Chronic diarrhea

CHRONIC DIARRHEA

Chronic diarrhea should first be defined as either small intestinal or large intestinal in origin, preferably by using the history and physical examination (Table 9-5 ). Occasionally, large and small intestines are concurrently involved. Patients with chronic diarrhea in which clinical disease is not severe are often treated with therapeutic trials before aggressive diagnostics are instituted. All patients should undergo at least three fecal examinations at 48-hour intervals. If these tests are negative, it is still acceptable to treat empirically for Giardia infection and whipworms before aggressive diagnostics are begun. Giardiasis may be particularly difficult to diagnose (see Fecal Giardia Detection) and medically manage. Adverse food reactions also cause chronic diarrhea. Dietary intolerances are a reaction to a particular substance in the diet, whereas true food allergies are immunologic reactions to specific antigens. Food reactions are common, especially in cats. Dietary food trials are indicated in suspected cases. Failing to respond to empiric therapy indicates the need for further diagnostics.

TABLE 9-5

Differentiation of Chronic Small Intestinal from Chronic Large Intestinal Diarrhea

	SMALL INTESTINAL DIARRHEA	LARGE INTESTINAL DIARRHEA
Weight loss (most important criteria)	Expected	Uncommon except with histoplasmosis, pythiosis, or cancer
Polyphagia	Often present	Uncommon
Vomiting	May occur	Occurs in 10% to 20% of patients
Volume of feces	May be normal or larger than normal	May be normal or smaller than normal
Frequency of defecation	Normal to slightly increased	Normal to markedly increased, may have many small defecations per bowel movement
Slate-gray feces (steatorrhea)	Occasionally	No
Hematochezia	No	Sometimes present
Melena	Sometimes	No
Mucoid stools	Rare (unless ileum is diseased)	Often present
Tenesmus/dyschezia	Rarely present	Sometimes present

Large Intestinal Diarrhea

Once parasitism, dietary-responsive disease, and clostridial colitis are eliminated, additional simple diagnostic steps, such as rectal mucosal scrapings (not swabs) with cytologic examination (see Color Plate 3B) or fecal culture for C. jejuni, Salmonella spp., Y. enterocolitica, verotoxin-positive E. coli, or a combination of these might be appropriate. Persistent large intestinal disease is usually an indication for colonoscopy plus biopsy, especially if the animal has hypoalbuminemia or has lost weight. Rigid colonoscopy of the descending colon is adequate for diagnosis in most cases. Flexible endoscopy allows access to the descending, transverse, and ascending colon; ileocolic valve; cecum; and ileum. If flexible endoscopy is unavailable, abdominal ultrasonography or a barium enema may reveal lesions in areas not accessible with rigid endoscopy.

Small Intestinal Disease

Chronic and severe small intestinal diarrhea necessitates differentiation of maldigestion, protein-losing enteropathy (PLE), and malabsorptive disease without protein loss (Figure 9-3 ). Weight loss and diarrhea are usually present, but some patients only have weight loss.

FIGURE 9-3

Diagnostic approach to chronic diarrhea in dogs and cats in which multiple fecal examination results are negative and empiric anthelmintic, antiprotozoal, and dietary therapy do not resolve the diarrhea. EPI, Exocrine pancreatic insufficiency; TLI, trypsin-like immunoreactivity.

Maldigestion

Maldigestion resulting from bile acid insufficiency as the result of biliary obstruction is rare. Intestinal lactase deficiency is uncommon, but a lactose-free diet may be tried in selected patients (especially cats). EPI is the most common cause of canine maldigestion but is rare in cats. Differentiation of EPI from malabsorptive disease is important. The diagnosis is often overlooked in afflicted dogs or may inappropriately be made in patients without the malady. Clinical trials using pancreatic enzyme preparations are commonly used to diagnose EPI. Unfortunately this method is unreliable. Powdered enzyme is often superior to tablet formulations, and some enzyme preparations are clearly superior to others. Even when appropriate enzymes are administered, some dogs with EPI also require a low-fat diet, antacid therapy (rare), or treatment for concurrent antibiotic-responsive enteropathy (ARE) (common) before the enzyme replacement therapy becomes effective. Too often, failure of the initial enzyme replacement therapy leads to unnecessary tests (i.e., exploratory laparotomy), because the correct diagnosis of EPI was incorrectly eliminated. No consistent hematologic or serum chemistry profile changes are seen, and the serum amylase and lipase values are usually normal. Undigested fats are often found in the feces; however, this is inconsistent. The fat absorption test is inexpensive but can yield false results. The TLI assay is the best test for canine EPI, and the fTLI assay is the best test for feline EPI. It is important to note that the tests are species specific. Measurement of trypsin proteolytic activity also is an accurate means of diagnosing feline EPI; however, it is more cumbersome and has limited availability.

Malabsorptive Disease Without Protein Loss

Once maldigestion has been accurately ruled out, malabsorption becomes the most likely diagnosis in diarrheic animals with weight loss. One must then decide whether to perform diagnostic therapeutic trials or diagnostic tests. A definitive diagnosis usually necessitates intestinal biopsy. Patients that are critically ill (i.e., are emaciated or have serum albumin <2.2g/dl) usually should next undergo abdominal ultrasonography and intestinal biopsies (preferably via endoscopy). Patients that are not critically ill may be managed first using therapeutic trials. Therapeutic trials may be chosen more rationally with the aid of minimal laboratory data such as a CBC, biochemical profile, and fecal examinations. The two major therapeutic trials are (1) food trials for dietary intolerance and (2) antibiotic trials for ARE.

ARE (previously called “small intestinal bacterial overgrowth”) may exist by itself or it may coexist with another GI malady. ARE may prevent therapy aimed at the underlying problem from resolving clinical signs. No consistent CBC or serum chemistry profile changes are seen in this syndrome. Fecal culture is not informative, and intestinal biopsy is seldom diagnostic. A barium contrast study may identify a segmental lesion or partial obstruction responsible for secondary ARE. Quantitated culture of duodenal or proximal jejunal fluid for aerobes and anaerobes is difficult to interpret, because clinically normal dogs may have as many or more bacteria than clinically affected dogs. Finding an increased concentration of unconjugated serum bile acids is believed to be supportive of ARE. Bacteria can deconjugate serum bile acids in the intestinal lumen, and these bile acids can be absorbed by the jejunum. However, the test is limited in its availability. Serum vitamin B₁₂ and folate concentrations have been used as screening procedures for ARE once EPI has been ruled out. Some patients with ARE have normal serum vitamin B₁₂ and folate concentrations, however. Response to empiric antibiotic therapy supports the diagnosis. Signs secondary to ARE usually respond to appropriate antibiotic therapy (e.g., tetracycline, tylosin, ampicillin, metronidazole) unless irreversible mucosal changes or a primary underlying intestinal disease are seen.

Dietary intolerance is relatively common, and hypoallergenic diets (e.g., fish and potato, turkey and potato, tofu and beans) are reasonable trials. At least 4 weeks (and preferably 6 to 8 weeks) should be allotted for such a dietary trial, during which time absolutely nothing else should be fed (including flavored treats or medications).

If dietary, antibiotic, and repeated anthelmintic and antiprotozoal therapies are ineffective, small intestinal biopsy is probably necessary. Laparotomy, laparoscopy, or endoscopy may be used. In most patients, the stomach, duodenum, ileum, and colon may be endoscopically sampled. Duodenal cytology is helpful in some disorders (e.g., eosinophilic enteritis, purulent enteritis, giardiasis, lymphoma). If laparotomy is performed, multiple representative full-thickness specimens (e.g., stomach, duodenum, jejunum, ileum, mesenteric lymph node) are indicated, because lesions can be sporadic. If endoscopy is performed, multiple specimens (e.g., ≥8) from each site are obtained. It is critical that the endoscopist be accomplished and trained in obtaining high-quality tissue samples. Many endoscopic biopsies obtain nondiagnostic samples because of the operator's lack of training in this area.

Protein-Losing Enteropathy

PLEs are often characterized by a decrease in serum concentrations of both serum albumin and globulin, which are lost through the GI tract. PLE is uncommon in cats but seen with some regularity in dogs. Dogs with inflammatory diseases causing hyperglobulinemia and some breeds (e.g., Basenji dogs) may have only hypoalbuminemia. This occurs because the serum globulin concentration is greatly increased, and even though much of this fraction is lost into the intestines, the amount remaining keeps concentrations in the normal range. If red blood cells (RBCs) are also being lost, iron-deficiency anemia may occur (see Chapter 3).

PLE may be the result of various GI diseases (e.g., hookworms, chronic intussusception, fungal infections, ulcers and erosions), but inflammatory bowel disease, alimentary lymphosarcoma, and lymphangiectasia are the most common causes in adult dogs. Intestinal lymphangiectasia causes severe PLE in dogs (it is not reported in cats) and can produce some of the lowest serum protein levels (serum albumin <1.0g/dl) that occur in alimentary disease. Because of the loss of lymph into the intestines, peripheral lymphocyte counts may be decreased; hypocholesterolemia and steatorrhea are common. If hepatic insufficiency and loss from the kidneys and skin have been eliminated in a hypoalbuminemic patient, PLE becomes the major differential diagnosis by process of elimination. If PLE is suspected in a patient that has another potential explanation for its hypoalbuminemia (e.g., renal protein loss or substantive hepatic insufficiency), then detecting abnormally high concentrations of alpha-1 protease inhibitor in the feces supports a diagnosis of GI protein loss. The relatively stable alpha-1 proteinase is resistant to GI degradation and consequently can be measured in the feces. Intestinal biopsy is usually the definitive test. Full-thickness biopsy may risk dehiscence if the serum albumin level is less than 1.5g/dl; however, serosal patch graft techniques decrease the risk of dehiscence. Gastroduodenoscopy-ileoscopy plus biopsy is safe and often (but not invariably) diagnostic. Occasionally the intestinal lesion is inaccessible via endoscopy. Although not recommended, dietary trial may be used in patients with PLE. An ultra-low–fat diet is reasonable if lymphangiectasia is suspected; however, therapeutic trials with steroids are potentially dangerous and are not recommended without a definitive diagnosis.

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FECAL CHARACTER

Mucoid feces should be approached as a large intestinal or a distal small intestinal problem. In dogs and cats that have large bowel disease but no weight loss or hypoalbuminemia, multiple fecal examinations, digital rectal examination, and therapeutic trials (i.e., dietary, antibacterial or anthelmintic [or both]) are often the best initial steps. If these are unsuccessful, then colonileoscopy plus biopsy generally becomes the most useful diagnostic tool. Hematochezia should also be considered as a large bowel problem. Melena signifies swallowed blood from any source, coagulopathy, or gastric and upper intestinal bleeding. Therefore before performing an exploratory laparotomy, one should consider all the possible causes of oral bleeding (e.g., coughing up blood from the respiratory tract, posterior nasal bleeding). Ingestion of bismuth subsalicylate (Pepto-Bismol) or liver can cause feces to appear melenic. Diet and changes in intestinal bacterial flora influence fecal color but do not generally signify disease.

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FECAL ENZYME-LINKED IMMUNOSORBENT ASSAY FOR PARVOVIRUS

Occasional Indications

Dogs suspected of having parvoviral enteritis (especially those not displaying classic signs); acute neutropenia of unknown cause.

Advantages

Quick, available, has good sensitivity and specificity if done at the appropriate time (e.g., approximately 1-3 days after onset of clinical signs).

Disadvantages

Dogs with parvoviral enteritis can have negative reactions, especially early in the course.

Analysis

Fresh feces, preferably taken from a dog that has begun to show signs in the last 24 to 36 hours, are used according to kit instructions (see Chapter 15). The instructions must be carefully followed or false results might be obtained.

Normal Values

Dogs should not have parvoviral antigen in feces.

Interpretation

A positive result supports canine parvoviral enteritis. Not all dogs affected with parvoviral enteritis have diarrhea and fever; some show only anorexia, vomiting, or fever. Theoretically, if coproantibody binds all of the antigen in the feces, a false-negative result may occur. If the test is performed too early in the disease, it may yield negative results. With such dogs, one should repeat the test in 36 to 48 hours. Shedding of viral particles decreases after the first week of disease, and a test performed too late in the disease might yield negative results. Modified-live vaccination results in transient fecal shedding and can give a weak positive fecal ELISA test result (5 to 15 days after vaccination).

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FECAL ANALYSIS FOR CLOSTRIDIAL TOXINS

Occasional Indications

Dogs with acute, nosocomial diarrhea or chronic large bowel diarrhea of unknown cause.

Advantages

Relatively easy to perform.

Disadvantages

Might be difficult to interpret results, especially of old fecal samples. Uncertain sensitivity and specificity for Clostridium perfringens —associated diarrhea.

Analysis

Fresh or frozen feces used according to the instructions on the test kit. Reversed passive latex agglutination (RPLA) and ELISA (i.e., Clostridium perfringens Enterotoxin Test, TechLab, Blacksburg, VA) methods are available for Clostridium perfringens enterotoxin. ELISA methodology is available to look for Clostridium difficil e toxin A (ImmunoCard Toxin A, Meridan Diagnostics, Cincinnati OH).

Interpretation

Finding Clostridium perfringens enterotoxin in feces plus clinical signs of clostridial diarrhea has been considered diagnostic of clostridial colitis. Results from ELISA methodology appear to correlate better with disease than do results from RPLA methodology. However, production of enterotoxin does not appear to be a consistent event (i.e., found in every bowel movement), especially in the later course of disease. In suspected cases with a negative toxin assay, it might be useful to wait and repeat the test again at the onset of recurrence of clinical signs or perform a therapeutic trial with amoxicillin or tylosin.

Fecal spore counts do not correlate well with Clostridium perfringens enterotoxin production or with the presence of diarrhea. Examining fecal smears (see Fecal Microscopic Cytology) to look for the presence of spores no longer seems to be an acceptable screening procedure (e.g., clinically normal dogs may have spores in their feces and be positive for enterotoxin by RPLA).

Finding evidence of Clostridium difficile toxin A in feces of diarrheic patients seems suggestive of a cause-and-effect relationship, but this is currently being investigated.

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FECAL CULTURE

Occasional Indications

Dogs and cats with persistent diarrhea (especially large bowel) of unknown origin, suspected contagious diarrhea, or a suspected infectious cause (e.g., diarrhea with concurrent fever, leukocytosis, neutrophilic fecal cytology, bloody diarrhea). Enteric pathogens include C. perfringens, Salmonella spp., C. jejuni, verotoxin-positive E. coli, Clostridium perfringens, Clostridium difficile, and Y. enterocolitica.

Disadvantages

Must specify which pathogens to culture, must provide the laboratory with fresh feces or feces submitted in appropriate transport media, and requires a microbiology laboratory familiar with the specific enrichment and isolation techniques for each pathogen for which a culture is attempted. Using culture swabs is not adequate for isolation of most enteric pathogens. Finally, growing a “pathogen” does not mean that it is responsible for clinical signs.

Analysis

Fresh feces must be promptly submitted to the laboratory, and the laboratory must know the specific pathogen(s) sought. To submit old feces or feces that have not been collected or handled properly or to request a “general culture for pathogens” is generally a waste of time and money. It requires laboratories that are properly equipped to culture for enteric pathogens. Culture for C. perfringens and Clostridium difficile in particular is not usually diagnostically useful.

Interpretation

Small numbers of any of the pathogens listed earlier might be found in normal pets, although Y. enterocolitica is particularly uncommon in the United States. Interpretation of the fecal culture must consider the history, physical examination, laboratory data, and sometimes numbers of pathologic organisms (i.e., number of bacterial colony-forming units per gram of feces) found. With diarrhea from any cause, the GI flora may change from a predominately anaerobic to a gram-negative aerobic population.

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FECAL ALPHA-1 PROTEASE INHIBITOR ACTIVITY

Infrequent Indications

Hypoalbuminemia of uncertain cause or suspected PLE.

Advantages

Specifically indicates the GI tract as the source of protein loss. Alpha-1 protease inhibitor is a plasma protein, which, if leaked into the intestinal lumen, is resistant to GI degradation and hence can be measured in the feces. The amount of alpha-1 protease inhibitor reflects the approximate loss of plasma proteins into the GI tract.

Disadvantages

Limited availability of the test. The magnitude of alpha-1 protease inhibitor in the feces is variable and may not reflect the severity of the disease.

Analysis

Three 1 g fecal samples from three different bowel movements are submitted in tubes provided by the laboratory. It is critically important that three samples (preferably from different days or at least different bowel movements) be submitted, that the feces be collected promptly after defecation, and that the feces not be collected by digitally removing them from the rectum. Samples must be frozen while one awaits shipping and must be shipped on a cold pack. Currently the only laboratory offering this test for dogs is GI Laboratory, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843-4474.

Normal Values

0.23 to 5.67 μg/g feces.

Causes of Abnormalities

Abnormally high values in the feces indicate loss of serum proteins into the alimentary tract and might indicate that PLE is the cause of hypoalbuminemia. Interpretation of the magnitude of the loss is as per the laboratory.

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FECAL MICROSCOPIC CYTOLOGY

Frequent Indications

Large or small intestinal diarrhea.

Advantages

Availability and ease of performing the test.

Disadvantages

Variable specificity for a particular causative factor.

Analysis

Thin, air-dried, fresh fecal smears are stained with NMB or Wright's stain and examined using high-power and oil immersion. Rectal and colonic mucosal scraping obtained with a curette is also a means of examining mucosal cells.

Normal Values

A mixed population of rod and cocci bacteria, few bacterial spores or yeast, occasional epithelial cells and amorphous debris.

Artifacts

Old fecal sample (white blood cells [WBCs] do not remain identifiable in feces for long times, and the bacterial population changes and bacterial spores may increase). Fecal debris may resemble degenerate WBCs.

Drug Therapy

Administration of barium and psyllium fiber may make interpretation difficult, and antibiotics change bacterial flora composition.

Causes of Abnormalities

Fecal WBCs (specifically neutrophils) are observed with bacterial (e.g., salmonellosis, campylobacteriosis) and inflammatory mucosal disease. Transmural colitides occasionally have increased fecal WBCs. Fecal WBCs are an indication to culture for specific bacterial pathogens or to biopsy colonic mucosa. Eosinophils may be visible with allergic or parasitic colitis. Increased numbers of yeast, fungal organisms, or a uniform population of bacteria may help identify the cause of diarrhea in a patient.

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FECAL OCCULT BLOOD

Rare Indications

To detect GI bleeding that is not apparent grossly (i.e., melena, hematochezia).

Disadvantages

See Artifacts.

Analysis

Fresh feces are smeared on a test pad. The patient must have been on a meat-free diet for at least 3 days before the feces are obtained. Sensitivity varies markedly between assays.

Normal Values

See Artifacts.

Artifacts

Falsely decreased: sampling unmixed feces (blood may not be distributed homogeneously throughout the feces) and vitamin C supplementation. Falsely increased: diets containing fresh meats (i.e., hemoglobin) or fresh uncooked vegetables (i.e., peroxidases), which cause a positive reaction.

Causes of Fecal Occult Blood

Bleeding into the GI tract at any level and as the result of any cause may result in fecal occult blood. GI blood loss of volumes of 2 ml blood/30 kg body weight will give positive results.

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TRYPSIN-LIKE IMMUNOREACTIVITY

Common Indications

Chronic small bowel diarrhea or weight loss.

Advantages

High sensitivity and specificity for EPI. Only need one serum sample that does not require special or cumbersome handling procedures, and most large veterinary diagnostic laboratories can perform this test for dogs.

Disadvantages

Currently the only laboratory offering the fTLI test (for cats) is the GI Laboratory, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843-4474.

Analysis

Performed on serum using ELISA. See Appendix I for availability.

Normal Values

Dogs, 5 to 35 μg/L (Figure 9-4 ); cats, 12 to 82 μg/L.

FIGURE 9-4

Typical ranges of trypsin-like immunoreactivity (TLI) values in normal dogs, dogs with small intestinal disease, and dogs with exocrine pancreatic insufficiency (EPI).

(Modified from Williams DA: Sensitivity and specificity of radioimmunoassay of serum trypsin-like immunoreactivity for the diagnosis of canine exocrine pancreatic insufficiency, J Am Vet Med Assoc 192:195, 1988.)

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Danger Values

None.

Artifacts

Theoretically, EPI caused by an obstructed pancreatic duct instead of acinar cell atrophy would yield a normal or even increased serum TLI value.

Drug Therapy That May Alter TLI

Drugs causing acute pancreatitis (see Table 9-3) might increase serum TLI. Oral pancreatic enzyme supplementation does not affect serum TLI concentrations.

Causes of Decreased TLI

A serum TLI concentration less than 2.5 μg/L (dog) or 8 μg/L (cat) is generally considered diagnostic for EPI, and TLI is considered to be the test of choice for EPI (see Figure 9-4). Subclinical canine EPI may be suspected by finding intermediate values (>2.5μg/L and <5.0μg/L). In such cases repeated testing should be performed. Some dogs will later develop EPI, whereas others will not.

Causes of Increased TLI

Values greater than 50 μg/L in dogs and greater than 100 μg/L in cats may occur with pancreatitis, renal failure, prerenal azotemia (may increase two times), and malnutrition. The fTLI test seems to be more specific for the diagnosis of pancreatitis in cats than amylase or lipase; however, the fTLI test is not clearly as sensitive or specific for feline pancreatitis as pancreatic biopsy. In dogs, TLI seems to increase early in pancreatitis but then returns to reference ranges.

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Serum Vitamin B₁₂ And Serum Folate

Occasional Indications

Chronic small bowel diarrhea, unexplained weight loss, or uncertain but suspected small intestinal disease.

Advantages

Need only one serum sample.

Disadvantages

Uncertain sensitivity and specificity for small intestinal disease, ARE, or EPI. This test should be used as an adjunct to other tests for maldigestion and malabsorption syndromes. The test is specific for cobalamin deficiency.

Analysis

Measured in serum by bioassay or immunoassay. “No boil” methods are unreliable in dogs. Serum should be transported in a covered tube.

Normal Values

Depend on the laboratory. Normal ranges vary widely between laboratories. The particular laboratory must validate the assay for dogs or cats.

Danger Values

None.

Artifacts

Falsely decreased vitamin B₁₂: degradation caused by exposure of serum to sunlight.

Drug Therapy That May Alter Serum Vitamin B₁₂ Concentrations

Dietary content or vitamin supplementation of vitamin B₁₂ and folate can affect serum concentrations. Drugs that affect intestinal bacterial concentrations (antibiotics or antacids) may also alter values.

Causes of Decreased Serum Vitamin B₁₂ Concentrations

The major recognized reasons for decreased serum B₁₂ concentrations in dogs and cats are ileal disease or resection (rare), EPI, intestinal mucosal disease, ARE, and in cats, hepatic disease. The major differentiation to be made is among EPI, mucosal disease, and ARE; therefore, decreased serum B₁₂ is an indication for serum TLI. Not all dogs with EPI, mucosal disease, or ARE have decreased serum vitamin B₁₂. Cats with EPI, severe small intestinal disease (e.g., lymphoma, inflammatory bowel disease), and some hepatic diseases (e.g., idiopathic hepatic lipidosis) can have very low B₁₂ concentrations. Finding a significantly decreased serum B₁₂ concentration can be an indication of small intestinal disease in animals that were previously not suspected to have such disease.

Causes of Increased Serum Vitamin B₁₂ Concentrations

Vitamin B₁₂ supplementation.

Causes of Decreased Serum Folate

Severe mucosal disease of the proximal small intestine decreases serum folate. Not all patients with such disease have decreased folate levels.

Causes of Increased Serum Folate

ARE, EPI, and dietary supplementation are probably the major causes. Many patients with these diseases do not have increased folate levels. The combination of low vitamin B₁₂ plus increased folate is an indication to treat for ARE.

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FECAL SMEAR (WET MOUNT) FOR PARASITES

Common Indications

A screen for parasites and parasitic ova; any patient with diarrhea, melena, hematochezia, fecal mucus, weight loss, or vomiting.

Advantages

Availability, ease of performing the test, and low cost.

Disadvantages

Need for fresh feces and the frequency with which parasites and their ova or cysts are not detected.

Analysis

A thin smear is made of very fresh (<5 minutes old) feces, usually mixed with a drop of saline solution and coverslipped to prevent dehydration. It should be examined immediately. If protozoa are visible and better cytologic detail is desired, a drop of Lugol's iodine or Dobell and O'Connor's iodine may be placed at the corner of the coverslip.

NOTE:

Iodine kills protozoa, thus stopping motility.

Normal Values

Dogs and cats, no parasites or ova.

Artifacts

Cooling of the slide or dehydration inhibits the motility of some protozoa and bacteria.

Drug Therapy That May Alter Results

Orally administered compounds containing kaolin, pectin, barium sulfate, bismuth, and other intestinally active compounds (e.g., cathartics, enemas) may make it difficult to find and identify parasites, ova, and cysts.

Parasites, Bacteria, and Ova That May Be Identified

This test is most useful in identifying Giardia spp., Tritrichomonas spp., Entamoeba histolytica, Balantidium coli, Strongyloides stercoralis, and Aleurostrongylus abstrusus. Any ova may be found, but this test may be useful for detecting Spirocerca lupi and Trichuris vulpis ova. With oil immersion, small motile bacterial spirochetes in conjunction with fecal WBCs suggest Campylobacter spp. as a possible cause.

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FECAL FLOTATION

Common Indications

As for fecal smear.

Advantages

Sensitivity, availability, and low cost.

Analysis

Feces are well mixed with either a saturated sugar solution or a zinc sulfate solution (^{Leib, 1999}). (Zinc sulfate solution is made by mixing 331 g ZnSO₄ • 7 H₂O in 1 L water to attain a specific gravity of 1.18 to 1.20 [as determined with a hydrometer]. This is supposedly the best fecal flotation technique for Giardia spp. because it does not distort the cysts.) Ova and cysts are allowed to rise to the surface and are retrieved with a coverslip. Samples for Giardia detection should be examined within 15 minutes to avoid distortion and lysis of cysts. Centrifugation of the sample increases the sensitivity of the procedure. Samples that will be sent to an outside laboratory for analysis may be refrigerated (not frozen) for 1 to 2 days or preserved by mixing 1 part feces with 3 parts sodium acetate—acetic acid—formalin. This is prepared by mixing 1.5 g sodium acetate + 2 ml glacial acetic acid + 4 ml 40% formaldehyde solution + 92.5 ml water (Kirkpatrick, 1987).

Normal Values

Dogs and cats, no ova or oocysts present.

Artifacts

Falsely decreased: Diarrhea may decrease ova concentration within a sample.

Parasite Ova and Cysts That May Be Identified

Ancylostoma spp., Toxocara spp., Toxascaris leonina, T. vulpis, S. lupi, Physaloptera rara (using dichromate solution),Capillaria aerophilia, Capillaria plica, Onciolo canis, Dioctophyme renale, Isospora spp., Giardia spp., Toxoplasma gondii, Cryptosporidium spp.,Paragonimus kellicotti, and some tapeworms.

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FECAL SEDIMENTATION

Rare Indications

Same as for fecal smear and flotation, especially if flukes are being considered. If feces contain excessive fat, formalin and ethyl acetate is probably better than water sedimentation.

Disadvantages

Requires more time than direct fecal smear or fecal flotation.

Analysis

Feces are mixed with the sedimentation solution (e.g., water), usually strained once or twice to remove large debris, and allowed to settle for 30 minutes to 2 hours. The sediment is then examined microscopically. When formalin and ethyl acetate is used, the strained feces are centrifuged, the pellet is resuspended in 9 ml of 5% formalin solution, 3 ml ethyl acetate is added, and the mixture is shaken vigorously. This is recentrifuged, the debris at the formalin and ethyl acetate interface is discarded, and the sediment is then examined (Kirkpatrick, 1987).

Normal Values

Dogs and cats, no ova.

Artifacts

Same as under Fecal Flotation.

Parasite Ova That May Be Identified

All the ova that may be found by fecal flotation, plus Alaria canis and Nanophyetus salmincola.

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FECAL GIARDIA DETECTION

Occasional Indications

Chronic diarrhea, unexplained weight loss, intermittent bilious vomiting, or when Giardia is suspected clinically and multiple (i.e., at least 3) zinc sulfate flotations using centrifugation are negative. Techniques include duodenal aspiration and cytology, fecal ELISA antigen test (e.g., ProSpecT Microplate ELISA Assay for Giardia, Alexon, Lenexa, KS), and IFA (e.g., MeriFlour Cryptosporidium/Giardia, Meridian Diagnostics, Cincinnati, OH) performed on feces.

Advantages

Provides additional methods for detection of Giardia.

Disadvantages

Duodenal aspirates require surgery or endoscopy.

Analysis

Duodenal fluid aspirates require fresh direct wet-mount observation of motile trophozoites. Fresh samples should be used for analysis with fecal ELISA and fecal IFA.

Normal Values

No trophozoites or fecal antigen present.

FECAL CRYPTOSPORIDIUM DETECTION

Rare Indications

Chronic diarrhea. Cats (especially with feline immunodeficiency virus [FIV] infection) may be more likely to have cryptosporidiosis than dogs, but the prevalence of this disorder is currently unknown.

Disadvantages

Oocysts are small and may be difficult to find.

Analysis

Fresh fecal samples should be sent to a referral laboratory experienced in finding Cryptosporidium. Special fecal flotation techniques, direct fecal smears stained with an acid-fast stain, or ELISA methodology (e.g., ProSpecT Cryptosporidium Microplate Assay, Alexon, Lenexa, KS) can be used. The ELISA methodology appears to be the most sensitive.

Normal Values

Dog and cat feces should be negative for Cryptosporidium.

Go to: Regurgitation and vomiting

Go to: Pancreatitis

Go to: Acute diarrhea

Go to: Liver disease

Go to: Liver enzymes and tests

Go to: Weight loss, anorexia, abdominal pain

Reference:

Published online 2009 May 15. doi: 10.1016/B0-72-168903-5/50014-8