Chronic Diarrhea

Chronic Diarrhea 

A 21 year-old male presents with a 6-week history of watery diarrhea

and crampy abdominal pain. He reports that the diarrhea has not been constant and has alternated with periods of constipation. For the past 2 weeks, the diarrhea has been blood-streaked and he has had several weeks of midepigastric pain. He spent the past 6 months in a rural community in Guatemala participating in a community service project sponsored by his college. He returned from Guatemala just 10 days ago. While there, he drank the water and ate the food available in the local community, and he did not routinely boil water for drinking. He denies antibiotic exposure but has taken mefloquine weekly for malaria prophylaxis. Two separate stool specimens taken by student health when he returned were

reported as negative for Salmonella, Shigella, Campylobacter, E. coli O157:H7, Yersinia, Aeromonas, and Pleisiomonas as well as Giardia lamblia. On physical examination he appeared well nourished and well developed but reports an 8–10 lb weight loss. 

LABORATORY TESTS

Just as with acute diarrhea, the history of a patient’s illness frequently

provides clues to the etiology of the disease. The length of illness and

travel history of this patient plus abdominal findings and weight loss

are key features. Diarrhea with blood narrows infectious causes to agents such as Shigella, Salmonella, Campylobacter, EHEC, EIEC, and Entamoeba histolytica. An evaluation for chronic diarrhea requires a stool culture (×3), ova and parasite exam of stool (×3), and guaiac test of stool for occult blood. Because of this patient’s abdominal findings, liver function tests such as alkaline phosphatase and serum transaminases should also be ordered. Whenever liver abscess is suspected, abdominal ultrasound or computed tomography (CT scan) should also be performed.

Because both bacteria and parasites can be shed intermittently in stool, multiple stool specimens should be submitted for both bacterial culture and ova and parasite examination. See Case 3 for information on stool collection and transport for bacterial culture. For parasite analysis, specimens should be taken on separate days (every other day if possible) to increase likelihood of detection. Stool specimens collected for parasite analysis should be submitted in preservation vial(s) designed for this purpose.

  All forms of parasites (ova, larvae, protozoa, worms) can be

maintained at room temperature for long periods of time (months) using preservation vials. In addition, concentration procedures to recover small numbers of protozoan cysts, eggs, and larvae can be performed using the vials, and permanent stained smears can be prepared as well. If preservation vials are not available, then stool should be collected in clean, dry, wide-mouthed containers with tight-fitting lids. The stool should not be contaminated with urine because the pH of urine can destroy motile parasites. Liquid stool specimens must be examined by the laboratory within 30 min after they were taken from the patient, or some parasitic forms will disintegrate. If this rapid transport time is not possible, then preservation vials should be used. Results of an initial ova and parasite stool examination showed that the specimen was positive for cysts of E. histolytica/E. dispar. With this additional information, a serology test for E. histolytica antibodies and an abdominal CT scan were ordered.

E. histolytica, the cause of intestinal amebiasis and amebic liver abscess, can be diagnosed in the laboratory using a variety of methods:

1. Microscopic exam (stool, liver abscess). Microscopic identification of E. histolytica cysts or trophozoite (ameboid) forms is the most common method used to diagnose the infection; however, it is both insensitive and nonspecific. The test is nonspecific because E. histolytica cysts cannot be morphologically distinguished from those of Entamoeba dispar, a harmless commensal, unless ingested RBCs are present inside the trophozoite. Microscopic examination of liver abscess material is a poor way to attempt the diagnosis of amebiasis. While the abscess material is known to have the appearance of “anchovy paste,” ameba are rarely visualized in the material because they have disintegrated.

2. Antibody detection (serum). Serology studies [indirect hemagglutination, gel diffusion, enzyme-linked immunosorbent assay (ELISA)] to detect antibody to E. histolytica are positive in >90% of patients who have invasive disease. In the vast majority of patients antibodies are detectable after 7–10 days. When patients no longer have detectable parasites in their stools, detection of antibodies is critical for diagnosis of amebic liver abscesses.

TREATMENT AND PREVENTION

Two classes of drugs are used to treat E. histolytica infections. (1) a luminal amebicide, such as iodoquinol, which destroys parasites in the lumen of the intestine but does not kill ameba in tissue; and (2) a tissue amebicide, such as metronidazole or chloroquine, which treats invasive amebiasis but is less effective in the lumen. Amebic dysentery may be treated with iodoquinol and metronidazole. Extraintestinal disease is treated with a combination of

metronidazole and chloroquine. To follow the clinical response of intestinal disease to therapy, a repeat stool exam for parasites should be done 2–4 weeks after treatment, and extraintestinal disease should be monitored by repeat CT scans. Repeat serology tests are of little use since antibody titers remain elevated in spite of response to therapy. Prevention of infection with E. histolytica involves drinking boiled or bottled water when traveling to developing nations, and avoiding uncooked foods that may have been washed in water, such as salad.

Vomiting and Diarrhea after a School Picnic

 Vomiting and Diarrhea after a School Picnic

 PATIENT HISTORY

   A 14-year-old male presented to his pediatrician for evaluation of vomiting,abdominal discomfort, and nonbloody diarrhea. Three days prior, he attended his school picnic, where he ate everything offered: barbecued chicken, potato salad, baked beans, tossed salad, and ice cream . Within 36 h of the picnic he noted mild abdominal discomfort, intermittent crampy abdominal pain, and three to five loose, watery bowel movements per day. He reported no blood in the stool, rash, pain on urination (dysuria), or blood in the urine (hematuria) and had no travel history, had no pets, and denied taking antibiotics. The school reports that at least 50 other students who attended the picnic are also reporting similar symptoms. 

LABORATORY TESTS

There are various interpretations of what is considered medically indicated for evaluating persons with acute diarrhea. Because most diarrheal illness is self-limited, the usefulness of stool cultures is questioned by some; however, early diagnosis can lead to interventions that both alleviate symptoms and prevent secondary transmission, which can have tremendous public health impact. In addition, detection of specific agents aids in the timely detection and control of outbreaks. Some causes of acute diarrhea can result in serious long-term sequelae such as Guillain–Barr´e syndrome (with

Campylobacter) or hemolytic uremic syndrome (HUS) due to EHEC, further justifying the need for performing stool culture. A stool specimen for culture should be obtained as early in the course of the disease as possible from all patients with bloody diarrhea, patients with fever, in persons with diarrhea who are immunosuppressed, from patients in whom the diagnosis of HUS is suspected, and from persons involved in possible outbreaks.

Pathogenic bacteria can be identified by isolating the organism by

culture and/or by identifying a characteristic marker for virulence such

as a toxin. Routine bacterial stool cultures can identify Campylobacter, Salmonella, Shigella,Yersinia enterocolitica, Aeromonas hydrophila, Pleisiomonas  shigelloides, and noncholera Vibrio spp. Special media are required to identify E. coli O157:H7 and Vibrio cholera, and laboratory personnel should be notified when such agents are suspected. In addition to culture, E. coli

O157:H7 can also be diagnosed using a toxin assay that detects shiga toxins produced by all EHEC types. Toxin assays rather than culture are routinely used for diagnosing Clostridium difficile diarrhea.

Because an outbreak was suspected from the school picnic our case

patient attended, a stool culture was performed despite the fact that he had a mild self-limited illness. A routine bacterial stool culture would be appropriate in this case since Salmonella, Shigella, or Campylobacter spp. would be the most likely causes. His lack of bloody diarrhea would make EHEC, such as E. coli O157:H7, less likely. His lack of travel history indicates that his specimen does not need to be screened for organisms found outside his geographic area, and the absence of antibiotic use makes testing for toxins of C. difficile less of a priority.

Because there is no specific antiviral treatment available, testing for viral causes of gastroenteritis is not routinely performed except in outbreak situations or hospital settings. Testing for rotavirus, a major cause of fever, vomiting, and watery diarrhea in infants and young children, is routinely performed in hospitals so that patients can be cohorted and infection control practices emphasized. Rotavirus is commonly seen during the winter months (October–March).

Feces should be submitted in a clean, dry, plastic or waxed cardboard container with a tight-fitting or screwcap lid. Once collected, the specimen can be maintained at room temperature during transport. Rectal swabs should be used only with infants and young children fromwhomcollecting feces may be difficult and again should be taken only during acute disease. For an adequate specimen, the swab should be inserted past the anal sphincter into the rectum, and feces should be obvious on the swab when

removed. If the specimen (feces or swab) will not be processed or reach the laboratory within 1 h, an enteric transport medium should be inoculated with the feces and this will be stable for as long as 72 h at room temperature. In addition to stool, blood cultures should also be obtained from patients who have fever and diarrhea.

 TREATMENT AND PREVENTION

 The first line of therapy is supportive treatment, to return the patient to fluid and electrolyte balance. The patient may drink an oral rehydration solution that contains water, salt, and sugar, or liquids such as Pedialyte, which have the appropriate electrolytes and fluids to replace those being lost. Most cases of gastroenteritis are self-limited and require no antibiotic therapy. In fact, antibiotics are contraindicated in some cases. Giving antibiotics for Salmonella gastroenteritis prolongs the carriage of the organism in the GI tract and can lead to the person retaining the organism for months. Treatment of E. coli O157:H7 may increase the risk of hemolytic

uremic syndrome (HUS) in children and should be avoided. Likewise, one should avoid using antimotility agents in cases with bloody diarrhea or proven EHEC infection.

Patients who are very young or immunosuppressed may require antibiotics to recover from their disease. Patients with Shigella gastroenteritis are more likely to be sicker and require antibiotic therapy than are patients with Salmonella or Campylobacter gastroenteritis. Ampicillin, SXT, or ciprofloxacin are common choices for antimicrobial therapy because they can be administered orally if the patient can tolerate drinking liquids. Since the organism may be resistant to one or more of these antimicrobials, susceptibility results for the patient’s organism should guide the physician’s choice.

According to surveillance by the Centers for Disease Control and Prevention (CDC), Campylobacter jejuni is the most common enteric pathogen seen in adult patients with diarrhea, whereas Salmonella is the most common in children. Campylobacter spp. are not susceptible to penicillins or cephalosporins. Ciprofloxacin and erythromycin are the drugs of choice.

If a patient is hospitalized with enteric fever (S. typhi), a thirdgeneration cephalosporin is usually given intravenously. Our case patient has an infection with Salmonella susceptible to ampicillin, SXT, and ciprofloxacin. Because he is a healthy young adult, only supportive treatment

was given.

Student with Dysuria

Student with Dysuria

 PATIENT HISTORY

A 20-year-old college student complained of burning when urinating and a strong desire to void frequently although she had little urine to void. She was not experiencing any pelvic pain or discharge. Her symptoms beganshortly after she returned from a weekend visit to her boyfriend’s school.

She went to her university health service for diagnosis and treatment. On exam she was without fever and had moderate suprapubic tenderness, but

no flank tenderness.

LABORATORY TESTS

Urine Dipstick

A urine specimen was collected from this patient by a noninvasive technique,a midstream clean catch. Screening tests can predict which urine specimens contain a high colony count of bacteria. The most frequently used screening test with urine is called a “dipstick test”. A dipstick consists of plastic strips that contain multiple pads with chemical indicators. Normal urine is sterile, without protein, white cells, blood, or nitrites. A positive test for nitrites indicates the presence of bacteria that produce nitrate reductase, changing nitrate to nitrite. A positive test for leukocyte esterase indicates the presence of polymorphonuclear neutrophils (PMNs) in the urine that produce the enzyme. Inflammatory cells are the host’s response to infection. The strip is dipped into the urine, and the indicator

pads turn colors that are read immediately and compared to a scale of +1 to +4 . A dipstick test performed at the university health center on the urine from our college student showed positive reactions for both nitrate and leukocyte esterase, so her urine was sent to the lab for culture. A urine culture should be performed in patients with suspected cystitis regardless of dipstick results.

 TREATMENT AND PREVENTION

Factors to consider when treating UTI include:

■ Patient’s age and sex

■ Symptomatic versus asymptomatic infection

■ Upper (pyelonephritis) versus lower (cystitis) urinary tract involvement

■ Community- versus hospital-acquired infection

■ Single event versus recurrent events

■ Patient’s underlying illness

For uncomplicated cystitis a 3-day course of treatment is recommended. Symptoms usually resolve over 1–3 days. Many antibiotics with a broad range of activity against gram-negative rods and/or gram-positive cocci are suitable for the treatment of UTI, whether they are bacteriostatic or bacteriocidal drugs because they are concentrated 10–30-fold in the urine. Choices for initial empiric treatment of uncomplicated UTI in women include trimethoprim–sulfamethoxazole, a fluoroquinolone, or nitrofurantoin. The choice of an empiric antibiotic should always be based on the local prevalence of resistance in one’s geographic area, and this should be

periodically reevaluated. Ampicillin, amoxicillin, and sulfonamides are no longer considered good empiric choices because of the higher resistance rates seen in Enterobacteriaceae and Enterococcus spp. isolated from adults. Follow-up urine cultures are not necessary for patients with uncomplicated cystitis who respond clinically to treatment. Pregnant women should receive a follow-up culture 1–2 weeks after treatment. Complicated UTIs are more often caused by bacteria that may be resistant to the antibiotics used to treat uncomplicated UTI, particularly in hospitalized patients. Until the results of urine cultures are available in these patients, a fluoroquinolone is an excellent antibiotic choice in adult patients. In

these patients, treatment should be continued for 7–14 days. If symptoms resolve, a follow-up urine culture is not generally recommended.

Liver blood test

 Liver blood test

An initial step in detecting liver damage is a simple blood test to determine the presence of certain liver enzymes (proteins) in the blood. Under normal circumstances, these enzymes reside within the cells of the liver. But when the liver is injured for any reason, these enzymes are spilled into the blood stream. Enzymes are proteins that are present throughout the body, each with a unique function. Enzymes help to speed up (catalyze) routine and necessary chemical reactions in the body.

Among the most sensitive and widely used liver enzymes are the aminotransferases. They include aspartate aminotransferase (AST or SGOT) and alanine aminotransferase (ALT or SGPT). These enzymes are normally contained within liver cells. If the liver is injured or damaged, the liver cells spill these enzymes into the blood, raising the enzyme levels in the blood and signaling the liver disease.

 Aminotransferases

The aminotransferases catalyze chemical reactions in which an amino group (amino acids are building blocks of proteins) is transferred from a donor molecule to a recipient molecule. Hence, the names "aminotransferases."

Medical terms can sometimes be confusing, as is the case with these enzymes.

·                          Another name for aminotransferase is transaminase. 

·                          The enzyme aspartate aminotransferase (AST) is also known as serum glutamic oxaloacetic transaminase (SGOT); and 

·                          alanine aminotransferase (ALT) is also known as serum glutamic pyruvic transaminase (SGPT).

To put matters briefly, AST = SGOT and ALT = SGPT.

 Normal levels of AST and ALT

The normal range of values for AST (SGOT) is from 5 to 40 units per liter of serum (the liquid part of the blood).

The normal range of values for ALT (SGPT) is from 7 to 56 units per liter of serum.

The ranges of AST and ALT numbers may differ slightly depending on the technique and protocols used by different laboratories. However, normal reference ranges are routinely provided by each laboratory and printed in the report.

Medications cause abnormal aminotransferase levels

A host of medications can cause abnormal liver enzymes levels.

Examples include:

Pain relief medications such as:

·                          aspirin, 

·                          acetaminophen (Tylenol), 

·                          naproxen (Narcosis, Nap élan, Anaprox, Aleve), 

·                          diclofenac (Voltaren, Cataflam, Voltaren-XR), and 

·                          phenylbutazone (Butazolidine)

Anti-seizure medications such as:

·                          phenytoin (Dilantin), 

·                          valproic acid (Depakote, Depakote ER, Depakene, Depacon), 

·                          carbamazepine (Tegretol, Tegretol XR, Equertro), and 

·                          phenobarbital

Antibiotics such as:

·                          tetracyclines, [for example, tetracycline (Achromycin)]

·                          sulfonamides, 

·                          isoniazid (INH) (Nydrazid, Laniazid)

·                          sulfamethoxazole (Gantanol), 

·                          trimethoprim (Trimpex; Proloprim, Primsol)

·                          nitrofurantoin (Macrodantin; Furadantin; Macrobid), 

·                          fluconazole (Diflucan ) and some other anti-fungals, etc.

Cholesterol lowering drugs such as:

·                          the statins:

o                                         lovastatin (Mevacor, Altocor), 

o                                         pravastatin (Pravachol), 

o                                         atorvastatin (Lipitor),

o                                         fluvastatin (Lescol),

o                                         rosuvastatin (Crestor),

o                                         simvastatin (Zocor), and

·                          niacin

Cardiovascular drugs such as:

·                          amiodarone (Cordarone),

·                          hydralazine (Apresoline) 

·                          quinidine (Quinaglute, Quinidex), etc.

Other drugs

·                          Antidepressant drugs of the tricyclic type

With drug-induced liver enzyme abnormalities, the enzymes usually normalize weeks to months after stopping the medications.

Acute Pharyngitis

 Acute Pharyngitis

 PATIENT HISTORY

The patient was a 6 year-old male who had been in good health with no significant medical problems. In late September he presented to his pediatrician’s office with a complaint of sore throat, fever, headache, and swollen glands in his neck for the past 36 h. On physical examination

(PE), he had a fever of 38◦C (100.4◦F), a red posterior pharynx, yellowish exudate on his tonsils, and multiple, enlarged, tender cervical lymph nodes.

 There were no other pertinent symptoms.

LABORATORY TESTS

  pain on swallowing, as well as erythema with or without exudate on the

tonsils and tender cervical lymph nodes. There are no clinical indicators

that would make it possible to accurately predict the cause of this child’s

pharyngitis. Laboratory tests are required to make a diagnosis.

When deciding whether to perform a laboratory test, clinical and epidemiological

features as well as the availability and usefulness of treatment

must be considered. While viruses are the most common cause

of acute pharyngitis in both adults and children, lab testing for viruses

is not warranted because antiviral agents are not used to treat acute

pharyngitis. Given the age of this patient, the absence of travel, and the

lack of suspicion of child abuse, GAS is the most likely etiologic agent.

Since GAS pharyngitis is the most commonly occurring form of pharyngitis

for which antibiotic therapy is indicated, lab testing should be directed

at ruling out GAS. Appropriate laboratory tests for this would

include:

Rapid strep test. This is not a culture; the test detects a unique carbohydrate

on the cell wall of GAS.

Throat culture. This test will grow the GAS organism from a throat

specimen taken from the patient and will require overnight incubation

at the minimum. Most labs offer a specific “rule out GAS”

throat culture.

The specimen required for each of these tests is a throat swab. Use of a

double-swab format allows one to obtain sufficient specimen to perform

both tests if necessary. As with any microbiology test, the quality of the

results is contigent on whether the laboratory receives a well-taken specimen.

The double swab should be firmly rubbed over much of the surface

of both tonsils and the posterior pharyngeal area and rolled to ensure

that there is ample specimen is on each swab tip. If exudate is present, it

should also be sampled on the same swabs. Care should be taken to avoid

touching other areas of the oropharynx, mouth, and tongue.

DirectGramstains fromthroat swabs are not at all useful becausemany

bacteria normally reside in the throat, including nonpathogenic streptococci

that have Gram stain appearance identical to that of GAS.

 TREATMENT AND PREVENTION

Treatment of group A streptococcal pharyngitis is important in order to

relieve the patient’s symptoms and to prevent the transmission to others.

Prompt treatment will also prevent complications such as peritonsillar abscess

and acute rheumatic fever. Symptoms will often disappear within

3–4 days even without antibiotics, but early antibiotics can shorten the

duration of symptoms. Pharyngitis caused by S. pyogenes can be effectively

treated with a penicillin. In children, like this patient, amoxicillin

is routinely prescribed. Patients must complete the course of antibiotic to

eradicate the organisms from the pharynx. For patients who are allergic

to penicillin, erythromycin would be an acceptable alternative. If left untreated,

patients with GAS infection may develop the sequellae of heart

valve damage (RF) or kidney damage (GN).

Susceptibility tests on GAS would not be performed since resistance

to penicillin has not been documented in these organisms to date. Carriers

maintain S. pyogenes in their throats despite appropriate antibiotic therapy;

it is not because the organisms are resistant to penicillin. Carriers are not

symptomatic but can spread the organism to others who may develop an

infection.

Alcoholism

Alcoholism

Definition

• Alcoholism and alcohol abuse

o Regular and excessive use of alcohol with concomitant social, interpersonal, legal, occupational, and/or physical problems or

o Repeated use in hazardous situations such as driving

• Alcohol dependence

o Repeated alcohol-related difficulties in at least 3 areas of functioning that cluster together over any 12-month period

o Regular use of alcohol has resulted in a state of physiologic tolerance.

Symptoms & Signs

• Most patients with alcoholism do not have dramatic physical symptoms.

o Instead present with psychosocial difficulties

 Marital difficulties

 Job problems (tardiness, absenteeism)

 Legal problems resulting from driving while intoxicated

o Patients may describe a host of difficulties but may deny that they have a problem with alcohol abuse.

o Denial is a characteristic symptom of alcoholism.

• "CAGE" questionnaire: any positive answer indicates a high probability of alcoholism

o Blackouts

 Episode of temporary anterograde amnesia associated with alcohol use

 Occurs in ~35% of drinkers

o Sleep disturbances

 Deficiency in rapid eye movement and deep sleep results in prominent and sometimes disturbing dreams later in the night.

o Sleep apnea

 75% of alcoholic men over age 60

 Relaxes muscles in the pharynx

o Impairment in judgment and coordination

 At least half of patients with physical trauma have evidence of substance-related impairment.

 In the U.S., 40% of drinkers have at some time driven while intoxicated.

o Peripheral neuropathy

 Chronic high doses of alcohol; occurs in 5–15% of alcoholics

o Cerebellar degeneration

1% of alcoholics

 Syndrome of progressive unsteady stance and gait often accompanied by mild nystagmus

2 Alcoholism

o Alcohol-induced mood disorder

 Intense sadness lasting for days to weeks in the midst of heavy drinking in 40% of alcoholics

o Alcohol-induced anxiety disorder

 Temporary severe anxiety in 10–30% of alcoholics

 Often begins during alcohol withdrawal

 Can persist for many months after cessation of drinking

o Alcohol-induced psychotic disorder

 Auditory hallucinations and/or paranoid delusions with a clear sensorium

• GI findings

o Esophagus and stomach

 Inflammation of the esophagus and stomach

 Epigastric distress

 GI bleeding

o Pancreas and liver

 Incidence of acute pancreatitis (~25 per 1000 per year) almost 3-fold higher than in the general population

 Repeated exposure to ethanol leads to:

 Fatty accumulation in the liver

 Alcohol-induced hepatitis

 Perivenular sclerosis

 Cirrhosis (15–20%)

 Chronic pancreatitis

• Cardiovascular findings

o Chronic heavy drinking

 Mild to moderate hypertension

 Cardiomyopathy

 One-third of cases of cardiomyopathy are alcohol induced.

 Atrial or ventricular arrhythmias, especially paroxysmal tachycardia

 Occurs after a drinking binge in individuals showing no other evidence of heart disease: "holiday heart"

• Genitourinary system changes; sexual function

o Acutely (modest alcohol dose: blood alcohol concentrations of ≤100 mg/dL)

 Increases sexual drive and decreases erectile capacity in men

o Chronic alcoholism in men

 Irreversible testicular atrophy with concomitant shrinkage of the seminiferous tubules, decreases in ejaculate volume, lower sperm count

o Repeated ingestion of high doses of ethanol by women

 Amenorrhea

 Decrease in ovarian size

 Absence of corpora lutea with associated infertility

 Spontaneous abortions

• Musculoskeletal findings

o Acute alcoholic myopathy

 Condition improves, but might not disappear with abstinence.

o Effects of repeated heavy drinking

 Alteration in calcium metabolism

 Lower bone density

 Increased risk for fractures and osteonecrosis of the femoral head

Alcoholism 3

• Alcohol-withdrawal syndrome

o Withdrawal symptoms generally begin within 5–10 hours of decreasing ethanol intake, peak in intensity on day 2 or 3, and improve by day 4 or 5.

o Anxiety, insomnia, and mild levels of autonomic dysfunction may persist to some degree for ≥6 months; may contribute to the tendency to return to drinking.