VIBRIO

CAMPYLOBACTER
HELICOBACTER

KATHLEEN ROSS S. CALIGAGAN, MD, FPSNM

GRAM (-) RODS

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 (<20-21% O2)
Alkaliphilic can live in a high pH environment (>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

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)

EXAMPLES OF DISEASES PERPETUATED BY

CONTAMINATED WATER
BACTERIA

VIRUSES

HELMINTHS &
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

Pleisomonas
shigelloides

Hemorrhagic fever (Flavirus Yellow,

Dengue, Lassa, Ebola, Marburg)

Microsporidia

Aeromonas sp.

Plasmodium sp
Ascaris sp.

VIBRIO

GRAM (-) RODS

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

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

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 (aeromonas
are resistant to O/129)

GRAM (-) RODS

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

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

VIBRIOS
MEDICALLY IMPORTANT VIBRIOS

ORGANISM

HUMAN DISEASE

V Cholerae serogroups
O1 & O139

Classic cholera (epidemic and

pandemic)

V cholerae serogroups
non-O1/non-O139

Cholera-like
Mild diarrhea
Extraintestinal infection
Gastroenteritis
Extraintenstinal infection

V parahaemolyticus
V mimicus, V vulnificus,
V hollisae, V fluvialis,
V damsela, V anginolyticus,
V metschnikovii

Ear wound
Soft tissue & other
extraintestinal infections

1. Vibrio cholerae

GRAM (-) RODS

1.

Vibrio cholerae

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

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

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

VIBRIO CHOLERAE
gram-negative, comma/curved/straight bacilli
with a single flagellum at one pole

GRAM (-) RODS

1.

Vibrio cholerae

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 integron
island has not yet been shown to be required for virulence in V. cholerae

(A) The two

chromosomes of Vibrio
cholerae

(B) Map of the CTX locus. The genes encoding the two subunits of cholera toxin are ctxA
and 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

GRAM (-) RODS

1.

Vibrio cholerae

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

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

TOXIGENIC VIBRIO CHOLERAE

SEROTYPE

O1

BIOTYPE

O139

CLASSICAL

EL TOR

RIBOTYPE

Ogawa

ANTIGENIC
DETERMINANTS

A, B

Inaba

A, C

Hikojima

A, B, C

Ogawa

A, B

Inaba

A, C

Hikojima

A, B, C

GRAM (-) RODS

1.

Vibrio cholerae

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

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

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

VIRULENCE FACTORS
Toxins

Exotoxin/Enterotoxin known as Cholera Toxin or Choleragen

HA Protease
RTX Toxin
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 hemagglutinin
o Toxin Co-regulated Pilus (TCP)
Integrons
o
o
o
o

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

GRAM (-) RODS

1.

Vibrio cholerae

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

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)

GRAM (-) RODS

1.

Vibrio cholerae

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

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

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
<5% may develop Cholera gravis

fever is uncommon (non-invasive)

GRAM (-) RODS

1.

Vibrio cholerae

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

Adult cholera gravis

patient with washer
womans hand sign

Severely
dehydrated
pediatric patient
with Cholera gravis

Rice-water
stool of Vibrio
cholerae

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

GRAM (-) RODS

1.

Vibrio cholerae

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

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

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

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

Yellow colonies
on TCBS agar

Oxidase-positive
on blood agar

GRAM (-) RODS

1.

Vibrio cholerae

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

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

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

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

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

GRAM (-) RODS

1.

Vibrio cholerae

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)

2. Vibrio parahaemolyticus

3. Vibrio vulnificus

GRAM (-) RODS

2.

Vibrio parahaemolyticus

Physiology and - Facultative anaerobe, curved gram-negative bacilli

Structure
- 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

GRAM (-) RODS

3.

Vibrio vulnificus

Physiology and - Facultative anaerobe, curved gram-negative bacilli; fermenter

Structure
- 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

edema; ecchymoses; and

hemorrhagic, serous bullae on
the lower legs

VIBRIO VULNIFICUS

Necrotizing fascitis

CAMPYLOBACTER

GRAM (-) RODS

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

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 immunocompromised

patients

GRAM (-) RODS

CAMPYLOBACTER

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

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

CAMPYLOBACTER
gram-negative, comma-/curved-/S-/gull-wingshaped bacilli with single flagellum

GRAM (-) RODS

CAMPYLOBACTER

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

PATHOGENESIS & PATHOLOGY

Ingestion of
contaminated food by
susceptible host

Toxin production
in the intestines

Massive inflammatory
response and increased
cytokines

Passage through
the stomach into
the intestines

Colonization and cell

invasion of the SI and LI
epithelial cells

Diarrheal disease
and blood in stool

GRAM (-) RODS

CAMPYLOBACTER

PATHOGENESIS & PATHOLOGY

COLONIZATION, VIRULENCE and CELL INVASION of SI and LI epithelial

cells is facilitated by:

1.
2.

3.

4.

Polysaccharide capsule
Lipooligosaccharide
display molecular mimicry of neuronal ganglioside of C. jejuni, which is
linked to Guillaine-Barre and Miller-Fischer syndrome
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
T4SS (Type 4 secretion system)
secretes effector proteins (eg. C. fetus, C. rectus)

GRAM (-) RODS

CAMPYLOBACTER

PATHOGENESIS & PATHOLOGY

5.

6.

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)
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

PATHOGENESIS & PATHOLOGY

TOXIN PRODUCTION:
1.

2.

3.

Interleukin-8
causes recruitement of dendritic cells, macrophages and neutophils
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
Hemolysin
lyse RBCs

GRAM (-) RODS

PATHOGENESIS & PATHOLOGY

CAMPYLOBACTER

GRAM (-) RODS

CAMPYLOBACTER

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. fetus

Bacteremia, meningitis, endocarditis, mycotic aneurysm,

diarrhea

Sheep, 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. upsaliensis

Diarrhea, bacteremia, abscesses, enteritis, colitis,

hemolyticuremia

Cats, 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 abscess

Poultry, raw milk, cats, dogs, cattle, swine, monkeys, water, human
oral cavity

C. gracilis

Head and neck abscess, abdominal abscess, empyema

C. cryaerophila

Diarrhea

swine

GRAM (-) RODS

CAMPYLOBACTER

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

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
Miller Fischer syndrome (ophthalmoplegia, arelexia, ataxia)

2.
3.
4.
5.

Reiter syndrome (arthritis, urethritis, bilateral conjunctivitis)

Irritable bowel syndrome
Reactive Arthritis

6.
7.

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

IgA nephropathy and immune complex glomerulonephritis

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

HELICOBACTER

GRAM (-) RODS

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

Helicobacter pylori

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 PYLORI
gram-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

GRAM (-) RODS

Helicobacter pylori

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

GRAM (-) RODS

Helicobacter pylori

GRAM (-) RODS

Helicobacter pylori

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

GRAM (-) RODS

Helicobacter pylori

DIAGNOSIS
1.

Gastric biopsy (gastroscopy) for

histologic examination
confirmatory test for H. Pylori infection

(most sensitive & specific)

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)

GRAM (-) RODS

Helicobacter pylori

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

GRAM (-) RODS

Helicobacter pylori

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

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, gramnegative rods with multiple flagella in

one pole

GRAM (-) RODS

Helicobacter pylori

DIAGNOSIS

Serology:

4.

Blood for serum antibody determination

H. pylori antigen test (sensitive and specific;

performed with stool specimens)

useful for demonstrating exposure to H. Pylori

GRAM (-) RODS

Helicobacter pylori

DIAGNOSIS

Urea breath test

5.

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

Drink.
13C or 14Clabeled urea
capsule

Exhale.
labeled CO2 into
a chamber

Measure.
exhaled labeled
CO2 from
chamber using a
heliprobe
machine

Interpret.
<25: negative
26-50: borderline
>51: positive

GRAM (-) RODS

Helicobacter pylori

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 urease

inhibitors, & enhances ulcer healing)
Omeprazole
option 1
metronidazole

GRAM (-) RODS

Helicobacter pylori

TREATMENT
option 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

OTHERS

GRAM (-) RODS

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

Aeromonas sps.

14 species but the 3 most important species

of primary clinical importance are:

Aeromonas hydrophila
Aeromonas caviae
Aeromonas veronii biovar sobria

CULTURE of Aeromonas hydrophila

on horse blood agar

CULTURE of Aeromonas hydrophila

on TCBS agar

ELECTRON PHOTOMICROGRAPH.
Aeromonas hydrophila

GRAM STAIN.
Aeromonas hydrophila

GRAM (-) RODS

Aeromonas sps.

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

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)

ELECTRON PHOTOMICROGRAPH.
Plesiomonas sp.

GRAM STAIN.
Plesiomonas sp.

GRAM (-) RODS

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

RICKETSSIAE

UNIQUE BACTERIA

GENERA
Rickettsia

Orientia
Coxiella
Ehrlichia

RICKETTSIACEAE

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

RICKETTSIACEAE

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)

1.
2.
3.

Adhere to endothelial cells lining the small blood vessels by parasite-induced phagocytosis
Once in the host cell, the bacteria lyse the phagosome membrane with a phospholipase and escape into the host cell
cytoplasm where they replicate.
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.

UNIQUE BACTERIA

RICKETTSIACEAE

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)

SPOTTED FEVER GROUP
-Rickettsia rickettsii
-Rickettsia akari
-Coxiella burnetii

TYPHUS GROUP
-Rickettsia prowazekii
-Rickettsia typhi
-Orientia (Rickettsia)

tsutsugamushi
-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

Ehrlichiae
- Ehrlichia chaffeensis
-Ehrlichia phagocytophilia
-Ehrlichia ewingii

UNIQUE BACTERIA

RICKETTSIACEAE

RICKETTSIAL DISEASES:
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

Epidemic/Louse-borne typhus

R. prowazekii

Louse

Humans, squirrel fleas,

flying squirrels

Endemic/Murine typhus

R. typhi

Flea

Wild rodents

Scrub typhus

R. tsutsugamushi

Mite

Mites, wild rodents

Human monocyte ehrlichiosis

E. chaffeensis

Tick

Deer

Human granulocyte ehrlichiosis

E. phagocytophila

Tick

Mouse, other mammals

E. ewingii

Tick

Dog

TYPHUS GROUP

ERLICHIAE

UNIQUE BACTERIA

(1)

RICKETTSIAL DISEASES

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 BACTERIA

(1)

RICKETTSIAL DISEASES

ROCKY MOUNTAIN SPOTTED FEVER

VECTORS

WOOD TICK
(Dermacentor
andersoni)

DOG TICK
(Dermacentor
variabilis)

BROWN DOG
TICK
(Rhipicephalus
sanguineus)

FEMALE LONE
STAR TICK
(Amblyomma
americanum)

UNIQUE BACTERIA

(1)

RICKETTSIAL DISEASES

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 BACTERIA

(1)

RICKETTSIAL DISEASES

ROCKY MOUNTAIN SPOTTED FEVER

2nd -5th day

appear first on
the extremities

Maculepainless, small (15 mm), flat nonitchy, faint pink

in color

6th day

moves
centripetally 2-5
days after onset
of illness

Maculopapularcharacteristic
red, spotted rash
on the 6th day

Petechia and
Purpurahemorrhage in
the center of the
lesion

UNIQUE BACTERIA

(2)

RICKETTSIAL DISEASES

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 BACTERIA

(2)

RICKETTSIAL DISEASES

RICKETTSIALPOX
First phase:
1 week after the bite

Papule
developes 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

Second phase:
2-3 days later
sudden onset of fever,
chills, headache,
vomiting, myalgia,
anorexia, and
photophobia

2-3 weeks later

generalized
papulovesicular
rash
distributed
centripetally

rash will crust

and heal
without
scarring

UNIQUE BACTERIA

(2)

RICKETTSIAL DISEASES

RICKETTSIALPOX
RESERVOIR

HOUSE MOUSE
(Mus musculus)

VECTOR

MOUSE MITE
(Liponyssoides sanguineus)

UNIQUE BACTERIA

(3)

RICKETTSIAL DISEASES

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 BACTERIA

RICKETTSIAL DISEASES

(3) EPIDEMIC/LOUSE-BORNE TYPHUS

VECTOR

FEMALE BODY LOUSE

(Pediculus humanus corporis)

UNIQUE BACTERIA

(3)

RICKETTSIAL DISEASES

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 BACTERIA

RICKETTSIAL 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 BACTERIA

RICKETTSIAL DISEASES

(4) ENDEMIC/MURINE/FLEA-BORNE TYPHUs

RESERVOIR

NORWAY RAT
(Rattus norvegicus)

VECTOR

RAT FLEA
(Xenopsylla cheopsis)

UNIQUE BACTERIA

(5)

RICKETTSIAL DISEASES

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 BACTERIA

(6)

RICKETTSIAL DISEASES

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 BACTERIA

(7)

RICKETTSIAL DISEASES

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 BACTERIA

(7)

RICKETTSIAL DISEASES

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 BACTERIA

(7)

RICKETTSIAL DISEASES

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 BACTERIA

RICKETTSIACEAE

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)

Giemza stain of tick

hemolymph cells
infected with R.
rickettsii

IFA reaction of a positive

human serum on
Rickettsia rickettsii grown
in chicken yolk sacs

UNIQUE BACTERIA

RICKETTSIACEAE

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

INTRODUCTION TO
IMMUNOLOGY
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