Vibrio cholerae

The epidemiology of cholera closely parallels the recognition of V cholerae transmission in

water and the development of sanitary water systems.
Morphology & Identification
Typical Organisms
Upon first isolation, V cholerae is a comma-shaped, curved rod 24 m long (Figure 18
1). It is actively motile by means of a polar flagellum. On prolonged cultivation, vibrios may
become straight rods that resemble the gram-negative enteric bacteria.
Figure 181.


Vibrio cholerae grown in broth showing slightly curved gram-negative rods.
Culture
V cholerae produces convex, smooth, round colonies that are opaque and granular in
transmitted light. V cholerae and most other vibrios grow well at 37 C on many kinds of
media, including defined media containing mineral salts and asparagine as sources of carbon
and nitrogen. V cholerae grows well on thiosulfate-citrate-bile-sucrose (TCBS) agar, on
which it produces yellow colonies that are readily visible against the dark-green background
of the agar. Vibrios are oxidase-positive, which differentiates them from enteric gram-
negative bacteria. Characteristically, vibrios grow at a very high pH (8.59.5) and are rapidly
killed by acid. Cultures containing fermentable carbohydrates therefore quickly become
sterile.
In areas where cholera is endemic, direct cultures of stool on selective media such as TCBS,
and enrichment cultures in alkaline peptone water are appropriate. However, routine stool
cultures on special media such as TCBS generally are not necessary or cost-effective in areas
where cholera is rare.
Growth Characteristics
V cholerae regularly ferments sucrose and mannose but not arabinose. A positive oxidase test
is a key step in the preliminary identification of V cholerae and other vibrios. Vibrio species
are susceptible to the compound O/129 (2,4-diamino-6,7-diisopropylpteridine phosphate),
which differentiates them from Aeromonas species, which are resistant to O/129. Most Vibrio
species are halotolerant, and NaCl often stimulates their growth. Some vibrios are halophilic,
requiring the presence of NaCl to grow. Another difference between vibrios and aeromonas is
that vibrios grow on media containing 6% NaCl, whereas aeromonas does not.
Antigenic Structure & Biologic Classification
Many vibrios share a single heat-labile flagellar H antigen. Antibodies to the H antigen are
probably not involved in the protection of susceptible hosts.
V cholerae has O lipopolysaccharides that confer serologic specificity. There are at least 139
O antigen groups. V cholerae strains of O group 1 and O group 139 cause classic cholera;
occasionally, non-O1/non-O139 V cholerae causes cholera-like disease. Antibodies to the O
antigens tend to protect laboratory animals against infections with V cholerae.
The V cholerae serogroup O1 antigen has determinants that make possible further typing; the
serotypes are Ogawa, Inaba, and Hikojima. Two biotypes of epidemic V cholerae have been
defined, classic and El Tor. The El Tor biotype produces a hemolysin, gives positive results
on the Voges-Proskauer test, and is resistant to polymyxin B. Molecular techniques can also
be used to type V cholerae. Typing is used for epidemiologic studies, and tests generally are
done only in reference laboratories.
V cholerae O139 is very similar to V cholerae O1 El Tor biotype. V cholerae O139 does not
produce the O1 lipopolysaccharide and does not have all the genes necessary to make this
antigen. V cholerae O139 makes a polysaccharide capsule like other non-O1 V cholerae
strains, while V cholerae O1 does not make a capsule.
Vibrio cholerae Enterotoxin
V cholerae produce a heat-labile enterotoxin with a molecular weight of about 84,000,
consisting of subunits A (MW 28,000) and B (see Chapter 10). Ganglioside GM
1
serves as
the mucosal receptor for subunit B, which promotes entry of subunit A into the cell.
Activation of subunit A
1
yields increased levels of intracellular cAMP and results in
prolonged hypersecretion of water and electrolytes. There is increased sodium-dependent
chloride secretion, and absorption of sodium and chloride is inhibited. Diarrhea occursas
much as 2030 L/dwith resulting dehydration, shock, acidosis, and death. The genes for V
cholerae enterotoxin are on the bacterial chromosome. Cholera enterotoxin is antigenically
related to LT of Escherichia coli and can stimulate the production of neutralizing antibodies.
However, the precise role of antitoxic and antibacterial antibodies in protection against
cholera is not clear.
Pathogenesis & Pathology
Under natural conditions, V cholerae is pathogenic only for humans. A person with normal
gastric acidity may have to ingest as many as 10
10
or more V cholerae to become infected
when the vehicle is water, because the organisms are susceptible to acid. When the vehicle is
food, as few as 10
2
10
4
organisms are necessary because of the buffering capacity of food.
Any medication or condition that decreases stomach acidity makes a person more susceptible
to infection with V cholerae.
Cholera is not an invasive infection. The organisms do not reach the bloodstream but remain
within the intestinal tract. Virulent V cholerae organisms attach to the microvilli of the brush
border of epithelial cells. There they multiply and liberate cholera toxin and perhaps
mucinases and endotoxin.
Clinical Findings
About 60% of infections with classic V cholerae are asymptomatic, as are about 75% of
infections with the El Tor biotype. The incubation period is 14 days for persons who
develop symptoms, depending largely upon the size of the inoculum ingested. There is a
sudden onset of nausea and vomiting and profuse diarrhea with abdominal cramps. Stools,
which resemble "rice water," contain mucus, epithelial cells, and large numbers of vibrios.
There is rapid loss of fluid and electrolytes, which leads to profound dehydration, circulatory
collapse, and anuria. The mortality rate without treatment is between 25% and 50%. The
diagnosis of a full-blown case of cholera presents no problem in the presence of an epidemic.
However, sporadic or mild cases are not readily differentiated from other diarrheal diseases.
The El Tor biotype tends to cause milder disease than the classic biotype.
Diagnostic Laboratory Tests
Specimens
Specimens for culture consist of mucus flecks from stools.
Smears
The microscopic appearance of smears made from stool samples is not distinctive. Dark-field
or phase contrast microscopy may show the rapidly motile vibrios.
Culture
Growth is rapid in peptone agar, on blood agar with a pH near 9.0, or on TCBS agar, and
typical colonies can be picked in 18 hours. For enrichment, a few drops of stool can be
incubated for 68 hours in taurocholate-peptone broth (pH 8.09.0); organisms from this
culture can be stained or subcultured.
Specific Tests
V cholerae organisms are further identified by slide agglutination tests using anti-O group 1
or group 139 antisera and by biochemical reaction patterns.
Immunity
Gastric acid provides some protection against cholera vibrios.
An attack of cholera is followed by immunity to reinfection, but the duration and degree of
immunity are not known. In experimental animals, specific IgA antibodies occur in the lumen
of the intestine. Similar antibodies in serum develop after infection but last only a few
months. Vibriocidal antibodies in serum (titer 1:20) have been associated with
protection against colonization and disease. The presence of antitoxin antibodies has not been
associated with protection.
Treatment
The most important part of therapy consists of water and electrolyte replacement to correct
the severe dehydration and salt depletion. Many antimicrobial agents are effective against V
cholerae. Oral tetracycline tends to reduce stool output in cholera and shortens the period of
excretion of vibrios. In some endemic areas, tetracycline resistance of V cholerae has
emerged; the genes are carried by transmissible plasmids.
Epidemiology, Prevention, & Control
Six pandemics (worldwide epidemics) of cholera occurred between 1817 and 1923, caused
most likely by V cholerae O1 of the classic biotype and largely originating in Asia, usually
the Indian subcontinent. The seventh pandemic began in 1961 in the Celebes Islands,
Indonesia, with spread to Asia, the Middle East, and Africa. This pandemic has been caused
by V cholerae biotype El Tor. Starting in 1991, the seventh pandemic spread to Peru and then
to other countries of South America and Central America. Cases also occurred in Africa.
Millions of people have had cholera in this pandemic. Some consider the cholera caused by
the serotype O139 strain to be the eighth pandemic that began in the Indian subcontinent in
19921993, with spread to Asia. The disease has been rare in North America since the mid
1800s, but an endemic focus exists on the Gulf Coast of Louisiana and Texas.
Cholera is endemic in India and Southeast Asia. From these centers, it is carried along
shipping lanes, trade routes, and pilgrim migration routes. The disease is spread by contact
involving individuals with mild or early illness and by water, food, and flies. In many
instances, only 15% of exposed susceptible persons develop disease. The carrier state
seldom exceeds 34 weeks, and the importance of carriers in transmission is unclear. Vibrios
survive in water for up to 3 weeks.
Vibrio cholerae lives in aquatic environments. And such environments are the vibrios natural
reservoir. Vibrio cholerae lives attached to algae, copepods, and crustacean shells. It can
survive for years and grow, but when conditions are not suitable for growth it can become
dormant.
Control rests on education and on improvement of sanitation, particularly of food and water.
Patients should be isolated, their excreta disinfected, and contacts followed up.
Chemoprophylaxis with antimicrobial drugs may have a place. Repeated injection of a
vaccine containing either lipopolysaccharides extracted from vibrios or dense vibrio
suspensions can confer limited protection to heavily exposed persons (eg, family contacts)
but is not effective as an epidemic control measure.
Vibrio parahaemolyticus & Other Vibrios
Vibrio parahaemolyticus is a halophilic bacterium that causes acute gastroenteritis following
ingestion of contaminated seafood such as raw fish or shellfish. After an incubation period of
1224 hours, nausea and vomiting, abdominal cramps, fever, and watery to bloody diarrhea
occur. Fecal leukocytes are often observed. The enteritis tends to subside spontaneously in 1
4 days with no treatment other than restoration of water and electrolyte balance. No
enterotoxin has yet been isolated from this organism. The disease occurs worldwide, with
highest incidence in areas where people eat raw seafood. V parahaemolyticus does not grow
well on some of the differential media used to grow salmonellae and shigellae, but it does
grow well on blood agar. It also grows well on TCBS, where it yields green colonies. V
parahaemolyticus is usually identified by its oxidase-positive growth on blood agar.
Vibrio vulnificus can cause severe wound infections, bacteremia, and probably gastroenteritis.
It is a free-living estuarine bacterium found in the USA on the Atlantic, Gulf, and Pacific
Coasts. Infections have been reported from Korea, and the organism may be distributed
worldwide. V vulnificus is particularly apt to be found in oysters, especially in warm months.
Bacteremia with no focus of infection occurs in persons who have eaten infected oysters and
who have alcoholism or liver disease. Wounds may become infected in normal or
immunocompromised persons who are in contact with water where the bacterium is present.
Infection often proceeds rapidly, with development of severe disease. About 50% of the
patients with bacteremia die. Wound infections may be mild but often proceed rapidly (over a
few hours), with development of bullous skin lesions, cellulitis, and myositis with necrosis.
Several of the first deaths in Louisiana and Texas following hurricane Katrina were caused by
Vibrio vulnificus. Because of the rapid progression of the infection, it is often necessary to
treat with appropriate antibiotics before culture confirmation of the etiology can be obtained.
Diagnosis is by culturing the organism on standard laboratory media; TCBS is the preferred
medium for stool cultures, where most strains produce blue-green (sucrose-negative)
colonies.
Tetracycline appears to be the drug of choice for V vulnificus infection; ciprofloxacin may be
effective also based on in vitro activity.
Several other vibrios also cause disease in humans: Vibrio mimicus causes diarrhea after
ingestion of uncooked seafood, particularly raw oysters. Vibrio hollisae and Vibrio fluvialis
also cause diarrhea. Vibrio alginolyticus causes eye, ear, or wound infection after exposure to
seawater. Vibrio damsela also causes wound infections. Other vibrios are very uncommon
causes of disease in humans.
Aeromonas


The Shigellae
The natural habitat of shigellae is limited to the intestinal tracts of humans and other
primates, where they produce bacillary dysentery.
Morphology & Identification
Typical Organisms
Shigellae are slender gram-negative rods; coccobacillary forms occur in young cultures.
Culture
Shigellae are facultative anaerobes but grow best aerobically. Convex, circular, transparent
colonies with intact edges reach a diameter of about 2 mm in 24 hours.
Growth Characteristics
All shigellae ferment glucose. With the exception of Shigella sonnei, they do not ferment
lactose. The inability to ferment lactose distinguishes shigellae on differential media.
Shigellae form acid from carbohydrates but rarely produce gas. They may also be divided
into those that ferment mannitol and those that do not (Table 163).
Table 163. Pathogenic Species of Shigella.

Present Designation Group and Type Mannitol Ornithine Decarboxylase
S dysenteriae A - -
S flexneri B + -
S boydii C + -
S sonnei D + +
Antigenic Structure
Shigellae have a complex antigenic pattern. There is great overlapping in the serologic
behavior of different species, and most of them share O antigens with other enteric bacilli.
The somatic O antigens of shigellae are lipopolysaccharides. Their serologic specificity
depends on the polysaccharide. There are more than 40 serotypes. The classification of
shigellae relies on biochemical and antigenic characteristics. The pathogenic species are
shown in Table 163.
Pathogenesis & Pathology
Shigella infections are almost always limited to the gastrointestinal tract; bloodstream
invasion is quite rare. Shigellae are highly communicable; the infective dose is on the order
of 10
3
organisms (whereas it usually is 10
5
10
8
for salmonellae and vibrios). The essential
pathologic process is invasion of the mucosal epithelial cells (eg, M cells) by induced
phagocytosis, escape from the phagocytic vacuole, multiplication and spread within the
epithelial cell cytoplasm, and passage to adjacent cells. Microabscesses in the wall of the
large intestine and terminal ileum lead to necrosis of the mucous membrane, superficial
ulceration, bleeding, and formation of a "pseudomembrane" on the ulcerated area. This
consists of fibrin, leukocytes, cell debris, a necrotic mucous membrane, and bacteria. As the
process subsides, granulation tissue fills the ulcers and scar tissue forms.
Toxins
Endotoxin
Upon autolysis, all shigellae release their toxic lipopolysaccharide. This endotoxin probably
contributes to the irritation of the bowel wall.
Shigella dysenteriae Exotoxin
S dysenteriae type 1 (Shiga bacillus) produces a heat-labile exotoxin that affects both the gut
and the central nervous system. The exotoxin is a protein that is antigenic (stimulating
production of antitoxin) and lethal for experimental animals. Acting as an enterotoxin, it
produces diarrhea as does the E coli verotoxin, perhaps by the same mechanism. In humans,
the exotoxin also inhibits sugar and amino acid absorption in the small intestine. Acting as a
"neurotoxin," this material may contribute to the extreme severity and fatal nature of S
dysenteriae infections and to the central nervous system reactions observed in them (ie,
meningismus, coma). Patients with Shigella flexneri or Shigella sonnei infections develop
antitoxin that neutralizes S dysenteriae exotoxin in vitro. The toxic activity is distinct from
the invasive property of shigellae in dysentery. The two may act in sequence, the toxin
producing an early nonbloody, voluminous diarrhea and the invasion of the large intestine
resulting in later dysentery with blood and pus in stools.
Clinical Findings
After a short incubation period (12 days), there is a sudden onset of abdominal pain, fever,
and watery diarrhea. The diarrhea has been attributed to an exotoxin acting in the small
intestine (see above). A day or so later, as the infection involves the ileum and colon, the
number of stools increases; they are less liquid but often contain mucus and blood. Each
bowel movement is accompanied by straining and tenesmus (rectal spasms), with resulting
lower abdominal pain. In more than half of adult cases, fever and diarrhea subside
spontaneously in 25 days. However, in children and the elderly, loss of water and
electrolytes may lead to dehydration, acidosis, and even death. The illness due to S
dysenteriae may be particularly severe.
On recovery, most persons shed dysentery bacilli for only a short period, but a few remain
chronic intestinal carriers and may have recurrent bouts of the disease. Upon recovery from
the infection, most persons develop circulating antibodies to shigellae, but these do not
protect against reinfection.
Diagnostic Laboratory Tests
Specimens
Specimens include fresh stool, mucus flecks, and rectal swabs for culture. Large numbers of
fecal leukocytes and some red blood cells often are seen microscopically. Serum specimens,
if desired, must be taken 10 days apart to demonstrate a rise in titer of agglutinating
antibodies.
Culture
The materials are streaked on differential media (eg, MacConkey's or EMB agar) and on
selective media (Hektoen enteric agar or salmonella-shigella agar), which suppress other
Enterobacteriaceae and gram-positive organisms. Colorless (lactose-negative) colonies are
inoculated into triple sugar iron agar. Organisms that fail to produce H
2
S, that produce acid
but not gas in the butt and an alkaline slant in triple sugar iron agar medium, and that are
nonmotile should be subjected to slide agglutination by specific shigella antisera.
Serology
Normal persons often have agglutinins against several Shigella species. However, serial
determinations of antibody titers may show a rise in specific antibody. Serology is not used to
diagnose shigella infections.
Immunity
Infection is followed by a type-specific antibody response. Injection of killed shigellae
stimulates production of antibodies in serum but fails to protect humans against infection.
IgA antibodies in the gut may be important in limiting reinfection; these may be stimulated
by live attenuated strains given orally as experimental vaccines. Serum antibodies to somatic
shigella antigens are IgM.
Treatment
Ciprofloxacin, ampicillin, doxycycline, and trimethoprim-sulfamethoxazole are most
commonly inhibitory for shigella isolates and can suppress acute clinical attacks of dysentery
and shorten the duration of symptoms. They may fail to eradicate the organisms from the
intestinal tract. Multiple drug resistance can be transmitted by plasmids, and resistant
infections are widespread. Many cases are self-limited. Opioids should be avoided in shigella
dysentery.
Epidemiology, Prevention, & Control
Shigellae are transmitted by "food, fingers, feces, and flies" from person to person. Most
cases of shigella infection occur in children under 10 years of age. S dysenteriae can spread
widely. Mass chemoprophylaxis for limited periods of time (eg, in military personnel) has
been tried, but resistant strains of shigellae tend to emerge rapidly. Since humans are the
main recognized host of pathogenic shigellae, control efforts must be directed at eliminating
the organisms from this reservoir by (1) sanitary control of water, food, and milk; sewage
disposal; and fly control; (2) isolation of patients and disinfection of excreta; (3) detection of
subclinical cases and carriers, particularly food handlers; and (4) antibiotic treatment of
infected individuals.
Rotaviruses
Rotaviruses are a major cause of diarrheal illness in human infants and young animals,
including calves and piglets. Infections in adult humans and animals are also common.
Among rotaviruses are the agents of human infantile diarrhea, Nebraska calf diarrhea,
epizootic diarrhea of infant mice, and SA11 virus of monkeys.
Rotaviruses resemble reoviruses in terms of morphology and strategy of replication.
Classification & Antigenic Properties
Rotaviruses have been classified into five species (AE), plus two tentative species (F and
G), based on antigenic epitopes on the internal structural protein VP6. These can be detected
by immunofluorescence, ELISA, and immune electron microscopy (IEM). Group A
rotaviruses are the most frequent human pathogens. Outer capsid proteins VP4 and VP7 carry
epitopes important in neutralizing activity, with VP7 glycoprotein being the predominant
antigen. These type-specific antigens differentiate among rotaviruses and are demonstrable
by Nt tests. Multiple serotypes have been identified among human and animal rotaviruses.
Some animal and human rotaviruses share serotype specificity. For example, monkey virus
SA11 is antigenically very similar to human serotype 3. The gene-coding assignments
responsible for the structural and antigenic specificities of rotavirus proteins are shown in
Figure 374.
Figure 374.


Rotavirus structure. A: Gel diagram showing the 11 segments of the genome. The structural
(VP) and nonstructural (NSP) proteins encoded by these segments are indicated. B: Surface
representation of the rotavirus structure from cryo-electron microscopic analysis. The two
outer layer proteins are VP4, which forms the spikes, and VP7, which forms the capsid
layer. C: Cut-away view showing the triple-layered organization of the virion, with the
intermediate VP6 layer and the innermost VP2 layer indicated. The enzymes required for
endogenous transcription (VP1) and capping (VP3) are attached as heterodimeric complexes
to the inner surface of the VP2 layer. D: Proposed organization of the double-stranded RNA
genome inside the VP2 layer along with transcription enzyme complexes (VP1/3) depicted
as balls. E: Exit of transcripts from the channels at the 5-fold vertices of actively
transcribing double-layered particles. F: Close-up view of one of the exit channels.
(Courtesy of BVV. Prasad.)

Molecular epidemiologic studies have analyzed isolates based on differences in the migration
of the 11 genome segments following electrophoresis of the RNA in polyacrylamide gels
(Figure 375). These differences in electropherotypes can be used to differentiate group A
viruses from other groups, but they cannot be used to predict serotypes.
Figure 375.


Electrophoretic profiles of rotavirus RNA segments. Viral RNAs were electrophoresed in
10% polyacrylamide gels and visualized by silver stain. Different rotavirus groups and RNA
patterns are illustrated: a group A monkey virus (SA11; lane A), a group A human rotavirus
(lane B), a group B human adult diarrhea virus (lane C), and a group A rabbit virus that
exhibits a "short" RNA pattern (lane D). Rotaviruses contain 11 genome RNA segments, but
sometimes two or three segments migrate closely together and are difficult to separate.
(Photograph provided by T Tanaka and MK Estes.)
Animal Susceptibility
Rotaviruses have a wide host range. Most isolates have been recovered from newborn
animals with diarrhea. Cross-species infections can occur in experimental inoculations, but it
is not clear if they occur in nature. Swine rotavirus infects both newborn and weanling
piglets. Newborns often exhibit subclinical infection due perhaps to the presence of maternal
antibody, whereas overt disease is more common in weanling animals.
Propagation in Cell Culture
Rotaviruses are fastidious agents to culture. Most group A human rotaviruses can be
cultivated if pretreated with the proteolytic enzyme trypsin and if low levels of trypsin are
included in the tissue culture medium. This cleaves an outer capsid protein and facilitates
uncoating. Very few non-group A rotavirus strains have been cultivated.
Pathogenesis
Rotaviruses infect cells in the villi of the small intestine (gastric and colonic mucosa are
spared). They multiply in the cytoplasm of enterocytes and damage their transport
mechanisms. One of the rotavirus-encoded proteins, NSP4, is a viral enterotoxin and induces
secretion by triggering a signal transduction pathway. Damaged cells may slough into the
lumen of the intestine and release large quantities of virus, which appear in the stool (up to
10
10
particles per gram of feces). Viral excretion usually lasts 212 days in otherwise healthy
patients but may be prolonged in those with poor nutrition. Diarrhea caused by rotaviruses
may be due to impaired sodium and glucose absorption as damaged cells on villi are replaced
by nonabsorbing immature crypt cells. It may take 38 weeks for normal function to be
restored.
Clinical Findings & Laboratory Diagnosis
Rotaviruses cause the major portion of diarrheal illness in infants and children worldwide but
not in adults (Table 372). There is an incubation period of 13 days. Typical symptoms
include watery diarrhea, fever, abdominal pain, and vomiting, leading to dehydration.
Table 372. Viruses Associated with Acute Gastroenteritis in Humans.
1


Virus Size
(nm)
Epidemiology Important as a
Cause of
Hospitalization
Rotaviruses
Group A 60
80
Single most important cause (viral or bacterial)
of endemic severe diarrheal illness in infants
and young children worldwide (in cooler
months in temperate climates).
Yes
Group B 60
80
Outbreaks of diarrheal illness in adults and
children in China.
No
Group C 60
80
Sporadic cases and occasional outbreaks of
diarrheal illness in children.
No
Enteric
adenovirus
70
90
Second most important viral agent of endemic
diarrheal illness of infants and young children
worldwide.
Yes
Caliciviruses
Norwalk 27
40
Important cause of outbreaks of vomiting and
diarrheal illness in older children and adults in
families, communities, and institutions;
frequently associated with ingestion of food.
No
Sapporo 27
40
Sporadic cases and occasional outbreaks of
diarrheal illness in infants, young children, and
the elderly.
No
Astroviruses 28
30
Sporadic cases and occasional outbreaks of
diarrheal illness in infants, young children, and
the elderly.
No


1
Modified from Kapikian AZ: Viral gastroenteritis. JAMA 1993;269:627.
In infants and children, severe loss of electrolytes and fluids may be fatal unless treated.
Patients with milder cases have symptoms for 38 days and then recover completely.
However, viral excretion in the stool may persist up to 50 days after onset of diarrhea.
Asymptomatic infections, with seroconversion, occur. In children with immunodeficiencies,
rotavirus can cause severe and prolonged disease.
Adult contacts may be infected, as evidenced by seroconversion, but they rarely exhibit
symptoms, and virus is infrequently detected in their stools. A common source of infection is
contact with pediatric cases. However, epidemics of severe disease have occurred in adults,
especially in closed populations, as in a geriatric ward. Group B rotaviruses have been
implicated in large outbreaks of severe gastroenteritis in adults in China (Table 372).
Laboratory diagnosis rests on demonstration of virus in stool collected early in the illness and
on a rise in antibody titer. Virus in stool is demonstrated by IEM, latex agglutination tests, or
ELISA. Genotyping of rotavirus nucleic acid from stool specimens by the polymerase chain
reaction is the most sensitive detection method. Serologic tests can be used to detect an
antibody titer rise, particularly ELISA.
Epidemiology & Immunity
Rotaviruses are the single most important worldwide cause of gastroenteritis in young
children. Estimates range from 3 billion to 5 billion for annual diarrheal episodes in children
under 5 years of age in Africa, Asia, and Latin America, resulting in as many as 1 million
deaths. Developed countries have a high morbidity rate but a low mortality rate. Typically, up
to 50% of cases of acute gastroenteritis of hospitalized children throughout the world are
caused by rotaviruses.
Rotavirus infections usually predominate during the winter season. Symptomatic infections
are most common in children between ages 6 months and 2 years, and transmission appears
to be by the fecal-oral route. Nosocomial infections are frequent.
Rotaviruses are ubiquitous. By age 3 years, 90% of children have serum antibodies to one or
more types. This high prevalence of rotavirus antibodies is maintained in adults, suggesting
subclinical reinfections by the virus. Rotavirus reinfections are common; it has been shown
that young children can suffer up to five reinfections by 2 years of age. Asymptomatic
infections are more common with successive reinfections. Local immune factors, such as
secretory IgA or interferon, may be important in protection against rotavirus infection.
Asymptomatic infections are common in infants before age 6 months, the time during which
protective maternal antibody acquired passively by newborns should be present. Such
neonatal infection does not prevent reinfection, but it does protect against the development of
severe disease during reinfection.
Treatment & Control
Treatment of gastroenteritis is supportive, to correct the loss of water and electrolytes that
may lead to dehydration, acidosis, shock, and death. Management consists of replacement of
fluids and restoration of electrolyte balance either intravenously or orally, as feasible. The
infrequent mortality from infantile diarrhea in developed countries is due to routine use of
effective replacement therapy.
In view of the fecal-oral route of transmission, wastewater treatment and sanitation are
significant control measures.
An oral live attenuated rhesus-based rotavirus vaccine was licensed in the United States in
1998 for vaccination of infants. It was withdrawn a year later because of reports of
intussusception (bowel blockages) as an uncommon but serious side effect associated with
the vaccine. In 2006, an oral bovine-based rotavirus vaccine was licensed in the United
States. A safe and effective vaccine remains the best hope for reducing the worldwide burden
of rotavirus disease.
Salmonella adalah suatu genus bakteri enterobakteria gram-negatif berbentuk tongkat yang
menyebabkan tifoid, paratifod, dan penyakit foodborne.
[1]
Spesies-spesies Salmonella dapat bergerak
bebas dan menghasilkan hidrogen sulfida.
[2]
Salmonella dinamai dari Daniel Edward Salmon,
ahlipatologi Amerika, walaupun sebenarnya, rekannya Theobald Smith (yang terkenal akan hasilnya
pada anafilaksis) yang pertama kali menemukan bakterium tahun 1885 pada tubuh babi.
[3][4]

Daftar isi
[sembunyikan]
1 Patogenitas
2 Media tumbuh
3 Referensi
4 Pranala luar
Patogenitas[sunting]
Salmonella adalah penyebab utama dari penyakit yang disebarkan melalui makanan (foodborne
diseases).
[5]
Pada umumnya, serotipe Salmonella menyebabkan penyakit pada organ
pencernaan.
[5]
Penyakit yang disebabkan oleh Salmonella disebut salmonellosis.
[5]
Ciri-ciri orang yang
mengalami salmonellosis adalah diare, keram perut, dan demam dalam waktu 8-72 jam setelah
memakan makanan yang terkontaminasi oleh Salmonella.
[5]
Gejala lainnya adalah demam, sakit
kepala, mual dan muntah-muntah.
[5]
Tiga serotipe utama dari jenis S. enterica adalah S. typhi, S.
typhimurium, dan S. enteritidis.
[6]
S. typhi menyebabkan penyakit demam tifus (Typhoid fever),
karena invasi bakteri ke dalam pembuluh darah dan gastroenteritis, yang disebabkan oleh keracunan
makanan/intoksikasi.
[6]
Gejala demam tifus meliputi demam, mual-mual, muntah dan kematian.
[6]
S.
typhi memiliki keunikan hanya menyerang manusia, dan tidak ada inang lain.
[6]
Infeksi Salmonella
dapat berakibat fatal kepada bayi, balita, ibu hamil dan kandungannya serta orang lanjut usia. Hal ini
disebabkan karena kekebalan tubuh mereka yang menurun.
[7]
Kontaminasi Salmonella dapat dicegah
dengan mencuci tangan dan menjaga kebersihan makanan yang dikonsumsi.
[7]

Media tumbuh[sunting]
Untuk menumbuhkan Salmonella dapat digunakan berbagai macam media, salah satunya adalah
media Hektoen Enteric Agar (HEA).
[8]
Media lain yang dapat digunakan adalah SS agar, bismuth
sulfite agar, brilliant green agar, dan xylose-lisine-deoxycholate (XLD) agar.
[9]
HEA merupakan media
selektif-diferensial.
[8]
Media ini tergolong selektif karena terdiri dari bile salt yang berguna untuk
menghambat pertumbuhan bakteri gram positif dan beberapa gram negatif, sehingga
diharapkan bakteri yang tumbuh hanya Salmonella.
[8]
Media ini digolongkan menjadi
media diferensial karena dapat membedakan bakteri Salmonella dengan bakteri lainnya dengan cara
memberikan tiga jenis karbohidrat pada media, yaitu laktosa, glukosa, dan salisin, dengan komposisi
laktosa yang paling tinggi.
[8]
Salmonella tidak dapat memfermentasi laktosa, sehingga asam yang
dihasilkan hanya sedikit karena hanya berasal dari fermentasi glukosa saja.
[9]
Hal ini
menyebabkan koloni Salmonella akan berwarna hijau-kebiruan karena asam yang dihasilkannya
bereaksi dengan indikator yang ada pada media HEA, yaitu fuksin asam dan bromtimol blue.
[9]