Lecture 5 - Microbio

Gram Positive Bacilli

Spore Forming Rods

  • Includes Bacillus and Clostridium.

  • Release potent exotoxins that cause disease.

Bacillus anthracis

  • Causative Agent: Anthrax.

  • Unique Features:

    • UNIQUE Protein capsule that is antiphagocytic.

      • usually capsule made out of carbohydrates

    • Growth conditions: aerobic.

    • Spores are stable and resistant to heat, drying, UV, and disinfectants.

  • Transmission: Humans exposed through contact with animals or soil.

    • Cutaneous and respiratory routes for spores

      • animal hides or soil

  • Use in Warfare: Known for potential bio-terrorism use.

Bacillus anthracis Exotoxin

  • Encoded on: pXO1 plasmid.

  • The plasmid contains virulence factors, optimal at 37°C with increased CO2 and serum proteins.

  • Exotoxin produced by pXO1 Components:

    • Edema factor (EF)

    • Protective antigen (PA)

    • Lethal factor (LF)

  • Combination of proteins is lethal; individually, they are not toxic.

  • Protein Capsule Genes: Encoded by pXO2 plasmid.

  • Plasmid Requirement: Both pXO1 and pXO2 necessary for virulence.

Prevention and Treatment of Anthrax

  • Speed is Crucial: Rapid treatment essential.

  • Recommended Antibiotics: Penicillin, doxycycline, ciprofloxacin, or levofloxacin.

  • Vaccine: Available against PA protein.

Bacillus cereus

  • Food Poisoning: Caused when spores enter food products.

  • Characteristics: Motile, non-encapsulated, resistant to penicillin.

  • Enterotoxins:

    1. Heat labile: causes nausea, abdominal pain, diarrhea-lasting 12-24 hours.

    2. Heat stable: leads to severe nausea and vomiting.

  • Antibiotic Treatment: Useless due to preformed toxins.

Clostridium

  • Anaerobic: Differentiates from other spore-forming bacilli.

  • Diseases: Includes botulism, tetanus, gas gangrene, and pseudomembranous colitis.

  • Exotoxins: Powerfully toxic; require rapid diagnosis.

Clostridium botulinum

  • Disease: Rapidly fatal food poisoning from lethal neurotoxin.

  • Effects: Neurotoxin inhibits acetylcholine (Ach) release, leading to flaccid muscle paralysis.

  • Symptoms:

    • Afebrile with bilateral cranial nerve palsies.

    • Double vision, trouble swallowing, muscle weakness.

    • Can lead to respiratory paralysis and death.

  • Treatment: Antitoxin and respiratory assistance.

    • antitoxin: antibody that binds to toxin and neutralizes its effects in the body, preventing further damage to the nervous system.

  • Sources: Smoked fish, improperly canned vegetables; proper cooking can destroy spores.

Infant Botulism

  • Cause: Honey contamination with spores.

  • “floppy baby syndrome”

  • Process: Spores germinate, bacteria colonizes intestine, neurotoxin released within

    • Constipation 2-3 days,

    • Trouble swallowing and muscle weakness.

Botox is type A

  • To treat two eye muscle disorders

  • treat uncontrollable blinking and misaligned eyes

  • excessive sweating

Clostridium tetani

  • Disease: Tetanus often through rusty nails in anaerobic conditions.

  • Exotoxin: Tetanospasmin leading to sustained contractions of skeletal muscles.

  • Symptoms: Severe muscle spasms (lockjaw); high mortality potential.

  • Prevention: Booster toxoid given every 10 years.

Stepping on a rusty nail does not give you tetanus. If its rusty there is a possibility that rust gets inside you (septicemia). But there has to be a spore to get tetanus. You get tetanus from anything that breaks the skin and contains a spore.

Clinical Manifestations of Clostridium tetani

  1. Entry: Wound infection.

  2. Spread of Toxin.

  3. Symptoms: Rigid paralysis, cardiac failure, respiratory failure.

Clostridium perfringens

anaerobic

  • Disease: Gas gangrene.

  • Types of Infection:

    1. Wound infection/cellulitis: Necrosis with moist, spongy skin. with crackly pockets

    2. Myonecrosis: Toxin secretion destroys muscles; fatal if untreated.

  • Treatment: Oxygen, penicillin, and removal of necrotic tissue.

Clostridium difficile

  • Disease: Antibiotic-associated pseudomembranous colitis.

  • Occurrence: More common in hospitals than tetanus, anthrax, or botulism.

  • Mechanism: Destruction of normal flora by antibiotics leads to infection.

  • Symptoms: Severe diarrhea and abdominal cramping, fever.

  • Treatment: Discontinue antibiotics, administer metronidazole or vancomycin.

    • these two antibiotics are good against C-diff because they stay in intestinal tract (don’t cross well into blood), therefore kill intestinal bacteria.

Clinical Manifestations of Clostridium difficile

  1. Entry: Overgrowth after broad-spectrum antibiotics.

  2. Spread: Toxin production.

  3. Symptoms: Diarrhea, pseudomembranous colitis.

Non-Spore Forming Rods

  • Key Bacilli: Listeria monocytogenes and Corynebacterium diphtheriae.

Listeria monocytogenes

  • Disease: Causative agent of listeriosis; high risk in immunocompromised.

  • Sources: Soft cheeses, unpasteurized milk, cold cuts, pâté.

  • Characteristics: Psychrophile; survives in refrigerator temperatures.

  • Symptoms: Vary: include malaise, diarrhea, meningitis, septicemia, stillbirth/abortions.

  • Intracellular: Crosses 3 protective barriers blood-brain, GI, and feto-placental barriers.

  • Treatment: Ampicillin or trimethoprim-sulfamethoxazole.

    No vaccine.

Clinical Manifestations of Listeria monocytogenes

  1. Entry: Pathogen enters body.

  2. Invasion: Travels within cells, evading immune response.

  3. Spread: Can lead to meningitis and encephalitis, septicemia.

High fatality rate (30-40%) whereas other pathogens 1-3%

Corynebacterium diphtheriae

  • Disease: Diphtheria; colonizes pharynx, releasing exotoxins.

  • Effects: Damages heart and neural cells.

  • Treatment Steps:

    1. Administer antitoxin.

    2. Treat with penicillin or erythromycin.

    3. Vaccination with DPT.

Can be lysogenized by a bacteriophage (virus that infects bacteria) - phage encodes toxin gene

Clinical Manifestations of Corynebacterium diphtheriae

  1. Disease: Pharyngeal diphtheria.

  2. Symptoms: Pharyngitis, hypoxia due to pseudomembrane obstruction.

  3. Complications: Toxic myocarditis and congestive heart failure.

Gram Negative Bacilli - Enterics

  • Normal Flora: Found in intestinal microbiota but can also cause disease.

  • 4 Major Groups: Enterobacteriaceae (e.g., Salmonellae, Shigellae, E. coli), Vibrionaceae (e.g., Vibrio, Campylobacter), Pseudomonadaceae, and Bacterioidaceae.

  • Organisms are divided based on biochemical (what do they eat) and antigenic properties

Biochemical Classifications

  • Lactose Fermentation: Identified using EMB and MacConkey media.

    • EMB: Dark purple for fermenters.

    • MacConkey: Pink-purple for fermenters.

  • Other Indicators: H2S production, urease hydrolysis, gelatin liquefaction, amino acid decarboxylation.

3 Surface antigens:

O - outside cell wall

K - to do with capsule

H - only in motile bacteria. flagellar sub-unit

Diseases Caused by Enterics

  • Type 1: Diarrhea without systemic invasion - toxin-induced, watery diarrhea with no fever (e.g., Vibrio cholerae).

  • Type 2: Diarrhea with intestinal cell invasion - bloody stools (e.g., Shigella).

  • Type 3: Diarrhea with invasion into lymph nodes/bloodstream - leads to more severe symptoms (e.g., Salmonella typhi).

Other Enteric Infections

  • Additional Infections: Urinary tract infections, pneumonia, sepsis.

  • Notable Pathogens: E. coli, Klebsiella pneumoniae, and others.

Salmonellae

  • Family: Enterobacteriaceae; unable to ferment lactose.

  • All have animal reservoirs except S. enterica serovar Typhi

  • Types: S. enterica (most infections) and S. bongori.

  • Infections: Include enterocolitis, enteric fever, and opportunistic infections.

Enterocolitis (tummy problems)

  • S. enterica serovar Enteritidis

  • S. enterica serovar Typhimurium

Typhoid (enteric) fever

  • S. enterica serovar Typhi

  • S enterica serovar Paratyphi

S. enterica serovar Enteritidis

  • Pathogenesis: Dependent on ingested doses, immune status, virulence.

  • Incubation: 6-48h; multiplication in small intestine.

  • Symptoms: Nausea, vomiting, diarrhea, abdominal pain; typically self-limiting.

  • Antibiotics not recommended, because some strains grow better in the presence of antibiotics.

Enteric Fever

  • Causative Agents: S. enterica serovar Typhi and others cause systemic infection.

  • Symptoms: Multiply in lymphoid tissue leading to ulceration and necrosis of intestinal tissue.

  • Untreated Mortality: 10%.

  • Chronic Carriers: Can excrete bacteria for prolonged periods.

Diagnosis and Prevention of Enteric Fever

  • Diagnosis: Isolation from blood, stool, and urine.

  • Transmission Sources: Contaminated food/water.

  • Prevention: Clean water, food safety, vaccination available.

  • Vaccine available, only effective against small bacterial load

Nomenclature for HSS1100 for Exam

  • Stomach Problems: Salmonella enteritidis or Salmonella typhimurium.

  • Typhoid Fever: Salmonella typhi or Salmonella paratyphi.

Escherichia coli

  • Roles: Major part of gut flora; pathogenic to other body parts, responsible for most bacteriuria.

  • lactose fermenting

  • pathogenic to other parts of the body.

    • responsible for 85% of bacteriuria

E. coli Gastroenteritis

  • enterotoxigenic E.coli

    • infant diarrhoea

    • travellers diarrhoea

    • enterotoxins

  • Enteroinvasive E.coli

    • similar symptoms to shigellosis

  • Enteropathogenic e.coli

    • older name for some serotypes causing infant diarrhoea

  • E.coli O157:H7

    • Haemorrhagic colitis

    • Hamburger disease

    • Proper food handling prevent illness

    • can cause HUS (hemolytic uremic syndrome)

  • E

Shigellae

Non lactose fermenters

  • Causes: Acute diarrhea with mucus and blood, highly infectious.

  • Symptoms: Watery diarrhea, cramps, fever; primarily affects children, especially in unsanitary conditions.

  • NO VACCINE

Vibrio cholerae

  • Effects: Causes cholera; profuse watery diarrhea can lead to severe dehydration.

  • Pathogenesis: Enterotoxin causes chloride secretion into the gut, accumulated water leads to loss.

  • Prevalence: Endemic in regions with poor sanitation.

  • Massive 10-15 litre water loss

Campylobacter

  • Species: C. jejuni and C. coli; major causes of enteritis.

  • Reservoirs: Normal flora in birds and domestic animals.

  • Symptoms: Fever, abdominal pain, bloody diarrhea.

#1 cause of foodborne related illness

Non enterics

Pseudomonas

  • Opportunistic Pathogen: Found in moist environments; treatment is complex due to antibiotic resistance.

Pseudomonas aeruginosa

  • Profile: Respiratory pathogen in cystic fibrosis patients, noted for infections in burn patients.

Pseudomonas cepacia

  • Role: Respiratory infections in cystic fibrosis; a common contaminant.

  • able to grow in low nutrient environements.

    • has `contaminated saline solns, and contact lens soln

Haemophilus influenzae

  • Normal Flora: Found in many adults; primary cause of invasive infections in children.

    • meningitis, pneumonia, joint infections

  • Vaccination Impact: Routine vaccination has decreased cases significantly.

Cronobacter spp.

  • Associated Infections: Nosocomial infections in several forms; linked to infant illness from contaminated formula.

Helicobacter pylori

  • Profile: Microaerophilic, spiral-shaped; causes stomach ulcers.

  • Historical Context: Initially thought to be due to stress; later linked to H. pylori by research.

  • Mechanism: Urease protects against stomach acidity.

  • Treatment: Triple therapy including antibiotics and H+ pump inhibitors.

Bordetella pertussis

  • Disease: Whooping cough characterized by a violent cough.

  • Virulence Factors: Include pertussis toxin and other factors aiding in infection persistence and toxin release.

  • Prevention: Vaccination using heat-killed organisms.

Legionella pneumophila

  • Cause: Legionnaires disease; opportunistic and may cause severe pneumonia.

  • Environmental Presence: Grows in water sources; aerosol exposure with no direct person-to-person transmission.