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Merck Manual Outlines Hideous Results Of Sodomy

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Old December 21st 04, 11:34 PM
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Intestinal Protozoa

Multiple pathogenic parasites and nonpathogenic commensals often are
present in the bowel. The most important pathogens are Entamoeba
histolytica, Giardia lamblia, Cryptosporidium, Isospora, Cyclospora,
and Microsporidia.

Intestinal protozoa are passed by the fecal-oral route, and infections
are widespread in developing countries with inadequate sanitation. They
are also common within the USA where fecal incontinence and poor
hygiene prevail, such as in mental institutions and day care centers.
Some amebas and GI protozoa are spread as sexually transmitted
diseases, especially among promiscuous male homosexuals, and several
protozoan species cause major opportunistic infections in patients with
AIDS. Asymptomatic infected persons are a major source of environmental
and person-to-person spread and should be treated.

Clinical diagnosis is unreliable; microscopic examination of suitable
stool specimens is necessary. Diagnosis may require several samples,
concentration methods, special stains, or semi-invasive diagnostic
techniques such as endoscopic biopsy (see Table 161-1).

Infection of the colon with Entamoeba histolytica, which is commonly
asymptomatic but may produce clinical manifestations ranging from mild
diarrhea to severe dysentery.
Etiology and Pathogenesis

Amebiasis is a protozoan infection of the lower GI tract. E.
histolytica exists in two forms: the trophozoite and the cyst. The
trophozoite is a motile stage that feeds on bacteria and tissue,
reproduces, colonizes the lumen and the mucosa of the large intestine,
and sometimes invades tissues and organs. Some trophozoites in the
colonic lumen become cysts that are excreted with feces. Trophozoites
predominate in liquid stools (no matter what causes the diarrhea) but
rapidly die outside the body. Cysts predominate in formed stools.

Cysts are resistant to the external environment. They may spread either
directly from person to person or indirectly via food or water.
Amebiasis is a sexually transmitted disease in male homosexuals.

Two species of Entamoeba are morphologically indistinguishable: E.
histolytica is pathogenic and E. dispar harmlessly colonizes the colon.
Amebas adhere to and kill colonic epithelial cells and cause dysentery
with blood and mucus in the stool. Amebas also secrete proteases that
degrade the extracellular matrix and permit invasion into the bowel
wall and beyond. Amebas can spread via the portal circulation and cause
necrotic liver abscesses. The infection may spread further by direct
extension from the liver or through the bloodstream to the lungs,
brain, and other organs.
Symptoms and Signs

Most infected persons are asymptomatic but chronically pass cysts in
stools. Symptoms that occur with tissue invasion include intermittent
diarrhea and constipation, flatulence, and cramping abdominal pain.
There may be tenderness over the liver and ascending colon, and the
stools may contain mucus and blood.

Amebic dysentery, common in the tropics but uncommon in temperate
climates, is characterized by episodes of frequent (semi)liquid stools
that often contain blood, mucus, and live trophozoites. Abdominal
findings range from mild tenderness to frank abdominal pain with high
fevers and systemic toxic symptoms. Tender hepatomegaly frequently
accompanies amebic colitis. Between relapses, symptoms diminish to
recurrent cramps and loose or very soft stools, but emaciation and
anemia continue. Symptoms of subacute appendicitis may occur. Surgery
in such cases may result in peritonitis.

Chronic infection commonly mimics inflammatory bowel disease and
presents as intermittent nondysenteric diarrhea with abdominal pain,
mucus, flatulence, and weight loss. Chronic infection may also present
as tender, palpable masses or annular lesions in the cecum and
ascending colon that resemble carcinomas (amebomas).

Metastatic disease originates in the colon and can involve any organ,
but a liver abscess, usually single and in the right lobe, is the most
common. It can present in patients without prior symptoms, is more
common in men than in women (ratio of 7:1 to 9:1), and may develop
insidiously. Symptoms include pain or discomfort over the liver, which
is aggravated by movement and occasionally referred to the right
shoulder; intermittent fever; sweats; chills; nausea; vomiting;
weakness; and weight loss. Jaundice is unusual and low-grade when
present. The abscess may perforate into the subphrenic space, right
pleural cavity, right lung, and other adjacent organs. Skin lesions
caused by direct implantation of trophozoites are occasionally
observed, especially around the perineum and buttocks and particularly
in traumatic and operative wounds.

Nondysenteric amebiasis is often misdiagnosed as irritable bowel
syndrome, regional enteritis, or diverticulitis. Amebic dysentery may
be confused with shigellosis, salmonellosis, schistosomiasis, or
ulcerative colitis. The stools in amebic dysentery are more fecal and
less frequent and watery than those in bacillary dysentery. They
characteristically contain tenacious mucus and flecks of both fresh and
altered blood. Unlike stools in shigellosis, salmonellosis, and
ulcerative colitis, amebic stools do not contain large numbers of WBCs.

Hepatic amebiasis and amebic abscess must be differentiated from other
hepatic infections, including bacterial abscesses and infected
echinococcus cysts.

Intestinal amebiasis is confirmed by finding E. histolytica in the
stool or tissues. Diagnosis may require examination of 3 to 6 stool
specimens and concentration methods (see Table 161-1). Antibiotics,
antacids, antidiarrheals, enemas, and intestinal radiocontrast agents
may interfere with recovery of the parasite and should not be given
until the stool has been examined. E. histolytica has to be
distinguished from nonpathogenic amebas and E. coli.

In symptomatic patients, proctoscopy often shows flask-shaped mucosal
lesions, which should be aspirated and the material examined for
trophozoites. Biopsy specimens from rectosigmoid lesions may also show

Extraintestinal amebiasis is more difficult to diagnose. Stool
examination is usually negative, and recovery of trophozoites from
aspirated pus is uncommon. A therapeutic trial of amebicides may be the
most helpful diagnostic tool for an amebic liver abscess.

Serologic tests are positive in almost all patients with amebic liver
abscess and in 80% of those with amebic dysentery. The tests are
positive in only about 10% of asymptomatic carriers. The indirect
hemagglutination and enzyme-linked immunosorbent assays (ELISA) are the
most sensitive tests available. Antibody titers may persist for months
or years.

When a liver abscess is present, x-rays may show elevation and fixation
or impaired excursion of the right diaphragm. Radioisotopic liver
scanning or CT may show the extent of the abscess, while ultrasound
scans may show it to be fluid-filled. The alkaline phosphatase level
may be elevated. Needle aspirations are usually reserved for lesions
10 cm, suspicion of imminent rupture, or poor response to 5 days of
drug therapy. The abscesses contain thick, semifluid material ranging
from yellow to chocolate-brown. A needle biopsy may show necrotic
tissue, but motile amebas are difficult to find in the abscess material
and cysts are not present.

Contamination of food and water with human feces must be prevented, a
problem complicated by the high incidence of asymptomatic carriers.
Chlorine levels sufficient to kill bacteria will not affect the cysts
of E. histolytica, but boiling or treating water with tetraglycine
hydroperiodide tablets (1 to 2 tablets per quart or liter) kills cysts.

General therapy relieves symptoms, replaces blood, and corrects fluid
and electrolyte losses. If symptoms of appendicitis are thought to be
of amebic origin, surgery may be delayed for 48 to 72 h to observe the
effects of chemotherapy.

Asymptomatic persons who pass cysts should be treated to prevent their
spreading the infection. One course of oral diloxanide furoate (500 mg
tid for 10 days in adults or 20 mg/kg/day in 3 divided doses for
children) is usually given. A suitable alternative is 20 days with
iodoquinol (650 mg po tid for adults or 30 to 40 mg/kg/day in 3 divided
doses for children, with a maximum of 2 g to avoid causing optic
neuritis). Metronidazole has a high failure rate in asymptomatic cyst
passers unless used at high doses.

For those with mild GI symptoms, 5 to 10 days of treatment with oral
metronidazole is recommended (750 mg tid for adults, 35 to 50 mg/kg/day
in 3 divided doses for children). Metronidazole should not be given to
pregnant women. For those with moderate GI symptoms, a course of
metronidazole may have to be followed by a second oral drug such as
iodoquinol or diloxanide furoate at the doses listed above or with
paromomycin (25 to 30 mg/kg/day in 3 divided doses for 7 days) to
prevent relapses. If symptoms are severe, oral drugs may be followed by
emetine 1 mg/kg/day (maximum 60 mg) or dehydroemetine 1 to 1.5
mg/kg/day (maximum 90 mg) given IM until symptoms are controlled
(maximum 5 days). Emetine and dehydroemetine are toxic, and patients
receiving them should be confined to bed and monitored by ECG. Therapy
should be stopped promptly if signs of toxicity appear, such as
tachycardia, hypotension, muscular weakness, marked GI effects, or
dermatoses. Contraindications include pregnancy and renal or cardiac

For extraintestinal amebiasis, metronidazole is the drug of choice and
is given as above. Alternatively, emetine or dehydroemetine can be
given for 5 days as described for severe amebic dysentery. Emetine or
dehydroemetine used to treat hepatic disease should be combined with
chloroquine (1 g/day po for 2 days, then 500 mg/day for 3 wk in adults;
10 mg/kg/day in children, with a maximum of 300 mg chloroquine
base/day). If E. histolytica is present in stool, iodoquinol may also
be given, as described above.

Stools should be reexamined for relapse 1, 3, and 6 mo after treatment,
if feasible.

Infection of the small intestine with the flagellated protozoan Giardia
lamblia, which can be asymptomatic or cause clinical manifestations
ranging from intermittent flatulence to chronic malabsorption.
Etiology and Pathogenesis

Giardia trophozoites firmly attach to the duodenal and proximal jejunal
mucosa and multiply by binary fission. Released organisms rapidly
transform into environmentally resistant cysts that are passed in stool
and spread by the fecal-oral route. Waterborne transmission is the
major source of giardiasis. Transmission can also occur by direct
person-to-person contact, especially in mental institutions, in day
care centers, or between sexual partners. Filtration of water through
soil removes Giardia cysts, but these remain viable in surface water
and are resistant to routine levels of chlorination. In addition to
humans, wild animals may serve as reservoirs. Thus, mountain streams as
well as chlorinated but poorly filtered urban water supply systems have
been implicated in waterborne epidemics.

The infection occurs worldwide, especially among children and where
sanitation is poor. In the USA, giardiasis is one of the most common
intestinal infections. Infection rates are high among travelers to many
countries, in promiscuous male homosexuals, and in patients who are
postgastrectomy, have chronic pancreatitis, or have
Symptoms and Signs

Most cases are asymptomatic. However, these persons pass infective
cysts and need to be treated. Symptoms of acute giardiasis generally
appear 1 to 3 wk after infection. Symptoms are usually mild and include
watery malodorous diarrhea, abdominal cramps and distention, flatulence
and eructation, intermittent nausea, and epigastric pain. Low-grade
fever, chills, malaise, and headaches may be present. Malabsorption of
fat and sugars can lead to significant weight loss in severe cases.
Blood and mucus usually are not found in stool.

The chronic phase may evolve from, or occur without, an acute illness.
Periodic loose foul stools, abdominal distention, and malodorous flatus
predominate. Chronic giardiasis occasionally is a cause of failure to
thrive in children.

Characteristic trophozoites or cysts in stool are diagnostic. These are
readily seen in acute infections, but parasite excretion is
intermittent and at low levels in chronic infections. Thus, diagnosis
may require repeated stool examinations or sampling of the upper
intestinal contents obtained with a nylon string or by endoscopic
aspiration. Immunofluorescent assays and ELISAs to detect parasites or
parasite antigens in stool are available. Specific DNA probes are under

Scrupulous personal hygiene may prevent person-to-person transmission.
Treatment of asymptomatic cyst passers reduces the spread of infection,
but whether treatment of asymptomatic infected children in day care
centers is cost-effective remains unclear. Water can be decontaminated
by boiling or heating to at least 70 C (158 F) for 10 min. Giardia
cysts resist routine levels of chlorination; iodine-based disinfection
must be carried out for at least 8 h to be effective. Some filtration
devices can remove Giardia cysts from contaminated water.

Oral metronidazole (250 mg tid for 5 days in adults; 15 mg/kg/day in 3
divided doses for 5 days in children) is effective, but it is not
currently licensed in the USA for use in giardiasis. Side effects
include nausea, headaches, and, less commonly, black urine,
paresthesia, and dizziness. Oral quinacrine (100 mg tid for 5 days in
adults; 2 mg/kg tid [maximum 300 mg/day] for 5 days in children) is
highly effective but may produce GI disturbances, dizziness, and
headaches and, rarely, exfoliative dermatitis and toxic psychosis. It
is no longer available in the USA. Oral furazolidone (100 mg qid for 7
to 10 days in adults; 6 mg/kg/day in 4 divided doses for 7 to 10 days
in children) is less effective than quinacrine and metronidazole but is
available as a suspension, making it useful in children.

Household and sexual contacts should be examined and treated if
infected. Treatment during pregnancy should be avoided if possible;
metronidazole should not be given to pregnant women. If therapy cannot
be delayed because of severe symptoms, a nonabsorbable aminoglycoside
such as paromomycin (25 to 35 mg/kg/day po in 3 divided doses for 7
days) can be used.

Infection with protozoa of the genus Cryptosporidium, causing diarrheal
Etiology and Pathogenesis

Cryptosporidia are coccidian protozoa that replicate intracellularly in
the brush border of the small intestine. Infective oocysts are shed
into the lumen and passed in the feces. After its ingestion by another
vertebrate, the oocyst releases sporozoites that transform into
trophozoites in the brush border, replicate, and then produce oocysts
after about 12 days.

C. parvum causes most cases. Infections result from zoonotic spread,
direct person-to-person contact, or waterborne transmission. The
disease occurs worldwide; children, travelers to foreign countries,
immunocompromised patients, and medical personnel caring for patients
with cryptosporidiosis are at high risk. Cryptosporidiosis is
responsible for up to 5% of all gastroenteritis in both industrialized
and developing countries. Outbreaks have occurred in day care centers;
nosocomial transmission has caused large waterborne outbreaks in
several U.S. cities.
Symptoms and Signs

The incubation period is about 1 wk, and clinical illness occurs in
80% of infected persons. The onset is acute, with profuse watery
diarrhea, abdominal cramping, and, less commonly, nausea, anorexia,
fever, and malaise. Symptoms generally persist 1 to 2 wk, rarely = 1
mo, and then abate. Fecal excretion of oocysts may continue for several
weeks after clinical symptoms have subsided. Asymptomatic shedding of
oocysts is common among older children in developing countries.

In the immunocompromised host, the onset of disease may be more
gradual, but diarrhea can be more severe. Unless the underlying immune
defect is corrected, infection is not cleared. Thus, profuse
intractable diarrhea may continue persistently or intermittently for
life, with fluid losses 5 to 10 L/day.

Identifying the acid-fast oocysts in stool confirms the diagnosis;
conventional methods of stool examination are unreliable. Using the
formalin-ethyl acetate sedimentation or the sugar flotation stool
concentration procedures enhances diagnosis. Cryptosporidium oocysts
can be identified by phase-contrast microscopy or by staining with the
Kinyoun modified acid-fast reagent. Fluorescein-labeled monoclonal
antibody and ELISA kits provide excellent detection of oocysts.
Intestinal biopsy is a last resort.
Prevention and Treatment

Stools of patients with cryptosporidiosis are highly infectious; strict
stool precautions should be observed. Boiling water is the most
reliable decontamination method; only filters with pore sizes = 1 m
remove Cryptosporidia.

In immunocompetent persons, cryptosporidiosis is self-limiting,
requiring only supportive treatment. No completely effective drug is
available, but paromomycin (500 to 750 mg po qid) has the highest
success rate; relapses are common. In some AIDS patients, symptoms of
cryptosporidiosis have abated after antiretroviral therapy. Supportive
measures, oral and parenteral rehydration, and hyperalimentation are
often vital in immunocompromised persons.

Infections with the coccidian protozoa Isospora belli or Cyclospora
cayetanensis, causing diarrhea.
Etiology and Pathogenesis

The life cycles of I. belli and C. cayetanensis are similar to that of
Cryptosporidium, except that oocysts must sporulate before becoming
infective. Human isosporiasis is most common in tropical and
subtropical climates. Transmission is by the fecal-oral route via
contaminated food or drink. Dogs and other mammals are believed to
harbor I. belli.
Symptoms and Signs

The main complaint is watery diarrhea; the onset may be sudden with
fever, malaise, and abdominal pain. The illness usually resolves
spontaneously in a few days or weeks, but it may persist for months or
years. Prolonged disease is associated with malabsorption and weight

In the immunocompromised host, isosporiasis and cyclosporiasis may
cause intractable, voluminous diarrhea similar to that observed in
cryptosporidiosis. Extraintestinal disease has been reported, including
cholangitis and disseminated infections.

Detection of characteristic oocysts by microscopic examination of the
stool establishes the diagnosis. Multiple stool specimens may be
needed; detection of oocysts is facilitated by staining stool samples
with the modified acid-fast stain. Diagnosis is sometimes made only
when intracellular parasite stages are detected in biopsies of
intestinal tissue. The stool of persons with I. belli infection often
contains Charcot-Leyden crystals derived from eosinophils; peripheral
blood eosinophilia is often present. Biopsies from patients infected
with these parasites show shortened villi and infiltrates of
lymphocytes, plasma cells, and eosinophils in the lamina propria.
Prevention and Treatment

Prevention is as for cryptosporidiosis. Treatment of choice for both
isosporiasis and cyclosporiasis is double-strength oral trimethoprim-
sulfamethoxazole (TMP-SMX) 160 mg TMP and 800 mg SMX qid for 10 days,
then bid for 3 wk. In AIDS patients, this should be followed by
lifelong suppressive treatment with 1 double-strength tablet of TMP-SMX
3 times/wk. Alternative treatments for isosporiasis include
pyrimethamine (25 mg/day po) plus sulfadiazine (500 mg/day po) with
leucovorin rescue; sulfonamide-sensitive patients may benefit from high-
dose pyrimethamine alone (50 to 75 mg/day with leucovorin rescue) or

Infection with Microsporidia, causing a spectrum of manifestations that
range from asymptomatic infection in immunocompetent persons to chronic
diarrhea, corneal disease, and myositis in patients with AIDS.
Etiology and Pathogenesis

Microsporidia are obligate intracellular spore-forming protozoan
parasites. In the lumen of the GI tract, they uncoil, harpoon a host
cell, and inoculate it with nucleated sporoplasm. Intracellular
division then produces sporoblasts that mature into spores, which
disseminate to other cells or pass into the environment via feces,
urine, or skin.

Little is known about routes of transmission or possible animal
reservoirs. Microsporidia probably are a common cause of subclinical or
mild self-limited illness in otherwise healthy persons. Serologic
surveys have shown that up to 50% of healthy populations, especially
those in tropical environments, have antibodies to the microsporidium
Enterocytozoon cuniculi, but only a few cases of human infection had
been reported in the pre-AIDS era. The organisms are important
opportunistic pathogens in persons with AIDS. Up to 30% of AIDS
patients with otherwise unexplained chronic diarrhea have intestinal
microsporidiosis. Others develop infections involving sites other than
the GI tract.
Symptoms and Signs

Clinical disease caused by microsporidia varies with the infecting
parasite species and the immune status of the host. In AIDS patients,
various species cause chronic diarrhea, cholangitis, punctate
keratoconjunctivitis, peritonitis, hepatitis, myositis, or sinusitis.
Infections of kidneys, gallbladder, and sinuses have been described.
Enterocytozoon bieneusi is present in AIDS patients both with and
without diarrhea and thus may not be the cause of diarrhea. Nosema
corneum can cause severe, vision-threatening stromal keratitis in
immunocompetent persons as well as in patients with AIDS.
Diagnosis and Treatment

Organisms must be demonstrated in specimens of affected tissue obtained
by biopsy, or in corneal scrapings. Microsporidia are best seen after
staining with Giemsa, PAS, Gram, or acid-fast stains. The small spores
may be detectable in feces, urine, or other secretions.

Albendazole (400 mg po bid) may be effective for controlling intestinal
infection with Septata intestinalis. The drug also reduces the number
of E. bieneusi in small-bowel biopsies but does not eliminate this
infection. No established treatment exists for ocular or disseminated
microsporidiasis, but some success with fumagillin eyedrops and
imidazole compounds (fluconazole, itraconazole) has been reported.
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