Microbiology unit 11 STUDY

Vibrio cholerae Gram stain morphology

Gram negative comma shaped rod

Vibrio cholerae disease

Cholera

Vibrio cholerae source/reservoir

Humans; infected carriers shed bacteria in feces

Vibrio cholerae transmission

Fecal-oral route through contaminated food or water

Vibrio cholerae carriers

Convalescent carriers shed bacteria up to a year; chronic carriers may shed for years

Vibrio cholerae detrimental conditions

Drying, sunlight, and acidic conditions kill the bacteria

Vibrio cholerae enterotoxin

Causes massive fluid and electrolyte loss from the intestinal lining

Cholera characteristic stool

Rice-water stools

Cholera symptoms

Abrupt onset of severe vomiting and diarrhea

Cholera fluid loss

May reach 20 liters per day

Cholera electrolyte losses

Sodium, potassium, chloride, and bicarbonate

Cholera hypovolemic shock

Massive fluid loss decreases blood volume and blood pressure

Cholera metabolic acidosis

Bicarbonate loss decreases the body's buffering capacity, causing acidosis

Untreated cholera mortality

Approximately 50%

Treated cholera mortality

Less than 1%

Vibrio cholerae laboratory identification

Gram-negative comma-shaped rod, oxidase-positive, lactose-negative; grows on simple agar media

Vibrio cholerae immunity

Long-lasting immunity after infection for most people

Cholera prevention and control

Oral cholera vaccines, proper sanitation, and hygiene

Cholera treatment

Prompt fluid and electrolyte replacement; tetracycline may reduce bacterial load and toxin release

Vibrio cholerae El Tor biotype

Milder disease, may be asymptomatic, survives longer in the body, and causes most global cases

Vibrio cholerae classical biotype

Relatively rare globally except in India and Bangladesh

Campylobacter jejuni disease

Gastroenteritis, accounting for 5–11% of diarrhea cases in the United States

Campylobacter jejuni source

Lower animals, including dogs and cats; birds may carry it without becoming ill

Campylobacter jejuni transmission

Undercooked poultry, unpasteurized dairy, contaminated water, or cross

Campylobacter jejuni infectious dose

Fewer than 500 organisms can cause illness

Campylobacter jejuni incubation period

2–10 days

Campylobacter jejuni symptoms

Fever, abdominal cramps, and bloody diarrhea

Campylobacter jejuni bloody diarrhea

Indicates intestinal invasion and inflammation

Campylobacter jejuni disease course

Usually self-limiting

Campylobacter jejuni treatment

Erythromycin is the preferred antibiotic according to the lecture

Campylobacter laboratory morphology

Curved and S-shaped Gram-negative rods

Campylobacter laboratory growth

Microaerophilic; requires high CO₂ and is killed by ambient oxygen levels

Campylobacter laboratory temperature

Preferred growth temperature is 42°C

Campylobacter laboratory media

Campy agar contains 10% blood and antibiotics; no growth on ordinary blood or MacConkey agar according to the lecture

Campylobacter biochemical identification

Nonfermentative, oxidase-positive, catalase-positive

Helicobacter pylori prevalence

More than 50% of the global population harbors H. pylori in the upper GI tract

Helicobacter pylori asymptomatic infection

Approximately 85% of infected people never experience symptoms

Helicobacter pylori transmission

Person-to-person through saliva or fecal contamination of food and water

Helicobacter pylori virulence factors

Motility, urease activity, and association with gastric mucosal cells\

Helicobacter pylori major diseases

Chronic gastritis and peptic ulcers\

Long-term Helicobacter pylori complications

Increased risk of gastric cancer and MALT lymphoma

Helicobacter pylori urease

Neutralizes gastric acid, helping the organism survive in the stomach\

Helicobacter pylori biopsy diagnosis

Endoscopy with biopsy; histologic stain and culture are described as the gold standard in the lecture\

Helicobacter pylori biopsy urease test

Rapid colorimetric test detecting urease activity in biopsy tissue\

Helicobacter pylori urea breath test

Labeled urea is metabolized by bacterial urease; labeled carbon is measured in exhaled CO₂\

Helicobacter pylori serum antibody test

Detects specific IgG antibodies; indicates current or previous infection\

Helicobacter pylori stool antigen test

Detects H. pylori antigens and indicates active infection; used for diagnosis and treatment monitoring\

Helicobacter pylori treatment

Antibiotics such as amoxicillin or tetracycline, plus an antacid or proton pump inhibitor\

Helicobacter pylori prevention

Handwashing, properly prepared food, and safe, clean drinking water\

Pseudomonas natural habitat

Soil and water; widespread in nature\

Pseudomonas species most associated with human disease

Pseudomonas aeruginosa\

Pseudomonas aeruginosa morphology

Aerobic Gram-negative rods

Pseudomonas aeruginosa carbohydrate metabolism

Nonfermentative; does not utilize glucose by fermentation\

Pseudomonas aeruginosa pigments

Pyocyanin and fluorescein\

Pseudomonas aeruginosa pigment appearance

Characteristic blue

Pseudomonas aeruginosa pyocyanin

Blue-green pigment that kills competing microbes, generates reactive oxygen species, inactivates catalase, and interferes with electron transport

Pseudomonas aeruginosa proteases

Cause tissue destruction, hemorrhage, and corneal damage\

Pseudomonas aeruginosa exotoxin A

Causes necrotizing activity at the site of colonization\

Pseudomonas aeruginosa hemolysins

Contribute to invasiveness, especially in pneumonia\

Pseudomonas aeruginosa source

Widespread in the environment and medical settings, including hospital water systems and dental water lines\

Pseudomonas aeruginosa transmission

Contaminated equipment, IV fluids, water, soap, and hospital personnel\

Pseudomonas aeruginosa susceptible patients

Burn patients, patients with malignancies, patients receiving invasive interventions, leukemia patients, and cystic fibrosis patients\

Pseudomonas aeruginosa major host defense

Innate immunity, especially phagocytosis\

Pseudomonas aeruginosa infection sites

Burns, wounds, cornea, lungs, urinary tract, and bloodstream\

Pseudomonas aeruginosa severe complication

Septicemia with high mortality\

Pseudomonas aeruginosa antimicrobial resistance

Intrinsic resistance to many antibiotics and acquired resistance to others\

Pseudomonas aeruginosa localized external infection treatment

Topical polymyxin B or colistin may be used cautiously because of kidney toxicity\

Pseudomonas aeruginosa wound management

Debride necrotic tissue and drain abscesses when present\

Pseudomonas aeruginosa systemic treatment

Intensive antimicrobial therapy selected according to local susceptibility patterns; combinations may be used\

Pseudomonas aeruginosa prevention

Aseptic technique when handling patients and equipment\

Pseudomonas aeruginosa vaccine

A heptavalent vaccine was developed for burn patients and shown to reduce infection incidence in the lecture\

Burkholderia pseudomallei disease

Melioidosis, also called Whitmore's disease\

Burkholderia pseudomallei source

Soil and water in tropical areas, especially Southeast Asia\

Burkholderia pseudomallei transmission

Inhalation or ingestion of contaminated dust or soil contamination of abraded skin\

Burkholderia pseudomallei high

risk groups

Burkholderia pseudomallei clinical features

Pneumonia, multiple abscesses, granulomatous disease, osteomyelitis, and possible septicemia\

Burkholderia pseudomallei disease course

Can remain latent for years and relapse due to reactivation\

Burkholderia pseudomallei mortality

Lecture reports a mortality rate of 40%\

Burkholderia pseudomallei treatment response

Often slow; relapses are common\

Haemophilus morphology

Small Gram-negative rods or coccobacilli

Haemophilus growth factors

Requires specific growth factors found in blood\

Haemophilus X

Hemin, an iron complex derived from hemoglobin

Haemophilus V

NAD

Haemophilus influenzae growth requirements

Both X-factor (hemin) and V-factor (NAD)

Haemophilus influenzae growth medium

Chocolate agar supplies X- and V-factors

Haemophilus influenzae serotyping

Six groups, A through F, based on capsular antigens\

Haemophilus influenzae type b

Important cause of acute, nonepidemic bacterial meningitis in infants and children\

Haemophilus influenzae source

Humans; upper respiratory tract\

Haemophilus influenzae transmission

Human-to-human transmission through inhaled infected respiratory droplets

Haemophilus influenzae respiratory diseases

Pharyngitis, otitis media, sinusitis, and pneumonia\

Haemophilus influenzae meningitis

Most serious disease described; may cause CNS deficits after recovery\

Haemophilus influenzae epiglottitis

Swelling of the epiglottis can close the airway and may require tracheotomy\

Haemophilus influenzae treatment

Ampicillin and chloramphenicol are listed in the lecture\

Haemophilus influenzae prevention

Hib vaccination\

Haemophilus aegyptius common name

Koch-Weeks bacillus

Haemophilus aegyptius disease

Conjunctivitis (pink eye), which may occur at epidemic levels in children\

Haemophilus aegyptius laboratory differentiation

Requires serological differentiation from H. influenzae because culture and biochemical characteristics are the same\

Haemophilus aegyptius treatment

Local ophthalmic antibiotic solution\

Haemophilus ducreyi common name

Chancroid bacillus\

Haemophilus ducreyi disease

Chancroid, a sexually transmitted disease\