(kat) vibrio etc.pdf
TRANSCRIPT
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KATHLEEN ROSS S. CALIGAGAN, MD, FPSNM
VIBRIOCAMPYLOBACTER
HELICOBACTER
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TERMINOLOGY
Halophilic requiring the presence of NaCl to grow
Thermophilic can live in high temp (up to 420C)
Microaerophilic require oxygen in concentration lower than room air (8.5 pH)
Anaerobic do not require oxygen
Facultative anaerobic may or may not require oxygen
Obligate intracellular pathogens that must live within the host cell (do not grow on artificial cultures, instead,
they should be inoculated into embryonated chicken
eggs, lab animals or cell cultures)
GRAM (-) RODS
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GRAM-NEGATIVE RODS
Gram-negative enteric eubacteria causing
diarrheal diseases other than Enterobacteriaciae
Vibrio (marine & surface water)
Campylobacter
Helicobacter
Aeromona (fresh water & cold-blooded animals)
Plesiomona (cold & warm blooded animal)
GRAM (-) RODS
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EXAMPLES OF DISEASES PERPETUATED BY CONTAMINATED WATER
BACTERIA VIRUSESHELMINTHS &
PROTOZOA
Escherichia coli Norovirus Dracunculi
Salmonella sp. Rotavirus Schistosoma
Shigella sp. Hepatitis A Cryptosporidium parvum
Yersinia enterolitica Adenovirus Giardia lamblia
Campylobacter sp. Astrovirus Leishmania
Vibrio sp. Calcivirus Trypanosoma sp.
Leptospira sp. Poliovirus Entamoeba histolytica
Brucella sp. Polyomavirus Taenia solium
Legionella Coronavirus Cyclospora
Pleisomonasshigelloides
Hemorrhagic fever (Flavirus Yellow, Dengue, Lassa, Ebola, Marburg)
Microsporidia
Aeromonas sp. Plasmodium sp
Ascaris sp.
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VIBRIO
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VIBRIOS
MORPHOLOGY & IDENTIFICATION
one of the most common organisms in
surface waters of the world.
they occur in both marine and freshwater
habitats and in associations with aquatic
animals (plankton and algae)
they survive in water for 3 weeks
GRAM (-) RODS
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VIBRIOS
MORPHOLOGY & IDENTIFICATION
gram-negative straight or curved or comma-shaped rods
motile by means of a single polar flagellum
non-spore former
facultatively anaerobic (may or may not require oxygen for growth)
capable of both respiratory & fermentative metabolism (ferments sucrose and mannose but not arabinose)
alkaliphilic, characteristically grow in very high pH (8.5-
9.5) & rapidly killed by acid
halophilic, requiring the presence of NaCl to grow (except for V. cholerae) (unlike aeromonas)
GRAM (-) RODS
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VIBRIOS
MORPHOLOGY & IDENTIFICATION
Catalase-positive
Oxidase-positive
which differentiates them from Enterobacteriaciae on
blood agar (a positive oxidase test is a key step in the preliminary identification of Vibrios)
Susceptible to 2,4-diamino-6,7-diisopropylteridine
phosphate (O/129)
which differentiates them from aeromonas (aeromonasare resistant to O/129)
GRAM (-) RODS
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VIBRIOS
MORPHOLOGY & IDENTIFICATION
Transport medium: Cary-Blair semi-solid agar
Enrichment medium: Alkaline peptone broth
Selective/differential culture medium: TCBS
(Thiosulfate Citrate Bile salts Sucrose) agar
GRAM (-) RODS
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VIBRIOS
MEDICALY IMPORTANT SPECIES OF VIBRIO
1. Vibrio cholera
is noninvasive, affecting the small intestine through
secretion of an enterotoxin
2. Vibrio parahemolyticus
is an invasive organism affecting primarily the colon
3. Vibrio vulnificus
is an emerging human pathogen
causes wound infections, gastroenteritis, or a syndrome
known as "primary septicemia
GRAM (-) RODS
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VIBRIOS
MEDICALLY IMPORTANT VIBRIOS
ORGANISM HUMAN DISEASE
V Cholerae serogroupsO1 & O139
Classic cholera (epidemic and pandemic)
V cholerae serogroupsnon-O1/non-O139
Cholera-like Mild diarrheaExtraintestinal infection
V parahaemolyticus GastroenteritisExtraintenstinal infection
V mimicus, V vulnificus, V hollisae, V fluvialis, V damsela, V anginolyticus, V metschnikovii
Ear woundSoft tissue & other extraintestinal infections
GRAM (-) RODS
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1. Vibrio cholerae
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causative agent of Cholera or Asiatic cholera or
Epidemic cholera
is a rapidly dehydrating diarrheal disease that can lead to death, if appropriate tx is not provided immediately.
human are the only known hosts
transmission to humans is by ingestion of
contaminated water or food (undercooked shellfish)
thru fecal-oral route or oral-oral route
natural reservoir of the organism is not known
GRAM (-) RODS
1. Vibrio cholerae
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EPIDEMIOLOGY
originated near Ganges Delta from India to
Bangladesh
responsible for seven global pandemics over the
past two centuries
the 7th pandemic is the most extensive and is caused by V. cholerae O1 El Tor.
Endemic in India & SEA, and pandemic in Africa
where sanitation is poor (very rare in industrialized countries)
has an annual global burden of >1M people
GRAM (-) RODS
1. Vibrio cholerae
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EPIDEMIOLOGY
long-term carriage does not occur
Risk factors in developing severe disease:
blood group O
decreased gastric acidity
malnutrition
immunocompromised state
absence of local intestinal immunity
GRAM (-) RODS
1. Vibrio cholerae
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VIBRIO CHOLERAEgram-negative, comma/curved/straight bacilli with a single flagellum at one pole
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GENOMIC STRUCTURE
The genome is approximately 4.0 Mb.
The genome unusual in having two circular chromosomes (rather than one) with distinct origins of replication, the oriC1 and oriC2.
Chromosome 1 (Large choromosome) CTX is an integrated filamentous bacteriophage that carries the genes for
cholera toxin.
VPI is a pathogenicity island carries genes for factors required for intestinal
colonization.
Chromosome 2 (small chromosome) Integron island is a structure that enables the sequential acquisition of
novel genes by facilitating the insertion of newly acquired DNA fragments downstream of a strong transcriptional prompter. Although this integronisland has not yet been shown to be required for virulence in V. cholerae
GRAM (-) RODS
1. Vibrio cholerae
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(B) Map of the CTX locus. The genes encoding the two subunits of cholera toxin are ctxAand ctxB. Other genes in the core region (ace and zot) are also involved in virulence. The two repeated flanking sequences RS2 and RS1 are involved in the chromosomal insertion of the bacteriophage genome
(A) The two chromosomes of Vibriocholerae
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ANTIGENIC STRUCTURE
1. H or flagellar antigen
- heat-labile, single, polar flagellum responsible for
motility
2. O or somatic lipopolysaccharide antigen on the
cell wall
- confers serologic specificity/used for specie identification
GRAM (-) RODS
1. Vibrio cholerae
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CLASSIFICATION: SEROGROUPS AND BIOTYPES
sub-classified into 200 serogroups based on the somatic O antigen
only two strains have been implicated in the cholera syndrome/epidemics (medically important somatic O antigens are):
1. O1 antigen
2. O139 antigen
O75 and O141 antigen are pathogenic and can
cause small outbreaks
GRAM (-) RODS
1. Vibrio cholerae
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ANTIGENIC
DETERMI-
NANTS
RIBOTYPE
BIOTYPE
SEROTYPE
GRAM (-) RODS
TOXIGENIC VIBRIO CHOLERAE
O1
CLASSICAL
Ogawa
A, B
Inaba
A, C
Hikojima
A, B, C
EL TOR
Ogawa
A, B
Inaba
A, C
Hikojima
A, B, C
O139
1. Vibrio cholerae
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V CHOLERAE O1 ANTIGEN
Genome is divided between a 2.4Mb large chromosome and a 1.6 Mb small chromosome.
Two biotypes: (based on biochemical test such as phenotyping)
1. CLASSIC
2. EL TOR distinguished from classic biotypes by the production
of hemolysin (which gives a positive Voges-Proskauer test)
causes milder disease than the classic biotype but is
able to survive in the body longer than classic biotype
resistant to polymyxin B
GRAM (-) RODS
1. Vibrio cholerae
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V CHOLERAE O139 ANTIGEN
genome is divided between a 2.96 Mb large chromosome
and a 1.07 Mb small chromosome
also known as Bengal, the 139th and latest serogroup of V cholerae to be identified
very similar to V cholerae O1 El Tor biotype
does not possess the characteristic lipopolysaccharide
O1 somatic antigen
makes a polysaccharide capsule like other non-O1 V
cholerae strain (V cholerae O1 does not make a capsule)
GRAM (-) RODS
1. Vibrio cholerae
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V CHOLERAE O139 ANTIGEN
This serovar is identified by:
1. absence of agglutination in O1 group specific
antiserum;
2. presence of agglutination in O139 group
specific antiserum;
3. presence of a capsule
GRAM (-) RODS
1. Vibrio cholerae
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VIRULENCE FACTORS
Toxins
o Exotoxin/Enterotoxin known as Cholera Toxin or Choleragen
o HA Protease
o RTX Toxin
o ACE and Zot
Adhesins
o Accessory Colonization Factors (ACF)o OmpU & other Omp Proteins (outer membrane proteins)o Mannose-fucose-resistant cell hemagglutinin & Mannose
sensitive hemagglutinino Toxin Co-regulated Pilus (TCP)
Integrons
GRAM (-) RODS
1. Vibrio cholerae
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GRAM (-) RODS
1. Vibrio cholerae
VIRULENCE FACTOR of V cholerae BIOLOGIC EFFECT
Cholera toxin or Choleragen Hypersecretion of electrolytes and water
Co-regulated pilus Adherence to mucosal cells
Accessory colonization Adhesin factor
Hemagglutination-protease
(mucinase)
Induces intestinal inflammation and degradation of tight
junctions
Neuraminidase Increased toxin receptors
Non-cholerae Vibrios VIRULENCE FACTORS
V. parahaeolyticus Thermostable direct hemolysin
V. vulnificus Serum resistance, antiphagocytic polysaccharides, cytolysins,
collagenase, protease, siderophores
V. alginolyticus Collagenase
V. hollisae Heat-stable and heat-labile enterotoxin, hemolysin
V. damsela cytolysin
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Cholera Enterotoxin or Choleragen(A2-5B)
main cause of the voluminous watery diarrhea that is
characteristic of cholera
an A-B type exotoxin
composed of protein, highly antigenic, heat-labile, and
highly potent
encoded by the bacteriophage, ctxAB genes
- ctxAB genes convert bacterial host from a nonpathogenic form
to a pathogenic form by providing the bacterium with virulence
genes, in a process called lysogenic phage conversion
structurally & functionally similar to ETEC LT
GRAM (-) RODS
1. Vibrio cholerae
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1. B-subunit binds to GM1 ganglioside
receptors in thesmall intestinal
epithelial cells or enterocytes
2. After binding, A subunit is released
into the cells, where it stimulates a
cascade of events: Reduction of
disulfide bond in A-subunit activates
A1 fragment that ADP-ribosylates
guanosine triphosphate (GTP)-binding
protein (Gs) by transferring ADP-ribose
from nicotinamide adenine
dinucleotide (NAD)
3. ADP-ribosylated GTP-binding protein
activates adenyl cyclase leading to an
increased cyclic AMP (cAMP) level
Increase in cAMP leads to increase
chloride secretion by the crypt cells,
which in turn leads to inhibition of
absorption of sodium and chloride by
the microvilli (hypersecretion of fluids
and electrolytes)
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PATHOGENESIS & PATHOLOGY
1. ENTRY: fecal-oral or oral-oral route
- Incubation period: 1-3 days (range: several hours to 5 days)
- Water (infectious dose = 109CFU); Food (infectious dose = 103CFU)
- can be transmitted from person-to-person
2. COLONIZATION: proximal small intestine
- Vibrios are sensitive to acid, and most die in the stomach but in order to survive in the
GI tract, they undergo changes such as:
- increased expression of genes required for nutrient acquisition
- downregulation of chemotactic response
- expression of motility
- adhere to and colonize in the alkaline environment of the proximal small bowel, where
they secrete the potent cholera enterotoxin causing massive secretion of electrolytes
and water into the intestinal lumen (diarrhea occurs as much as 20-30 L/day )
GRAM (-) RODS
1. Vibrio cholerae
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PATHOGENESIS & PATHOLOGY
3. DISEASE:
- rapid and massive loss of electrolyte rich isotonic fluid in the small intestine that
exceeds the absorptive capacity of the colon resulting to rapid and profound
dehydration and depletion of electrolytes (sodium, chloride, bicarbonate and
potassium) leading to metabolic acidosis, hypokalemia, anuria, hypovolemic shock, and
circulatory collapse
- not an invasive infection (do not reach the bloodstream)
4. EXIT: anus
GRAM (-) RODS
1. Vibrio cholerae
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CLINICAL FINDINGS
most patients are asymptomatic
some may have mild to moderate diarrhea, associated
with abdominal pain and muscle cramping for 3-7 days
rice water - characteristic stool - colorless with fishy odor, small flecks of mucus, and contains
epithelial cells & large nos of vibrios, and high concentration of
sodium, potassium, chloride and bicarbonate
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CLINICAL FINDINGS
Cholera gravis
most severe form of the disease
sudden onset of massive, profuse watery diarrhea (20-30 L/day
or 500-1000ml/hr) with or without abdominal cramps, nausea &
vomiting
characteristic rice water stool severe dehydration (lethargic appearance, sunken eyes/fontanels,
absence of tears, dry oral mucosa, poor skin turgor/skin pinch goes back very slowly, unable to drink or feed, poor capillary refill)
Washerwomans hands (shriveled hands and feet) Kussmaul breathing (rapid, deep breathing due to metabolic acidosis),
decreased urine output
thready pulse and tachycardia
hypotension and hypovolemicshock
GRAM (-) RODS
1. Vibrio cholerae
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Adult cholera gravis patient with washer womans hand sign
Severely dehydrated pediatric patient with Cholera gravis
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Rice-water stool of Vibriocholerae
Cholera cot:
- Made of folding canvas with 9 hole just above
the middle
- Bucket under the opening to collect stool
- Dip-stick calibrated to measure stool volume
directly from the pail
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COMPLICATIONS:
delayed /inadequate rehydration may lead to:
renal failure due to prolonged hypotension
hypokalemia may lead to nephropathy and focal myocardial
necrosis
hypoglycemia may lead to seizures or coma
may progress from the first liquid stool to shock in 4-12 hours,
with death following in 18 hours to several days.
in its extreme manifestation with no treatment, it is one
of the most rapidly fatal illnesses known with 50-60%
mortality rates (hypotention within an hour of the onset of symptoms and death within 2-3 hours)
GRAM (-) RODS
1. Vibrio cholerae
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HOST DEFENSES
Nonspecific: Gastric acid, mucus secretion, and
intestinal motility
Specific: involves primarily secretory IgA, as well
as IgG antibodies against vibrios, somatic antigen,
outer membrane protein, and/or the enterotoxin
and other products.
Breastfeeding in endemic areas is important in
protecting infants from disease
GRAM (-) RODS
1. Vibrio cholerae
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DIAGNOSIS
1. Microscopy: (using stool specimen)
Gram-negative, comma-shaped, curved bacilli,
2-4 um long (on prolonged isolation, may become straight rods that resemble the gram-negative enteric bacteria) not distinctive
Dark-field microscopy for rapid diagnosis, a
wet mount of liquid stool may show the
characteristic darting motility of vibrios(which is stopped by specific antisomatic antibody)
GRAM (-) RODS
1. Vibrio cholerae
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DIAGNOSIS
2. Culture: (gold standard for diagnosis)
specimen/s: stool, vomitous or rectal swabs
Selective medium TCBS (Thiosulfate citrate bile salt sucrose
agar) produces yellow colonies that are convex, smooth, round,
and opaque & granular in transmitted light
Transport medium Cary-Blair agar if cannot be processed
immediately
enrichment medium in alkaline peptone broth (up to pH 9)
blood agar with pH9 (oxidase-positive)
Definitive diagnosis not required for initiation of treatment, laboratory confirmation is necessary for epidemiologic surveillance
GRAM (-) RODS
1. Vibrio cholerae
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Yellow colonies on TCBS agar
Oxidase-positive on blood agar
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DIAGNOSIS
3. Direct antigen detection dipstick tests
extremely useful since results are available within minutes
4. Slide agglutination tests using anti-O group 1 and
139 antiserum
5. Biochemical tests
6. Serotyping/serogrouping
four-fold increase in antibody titer between acute and convalescent serum
7. PCR and DNA rpobes
GRAM (-) RODS
1. Vibrio cholerae
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DIAGNOSIS
6. Others:
fecalysis may only show few leukocytes and
erythocytes because of absence of inflammation
elevated urine specific gravity (concentrated urine)
hemoconcentration
hypoglycemia
metabolic acidosis
GRAM (-) RODS
1. Vibrio cholerae
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TREATMENT
1. Water and electrolyte replacement is the first priority in
the treatment of cholera. Rehydration is accomplished in 2
phases: rehydration and maintenance.
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 the solution of choice, preferred over isotonic
sodium chloride solution because saline does not correct metabolic acidosis. If normal
saline is used, ORS should be given simultaneously to supplement base and potassium.
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.
GRAM (-) RODS
1. Vibrio cholerae
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TREATMENT
2. Antibiotics:
reduce toxin production,shorten duration of illness, decrease fecal excretion of vibrio,
decrease volume of diarrhea, and reduce fluid requirement during rehydration
Antibiotic of choice:
Doxycycline (for adults and older children) 300 mg OD
Tetracycline 12.5 mg/kg/dose (up to 500 mg/dose) QID x 3 days
Trimethoprim-sulfamethoxazole/Cotrimoxazole (for children)
Furazolidone (for pregnant women)
Alternative:
Erythromycin (for adults and children) 12.5 mg/kg/dose (up to 250 mg/dose) QID x 3 days
GRAM (-) RODS
1. Vibrio cholerae
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TREATMENT
3. Zinc supplementation
for re-epithelialization of intestinal villi
shown to lessen stool output
antibiotics and zinc should be given as soon as vomiting stops.
any medication or condition that decreased the stomach acidity makes a person more susceptible to infection
Antimotility, antiemetics, adsorbents and analgesics are not recommended
GRAM (-) RODS
1. Vibrio cholerae
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GRAM (-) RODS
1. Vibrio cholerae
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EPIDEMIC CONTROL MEASURES
information dissemination, improvement of sanitation, adequate
supply of water, disinfection of excreta, isolation of patients,
contacts follow up
Good food hygiene
- thoroughly cooking food
- eating food while its hot
- preventing cooked foods from contacting raw foods (including water or ice)
- avoiding raw fruits or vegetables
- washing hands after defecation & before cooking
LIMITED ROLE: (not effective as an epidemic control measure)
- Chemoprophylaxis with antimicrobial drugs
- Repeated vaccination with either LPS extracted from vibrio or dense vibrio suspension
(valid only for 6 months)
GRAM (-) RODS
1. Vibrio cholerae
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2. Vibrio parahaemolyticus
3. Vibrio vulnificus
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GRAM (-) RODS
2. Vibrio parahaemolyticus
Physiology and
Structure
- Facultative anaerobe, curved gram-negative bacilli
- Fermenter
- Simple nutirtional requirements but requires salt for growth
Virulence - Hemolysin and Adhesin (does not produce enterotoxin)
Epidemiology - Organism found in estuarine and marine environments worldwide
- Associated with consumption of contaminated shell-fish
- Major pathogen in countries where raw fish is eaten
Disease - Incubation period of 12-24 hr
- Diarrhea ranging from mild disease to a cholera-like illness
- Typical presentation is an explosive, watery to bloody diarrhea with
abdominal cramps and fever
- Less commonly associated with wound infections and bacteremia
Diagnosis - Produces green colonies on TCBS agar
Treatment,
Prevention and
Control
- Self-limiting
- Rehydration and antibiotics can shorten symptoms and fluid loss
- Disease prevented by proper cooking of shellfish
- No vaccine available
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GRAM (-) RODS
3. Vibrio vulnificus
Physiology and
Structure
- Facultative anaerobe, curved gram-negative bacilli; fermenter
- Simple nutritional requirements but requires salt for growth
Virulence - Antiphagocytic capsule
- Production of hydrolytic enzymes (cytolysin, collagenase, proteases)
- Resistant to complement and antibody-mediated serum killing
Epidemiology - Free-living estuarine bacterium found in oyster during warm months
- Infection associated with exposure to contaminated salt water or
ingestion of improperly cooked shellfish
Disease - Wound infection that can progress rapidly to formation of bullae and
tissue necrosis
- Bacteremia/septicemia and gastroenteritis following ingestion of
contaminated shellfish with fever and watery to bloody diarrhea
- Life-threatening with high mortality rate (50%)
Diagnosis - produces blue-green colonies on TCBS agar; sucrose-negative
Treatment,
Prevention and
Control
- Prompt antibiotic treatment with Tetracycline or Aminoglycosides (DOC)
- Rehydration
- Aggressive wound treatment
- No vaccine available
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VIBRIO VULNIFICUS
edema; ecchymoses; and hemorrhagic, serous bullae on
the lower legsNecrotizing fascitis
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CAMPYLOBACTER
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CAMPYLOBACTER
among the most common widespread causes
of infection in the world in human, domestic
animals, and wild bird
causes both diarrheal and systemic diseases
ranging from mild to severe infection
recently, Campylobacter infections have
been identified as the most common
antecedent to an acute neurological disease,
the Guillain-Barr syndrome.
GRAM (-) RODS
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CAMPYLOBACTER
MEDICALY IMPORTANT SPECIES OF CAMPYLOBACTER
1. Campylobacter jejuni
2. Campylobacter coli
both C. jejuni and C. coli are usually associated with gastroenteritis
3. Campylobacter fetus
an opportunistic pathogen that causes extraintestinal, bacteremia, and systemic infections in immunocompromisedpatients
GRAM (-) RODS
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EPIDEMIOLOGY
endemic worldwide and hyperendemic in
developing countries
infants and young adults are most often
infected
incidence peaks in the summer
outbreaks are associated with contaminated
animal products or water
GRAM (-) RODS
CAMPYLOBACTER
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MORPHOLOGY & IDENTIFICATION
gram-negative, thin (0.2-0.4 um wide) short rods
(1.5-3.5 um long), that usually have tapered ends
and have various morphology including
comma, curved, S, or gull-wing shapes
they are motile with single flagellum
microaerophilic, thermophilic
unable to oxidize or ferment carbohydrates
oxidase- and catalase-positive
GRAM (-) RODS
CAMPYLOBACTER
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CAMPYLOBACTERgram-negative, comma-/curved-/S-/gull-wing-shaped bacilli with single flagellum
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PATHOGENESIS & PATHOLOGY
amount of organism to cause infection: 104
INCUBATION PERIOD: 1-7 days
TRANSMISSION:
oral ingestion of contaminated poultry, raw milk, water
direct contact with infected farm and pet animals
airborne transmission (common among farm workers)
person-to-person spread occurs occasionally
GRAM (-) RODS
CAMPYLOBACTER
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PATHOGENESIS & PATHOLOGY
GRAM (-) RODS
CAMPYLOBACTER
Ingestion of contaminated food by
susceptible host
Passage through the stomach into
the intestines
Colonization and cell invasion of the SI and LI
epithelial cells
Toxin production in the intestines
Massive inflammatory response and increased
cytokines
Diarrheal disease
and blood in stool
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PATHOGENESIS & PATHOLOGY
COLONIZATION, VIRULENCE and CELL INVASION of SI and LI epithelial
cells is facilitated by:
1. Polysaccharide capsule
2. Lipooligosaccharide
display molecular mimicry of neuronal ganglioside of C. jejuni, which is
linked to Guillaine-Barre and Miller-Fischer syndrome
3. Flagellin/Flagellum
acts as secretion apparatus for antigens invasion
for motility bacteria can translocate across intestinal epithelial cells via:
a) Transcellular route (eg. C. fetus)
b) Paracellular route (eg C. concisus) by breaking down tight junctions
4. T4SS (Type 4 secretion system)
secretes effector proteins (eg. C. fetus, C. rectus)
GRAM (-) RODS
CAMPYLOBACTER
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PATHOGENESIS & PATHOLOGY
5. Surface glycans
a) O-linked glycosylation
modifies the flagellin needed for flagellar assembly
b) N-linked glycosylation
modifies periplasmic and outer-membrane proteins (bacterial surface)
6. S-layer protein (Surface layer)
high molecular weight capsule-like structure found on the surface of C. fetus
and C. rectus that mediates high-level resistance to serum-mediated killing
and phagocytosis by inhibiting stable complement deposition onto bacterial
cell surface during the systemic phase of infection
responsible for bacteremia.
GRAM (-) RODS
CAMPYLOBACTER
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PATHOGENESIS & PATHOLOGY
TOXIN PRODUCTION:
1. Interleukin-8
causes recruitement of dendritic cells, macrophages and neutophils
2. Tripartite cytolethal distending toxin
mediated by CdtA and CdtC followed by CdtB
initiates cell cycle arrest and DNA damage
produce by C. fetus, C. coli, C. lari, C. upsaliensis and C. hyointestinalis
3. Hemolysin
lyse RBCs
GRAM (-) RODS
CAMPYLOBACTER
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PATHOGENESIS & PATHOLOGY
GRAM (-) RODS
CAMPYLOBACTER
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CAMPYLOBACTERGRAM (-) RODS
CAMPYLOBACTER SPECIES ASSOCIATED WITH HUMAN DISEASE
SPECIES DISEASES IN HUMANS COMMON SOURCES
C. jejuni Gastroenteritis, bacteremia, Guillain-Barre Syndrome Poultry, raw milk, cats, dogs, cattle, swine, monkeys, water
C. coli Gastroenteritis, bacteremia Poultry, raw milk, cats, dogs, cattle, swine, monkeys, water, oyster
C. fetusBacteremia, meningitis, endocarditis, mycotic aneurysm,
diarrheaSheep, cattle, birds
C. hyointestinalis Diarrhea, bacteremia, proctitis Swine, cattle, deer, hamster, raw milk, oyster
C. lari Diarrhea, colitis, appendicitis, bacteremia, UTI Seagulls, water, poultry, cattle, dogs, cats, monkeys, oyster, mussels
C. upsaliensisDiarrhea, bacteremia, abscesses, enteritis, colitis,
hemolyticuremiaCats, other domestic pets
C. concisus Diarrhea, gastritis, enteritis, periodontitis Human oral cavity
C. sputorum Diarrhea, bedsores, abscesses, periodontitis Human oral cavity, cattle, swine
C. rectus Periodontitis
C. mucosalis Enteritis swine
C. doylei Diarrhea, colitis, appendicitis, bacteremia, UTI Swine
C. curvus Gingivitis, alevolar abscessPoultry, raw milk, cats, dogs, cattle, swine, monkeys, water, human
oral cavity
C. gracilis Head and neck abscess, abdominal abscess, empyema
C. cryaerophila Diarrhea swine
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HOST DEFENSES
Nonspecific: Gastric acid, mucus secretion, and
intestinal motility
Specific: intestinal immunoglobulin (IgA) and
systemic antibodies
Persons deficient in humoral immunity develop
severe and prolonged illnesses.
GRAM (-) RODS
CAMPYLOBACTER
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CLINICAL MANIFESTATIONS
1. Acute gastroenteritis
90-95% is caused by C. jejuni and C.coli
prodrome of fever, headache, abdominal pain and myalgia, and within
a day develop loose, watery stool, may be bloody in severe cases.
mild disease lasts 1-2 days (resembles viral gastroenteritis)
Severe/persistent disease can mimic Shigella dysentery and acute
inflammatory bowel disease (IBD)
most patients recover in less than a week (20-30% remain ill for 2
weeks)
fatalities are rare
GRAM (-) RODS
CAMPYLOBACTER
-
CLINICAL MANIFESTATIONS
2. Bacteremia/Septicemia
From C. jejuni/coli:
common among malnourished children, patients with chronic illnesses
or immunodeficiency, and at extremes of ages
usually asymptomatic
if symptomatic, may cause enteric fever (headache, malaise, abdominal
pain, relapsing fever, night sweat, chills), weight loss, lethargy,
confusion, and even cough
From C. fetus:
occurs in adults with or without identifiable focal infections usually in
patients with malignancy and DM
GRAM (-) RODS
CAMPYLOBACTER
-
CLINICAL MANIFESTATIONS
3. Focal Extraintestinal Infections
commonly caused by C. fetus among neonates and
immunocompromised patients; and rarely caused by C. jejuni/coli
usually associated with vascular endothelium causing endocarditis,
pericarditis, thrombophlebitis, and mycotic aneurysms
can also cause meningitis, septic arthritis, osteomyelitis, UTI, lung
abscess and cholangitis
GRAM (-) RODS
CAMPYLOBACTER
-
CLINICAL MANIFESTATIONS
4. Perinatal infections
commonly caused by C. fetus and rarely by C. jejuni/coli
may result to abortion, stillbirth, premature delivery or neonatal
infection with bloody diarrhea, sepsis and meningitis
GRAM (-) RODS
CAMPYLOBACTER
-
COMPLICATIONS
1. Guillain-Barr syndrome (Acute Idiopathic Polyneuritis)
because of molecular mimicry between nerve tissue and Campylobacter jejuni
surface antigen
2. Miller Fischer syndrome (ophthalmoplegia, arelexia, ataxia)
3. Reiter syndrome (arthritis, urethritis, bilateral conjunctivitis)
4. Irritable bowel syndrome
5. Reactive Arthritis
seen in adolescents and adults who are positive for HLA-B27
appears 5-40 days after onset of diarrhea
involves large joints, typically migratory and resolves without sequelae
6. IgA nephropathy and immune complex glomerulonephritis
7. Hemolytic anemia
GRAM (-) RODS
CAMPYLOBACTER
-
DIAGNOSIS
1. Culture: (using stool specimen)
Selective media: Skirrows, Butzlers, Campy-BAP
Incubate at reduced oxygen (5% O2), increased carbon
dioxide (10% CO2), and 42oC (growth of other bacteria present in the feces are inhibited at 42oC temp, thus simplifying ID of C jejuni)
colonies are colorless or gray. May either be
watery and spreading or round and convex
contains vancomycin, polymixin B and
Trimethoprin (these inhibit growth of other bacteria)
GRAM (-) RODS
CAMPYLOBACTER
-
DIAGNOSIS
2. Microscopy: (using stool specimen)
gram-negative rods with thin, comma/curved,
S, or gull-wing shapes (insensitive)
dark-field microscopy may show typical
darting motility (rapid, presumptive test)
3. Antigen detection by ELISA
4. PCR and DNA probes
GRAM (-) RODS
CAMPYLOBACTER
-
DIAGNOSIS
5. Others:
fecal leukocytes in 75% of cases
fecal blood in 50% of cases
GRAM (-) RODS
CAMPYLOBACTER
-
TREATMENT
Mild gastroenteritis
self-limiting for a period of 5-8 days
managed by fluid and electrolyte replacement
Severe gastroenteritis and septicemia
Erythromycin (drug of choice)
Tetracyclines
fluoroquinolones
GRAM (-) RODS
CAMPYLOBACTER
-
CONTROL
information dissemination
public health control measures
GRAM (-) RODS
CAMPYLOBACTER
-
HELICOBACTER
-
Helicobacter pylori
found deep in the mucous layer of gastric mucosa.
most commonly affects pylorus and antrum along
lesser curvature
overlies gastric type epithelial cells but not
intestinal epithelial cells
classified as type I carcinogen by WHO
GRAM (-) RODS
-
Helicobacter pylori
associated with:
antral gastritis and a/hypochlorhydria
duodenal/peptic ulcer disease (90%)
gastric ulcers (50-80%)
gastric adenocarcinoma
gastric mucosa-associated lymphoid tissue (MALT) B-
cell lymphomas
GRAM (-) RODS
-
Helicobacter pylori
worldwide distribution; about 1/3 of the world's
population is infected
prevalence of infection increases with age
reservoir is humans but the exact modes of
transmission are not known
person-to-person transmission is common
H pylori has now been isolated from feces and
dental plaque
acute epidemics of gastritis suggest a common
source of H pylori
GRAM (-) RODS
-
MORPHOLOGY & IDENTIFICATION
gram-negative, spiral-shaped bacilli
motile with multiple flagella at one pole
grows in 3-6 days at 370c in a micro-
aerophilic environment
has very high urease production
oxidase and catalase positive
grows optimally at pH 6-7
Helicobacter pyloriGRAM (-) RODS
-
HELICOBACTER PYLORIgram-negative, spiral-shaped bacilli with multiple flagella at one pole
-
Electron photomicrograph of
Helicobacter pylori
Electron photomicrograph of H. pylori adherence to gastric
mucosa epithelium
-
PATHOGENESIS & PATHOLOGY
under normal condition, gastric mucus is relatively impermeable
to acid and has a strong buffering capacity. pH is low (1-2) on the
mucus side of the lumen while pH is physiologic (7.4) on the
epithelial side of the lumen.
H pylori produces a protease that modifies the gastric mucus and
further increases the ability of acid to diffuse through the mucus
H pylori produces potent urease activity, which yields production
of ammonia and further buffering of acids causing direct damage
to the epithelial cells
Toxins and LPS may damage the cells also
Helicobacter pyloriGRAM (-) RODS
-
Helicobacter pyloriGRAM (-) RODS
-
CLINICAL FINDINGS
Clinical manifestations
fever
crampy abdominal pain
nausea
vomiting of acid-free gastric juice (hypo/achlorhydria)
putrid breath
acute symptoms may last for 1-2 weeks. But
once colonized, may persists for years or
even a lifetime
Helicobacter pyloriGRAM (-) RODS
-
DIAGNOSIS
1. Gastric biopsy (gastroscopy) for
histologic examination
confirmatory test for H. Pylori infection
(most sensitive & specific)
Helicobacter pyloriGRAM (-) RODS
-
H. pyloripositive patient (left) and an H. pylorinegative patient (right):-H pylori positivity is associated with risk of gastric cancer, whereas H. pylori negativity is associated with risk of esophageal adenocarcinoma or EAC.-The presence of H. pylori (left) is indicated by the dark curved bacilli in the mucus layer adjacent to the epithelial cell surfaces. - The H. pylori (+) biopsy shows deeper staining of the epithelial cells, indicating tissue reactivity, and the lamina propria shows increased mononuclear cell numbers (compared with the H. pylori (-)biopsy)
-
DIAGNOSIS
2. Culture: (using stool specimen)
Skirrows & Chocolate agar (Colonies are translucent 1-2 mm)
incubation in microaerophilic conditions
growth is slow
relatively insensitive unless multiple biopsies are
cultured
Helicobacter pyloriGRAM (-) RODS
-
DIAGNOSIS
3. Microscopy: (specimen from gastric biopsy)
spiral-shaped, gram-negative rods with multiple
flagella in one pole
Giemsa or special silver stains
Dark-field microscopy may show motility
Helicobacter pyloriGRAM (-) RODS
-
CULTURE. Heavy growth of H. pylori from an antral biopsy specimen from a patient with duodenal ulcer. (larger white colonies are commensal flora of the mouth)
GRAM STAIN. spiral-shaped, gram-negative rods with multiple flagella in one pole
-
DIAGNOSIS
4. Serology:
Blood for serum antibody determination
H. pylori antigen test (sensitive and specific; performed with stool specimens)
useful for demonstrating exposure to H. Pylori
Helicobacter pyloriGRAM (-) RODS
-
DIAGNOSIS
5. Urea breath test
relatively sensitive and highly specific
non-radioactive 13C or radioactive 14C-labeled urea
capsule is ingested by patient.
Principle: H. pylori produces an enzyme urease which converts urea to ammonia and carbon dioxide. When H. pylori is present in the stomach, the enzyme urease, produced by Helicobacter pylori, will convert 13C or 14C-labeled urea in the test drink into ammonia and carbon dioxide. The generated labeled CO2 from patients exhaled breath is measured using a heliprobe machine
Helicobacter pyloriGRAM (-) RODS
-
Drink. 13C or 14C-labeled urea capsule
Exhale.labeled CO2 into a chamber
Measure.exhaled labeled CO2 from chamber using a heliprobemachine
Interpret.51: positive
-
TREATMENT
1. Triple antimicrobial therapy for 14 days (eradicates infection in 70-95% of patients)
Bismuth subsalicylate or bismuth subcitrate
Metronidazole
Amoxicillin or Tetracycline or Clarythromycin
2. Proton-pump inhibitors (directly inhibit H pylori, potent ureaseinhibitors, & enhances ulcer healing)
Omeprazole
option 1
metronidazole
bismuth (Pepto-bismol)
Helicobacter pyloriGRAM (-) RODS
-
TREATMENToption 1 (BMT or BMA)
Bismuth (Pepto-bismol)
Metronidazole
either Tetracycline or Amoxicillin
option 2
Metronidazole
Clarithromycin
Omeprazole
80-95% PPI+ clarythro+amox
90-99% PPI+bismuth+metro+tetra or amox
Helicobacter pyloriGRAM (-) RODS
-
OTHERS
-
Aeromonas sps.
gram-negative, facultative anaerobic rod
oxidase-positive
ubiquitous and free-living in fresh and
brackish water
TRANSMISSION:
oral ingestion of contaminated water & food
direct contact with contaminated water & food (medicinal leech therapy)
GRAM (-) RODS
-
14 species but the 3 most important species
of primary clinical importance are:
Aeromonas hydrophila
Aeromonas caviae
Aeromonas veronii biovar sobria
GRAM (-) RODS
Aeromonas sps.
-
CULTURE of Aeromonas hydrophilaon horse blood agar
CULTURE of Aeromonas hydrophilaon TCBS agar
-
ELECTRON PHOTOMICROGRAPH. Aeromonas hydrophila
GRAM STAIN. Aeromonas hydrophila
-
Clinical diseases:
1. Gastroenteritis
- most common clinical manifestation
2. Wound infections (with or without bacteremia)
3. Primary and secondary septicemia (in immunocompromised
persons)
4. Peritonitis, meningitis, and infections of the eye, joints, and
bones (less well described illnesses)
GRAM (-) RODS
Aeromonas sps.
-
Treatment (Antimicrobial therapy is necessary in patients with chronic diarrheal disease or systemic infection)
Ciprofloxacin
Gentamicin
Amikacin
Trimethoprim-sulfamethoxazole
GRAM (-) RODS
Aeromonas sps.
-
Plesiomonas shigelloides
gram-negative rod
motile with multiple polar flagellum
non-lactose fermenter
oxidase-positive (some Plesiomonas strains share antigens with Shigella sonnei, and cross-reactions with Shigella antisera occur thus the name shigelloides. Plesiomonas can be distinguished from Shigella in diarrheal stools by an oxidase test. Shigella sps. are oxidase-negative)
DNase-positive (aeromonas Dnase-negative)
GRAM (-) RODS
-
ELECTRON PHOTOMICROGRAPH. Plesiomonas sp.
GRAM STAIN. Plesiomonas sp.
-
Plesiomonas shigelloides
primarily a freshwater aquatic organism
generally found in fresh or estuarine (brackish)
waters rather than marine environments
most common in tropical and subtropical areas
acquired from contaminated freshwater fish and
animals resulting to diarrhea
GRAM (-) RODS
-
Plesiomonas shigelloides
Acquired by ingestion of or exposure to
contaminated water or seafood or by exposure to
amphibians or reptiles
Self-limited gastroenteritis: secretory colitis or
chronic forms
Variety of uncommon extra-intestinal infections
GRAM (-) RODS
-
RICKETSSIAE
-
RICKETTSIACEAE
GENERA
Rickettsia
Orientia
Coxiella
Ehrlichia
UNIQUE BACTERIA
-
RICKETTSIACEAE
MORPHOLOGY & IDENTIFICATION
small (0.3-0.5 x 0.8-2.0 um), gram-negative, pleomorphic,
coccobacilli (lack flagella, non-motile)
obligate intracellular (Energy Parasites) except for Coxiella
divide by binary fission
reside within the cytoplasm or within the nucleus of the
cell that they invade
they metabolize host-derived glutamate via aerobic
respiration and the citric acid (TCA) cycle
UNIQUE BACTERIA
-
RICKETTSIACEAE
MORPHOLOGY & IDENTIFICATION
reservoir are animals and arthropds (humans are accidentally infected with these organisms)
all are transmitted by arthropod vectors(e.g., ticks, mites, lice or fleas) except Coxiella
typically manifested by fever, rashes and vasculitis
except for Coxiella
UNIQUE BACTERIA
-
PATHOGENESIS
MOT: inoculated into the dermis of the skin by a tick bite
or through damaged skin from the feces of lice or fleas
TARGET CELLS: spread through the bloodstream and infect
the endothelial cells lining of small blood vessels of all
major tissues and organs. - Destruction of endothelial cells results in leakage of blood and subsequent organ
and tissue damage due to loss of blood into the tissue spaces
VIRULENCE FACTORS
Adhesins: OmpA (outer membrane protein A)
UNIQUE BACTERIA
RICKETTSIACEAE
-
1. Adhere to endothelial cells lining the small blood vessels by parasite-induced phagocytosis2. Once in the host cell, the bacteria lyse the phagosome membrane with a phospholipase and escape into the host cell
cytoplasm where they replicate. 3. The mode of exit from the host cell varies depending upon the species
- R. prowazekii exits by cell lysis- R. rickettsii get extruded from the cell through local projections (filopodia). F actin in the host cell associates with R. rickettsii
and the actin helps to "push" the bacteria through the filopdia- O. tsutsugamushi exits by budding through the cell membrane and remains enveloped in the host cell membrane as it infects
other cells.
-
HOST DEFENSES
Humoral immunity
- antibody-opsonized Rickettsia are phagocytosed and killed by
macrophages
C-cell mediated immunity
Delayed type hypersensitivity develops following
rickettsial infections.
UNIQUE BACTERIA
RICKETTSIACEAE
-
THREE MAJOR GROUPS: (based on clinical characteristics of disease)
UNIQUE BACTERIA
SPOTTED FEVER GROUP TYPHUS GROUP Ehrlichiae
-Rickettsia rickettsii
-Rickettsia akari
-Coxiella burnetii
-Rickettsia prowazekii
-Rickettsia typhi
-Orientia (Rickettsia)
tsutsugamushi
- Ehrlichia chaffeensis
-Ehrlichia phagocytophilia
-Ehrlichia ewingii
-R. aeschlimannii
-R. africae
-R. australis
-R. conorii
-R. felis
-R. honei
-R. helvitica
-R. japonica
-R. japonica
-R. massilae
-R.
mongolotimonae
-R. montanensis
-R. parkeri
-R. peacockii
-R. rhipicephali
-R. sibirica
-R. slovaca
-R. felis
- R. bellii
-R. canadensis
RICKETTSIACEAE
-
RICKETTSIAL DISEASES:
UNIQUE BACTERIA
Disease Organism Vector Reservoir
SPOTTED FEVER GROUP
Rocky Mountain spotted fever R. rickettsii Tick Ticks, wild rodents
Rickettsialpox R. akari Mite Mites, wild rodents
Q fever C. burnetii Inhalation of contaminated dust
TYPHUS GROUP
Epidemic/Louse-borne typhus R. prowazekii LouseHumans, squirrel fleas,
flying squirrels
Endemic/Murine typhus R. typhi Flea Wild rodents
Scrub typhus R. tsutsugamushi Mite Mites, wild rodents
ERLICHIAE
Human monocyte ehrlichiosis E. chaffeensis Tick Deer
Human granulocyte ehrlichiosis E. phagocytophila Tick Mouse, other mammals
E. ewingii Tick Dog
RICKETTSIACEAE
-
(1) ROCKY MOUNTAIN SPOTTED FEVER
caused by Rickettsia rickettsii
most severe and most frequently reported rickettsial disease in
the United States
first recognized in 1896 in the Snake River Valley of Idaho and was originally
called "black measles" because of the characteristic rash
3-5% mortality (death may occur during the end of the second week due to kidney or heart failure)
PRIMARY RESERVOIR: wild rodents
VECTOR: hard ticks (Ixodes sp.); dog ticks (Dermacentor sp.)
INCUBATION PERIOD: 7 days (range 2-14 days)
UNIQUE BACTERIARICKETTSIAL DISEASES
-
(1) ROCKY MOUNTAIN SPOTTED FEVER
VECTORS
UNIQUE BACTERIA
WOOD TICK
(Dermacentorandersoni)
DOG TICK
(Dermacentorvariabilis)
BROWN DOG TICK
(Rhipicephalussanguineus)
FEMALE LONE STAR TICK
(Amblyommaamericanum)
RICKETTSIAL DISEASES
-
(1) ROCKY MOUNTAIN SPOTTED FEVER
CLINICAL MANIFESTATIONS:
the classic triad of findings: fever, rash, and history of
tick bite (rash fails to develop in 20% of cases)
severe headache, muscle pain, nausea, vomiting,
abdominal pain, and cough
thrombocytopenia, anemia and hyponatremia
WBC is typically normal
lasts as long as 3 weeks
COMPLICATIONS:
CNS, cardiac, pulmonary, GI and renal involvement
DIC > shock > death
UNIQUE BACTERIARICKETTSIAL DISEASES
-
(1) ROCKY MOUNTAIN SPOTTED FEVER
UNIQUE BACTERIARICKETTSIAL DISEASES
appear first on the extremities
Macule-
painless, small (1-5 mm), flat non-itchy, faint pink
in color
moves centripetally 2-5 days after onset
of illness
Maculopapular-characteristic
red, spotted rash on the 6th day
Petechia and Purpura-
hemorrhage in the center of the
lesion
2nd -5th day 6th day
-
(2) RICKETTSIALPOX
caused by Rickettsia akari
RESERVOIR: house mite (Mus musculus) & wild rodents
VECTOR: mouse mite (Liponsyssoides sanguineus)
INCUBATION PERIOD: 9-14 days
non-communicable
rarely associated with complications
rare fatalities
UNIQUE BACTERIARICKETTSIAL DISEASES
-
(2) RICKETTSIALPOX
UNIQUE BACTERIARICKETTSIAL DISEASES
Papuledevelopes at
the site of the bite
Papule ulcerates and forms a black Eschar (punched-out
ulcer covered with blackened scab).
Regional LN in the area becomes enlarged
sudden onset of fever, chills, headache,
vomiting, myalgia, anorexia, and photophobia
generalized papulovesicular
rash
distributed centripetally
rash will crust and heal without scarring
First phase:
1 week after the bite
Second phase:
2-3 days later 2-3 weeks later
-
(2) RICKETTSIALPOX
UNIQUE BACTERIA
HOUSE MOUSE
(Mus musculus)
MOUSE MITE
(Liponyssoides sanguineus)
VECTORRESERVOIR
RICKETTSIAL DISEASES
-
(3) EPIDEMIC/LOUSE-BORNE TYPHUS
caused by Rickettsia prowazekii
occurs among people living in crowded, unsanitary
conditions such as those found in wars, famine and
natural disasters
RESERVOIR: humans (primary), squirrel, fleas
VECTOR: human body louse (Pediculus humanus corporis)
INCUBATION PERIOD: 8 days
UNIQUE BACTERIARICKETTSIAL DISEASES
-
(3) EPIDEMIC/LOUSE-BORNE TYPHUS
UNIQUE BACTERIA
FEMALE BODY LOUSE
(Pediculus humanus corporis)
VECTOR
RICKETTSIAL DISEASES
-
(3) EPIDEMIC/LOUSE-BORNE TYPHUS
CLINICAL SYNDROMES
a. Epidemic typhus
- is characterized by sudden onset of fever, chills, headache, myalgia and
arthralgia.
- after 4-7 days, maculopapular rash appears, becomes petechial or
hemorrhagic, then develops brownish pigmented areas. Rashes spread
centrifugally from the trunk first then spreads to the extremities (unlike the
Spotted fever group)
b. Brill-Zinsser disease
- is recrudescent epidemic typhus. It occurs decades after the initial infection.- clinical course of the disease is similar to epidemic typhus but is milder and
recovery is faster. The skin rash is rarely seen.- diagnosis is made on the basis of a fever with unknown origin and a history
of previous exposure to epidemic typhus.
UNIQUE BACTERIARICKETTSIAL DISEASES
-
(4) ENDEMIC/MURINE/FLEA-BORNE TYPHUS
caused by Rickettsia typhi
occurs worldwide
RESERVOIR: Norway rat (Rattus norvegicus;); & cat flea
VECTOR: rat flea (Xenopsylla cheopsis)
INCUBATION PERIOD: 1-2 weeks
CLINICAL SYNDROMES- fever, chills headache and myalgia.
- macular or maculopapular rash appears on 4-7 days after onset of illness
which begins on the trunk and spreads to the extremities (centrifugal
spread), and lasts for 4-8 days. Rash remains discrete, with sparse lesions
and no hemorrhage
- disease is mild and resolves within 3 weeks even if untreated.
UNIQUE BACTERIARICKETTSIAL DISEASES
-
(4) ENDEMIC/MURINE/FLEA-BORNE TYPHUs
UNIQUE BACTERIA
NORWAY RAT
(Rattus norvegicus)
RAT FLEA
(Xenopsylla cheopsis)
VECTORRESERVOIR
RICKETTSIAL DISEASES
-
(5) SCRUB TYPHUS
caused by Orientia (Rickettsia) tsutsugamushi
occurs in Asia, Australia and the Pacific Islands
RESERVOIR: mites and wild rodents
VECTOR: chiggers, the larval form of a mite
INCUBATION PERIOD: 1-3 weeks
CLINICAL SYNDROMES- characterized by sudden onset of fever, chills headache and myalgia.
- maculopapular rash develops 2 - 3 days later. The rash appears first on the
trunk and spreads to the extremities (centrifugal spread).
- also characterized by an eschar (50% of cases) at the inoculation bite.
UNIQUE BACTERIARICKETTSIAL DISEASES
-
(6) Q FEVER
caused by Coxiella burnetti
resembles influenza, pneumonia, hepatitis or
encephalopathy rather than typhus
not characterized by rash and not transmitted by vector
TRANSMISSION: inhalation of contaminated dust
found in ticks, which transmit the bacteria to sheep, goats
and cattle
may develop infective endocarditis
UNIQUE BACTERIARICKETTSIAL DISEASES
-
(7) HUMAN EHRLICHIOSIS
DISEASES:
a. Human Monocytotropic Ehrlichiosis (HME)
- caused by Ehrlichia chaffeensis (in US) and Ehrlichia
sennetsu (in Japan and Malaysia)
b. Human Granulocytotropic Ehrlichiosis (HGE)
- caused by Ehrlichia (Anaplasma) phagocytophilia and
Ehrlichia ewingii
UNIQUE BACTERIARICKETTSIAL DISEASES
-
(7) HUMAN EHRLICHIOSIS
CLINICAL MANIFESTATION
acute, systemic, febrile illnesses associated with headache, chills, malaise, myalgia, arthralgia, nausea, vomiting, anorexia and weight loss
clinically similar to RMSF but differ in that infections often demonstrate the following:
- leukopenia, absolute lymphopenia and neutropenia (HME)- neutropenia (HGE)- anemia- hepatitis- lack of vasculitis- rash less commonly
UNIQUE BACTERIARICKETTSIAL DISEASES
-
(7) HUMAN EHRLICHIOSIS
COMPLICATIONS:
- pulmonary, liver and kidney failure, bone marrow hypoplasia, encephalopathy, meningitis, DIC, spontaneous hemorrhage
- anemia, hyponatremia, thrombocytopenia, transaminasemia
VECTOR: tick vectors
RESERVOIR: deer, mouse, dogs and other mammals
INCUBATION PERIOD: 5-10 days after the tick bite and last
for 1-2 weeks
UNIQUE BACTERIARICKETTSIAL DISEASES
-
DIAGNOSIS
- Clinical diagnosis:
- Laboratory diagnosis:
- culture of blood or CSF
- direct detection after skin punch tissue biopsy: Giemsa stain
Direct/indirect fluorescent antibody test (4-fold or greater change in antibody titer between acute and convalescent serum)
- PCR
- Weil-Felix test (agglutinate OX strains of Proteus vulgaris; no longer recommended)
UNIQUE BACTERIA
RICKETTSIACEAE
-
IFA reaction of a positive human serum on Rickettsia rickettsii grown in chicken yolk sacs
Giemza stain of tick hemolymph cells infected with R. rickettsii
-
TREATMENT
- antibiotic treatment should be initiated immediately
- Doxycycline- Drug of choice
- 100 mg every 12 hours for adults or 4 mg/kg body weight per day in two divided doses for
children under 45 kg for a minimum total course of 5 to 10 days
- Tetracyclines- contraindicated in pregnant women because of risks associated with malformation of teeth
and bones in unborn children
- Chloramphenicol- is an alternative drug
UNIQUE BACTERIA
RICKETTSIACEAE
-
PREVENTION
prevention of tick bites
- protective clothing, insect repellents, etc.
tick control
no vaccine is available
UNIQUE BACTERIA
RICKETTSIACEAE
-
THANK YOU
INTRODUCTION TO IMMUNOLOGY