Sample Final Exam




Actinobacillus actinomycetemcomitans 

Actinomyces israelii;  A. naeslundii

Aeromonas hydrophila;  A. sobria

Bacillus anthracis       

Bacillus cereus

Bacteroides fragilis group

Bordetella bronchiseptica

Bordetella pertussis, Bordetella parapertussis

Borrelia recurrentis                            

Borrelia burgdorferi

Brucella abortus;  B. melintensis;  B. suis;  B. canis

Burkholderia cepacia

Burkholderia pseudomallei          

Campylobacter jejuni;  C. coli

Corynebacterium diphtheriae

Corynebacterium jeikeium, Stenotrophomonas maltophilia

Clostridium botulinum

Clostridium difficile

Clostridium perfringens   

Clostridium tetani

Opportunistic Escherichia coli

Enterotoxigenic Escherichia coli (ETEC)

Enterohemorrhagic Escherichia coli (EHEC) O157:H7

Enterococcus faecium;  E. faecalis         

Francisella tularensis      

Haemophilus ducreyi          

Haemophilus influenzae

Helicobacter pylori 

   Return to Exam Pathogen Key

Klebsiella pneumoniae             

Leptospira interrogans               

Listeria monocytogenes

Mycobacterium avium-intracellulare complex                     

Mycobacterium bovis

Mycobacterium leprae

Mycobacterium tuberculosis  

Neisseria gonorrhoeae            

Neisseria meningitidis 

Pasteurella multocida

Plesiomonas shigelloides

Propionibacterium acnes

Pseudomonas aeruginosa

Salmonella enterica (non-enteric fever Salmonella spp.)

Salmonella typhi

Shigella sonnei;  S. flexneri, S. dysenteriae;  S. boydii        

Staphylococcus aureus

Staphylococcus epidermidis

Stenotrophomonas maltophilia, Corynebacterium jeikeum

Streptococcus pyogenes (Group A streptococci)

Streptococcus agalactiae (Group B streptococci)

Streptococcus mutans (viridans group)

Streptococcus pneumoniae

Treponema pallidum ssp. pallidum

Treponema pallidum ssp. endemicum;  ssp. pertenue;  T. carateum

Vibrio cholerae

Vibrio parahaemolyticus

Vibrio vulnificus

Yersinia enterocolitica

Yersinia pestis


   Return to Exam Pathogen Key


I. DEFINITIONS:  Match the appropriate term from the Terminology Key  (not shown) with it’s definition.  Each definition matches only one term and each term is defined one time.


Know your MAJOR definitions.


II.  PHYSIOLOGY, STRUCTURE & MORPHOLOGY:  Match the organism from the Pathogen Key to the description.  Each description matches only one organism and each organism is described only one time in this section.

Facultatively anaerobic or strictly anaerobic, irregularly staining, beaded, gram-positive, partially acid-fast bacilli with highly developed branching filament formation (aerial and substrate), resembling fungi.;  “Molar tooth” appearance of colonies after prolonged incubation;  Delicate, filamentous bacilli concentrate in sulfur granules in sinus tracts.

Catalase negative, encapsulated (specific soluble substance, SSS), lancet-shaped, gram-positive cocci arranged in pairs (diplococci) or short chains in sputum;  Cell wall of teichoic acid (C-substance), phosphate, and choline;  a-hemolytic colonies on blood agar that undergo autolysis with aging (center collapses), but may be b-hemolytic when grown anaerobically.  

Aerobic or facultatively anaerobic, small, pleomorphic, gram-positive bacilli that appear in short chains (“V” or “Y” configurations) or in clumps resembling “Chinese letters;”  Cells contain metachromatic granules;  Cell wall contains meso-diaminopimelic acid, arabino-galactan polymers, and short-chain mycolic acids;  Lysogenic bacteriophage encodes for potent exotoxin in virulent strains.

Oxidase-positive, short, gram-negative curved (comma-shaped) bacilli that are comma-shaped on initial isolation and motile by a single polar flagellum;  Grow aerobically or anaerobically a variety of alkaline, but not acidic simple media (e.g., alkaline peptone enrichment broth), with a broad temperature range (18oC to 37oC);  Yellow colonies on TCBS agar;  Serologically divided into six groups (O1 and non-O1 serogroups);  Serogroup O1 further subdivided into two biotypes and two serological subgroups.

Small, oxidase-positive, microaerophilic, gram-negative, helically curved (spiral) or comma-shaped bacilli in young cultures that have characteristic “darting motility” by single polar or bipolar flagellum;  Coccoid and elongated forms in older cultures;  Grows faster at 42oC than at 37oC;  Metabolize amino acids, but do not oxidize nor ferment carbohydrates;  More than 90 different heat-stable, somatic O polysaccharides antigens (Penner serotypes) and more than 50  heat-labile, capsular and flagellar antigens (Lior serotypes).

Large, uniformly rectangular, nonmotile, anaerobic, gram-positive bacilli that can produce ovoid subterminal spores, but spores are rarely observed in vivo  or in fresh culture;  Although nonmotile, rapid, spreading growth on culture media resembles that of motile organisms;  Typical double zone of hemolysis, a b-hemolytic zone surrounded by a larger zone of incomplete hemolysis;  Lecithinase hydrolyzes phospholipids in egg yolk agar (Nagler reaction).

Small, motile, anaerobic, spore-forming bacilli;  Gram-positive in young culture, but may stain gram-negative in older cultures or in smears from wounds;  Round, terminal spore giving vegetative cell a “drumstick” or “tennis racket” appearance.

Non-motile, facultatively anaerobic, catalase positive, gram-positive cocci growing in irregular clusters  with a capsule or polysaccharide slime layer, protein A, ribitol teichoic acid with N-acetylglucosamine residues (polysaccharide A), and bound coagulase (clumping factor).  

Small, sometimes pleomorphic, gram-negative bacilli with many strains of this species, but not all, covered with a polysaccharide capsule comprising six antigenic serotypes (“a” through “f”), with type b antigen associated with the highest level of virulence;  In vitro growth requires supplementation of media with growth factors hematin and NAD or NADP.

Very small, nonmotile, strictly aerobic, fastidious, gram-negative coccobacillus that does not grow on common laboratory media without supplementing with nicotinamide and charcoal, starch, blood, or albumin to absorb toxic substances;  Oxidizes amino acids, but does not ferment carbohydrates;  Fimbriae present, but not primarily involved in adherence; Exotoxin and hemagglutinin mediate attachment.

Extremely small, nonmotile, fastidious, slow-growing (2-3 days) gram-negative coccobacillus with a thin, lipid capsule present in pathogenic strains;  Two biochemical varieties, tularensis (Jellison Type A) and palaearctica  (Jellison Type B).

Nonmotile, aerobic, fastidious, very slow-growing (12-30 days), acid-fast bacilli with a complex cell wall rich in lipids;  Surface glycolipids include waxes, mycosides and cord factor (mycolic acids), the latter, responsible for the parallel arrangement of rows of bacilli in virulent strains (“cord formation”);  Surface protein (15% of cell wall weight) stimulates host cell mediated immunity and is purified and used as a reagent to evaluate hypersensitivity in a skin test.

Very thin, very long, helically-coiled (spiral), motile, gram-negative “spirochetal” bacillus that is a strict human pathogen (although, experimental disease has been established in a rabbit testes model) that cannot be grown in cell-free culture;  Periplasmic flagella (axial fibrils) outside of protoplasmic core and surrounded by an outer envelope or sheath that are anchored at either end of the cell by insertion pores;  Too thin to be able to be seen by light microscopy, so darkfield microscopy or fluorescent antibody staining are required;  Once considered strict anaerobes, but are now known to be able to oxidatively metabolize glucose.


   Return to Exam Pathogen Key


III. PATHOGENESIS & IMMUNITY:  Match the organism from the Pathogen Key to the description of the virulence factors and/or immune response.  Each description matches only one organism and each organism is described no more than one time in this section.

Encapsulation responsible for virulence resulting in anaerobic abscess formation, puri- fied capsular polysaccharide will cause sterile intraabdominal abscess, nonencapsulated strains can still cause abscess in presence of polymicrobic mixture of endogenous organisms;  LPS, agglutinins, enzymes and oxygen tolerance also play a role in pathogenicity.

Range of clinical presentation is dependent on patient’s immune response;  At one end of the spectrum, patients have a strong delayed hypersensitivity reaction and weak humoral antibody response with infected foci characterized by large numbers of lymphocytes and granulomas and relatively few bacilli in the tissues due to cytokine-mediated macrophage activation;  At the other end of the spectrum, patients have a strong antibody response, but a specific defect in their cellular response with large numbers of organisms in dermal macrophages and Schwann cells of the peripheral nerves.  

Antiphagocytic hyaluronic acid capsule, lipoteichoic acid, M-protein, F-protein (receptor for fibronectin), hemolysins (streptolysins O and S), pyrogenic exotoxins (erythrogenic toxins) (A through C), streptokinases (A and B), deoxyribonucleases (A through D), hyaluronidase, DPNase, cardiohepatic toxin.

Capsule (smooth and rough variants), neuraminidase, toxins (pneumolysin O, purpura producing principle), adherence.

Prototype A-B exotoxin encoded by tox gene introduced by lysogenic bacteriophage.

Capacity to invade intact mucus membranes or skin with abrasions;  Most common sites of inoculation are the vagina or cervix in the female and the penis in the male;  Only piliated cells (formerly, colony types T1 and T2) are virulent by attaching to intact mucus membranes, penetrating into and passing through mucosal cells, and establishing infection in the sub-epithelial layer.

Outer membrane proteins associated with adherence, hyaluronidase facilitates perivascular infiltration (the hallmark presentation lesions at all stages of this disease, e.g., endarteritis and periarteritis), virulent strains capable of coating the bacterial cell with host cell fibronectin and effectively “masking” themselves, organisms frequently survive following ingestion by phagocytic cells.

Plasmid-mediated enterotoxins (heat-labile (LT), and/or heat-stable (ST)) stimulate guanylate or adenylate cyclase activity in the small intestine, specific adhesive pili (colonization factor antigens (CFA/I and CFA/II) in humans, K88 in piglets, K99 in calves).

Following transmission by infected arthropods, these organisms are disseminated in the bloodstream and seeded intracellularly in multiple organs where they are able to undergo antigenic variation as a means of avoiding the host immune response and resulting in periodic febrile and afebrile episodes, with each subsequent relapse generally less severe and of shorter duration.

A-B enterotoxin (B is pentameric) binds to GM1 ganglioside receptors in the small intestine, increasing adenyl cyclase activity and increasing cAMP production with rapid fluid and electrolyte loss;  Also produce heat-stable and heat-labile enterotoxins, cytotoxin, flagellum, adhesins, mucinase.

Invasiveness, Shiga toxin (neurotoxic, cytotoxic, and enterotoxic)

Rapid growth with production of four major lethal toxins (alpha toxin (lecithinase C), beta toxin, epsilon toxin, iota toxin), an enterotoxin, and minor toxins (delta, theta, kappa, lambda, mu, nu, neuraminidase), metabolically very active.

Production of neurotoxin (seven antigenically distinct types) specific for cholinergic nerves by blocking release of excitatory neurotransmitter, acetylcholine, with irreversible binding to specific receptors on the nerve endings.

Loose fitting capsule or slime layer (exopolysaccharide, glycocalyx), specific protein receptors for binding mammalian proteins, extracellular enzymes (coagulases (free and bound), catalase lipases, hyaluronidase, staphylokinase (fibrinolysin), nuclease, penicillinase), toxins (cytolytic toxins (alpha hemolysin, beta toxin, delta toxin, gamma toxin, leukocidin) enterotoxins (A, B, C, C2 , D, and E), exfoliative toxins, pyrogenic exotoxins (toxic shock syndrome toxin-1).

Pili, polysaccharide capsule, endotoxin, exotoxin A, exoenzyme S, elastase, alkaline protease, phospholipase C, leukocidin.

Pertussis toxin (a.k.a., histamine sensitizing factor, lymphocytosis promoting factor, islet cell activating factor and pertussigen), adenylate cyclase toxin, tracheal cytotoxin, dermonecrotic toxin, filamentous hemagglutinin, LPS (lipid A and lipid X).

Pili-mediated, receptor-specific colonization of nonciliated cells of nasopharynx, antiphagocytic polysaccharide  capsule allows systemic spread, toxic effects mediated by hyperproduction of lipooligosaccharide.

Antiphagocytic polypeptide capsule, three component exotoxin (protective antigen, edema factor, lethal factor), heat-resistant spore formation.

Inflammatory low molecular weight peptide attracts leukocytes to the sebacious follicles causing release of hydrolytic enzymes and together with bacterial lipases, proteases, neuraminidase, and hyaluronidase precipitate the inflammation that results in rupture of the sebaceous follicle;  Because the organisms establish a niche in the follicles, no amount of washing with soap and water can eradicate the infection.

Urease production produces cloud of ammonia that protects the organism by neutralizing stomach acidity, motility and mucinase production allow the organism to pass through the mucus layer, adherence factors anchor the bacteria in the gastric pits. 

Facultative intracellular  pathogen capable of escaping the  phagolysosome complex following phagocytosis and multiplying inside cells of the reticuloendothelial system (RES) presumably through the action of listeriolysin O, formation of actin filaments and pseudopodial extensions facilitate transfer to other phagocytes.

Acquisition of nonvenereal treponemal diseases is by contact with contaminated eating utensils (bejel), or by direct contact with infectious lesions (yaws, pinta)


   Return to Exam Pathogen Key


IV.  EPIDEMIOLOGY:  Match the organism from the Pathogen Key to the description of the epidemiological factors.  Each description matches only one organism and each organism is described no more than one time in this section.

Survive in soil and on vegetation for prolonged periods due to spore formation, herbivores are natural hosts and humans accidental hosts;  Human disease acquired by inoculation (95% of cases), inhalation (Woolsorter’s disease), or ingestion.

Most common cause of traumatic eye injury, inoculating organisms from soil contamination of the penetrating object or endogenous flora colonizing the surface of the eye;  Panopthalmitis rapidly progresses with complete loss of light perception within 48 hours with massive destruction of the vitreous and retinal tissues with three toxins implicated (necrotic toxin, cereolysin, and phospholipase C)

Animals are main reservoir for human disease;  Gastroenteritis with septicemia generally recognized in large, point-source foodborne outbreaks following a 6 to 48 hour incubation period after ingestion of improperly prepared foods (especially poultry, eggs, dairy products) contaminated with large numbers of this organism

Isolated from soil, water, vegetation, and a variety of mammals, birds, fish, insects, and other animals and transmitted to humans either by direct contact, ingestion of contaminated food products, or transplacentally (early-onset) or during birth or soon after (late-onset);  Focal epidemics have been associated with contaminated milk, soft cheeses, undercooked meat (e.g., turkey franks, cold cuts), unwashed raw vegetables;  Organisms able to grow and multiply at cold “refrigeration” temperatures

Simple taxonomic classification with four species, most common species differs between developing and developed countries;  As few as 200 organisms can establish disease, generally by a fecal-oral route and therefore spreading rapidly in communities with poor sanitary conditions or personal hygiene or epidemics in day-care centers, nurseries, or custodial institutions

Obligate parasites on mucus membranes of humans and animal species,  prior to introduction of successful pediatric immunization program, most common cause of acute bacterial meningitis in infants and young children, as well as, other serious pediatric diseases, e.g.,  epiglottitis, cellulitis, as well as, chronic pulmonary disease in adults;  Primary risk factor for invasive disease is the absence of protective antibody against the polysaccharide capsule

Seriously underreported, sexually transmitted disease found only in humans with strikingly different epidemiological presentations for females and males, major reservoir is asymptomatic carriage in females.

Source of most infections is ingestion of water or food products contaminated with large numbers of organisms by infected, but usually asymptomatic, food handler;  Majority of cases in the U.S. are attributable to foreign travel;  Reservoir for chronic asymptomatic carriage is often the gall bladder.

Halophilic marine vibrio is major cause of diarrheal disease in Japan where consumption of raw fish is common.

Endogenous infection with disease presentation dependent upon source of organisms;  Cervicofacial infections derive from poor oral hygiene, invasive dental procedure, or oral trauma;  Thoracic infections general aspirate the organisms into the lung and then dissemination is from there;  Abdominal infections generally proceeded by surgery or trauma to the bowel;  Pelvic infections can be secondary to abdominal infections or a primary infection in women with contaminated intrauterine devices.

Antibiotic use results in disruption of normal gastrointestinal flora and allows for overgrowth of endogenous organisms or greater susceptibility to infection with exogenous strains, resultant overgrowth of these toxigenic organisms can result in range of antibiotic-associated diseases from mild diarrhea to potentially fatal, pseudomembranous enterocolitis.

Halophilic marine vibrio responsible for a particularly severe bacteremia following ingestion of raw or improperly handled seafood (shellfish like oysters) or progressive wound infections after exposure to contaminated seawater.

Similarly to Aeromonas spp., found in fresh and brackish (estuarine) waters and clinically presenting as diarrhea, vomiting, and abdominal cramps;  Acquired through contact with water, consumption of contaminated seafood, or contact with amphibians or reptiles (e.g., pet turtles);  Presence of blood/leukocytes in stool with invasive pathogenesis

An estimated 1.7 billion people are infected worldwide and 10 million in the U.S.;  Humans are the only natural reservoir with transmission via inhalation of infectious aerosols associated with close person-to-person contact;  Spread to health care workers and the rise in antibiotic resistant and multiple-resistance strains pose particular public health hazards.

Estimates of more than 2,000,000 cases per year in the U.S., mostly sporadic, and more than half from consumption of undercooked or improperly handled chicken;  More common than total infections caused by Salmonella  and  Shigella;  Unlike developed countries, in hyperendemic underdeveloped countries, children develop multiple episodes during the first few years of life and then appear to develop lifelong immunity.

Ubiquitous, opportunistic pathogens that occupy a variety of moist environmental habitats with minimal nutritional requirements, an ability to tolerate a wide range of temperatures (4oC to 42oC), and resistance to most antibiotics and disinfectants;  found throughout hospitals in moist reservoirs;  Immunocompromised patients, burn patients, IV drug abusers at highest risk.

Natural reservoir is upper respiratory tract of domestic animals (e.g., dogs, cats) with humans acquiring the infection with an animal bite or scratch;  Subsequent suturing of the wound can exacerbate the infection, allowing for a reduction in the pO2 and growth of the facultative anaerobe. 

Common cause of enterocolitis in Scandinavian and colder areas of North America, some studies show increased incidence during colder months which leads to the speculation that this organism may be more clinically active in cold climates, a hypothesis that parallels the observed increased metabolic activity at 22oC to 25oC;  Epidemic outbreaks have been associated with contaminated meat or milk;  In 1987, blood-transfusion related bacteremia and endotoxic shock was reported with organisms apparently able to survive and grow in nutritionally rich blood products that are stored by prolonged refrigeration.

Often appear as specimen contaminants due to typical colonization of skin, but can cause endocarditis with infections of native heart valves and artificial valves or infections associated with other prosthetic devices (e.g., CNS shunts, prosthetic hips and joints, vascular grafts, peritoneal dialysis).

Initially recognized as a cause of peurperal sepsis, but now understood as a significant cause of septicemia, pneumonia, and meningitis in newborn children;  Organisms colonize the upper respiratory tract, lower gastrointestinal tract, and vagina (transient in as many as 40% of pregnant women);  Infection with subsequent development of disease in the neonate can occur in utero or during birth (early-onset neonatal disease), or during the first few months of life (late-onset neonatal disease) (approximately 60% of infants become colonized with the same serotype organism as colonizes the mother), or postpartum sepsis can occur in the mother, generally seen as endometritis or a wound infection.


   Return to Exam Pathogen Key


V.  CLINICAL SYNDROMES:  Match the organism from the Pathogen Key to the description of the clinical syndromes.  Each description matches only one organism and each organism is described no more than one time in this section.

Clinical disease associated with contact with infected cattle, cattle products, or dogs is a milder form than that associated with contact with goats and sheep (acute, severe, complications common) or swine (chronic, suppurative, destructive) with localization in cells of the reticuloendothelial system (RES).

Differences in clinical and immunological manifestations (type and number of skin lesions, histopathology, infectivity, and immune response including delayed hypersensitivity, immunoglobulin levels, and presence or absence of erythema nodosum leprosum) are used to identify the form of this disease that is diagnosed on a continuum from one end of the range to the other.

Genital ulcers (chancroid) are most commonly diagnosed in males (perhaps due to asymptomatic carriage in females) appearing 5 to 7 days after exposure with the lesion progressing to a painful ulcer and inguinal lymphadenopathy; Syphilis and herpes simplex disease must be excluded prior to diagnosis.

Clinical infection occurs either as i) cellulitis and lymphadenitis with pain and swelling from bites or scratches, ii) septicemia with systemic infection in immunocompromised patients, or iii) further pulmonary complications in patients with chronic respiratory disease.

Causes infection also known as , tick fever, borreliosis, famine fever.  An acute infection characterized by a 2-14 day (usually 6 day) incubation period followed by recurring febrile episodes, constant spirochaetemia  that worsens during febrile stages.          

Disease characterized by three stages;  i) Initially a unique skin lesion (erythema chronicum migrans (ECM)) with general malaise,  lesions periodically reoccur;  ii) Subsequent stage (in 5-15% of patients) have neurological or cardiac involvement;  iii) Third stage involves migrating episodes of non-destructive, but painful arthritis.

Primary pulmonary infection with secondary infection of pulmonary or extra-pulmonary sites with host cellular immunity resulting in tissue destruction and fibrosis (fibrous walling off of lesions, i.e. granulomatous reaction), caseation, calcification, and ultimately cavitation caused by host response to infection.

Formerly important cause of bovine tuberculosis transmitted by ingestion of contaminated milk.  Is uncommon in the United States, since the advent of pasteurization and herd surveillance.  Now important as species from which attenuated strain (Bacillus of Calmette and Guerin (BCG)) is used for preparation of tuberculosis BCG vaccine.

Disease with three clinical manifestations:  i) asymptomatic carriage in healthy children and adults, ii)  infection of fetus (granulomatosis infantisepticum) or newborn from infected mother, iii) infection of immunocompromised patients.

Clinical syndromes classified as (i) classical or foodborne (1 to 2 day incubation period culminating in flaccid paralysis and death attributed to respiratory paralysis), (ii) infant (with in vivo production of neurotoxin after consumption of spores), or (iii) wound (4 days or more incubation period with in vivo production of neurotoxin following direct inoculation of spores or vegetative organisms).

Primary disease process involves invasion of mucus membranes, rapid multiplication, wide dissemination through perivascular lymphatics and systemic circulation occur prior to development of the primary lesion;  10-90 days (usually 3-4 weeks) after initial contact the host mounts an inflammatory response at the site of inoculation resulting in the hallmark lesion, called the chancre (changes from hard to ulcerative), with profuse shedding of spirochetes; swelling of capillary walls and regional lymph nodes with draining;  primary lesion is resolved by fibrotic walling-off.

Strains with prominent capsules are major cause of community-acquired primary lobar pneumonia with necrotic destruction of alveolar spaces, cavity formation and blood-tinged sputum particularly in alcoholics and those with compromised pulmonary functions unable to clear aspirated oral secretions from the lower respiratory tract;  May also cause wound, soft tissue and urinary tract infections.

Causes mild flu-like febrile illness or severe systemic disease also called Weil’s disease (icteric form), characterized by renal and hepatic failure due to damage to the endothelium of small blood vessels with shedding of the abundant organisms in the urine;  Acute febrile jaundice and nephritis that is transmitted to humans from a variety of animal hosts (both wild and domestic mammals, e.g., dogs in the U.S.).

Two forms of food poisoning mediated by heat stable enterotoxin (usually in improperly stored, cooked rice) causing vomiting (emetic form) or heat labile enterotoxin causing diarrhea.

Plague with characteristic lymph node (buboes) swelling.

Human disease acquired by one of three routes: direct inoculation, inhalation, or ingestion of spores from contaminated soil or infected animal products.

Burn wound infections, bacteremia, endocarditis, pulmonary infections, complication of cystic fibrosis, ear infections, urinary tract infections, gastroenteritis, eye infections, musculoskeletal infections.  

Chronic type B gastritis, gastric and duodenal ulcers;  Possible gastric adenocarcinomas.

Bacteremia, histotoxicity with myonecrosis (gas gangrene), cellulitis, fasciitis, soft tissue infections, food poisoning (8 to 24 hour incubation period), or enteritis necroticans.

Overwhelming disseminated infections in immunocompromised patients, particularly common in AIDS patients in the terminal stages of their disease as CD4 lymphocyte levels wane;  may be referred to as atypical tuberculosis. 

Traveller’s diarrhea and infant diarrhea in developing countries generally presenting as a watery diarrhea with cramps, nausea, and low-grade fever due to effect of enterotoxin(s) on small intestine.

Hemorrhagic colitis with severe abdominal cramps, watery diarrhea followed by bloody diarrhea, little or no fever;  Can progress to hemolytic uremic syndrome (HUS) with acute renal failure and thrombocytopenia, particularly in young children;  Mediated by cytotoxic “verotoxin” or Shiga-like toxin action in the large intestine.

Meningitis, meningococcemia, pneumonia, arthritis, urethritis following dissemination of virulent organisms from the nasopharynx.

Infections including gram-negative sepsis, urinary tract infections, pneumonia, abdominal sepsis, meningitis, spontaneous bacterial peritonitis, and endocarditis.

Two-stage bacillary dysentery involving both small and large intestine;  Watery diarrhea in early stage changing to frequent, small volume stools with blood and mucus, tenesmus.

Disease is highly communicable (highly infectious),  person-to-person spread via inhalation of infectious aerosols.   Three distinct stages of disease: i) catarrhal, ii) paroxysmal, and iii) convalescent;  incidence in U.S.A. significantly reduced with required DPT vaccine

Suppurative disease including pharyngitis, scarlet fever, toxic shock-like syndrome, erysipelas, pyoderma, (puerperal sepsis, lymphangitis, pneumonia now rare in antibiotic area);  Post-infection, nonsuppurative sequelae often include acute rheumatic fever, rheumatic heart disease, and acute glomerulonephritis.

Opportunistic infections in hospitalized patients, particularly highly immunocom- promised patients receiving broad-spectrum antibiotics (e.g., hematological disorders, intravascular catheterization);  Opportunistic nosocomial infections include bacteremia/septicemia, soft tissue infections, pneumonia, meningitis, or urinary tract infections;  Therapy complicated by resistance to multiple antibiotics.

Dental caries (cavities) initiated by adherence to the enamel surface with the production of insoluble dextrans (adherent extracellular polysaccharide) from glucose that establishes a foundation layer for the formation of a complex biofilm known as dental plaque, enabling other oral flora to initiate colonization;  Acidogenic (production of acid) and aciduric (resistance to acid) properties are responsible for tooth decay.


   Return to Exam Pathogen Key


VI. Diagnosis, Treatment, Prevention & Control:  Match the organism from the Pathogen Key to the description.  Each description matches only one organism and each organism is described no more than one time in this section.

500,000 human cases per year caused by this organism with worldwide distribution, but less than 100 annual cases in the U.S. due to successful control of the disease in livestock and the animal reservoir (cattle, goats, sheep, swine, buffalo, bison, dogs, foxes, coyotes) including identification and destruction of infected animals/herds and animal vaccination;  Protective clothing for abattoir workers, avoidance of unpasteurized dairy products.

Grown on chocolate agar;  blood is heated to inactivate inhibitors and to release factors from red blood cells required for growth of organisms;  requirement for heat-labile V-factor (NAD, NADP coenzymes) and heat-stable X-factor (precursor of hemin)

Transmitted by direct sexual contact;  STD has long incubation period during which time host is non-infectious;  Useful epidemiologically for contact tracing and administration of preventative therapy;  Prostitution for drugs or for money to purchase drugs remains central epidemiologic aspect of transmission.

Large numbers (>107 organisms/ml) of encapsulated, small, gram-negative diplococci in the presence of  polymorphonuclear leukocytes (PMN’s) in cerebrospinal fluid (CSF);  Serogroups A, B, C, Y, W135;  Transparent, non-pigmented, oxidase-positive, nonhemolytic colonies on chocolate blood agar with enhanced growth in moist atmosphere with 5% CO2;  Although patients with systemic disease generally are bacteremic, commercial blood culture bottles contain toxic additives that may inhibit growth;  Differentiated from other species in the genus by acid production from glucose and maltose, but not sucrose or lactose.

Microscopy reveals encapsulated, small, gram-negative diplococci in side polymorphonuclear leukocytes (PMN’s) in urethral purulent discharge;   Penicillin is no longer the drug of choice because MIC has steadily increased, and plasmid-mediated enzymatic hydrolysis and chromosomally-mediated resistance has risen to >10% of all strains;  Ceftriazxone, cefixime, or a fluoroquinolone for uncomplicated cases and in combination with doxycycline or azithromycin for dual infections.

MRSA and VRE are abbreviations for two very important public health threats that are of particular concern in hospital settings.

Identify the pathogen to which MRSA is referring and also provide in your answer, the two words to which “MR” refers.

Identify the pathogen to which VRE is referring and also provide in your answer, the two words to which “VR” refers.

Microscopic detection of acid-fast bacilli in clinical specimens (particularly early morning sputum respiratory secretions) can be accomplished by carbol fuchsin stain (e.g.,  Kinyoun or Ziehl-Nielsen), fluorescent auramine-rhodamine dyes (Truant fluorochrome), followed by decolorization in an acid-alcohol solution, and counter staining.


   Return to Exam Pathogen Key


VII. General Concepts. Consider the following partial list of general concepts as potential topics for exam questions.

Host-parasite interactions

Koch’s Postulates

Immune response against pathogenic infection/disease, including:



            Non-specific defenses

            Specific immunity

Morphology, including:

Cell walls and cell membranes


Outer membrane proteins

Motility and flagella


Virulence factors, including:



Lipopolysaccharide and endotoxin


Microbial defenses against host immunological clearance

Anaerobic infections

Antibiotics & chemotherapy, including:

Basic mechanisms of antibiotic action

Basic microbial mechanisms of antibiotic resistance

Minimal Inhibitory Concentration (MIC) & Minimal Bactericidal Concentration (MBC)

Sensitivity and specificity of a diagnostic test


   Return to Exam Pathogen Key


   Go to Pathogen List



BSCI 424 — Pathogenic Microbiology — BSCI 424 HomePage

Lecture Syllabus General Course Information Grade Determination
Laboratory Syllabus Interesting WebSite Links Lab Safety

Designed & Maintained by David M. Rollins
Copyright © 2000, D.M. Rollins and S.W. Joseph
Revised: August 2000