direct examination of a fecal smear or by flotation. The infection is often self-limiting, but sulfadimethoxine (50 mg / kg given orally once daily for 10 days) or trimethoprim-sulfa (15 to 30 mg / kg given orally once daily for 5 days) can be used when clinical signs warrant treatment. The prognosis for recovery is good.

Cryptosporidium sp.

Cryptosporidium parvum, a significant pathogen in humans, is not a single species but is composed of genetically distinct genotypes. Transmission occurs by the fecal-oral route. Molecular studies have shown that dogs may transmit the catde genotype to humans but that specific cat and dog genotypes also exist. C. parvum has been associated with self-limiting diarrhea in dogs and cats and severe hemorrhagic diarrhea in immunocompromised animals.

Cryptosporidial oocysts are extremely small (approximately 1 / 10 the size of Isospora oocysts) and require identification by fecal flotation and oil immersion microscopy or by intestinal biopsy.

Paromomycin was reported to be effective against Cryptosporidium organisms in a cat. However, more recent studies have demonstrated that the drug’s efficacy is poor and that it may cause acute renal failure. No other drugs are consistently efficacious, although nitazoxanide may prove to be effective. Fortunately, the disease is usually self-limiting in immunocompetent animals.

Giardia sp.

Giardia sp. can affect both dogs and cats. The prevalence of infection in canine studies ranges from less than 2% to 100% in kennels. Cats are less commonly infected than dogs. The parasite is usually transmitted via the fecal-oral route. Ingested oocysts excyst in the upper small intestine, and trophozoites attach to the intestinal mucosa from the duodenum to the ileum. After multiplication of trophozoites, oocysts are passed in the feces at 1 to 2 weeks after infection. Molecular epidemiologic studies indicate that giardiasis may be a zoonosis.

Clinical Findings

Most infections are not associated with clinical signs. Clinical signs range from mild, self-limiting, acute diarrhea to severe or chronic small bowel diarrhea associated with intestinal protein loss and weight loss.


Giardia infection can be diagnosed by demonstration of motile trophozoites in duodenal juice or on a fresh fecal smear or by demonstration of cysts by zinc sulfate fecal flotation. Shedding of cysts occurs intermittendy, and three fecal analyses are 95% sensitive. Giardia antigen can also be detected by means of a fecal enzyme-linked immunosorbent assay, and this is the preferred method of diagnosis compared to zinc sulfate flotation performed by inexperienced technicians.


Metronidazole is the drug most commonly used to treat Giardia infection in small animals. The standard dosage recommended for dogs is 25 mg / kg given orally twice daily for 5 days; the standard dosage for cats is 10 to 25 mg / kg given orally twice daily for 5 days. The drug is effective at eliminating Giardia infection in two thirds of infected dogs but may cause side effects at these high doses.

Albendazole (25 mg / kg given orally twice daily for 2 days) and fenbendazole (50 mg / kg given orally twice daily for 3 days) also eliminate Giardia infection. Fenbendazole is preferred, because albendazole has been associated with bone marrow toxicosis. Febantel (in a combination product with praziquantel and pyrantel pamoate) is also effective in dogs.

Decontamination of the patient’s coat by bathing and the patient’s habitat by steam cleaning or cleaning with quaternary ammonium compounds is advised to prevent reinfection. A Giardia vaccine is available for use in high-risk areas, and it has been shown to be effective in clearing infection from dogs that failed to respond to standard drug therapy.


The prognosis is usually good. Some patients may require several treatments to eliminate infection, because reinfection is a significant problem.