CHOLERA
Cholera is an acute diarrhoeal disease caused by Vibrio cholerae.
Records from Hippocrates (460-377 BCE) and the Indian peninsula describe
an illness that might have been cholera.
Although not the first description, the discovery of the cholera organism is
credited to German bacteriologist Robert Koch, who independently identified
V cholerae in 1883 during an outbreak in Egypt; the genus name refers to the
fact that the organism appears to vibrate when moving.
The hallmark of the disease is profuse secretory diarrhea.
Cholera can be endemic, epidemic, or pandemic.
Pathophysiology
Cholera, caused by the bacteria Vibrio cholerae, is a comma-shaped, gram-negative
aerobic or facultatively anaerobic bacillus that varies in size from 1-3 µm in length by
0.5-0.8 µm in diameter.
The clinical and epidemiologic features of disease caused by V cholerae
O139 are indistinguishable from those of disease caused by O1 strains; both
serogroups cause clinical disease by producing an enterotoxin that promotes
the secretion of fluid and electrolytes into the lumen of the small intestine.
To reach the small intestine, however, the organism has to negotiate the
normal defense mechanisms of the GI tract; because the organism is not
acid-resistant, it depends on its large inoculum size to withstand gastric
acidity.
The use of antacids, histamine receptor blockers, and proton pump inhibitors
increases the risk of cholera infection and predisposes patients to more
severe disease as a result of reduced gastric acidity.
Fluid loss originates in the duodenum and upper jejunum; the ileum is less
affected.
The colon is usually in a state of absorption because it is relatively insensitive
to the toxin; however, the large volume of fluid produced in the upper intestine
overwhelms the absorptive capacity of the lower bowel, resulting in
severe diarrhea.
Unless the lost fluid and electrolytes are replaced adequately, the infected
person may develop shock from profound dehydration and acidosis from loss
of bicarbonate.
The enterotoxin acts locally and does not invade the intestinal wall. As a
result, few neutrophils are found in the stool.
Causes
Cholera can be an endemic, epidemic, or a pandemic disease.
Environmental factors. Primary infection in humans is incidentally acquired.
Risk of primary infection is facilitated by seasonal increases in the number of
organisms, possibly associated with changes in water temperature and algal
blooms; secondary transmission occurs through fecal-oral spread of the
organism through person-to-person contact or through contaminated water
and food.
Host factors. Malnutrition increases susceptibility to cholera. Because gastric
acid can quickly render an inoculum of V cholerae noninfectious before it
reaches the site of colonization in the small bowel, hydrochlorhydria or
achlorhydria of any cause (including Helicobacter pylori infection,
gastric surgery, vagotomy, use of H2 blockers for ulcer disease) increases
susceptibility; infection rates of household contacts of cholera patients range
from 20-50%. Rates are lower in areas where infection is endemic and
individuals, especially adults, may have preexisting vibriocidal antibodies from
previous encounters with the organism.
Statistics and Incidences
In the United States, cholera has virtually been eliminated because of
improved hygiene and sanitation systems.
The frequency of cholera among international travelers returning to the United
States has averaged 1 case per 500,000 population, with a range of 0.05-3.7
cases per 100,000 population, depending on the countries visited.
In 1990, fewer than 30,000 cases were reported to the WHO.
From 2005 to 2008, 178,000-237,000 cases and 4000-6300 deaths were
reported annually worldwide.
In nonendemic areas, the incidence of infection is similar in all age groups,
although adults are less likely to become symptomatic than children.
CLINICAL MANIFESTATIONS
After a 24- to 48-hour incubation period, symptoms begin with the sudden onset of
painless watery diarrhea that may quickly become voluminous and is often followed
by vomiting.
Diarrhea. Profuse watery diarrhea is a hallmark of cholera; cholera should be
suspected when a patient older than 5 years develops
severe dehydration from acute, severe, watery diarrhea (usually
without vomiting) or in any patient older than 2 years who has acute watery
diarrhea and is in an area where an outbreak of cholera has occurred.
Vomiting. Vomiting, although a prominent manifestation, may not always be
present; early in the course of the disease, vomiting is caused by decreased
gastric and intestinal motility; later in the course of the disease it is more likely
to result from acidemia.
Dehydration. If untreated, the diarrhea and vomiting lead
to isotonic dehydration, which can lead to acute tubular necrosis and renal
failure; because the dehydration is isotonic, water loss is proportional between
3 body compartments, intracellular, intravascular, and interstitial.
Assessment and Diagnostic Findings
Definitive diagnosis is not a prerequisite for the treatment of patients with cholera.
Stool examination. Although observed as a gram-negative organism, the
characteristic motility of Vibrio species cannot be identified on a Gram stain,
but it is easily seen on direct dark-field examination of the stool.
Stool culture. V cholerae is not fastidious in nutritional requirements for
growth; however, it does need an adequate buffering system if fermentable
carbohydrate is present because viability is severely compromised if the pH is
less than 6, often resulting in autosterilization of the culture.
Serotyping and biotyping. Specific antisera can be used in immobilization
tests; a positive immobilization test result (ie, cessation of motility of the
organism) is produced only if the antiserum is specific for the Vibrio type
present; the second antiserum serves as a negative control.
Hematologic tests. Hematocrit, serum-specific gravity, and serum protein are
elevated in dehydrated patients because of resulting hemoconcentration;
when patients are first observed, they generally have a leukocytosis without a
left shift.
Metabolic panel. Serum sodium is usually 130-135 mmol/L, reflecting the
substantial loss of sodium in the stool; serum potassium usually is normal in
the acute phase of the illness, reflecting the exchange of
intracellular potassium for extracellular hydrogen ion in an effort to correct the
acidosis; hyperglycemia may be present, secondary to systemic release
of epinephrine, glucagon, and cortisol due to hypovolemia; patients have
elevated blood urea nitrogen and creatinine levels consistent
with prerenal azotemia.
Medical Management
Rehydration is the first priority in the treatment of cholera. Rehydration is
accomplished in 2 phases: rehydration and maintenance.
Rehydration phase. The goal of the rehydration phase is to restore normal
hydration status, which should take no more than 4 hours; set the rate of
intravenous infusion in severely dehydrated patients at 50-100 mL/kg/hr;
Lactated Ringer solution is preferred over isotonic sodium chloride solution
because saline does not correct metabolic acidosis.
Maintenance phase. The goal of the maintenance phase is to maintain
normal hydration status by replacing ongoing losses; the oral route is
preferred, and the use of oral rehydration solution (ORS) at a rate of 500-1000
mL/hr is recommended.
Cholera cots. In areas where cholera is endemic, cholera cots have been
used to assess the volume of ongoing stool losses; a cholera cot is a cot
covered by a plastic sheet with a hole in the center to allow the stool to collect
in a calibrated bucket underneath.
Diet. Resume feeding with a normal diet when vomiting has stopped;
continue breastfeeding infants and young children.
Pharmacological Management
Antimicrobial therapy for cholera is an adjunct to fluid therapy and is not an essential
therapeutic component.
Antibiotics. Empiric antimicrobial therapy must be comprehensive and
should cover all likely pathogens in the context of the clinical setting; although
not necessarily curative, treatment with an antibiotic to which the organism is
susceptible diminishes the duration and volume of the fluid loss and hastens
clearance of the organism from stool.
Vaccines. In June, 2016, the first U.S. cholera vaccine was approved by the
FDA; contains live attenuated cholera bacteria that replicate in the
gastrointestinal tract of the recipient to provide immunity; it is indicated for
active immunization against disease caused by Vibrio cholerae serogroup O1
in adults aged 18-64 y traveling to cholera-affected areas.
Nursing Management
The nursing care of a client with cholera include the following:
Nursing Assessment
Assessment of the patient with cholera are as follows:
Assess for dehydration. Assess the status of dehydration ( skin color,
temperature, skin turgor, mucous membranes, eyes, crown, body
temperature, pulse, respiration, behavior, weight loss).
Observe for diarrhea. Observe for a sudden attack of
diarrhea, fever, anorexia, vomiting, nausea, abdominal cramps,
increased bowel sounds, and bowel movements more than 3 times a day, with
liquid stool consistency, with or without mucus or blood.
Assess the level of knowledge of the family. Assess for the knowledge of
diarrhea at home, dietary knowledge, and knowledge about the prevention of
recurrent diarrhea.
Nursing Diagnosis
Based on the assessment data, the major nursing diagnosis for cholera are:
Deficient fluid volume related to excessive fluid loss through the stool or
emesis.
Imbalanced Nutrition: less than body requirements related to loss of fluids
through diarrhea, inadequate intake.
Risk for infection related to microorganisms that penetrate the
gastrointestinal tract.
Impaired Skin Integrity: perianal, related to irritation from diarrhea.
Anxiety related to separation from parents, unfamiliar environment, a
stressful procedure.
Nursing Care Planning and Goals
The major nursing care planning goals for cholera:
Patient will maintain adequate hydration.
Patient will consume adequate nutritional requirements.
Patient will prevent onset of infection.
Patient will maintain skin integrity.
Patient will prevent anxiety.
Nursing Interventions
The nursing interventions on a patient diagnosed with cholera are:
Monitor intake and output. Note number, character, and amount of stools;
estimate insensible fluid losses like diaphoresis; measure urine specific
gravity and observe for oliguria.
Weigh daily. Daily weight is an indicator of overall fluid and nutritional status.
Maintain hydration. Replace ongoing fluid losses until diarrhea stops.
Administer medications as indicated. Give an oral antibiotic to the patient
with severe dehydration as prescribed.
Evaluation
Nursing goals are met as evidenced by:
Patient was able to maintain adequate hydration.
Patient was able to consume adequate nutritional requirements.
Patient was able to prevent onset of infection.
Patient was able to maintain skin integrity.
Patient was able to prevent anxiety.
