Balantidiasis (also known as balantidiosis) is defined as large-intestinal infection with Balantidium coli, which is a ciliated protozoan (and the largest protozoan that infects humans). B coli is known to parasitize the colon, and pigs may be its primary reservoir. See the image below.
View Image | Trophozoite of Balantidium coli in colon. This photograph shows the large macronucleus and the thin cell membrane covered with cilia (X820). Courtesy .... |
See Common Intestinal Parasites, a Critical Images slideshow, to help make an accurate diagnosis.
Balantidiasis is a zoonotic disease transmitted from pigs to humans and nonhuman primates via the fecal-oral route. Humans acquire this infection through water and food contaminated with pig or human feces.[1] Human-to-human transmission is also possible. Infected pigs remain asymptomatic, while humans can either remain asymptomatic or develop dysentery.
B coli was first described by Malmsten in 1857 in two patients presenting with symptoms of dysentery. It was initially named under the genus Paramoecium. It was then simultaneously reported by Leuckart and Stein 1861 and 1862, respectively, and they renamed the genus Balantidium. It is more common in warmer regions than in cooler ones.[2]
B coli exists as a trophozoite and a cyst and usually affects the large intestine, from the caecum to the rectum. The trophozoites replicate by binary fission and conjugation, and they subsist on bacteria. Humans ingest infective cysts, which then migrate to the large intestine, cecum, and terminal ileum. The organisms primarily dwell in the lumen but can also penetrate the mucosa and cause ulcers.[3]
The invasion of the intestinal mucosa is facilitated by the following:
The proteolytic activity of this parasite may also cause the tissue invasion and intestinal perforation.[4, 5]
Balantidium ulcers
Intestinal ulcers similar to those caused by intestinal amoebiasis are found in cecum, ascending colon, sigmoid colon, and rectum. However, in contrast to amebic ulcers, Balantidium ulcers do not invade muscular layers of intestine. The trophozoites can be demonstrated in the edges of the ulcer and in the pus.[2]
United States
Balantidiasis is found worldwide and has an overall estimated prevalence of 1%. Balantidiasis epidemics have occurred in psychiatric hospitals in the United States.
India
Cases of B coli infection from cattle, pigs,[6] and rats, among others, have also been previously reported from India. Very few cases of human Bcoli infection have been reported in India. Kumar et al reported a case of B coli infection in a 37-year-old man with tuberculosis; he presented with fever, anorexia, mild abdominal pain, and episodes of loose stools for one week.[7]
In 2014 in India, urinary balantidiasis was reported in an elderly farmer with diabetes and chronic kidney disease.[8]
Umesh demonstrated a case of urinary balantidiasis in a 29-year-old woman in Mumbai, India, but this report failed to demonstrate B coli on stool examination, required to confirm the hypothesis of extraintestinal Bcoli infection in humans.[9]
In a 2002 study by Kaur et al, diarrhea in children in New Delhi were determined to be parasitic based on direct wet mount examination.[10] In 2016, Kapur et al described a case of liver abscess with B coli trophozoites on wet mount of pus aspirate.[11]
International
Balantidiasis tends to be more common among persons who handle pigs. The disease is reported most commonly in Latin America; Southeast Asia; and Papua, New Guinea. In 1971, a balantidiasis outbreak involving 100 people occurred in Truk following a typhoon.[12] In France, a pork butcher with immunosuppression due to alcohol use developed occupational balantidiasis.[13]
Most cases of balantidiasis in immunocompetent individuals are asymptomatic. Mortality rates associated with acute and fulminating types of balantidiasis were as high as 30% in untreated patients prior to the introduction of antibiotics. Pneumonia has been described in patients with cancer-related immunosuppression[14] and has not always been associated with direct contact with pigs.
In the antibiotic era, severe balantidiasis carries an improved prognosis, and most affected patients now recover.
Patients should be counseled on the importance of good handwashing, particularly after being exposed to environments where likelihood of infection is high.
Balantidium mostly causes asymptomatic and self-limiting infections. Clinical presentations of balantidiasis range from mild to severe symptoms. Asymptomatic hosts serve as reservoirs of infection in the community. Individuals with chronic infection usually present with diarrhea, cramping, abdominal pain, and halitosis.[15, 16]
Ciliate dysentery
B coli infection causes ciliate dysentery. Intermittent diarrhea alternating with constipation is the typical symptom in mild infections.
Individuals with fulminating balantidiasis present with frequent mucoid, bloody stools.
The clinical presentations of ciliate dysentery are similar to those of amoebic dysentery. Such a fulminant infection has a high case fatality rate, especially in immunocompromised and malnourished patients.
The most severe presentation of B coli infection consists of weight loss, tenesmus, and bloody stools.[15] Intestinal hemorrhage and perforation can also occur and are mediated by the production of B coli proteolytic enzymes. Hemorrhage and perforation were reported in fatal cases of B coli infection.[17]
Extraintestinal infections, although rare, have been reported to affect the appendix, liver, and lungs.[17, 18]
Patients with balantidiasis may present with abdominal tenderness, fever, and prolonged diarrhea, which may result in signs of dehydration.
Balantidiasis is caused by ingestion of food or water that has been contaminated with fecal matter from humans or animals. The fecal matter can contaminate food or water with B coli cysts.
Risk factors for balantidiasis include contact with pigs, handling fertilizer contaminated with pig excrement, and living in areas where the water supply may be contaminated by the excrement of infected animals. Poor nutrition, achlorhydria, alcoholism, and immunosuppression may also be contributing factors.
Intestinal perforation and peritonitis are the most common causes of death associated with balantidiasis.[19]
Intestinal perforation and extraintestinal spread to liver and mesenteric lymph nodes are rare.
Pulmonary involvement has been reported and appears to be more common in patients with underlying illnesses such as diabetes, cancer, or impaired lymphocyte function.
The specimen of choice for diagnosing balantidiasis is stool. At least three stool samples should be collected at intervals since parasites are excreted intermittently.
In cases of low parasite load, concentration methods such as flotation and sedimentation may help in the recovery of cysts.
Trophozoites
Motile trophozoites (active, feeding, replicative stage) can be visualized via microscopy in saline wet mount of fresh diarrheic stool samples, as well as bronchoalveolar wash fluid. The size of the trophozoite varies from 30-300 µm in length and 30-100 µm in breadth. It is covered with cilia and is oval in shape with a pointed anterior end and rounded posterior end. A cytostome (mouth) is located at the anterior end of the trophozoite and a cytopyge (anus) at the posterior. Trophozoites consist of a macronucleus and a micronucleus.[19]
Pulmonary infection is difficult to diagnose because the ciliated pulmonary epithelial cells are difficult to distinguish from ciliated trophozoites. However, they can be differentiated based on size, shape, and motility. Balantidium trophozoites are larger and ovoid-shaped, while epithelial cells and ciliates show a classic spiraling motility. Phase-contrast microscopy helps to differentiate the features clearly.[20]
Cyst
The cyst represents the nonreplicating infective stage. B coli forms a large spherical cyst that may grow to 60 µm in diameter. The cyst contains a macronucleus, a micronucleus, and a granular cytoplasm. Cilia may be found in young cysts but never in mature cysts.[4] The cysts can be demonstrated in semiformed and fully formed stools.
Both trophozoites and cysts can be easily visualized in fixed samples. Other staining methods such as hematoxylin-eosin or trichrome are also useful.
In samples from cattle and buffalo, diagnosis based on cyst identification should not be considered confirmatory because other ciliates (namely B sulcata) with morphologically identical cysts could also be present. Complementary genetic analysis should be made in these cases.[3, 21, 22]
See the images below.
View Image | Trophozoite of Balantidium coli in colon. This photograph shows the large macronucleus and the thin cell membrane covered with cilia (X820). Courtesy .... |
View Image | Cyst of Balantidium coli in feces. This photograph demonstrates a thick cyst wall and a large macronucleus (X820). Courtesy Armed Forces Institute of .... |
Chest radiography may show pulmonary parenchymal involvement in patients with balantidiasis.
Computed tomography (CT) scanning may reveal pulmonary parenchymal and lymph node involvement, as well as involvement of other organ systems.
Colonoscopy: Perform an endoscopic examination of the colon to obtain a biopsy of ulcers, thereby aiding in diagnosis of balantidiasis. Obtain the specimens from the periphery of ulcers.
Bronchoalveolar lavage (BAL) can identify organisms on wet mount of bronchial secretions.
B coli can invade the mucosa and submucosa, causing ulceration and infiltration with polymorphonuclear cells, lymphocytes, and eosinophils. Trophozoites can be observed at the invading edge of ulcers or at the periphery of submucosal abscesses.
Special attention should be paid to volume replacement and electrolyte repletion in patients with balantidiasis who have severe diarrhea.
Balantidiasis rarely manifests as acute appendicitis, which requires appendectomy.[23]
Consult a surgeon for management of acute abdomen problems (eg, appendectomy, laparotomy).
Consult a gastroenterologist for patients who require colonoscopy.
Therapy in an intensive care unit may be required for patients with balantidiasis who show signs of clinical deterioration despite receipt of appropriate antibiotics.
A starch-free diet is advisable for patients with balantidiasis.[24] A diet consisting of milk, gruel, eggs, scraped beef, toast, and cereals has been shown beneficial.[25]
B coli infection can be prevented with the following measures:[4]
Patients with balantidiasis should have a follow-up visit after treatment to document the resolution of symptoms. Also, obtain a stool specimen and a wet smear to check for organisms.
The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Prolonged courses of therapy may be required to cure balantidiasis in patients who are infected with HIV or who are otherwise immunosuppressed.
Clinical Context: Isolated from a strain of Streptomyces aureofaciens. Exerts a bacteriostatic effect by reversibly binding to 30S and 50S ribosomal subunits of susceptible organisms, thereby inhibiting protein synthesis.
Clinical Context: Synthetic drug with antiprotozoal and antibacterial action used to treat symptomatic patients with diarrhea.
Clinical Context: Contact amebicide works in the lumen of intestine.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. Tetracycline is the treatment of choice, with metronidazole being the primary alternative. Tetracycline 500 mg PO is given four times a day for 10 days. Iodoquinol, puromycin, and nitazoxanide are also effective against balantidiasis.