(kat) VIBRIO etc.pdf

KATHLEEN ROSS S. CALIGAGAN, MD, FPSNM

VIBRIOCAMPYLOBACTER

HELICOBACTER

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

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

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.

VIBRIO

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


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


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

VIBRIOS


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

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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

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

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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

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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

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1. Vibrio cholerae

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

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

(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

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

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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

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1. Vibrio cholerae

ANTIGENIC

DETERMI-

NANTS

RIBOTYPE

BIOTYPE

SEROTYPE

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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

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


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


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

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

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1. Vibrio cholerae

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

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

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)

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


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

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

Adult cholera gravis patient with washer womans hand sign

Severely dehydrated pediatric patient with Cholera gravis

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

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

GRAM (-) RODS

1. Vibrio cholerae

Yellow colonies on TCBS agar

Oxidase-positive on blood agar

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)

GRAM (-) RODS

1. Vibrio cholerae

2. Vibrio parahaemolyticus


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

GRAM (-) RODS


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

VIBRIO VULNIFICUS

edema; ecchymoses; and hemorrhagic, serous bullae on

the lower legsNecrotizing fascitis

CAMPYLOBACTER

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 immunocompromisedpatients

GRAM (-) RODS

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


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

CAMPYLOBACTERgram-negative, comma-/curved-/S-/gull-wing-shaped bacilli with single flagellum


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


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


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


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


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


GRAM (-) RODS

CAMPYLOBACTER

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

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


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


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


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


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


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


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


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)

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


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, 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


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


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)


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


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.


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


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


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


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


VECTORS

UNIQUE BACTERIA

WOOD TICK

(Dermacentorandersoni)

DOG TICK

(Dermacentorvariabilis)

BROWN DOG TICK

(Rhipicephalussanguineus)

FEMALE LONE STAR TICK

(Amblyommaamericanum)

RICKETTSIAL DISEASES


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




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


(2) RICKETTSIALPOX


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


(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 BACTERIA

FEMALE BODY LOUSE

(Pediculus humanus corporis)

VECTOR



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.


(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.


(4) ENDEMIC/MURINE/FLEA-BORNE TYPHUs

UNIQUE BACTERIA

NORWAY RAT

(Rattus norvegicus)

RAT FLEA

(Xenopsylla cheopsis)

VECTORRESERVOIR


(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.


(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


(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



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



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


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

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