Host Microbe Interactions and Mechanisms in Pathogenesis Vocabulary

Flashcards based on lecture notes about Host Microbe Interactions and Mechanisms in Pathogenesis. Terms focus on vocabulary.

Normal Flora

Population of microbes inhabiting skin and mucosal surfaces of healthy organism, primarily bacteria.

Resident Flora

Fixed number and type of organisms, variable for geographic location and age.

Transient Flora

Inhabit organism for days, weeks, months; environmental microbes, won’t establish permanent residence.

Microbial Antagonism

Prevents colonization of potential pathogens by competing for nutrients and producing inhibitory compounds.

Colicins

Compounds that kill potential pathogens produced by normal flora.

Improper Location Example

Streptococci in the mouth entering the bloodstream causing endocarditis if valve artificial or defective.

Bacteroides species

Common in the intestine, rupture due to trauma releases to peritoneal cavity, causes potentially lethal sepsis.

E. coli

Normal in the intestine, common cause of UTI.

Staphylococci

Normal on skin, entry into blood causes serious problem with prosthetic implants.

Dominant Resident Bacteria on Skin

Aerobic and anaerobic diphtheroid bacteria (corynebacterium, propionibacterium).

Types of Staphylococci on Skin

Non-hemolytic and a-hemolytic staphylococci (S. epidermidis, S. aureus).

Spore Forming Bacteria on Skin

Gm (+) aerobic spore forming bacteria, ubiquitous in water and air (B. subtilis).

Skin Secretions

Reduces pH due to sebum (fatty acids) in oil.

Lysozyme

Actively kill potential pathogens in skin secretions.

Sweat

Wash off potential pathogens.

Streptococci species

Colonize nasal passages shortly after birth and remain dominant.

Bacteria Colonization

Tooth growth allows colonization of anaerobic spirochetes, prevotella species, fusobacterium species, rothia species, capnocytophaga species, anaerobic vibrios, lactobacilli, actinomyces, and yeasts.

Infections of Mouth and URI

Usually involve anaerobic bacteria.

Periodontal infections, abscesses, sinusitis, and mastoiditis

Caused by Prevotella malaninogencia, fusobacterium, and peptostreptococci.

Aspiration of saliva

May cause URI, consequences potentially severe such as necrotizing pneumonia, lung abscess, empyema.

Dental Caries

Disintegration of teeth beginning at the surface, progresses inward.

Formation of Plaque

S. mutans and S. sobrinus produces gelatinous substance, protein and carbohydrate components.

Intestine at birth

Colonized by breast milk or bacteria in formula; method of feeding dictates type of bacteria.

Flora of esophagus

Resembles that of mouth and food.

Stomach flora

Fairly light microbial flora 103-105/gram of material, due to gastric acid.

Intestinal Flora

Many organisms inhabit alkaline pH, 103-106/gram in duodenum, 105-108/gram in ileum, 108-1010/gram in large intestine.

Fecal matter

10-30% bacteria (1011/gram of matter).

Types of Bacteria in Intestine

Vast majority (96-99%) are anaerobes - bacteroides, fusobacterium, anaerobic lactobacilli, clostridia, anaerobic Gm (+) cocci.

Facultative Anaerobes in Intestine

Gm (-) coliforms, enterococci, proteus, pseudomonal, lactobacilli, candida.

Metabolic Functions of Gut Bacteria

Produce vitamin K, metabolize bile, assist absorption of nutrients, antagonize microbial pathogens.

Antimicrobial Drugs Used preoperatively for bowel surgery

Decreases chance for contamination of peritoneum.

Depletion By Antimicrobial Drugs

May lead to colonization with antibiotic resistant bacteria.

Infectious Peritonitis

Anaerobic bacteria primarily responsible for infectious peritonitis if bowel ruptures.

Bacteria in Urethra

Typically detect 102 -104 urease producing organism per ml.

Lactobacilli in birth canal

Major contributors to acidic pH, due to fermentation of carbohydrates (glycogen).

Cervical mucous

Contain lysozyme that thwarts infection.

The Eye (Conjunctiva)

Tears wash constantly, contain lysozyme.

Pathogenesis

Infection of host followed by damage to tissues and/or organs.

Colonization

Attachment to host.

Evasion of Immune System

Several mechanisms exist such as adhesins, capsules, cellular invasion, survival following phagocytosis.

Damage to Host

Multiple mechanisms such as toxins, cellular damage following invasion, induction of host damage to self.

Severity of Infection/Symptomology Depends On

Host immune system, virulence determinants for pathogen, delivered infectious dose.

Etiology of Disease

Determination of cause (infectious agent) of disease.

Koch's Postulate #1

Isolate and identify causative agent from afflicted organism.

Koch's Postulate #2

Introduce causative agent to heal healthy organism.

Koch's Postulate #3

Determine if healthy organism exhibits symptoms.

Koch's Postulate #4

Isolate causative agent from test organism.

Exceptions to Koch’s Postulates

Some cannot be cultivated in vitro.

Polymerase chain reaction (PCR)

Allows detection of organisms that cannot be cultivated in vitro.

Pathogen

Presence of organism abnormal, always causes disease.

Opportunistic Pathogen

Normally present in host, cause disease under unusual circumstances, improper localization or immuno-compromised of host.

Nonpathogen

Bacteria incapable of causing disease in specified host.

Reservoir

Source of organism causing disease.

Salmonella typhimurium, Clostridium botulinum

Often produce no symptoms in animal reservoir.

Environmental Reservoir

Often times a body of water.

Vector

Living organisms transmit pathogen.

Fomite

Inanimate mode of transmission.

Portal of Entry

Organisms have preferred entry points.

The Infectious Process - Step 1

Bacteria must first attach (colonize) the host.

The Infectious Process - Step 2

Disseminate to tissue/organ suitable for multiplication.

The Infectious Process - Step 3

Multiply, damage host, cause symptoms.

Clonal Nature of Bacterial Pathogens

Bacteria - haploid organisms, limited opportunities for acquisition of genetic material.

Clonal Typing

Useful for determination of origin of outbreak, certain clones specific to certain geographic locations.

Regulation of Expression of Virulence Factors

Virulence determinants only required for survival in host, expression in reservoir wastes metabolic energy.

Adhesins

Attachment first stage of infection.

Fimbriae

Short proteinacous appendages from cell, attach to surface carbohydrates on target cell.

Pili

Longer proteinacous appendages, may be associated with lipoteichoic acid, attaches to extracellular matrix proteins of host (fibronectin).

Invasion

Physically entering host cells - active role for bacteria, active or passive role for host cell.

Invasion of Phagocytic Cells (MF)

Fusion of phagosome with lysosome destroys most organism, two known mechanisms permit growth within MF.

Mechanism #1 for MF Invasion

Prevents fusion between phagosome and lysosome (Mycobacterium tuberculosis).

Mechanism #2 for MF Invasion

Organisms escapes from phagosome before fusion with lysosome (Listeria monocytogenes).

Invasion of Non-phagocytic Cells

Best characterized in Shigella dysenteriae and Yersinia enterocolitica.

Type III secretion of effectors

Forces cell to generate pseudopods and consume organism.

Anti-Phagocytic Factors

Many organisms resist phagocytosis by PMNs and MF.

Anti-Phagocytic Factor Example #1

Some organisms express IgG Fc binding proteins on surface, prevents opsonization.

Anti-Phagocytic Factor Example #2

Some produce polysaccharide capsules, prevents phagocytic cell from attaching.

Anti-Phagocytic Factor Example #3

Some produce adhesins, allow avid attachment to surfaces, prevents phagocytosis.

Enzymes - Virulence Determinants

Many pathogens secrete enzymes, not toxins, important to virulence.

Collagenase

Degrades collagen, ECM protein, allows penetration into tissues.

Hyaluronidase

Digests hyaluronic acid, major component of connective tissue, allows penetration into tissues.

Fibrinolysin

Degrades fibrin, breaks clots, allows dissemination.

Coagulase

Promotes formation of fibrin clots, limits immune system access to pathogen.

Hemolysin

Lyses red blood cells, important for acquisition of iron and cofactors for enzymes.

Leukocidins

Lyse white blood cells (leukocytes).

Superoxide dismutase

Scavenges H2O2 generated by PMNs and MF.

IgA1 protease

Degrades IgA1 at hinge region of antibody, prevents neutralization/coagulation of bacteria.

Exotoxins

Produced by both Gm (+) and Gm (-), secreted factors, variable size 10-900 kDa.

Exotoxin Use

Primary targets for vaccine development (toxoids), elicit strong antibody response.

Diphtheria toxin

Catalyzes ADP ribosylation of elongation factor 2.

Tetanus toxin

Infects motor neurons, travels to brain stem.

Clostridium botulinum

Targets motor neurons - prevents release of acetylcholine.

Staphylococcus aureus - toxic shock syndrome toxin-1

Super antigen - stimulates production of cytokines (IL-1 and TNFa).

Vibrio cholera

AB family of toxins, induces production of cAMP.

S. aureus - enterotoxin

Neural receptors in gut, transmits signal to brain, stimulates vomiting center.

Endotoxins

Major component of Gm (-) cell wall, do not exist in Gm (+).

Toxic Component of Endotoxins

Lippopolysaccharide complex, lipid portion toxic component.

Endotoxin Property

Potent pyogens - induce fever (IL-1 production).

Peptidoglycan Cell Wall

Peptidoglycan cell wall of Gm (+) organisms may produce similar symptoms, not a true endotoxin.

Intracellular Pathogenicity

Some pathogens thrive within phagocytic cells - escape phagosome, prevent fusion of phagosome, resistant to lysosomal enzymes.

Antigenic Variation

Multiple serotypes of E. coli - vary LPS carbohydrate.