Transmission/virulence Factors/pathogenesis

Front 1

Actinomyces

Back 1

Transmission: N/A (endogenous infections)
Virulence factors: none known; opportunistic pathogens that cause disease when normal barriers disrupted by trauma, surgery, etc.
Pathogenesis: direct damage to infected tissues

Front 2

Bacillus anthracis

Back 2

Transmission: contact with infected animals, inhalation of spores from animal hair or wool, inhalation of spores from act of bioterrorism
Virulence factors: edema factor (increase in intracellular levels of cAMP & excretion of H2O), lethal factor (interferes with cell signaling pathways and → cell death & tissue damage), capsule (prevents phagocytosis)
Pathogenesis: spores in alveoli transported to mediastinal lymph nodes; growth in lymph nodes & excretion of toxins cause most symptoms

Front 3

Bacillus cereus

Back 3

Habitat: grains such as rice
Transmission: ingestion of contaminated foods (usually rice; boiling or flash frying does not kill spores)
Virulence factors: heat-labile toxin (similar to cholera toxin; causes increase in cAMP in affected cells); heat-stable toxin (mechanism unknown)
Pathogenesis: toxins cause disease symptoms

Front 4

Campylobacter jejuni

Back 4

Transmission: fecal-oral route
Virulence factors: none known
Pathogenesis: histologic damage to mucosal surfaces of jejunum, ileum, and colon; actual mechanisms not understood

Front 5

Chlamydia trachomatis

Back 5

Transmission: via sexual contact in adults, neonates infected during passage through birth canal, eye infections mostly by hand-to-eye contact
Virulence factors: none known
Pathogenesis: replicates in & kills epithelial cells (LGV biovar also replicates in mononuclear phagocytes); stimulates proinflammatory cytokine response

Front 6

Clostridium difficile

Back 6

Transmission: fecal-oral route; spores difficult to eliminate from hospital environment – can cause nosocomial infections
Virulence factors: toxin A (enterotoxin → increased permeability of intestinal wall), toxin B (cytotoxin → depolymerization of actin → apoptosis and death of enterocytes)
Pathogenesis: increased permeability of intestinal wall → diarrhea; death of enterocytes → development of pseudomembranes in colon

Front 7

Clostridium perfringens

Back 7

Transmission: contamination of open wound (gas gangrene), ingestion of contaminated food (food poisoning)
Virulence factors: multiple toxins – especially alpha toxin (phospholipase C; lyses several types of human cells, → increased vascular permeability and bleeding, tissue destruction; gases (CO2, H2; bubbles compress small blood vessels in surrounding healthy tissue & → ischemia & necrosis; enterotoxin (alters membrane permeability in intestinal epithelial cells; superantigen)
Pathogenesis: gas gangrene: toxins cause extensive tissue damage; food poisoning: enterotoxin causes symptoms; gas gangrene:

Front 8

Escherichia coli

Back 8

Transmission: community-acquired UTIs usually caused by patient’s own strains, GI diseases transmitted via indirect fecal-oral route, nosocomial UTIs usually catheter-related, neonatal meningitis acquired during birth
Virulence factors: endotoxin (LPS), pili (adhesin), capsule (inhibits phagocy-tosis), enterotoxins (certain strains), Shiga toxin (serotype O157:H7), type III secretion system
Pathogenesis: endotoxin → sepsis, shock; enterotoxins & Shiga toxin → GI diseases; UTIs result from colonization of bladder and/or kidneys

Front 9

Haemophilus influenzae & H. influenzae type b

Back 9

Transmission: droplet infection
Virulence factors: polysaccharide capsule (type b only; inhibits phagocyto-sis), IgA protease, adhesins (pili), endotoxin (LPS)
Pathogenesis: unencapsulated strains cause mucosal infections but are not invasive; encapsulated (type b) strains invade → epithelium → bloodstream, etc.

Front 10

Helicobacter pylori

Back 10

Transmission: ingestion
Virulence factors: cytotoxins (Cag A, Vac A), Pic B (→ cytokine production), urease (urea → NH3 + CO2), proteases & lipases (damage mucous gel)
Pathogenesis: ammonia (from urease) & cytotoxins damage epithelium, damage to mucus gel exposes epithelium to acid; very strong inflammatory response greatly adds to damage (combination of factors → ulceration)

Front 11

Francisella tularensis

Back 11

Transmission: arthropod vector (ticks), exposure to aerosols, ingestion of contaminated meat, entry through open wounds, etc.
Virulence factors: unknown
Pathogenesis: organism localizes in reticuloendothelial cells

Front 12

Listeria monocytogenes

Back 12

Transmission: across placenta or during delivery (neonatal disease); inges-tion of contaminated foods (most cases in immunocompromised hosts)
Virulence factors: internalin (induces phagocytosis); listeriolysin O and phospholipases (escape from phagosome, movement into adjacent cells)
Pathogenesis: direct damage to infected tissues

Front 13

Mycobacterium leprae

Back 13

Transmission: direct skin contact with respiratory secretions and wound exudates; possibly via inhalation of aerosols
Virulence factors: none known
Pathogenesis: tuberculoid form: direct damage to skin & peripheral nerves, granuloma formation; lepromatous form: direct damage to skin, peripheral nerves, cartilage, bone, etc.

Front 14

Mycobacterium tuberculosis

Back 14

Transmission: droplet transmission
Virulence factors: no exotoxins or endotoxin
Pathogenesis: granulomas and caseation mediated by cellular immunity

Front 15

Neisseria gonorrhoeae (“Gonococcus”)

Back 15

Transmission: via sexual contact in adults; neonates infected during passage through birth canal
Virulence factors: pili and Opa protein (attachment to epithelial cells), Por protein (prevents phagolysosome fusion in neutrophils), lipooligosaccharide (mild endotoxin activity)
Pathogenesis: attaches to mucosal cells, replicates in mucosal cells, passes through mucosal cells & establishes infection in subepithelial space

Front 16

Nocardia

Back 16

Transmission: exposure to environmental source via inhalation, puncture wound, etc.
Virulence factors: none known; opportunistic pathogen that causes disease only in immunocompromised hosts
Pathogenesis: direct damage to infected tissues

Front 17

Propionibacterium acnes

Back 17

Transmission: N/A (endogenous infections)
Virulence factors: none known
Pathogenesis: phagocytosis of bacteria in sebaceous follicles releases sub-stances that → localized inflammatory response

Front 18

Pseudomonas aeruginosa

Back 18

Transmission: water aerosols, aspiration, fecal contamination
Virulence factors: endotoxin, adhesins (pili, LPS, etc.), exotoxins (exotoxin A, pyocyanin), various tissue-damaging enzymes (LasA, LasB, alkaline protease, phospholipase C, exoenzymes S & T)
Pathogenesis: direct damage to tissues via effects of virulence factors

Front 19

Rickettsia akari

Back 19

Transmission: arthropod vector (urban mite)
Virulence factors: none known
Pathogenesis: replication at site of inoculation → ulcer with eschar; patho-genesis of other symptoms not well understood

Front 20

Rickettsia rickettsii

Back 20

Transmission: arthropod vector (ticks)
Virulence factors: none known
Pathogenesis: replication in endothelial cells → vasculitis; inflammatory and cell-mediate immune responses cause most damage & symptoms

Front 21

Salmonella enterica

Back 21

Transmission: fecal-oral route
Virulence factors: type III secretion systems (aids invasion of mucosa)
Pathogenesis: invades mucosa of small and large intestines (→ M cells), inflammatory response stimulates production of cAMP & secretion of fluid into lumen; can be released into blood or lymphatic circulation

Front 22

Salmonella Typhi & Paratyphi

Back 22

Transmission: fecal-oral route
Virulence factors: capsule (interferes with phagocytosis)
Pathogenesis: infects cells of reticuloendothelial system (especially in liver and spleen); chronic carrier state established in gall bladder

Front 23

Shigella

Back 23

Transmission: fecal-oral route
Virulence factors: Shiga toxin (S. dysenteriae only) – A-B exotoxin that blocks protein synthesis (targets intestinal villus epithelial and renal endothelial cells)
Pathogenesis: invades mucosa of ileum & colon but generally doesn’t penetrate further; induces apoptosis & release of IL-1β → destabilization of intestinal wall

Front 24

Staphylococcus aureus

Back 24

Virulence factors: cell components (capsule, peptidoglycan, adhesins), toxins (cytolytic, exfoliative, enterotoxins, toxic shock syndrome toxin), enzymes (coagulase, hyaluronidase, lipases)
Pathogenesis: toxin activity (scalded skin syndrome, food poisoning, toxic shock syndrome), abscess formation & direct tissue damage (endocarditis, skin infections, pneumonia, empyema, osteomyelitis, etc.)

Front 25

Staphylococcus agalactiae (Group B Strep)

Back 25

Transmission: in utero (ascending infection) or exposure during birth
Virulence factors: none known; opportunistic pathogen
Pathogenesis: direct damage to tissues

Front 26

Staphylococcus epidermidis

Back 26

Transmission: most infections caused by patient’s own strains, transfer on hands possible
Virulence factors: no major virulence factors (opportunistic pathogen)
Pathogenesis: uses extracellular polysaccharide capsule material to attach to artificial surfaces (biofilm formation)

Front 27

Streptococcus pyogenes

Back 27

Transmission: droplet infection
Virulence factors: mechanisms for avoiding phagocytosis (hyaluronic acid capsule, M protein, C5a peptidase), adhesins & invasins (M & F proteins), enzymes (streptolysins, strepokinases, DNases), pyrogenic toxins
Pathogenesis: pyogenic infections involve direct tissue damage & inflam-matory responses; rheumatic heart disease results from immunologic cross-reactivity; acute glomerulonephritis caused by immune complexes

Front 28

Vibrio cholerae

Back 28

Transmission: fecal-oral route
Virulence factors: cholera toxin (A-B exotoxin; causes elevated cAMP and secretion of water & electrolytes), accessory cholera enterotoxin (increased intestinal fluid secretion), zonula occludans toxin (increased intestinal permeability), chemotaxis proteins (adherence to intestinal mucosa)
Pathogenesis: toxins → severe diarrhea, vomiting, and severe dehydration; no invasion of tissues

Front 29

Vibrio parahaemolyticus

Back 29

Transmission: ingestion of raw or undercooked shellfish, especially oysters (gastroenteritis); exposure of open wound to seawater (wound infections)
Virulence factors: Kanagawa hemolysin (induces chloride ion secretion → diarrhea)
Pathogenesis: toxin causes gastroenteritis

Front 30

Yersinia pestis

Back 30

Transmission: arthropod vector (flea), pneumonic plague transmitted by droplet infection
Virulence factors: endotoxin (LPS), type III secretion systems (apoptosis of macrophages), capsule protein (resistance to phagocytosis), plasminogen activator protein (degrades complement C3b and C5a, fibrin clots)
Pathogenesis: infection of lymph nodes → buboes; bacteremia & release of endotoxin → septic shock

Front 31

Coxsackie Viruses

Back 31

Diseases: aseptic meningitis, herpangina (Coxsackie A), pleurodynia, myco-carditis, hand-foot-and-mouth disease (Coxsackie A15)
Transmission: fecal-oral route
Pathogenesis: replication (lytic) in epithelial tissue → viremia → various organs (depending on specific strain of virus)

Front 32

Cytomegalovirus (CMV; HHV5)

Back 32

Diseases: congenital abnormalities; pneumonia & hepatitis in immunocom-promised patients; various infections in organ transplant recipients placed on immunosuppressant drugs
Transmission: across placenta, in various body fluids, by organ transplanta-tion
Pathogenesis: initial infection in oropharynx; virus spread to many organs in fetus; disseminated infections in immunocompromised individuals

Front 33

Filoviruses (Ebola, Marburg)

Back 33

Diseases: hemorrhagic fevers
Transmission: direct contact with infected animal fluid or tissue, accidental needle sticks, etc.
Pathogenesis: growth of virus (lytic infection) in multiple tissues → exten-sive damage & necrosis

Front 34

Hepatitis A Virus

Back 34

Diseases: hepatitis A (infectious hepatitis)
Transmission: fecal-oral route
Pathogenesis: replication in GI tract → viremia → liver; hepatocellular injury caused by immune attack by cytotoxic T cells

Front 35

Hepatitis B Virus

Back 35

Diseases: hepatitis B (serum hepatitis)
Transmission: sexual intercourse, blood-to-blood (parenteral), perinatal
Pathogenesis: replication in hepatocytes; hepatocellular injury caused by immune attack by cytotoxic (CD8) T cells

Front 36

Hepatitis C Virus

Back 36

Diseases: hepatitis C (“non-A, non-B hepatitis”)
Transmission: blood-to-blood (parenteral); sexual transmission and trans-mission from mother to child possible
Pathogenesis: hepatocellular injury probably caused by cytotoxic T cells

Front 37

Herpes Simplex Virus Type 1 (HSV-1, HHV1)

Back 37

Diseases: cold sores, keratitis, encephalitis, genital herpes (but most cases causes by HSV-2), herpes whitlow, herpes gladiatorum
Transmission: saliva-to-saliva contact; direct contact with virus in lesions
Pathogenesis: replication (lytic) in epithelial tissue → lesions; latent infec-tion in trigeminal ganglia; recurrences possible on reactivation of virus

Front 38

Herpes Simplex Virus Type 2 (HSV-2, HHV2)

Back 38

Diseases: genital herpes, meningitis, neonatal infections, cold sore (but most cases caused by HSV-1)
Transmission: sexual contact (adults), passage through birth canal (neonatal infections)
Pathogenesis: replication (lytic) in epithelial tissue → lesions; latent infec-tion in lumbar or sacral ganglia; recurrences possible on reactivation of virus

Front 39

Human Herpesviruses 6 & 6 (HHV6, HHV7)

Back 39

Diseases: roseola infantum
Transmission: droplet infection
Pathogenesis: detailed mechanism not well understood

Front 40

Human Papilloma Virus (HPV)

Back 40

Diseases: warts, condylomata acuminata (genital warts); associated with carcinoma of cervix and penis (especially HPV-16 and HPV-18)
Transmission: direct contact with skin or genital lesion
Pathogenesis: replication in squamous epithelium of skin or mucous mem-branes stimulates rapid proliferation of cells

Front 41

JC Virus

Back 41

Diseases: progressive multifocal leukoencephalopathy (PML)
Transmission: droplet infection (?)
Pathogenesis: infection during childhood → latent infection; reactivation of virus in immunocompromised host → replication in CNS → demyelination of CNS tissues

Front 42

Mumps Virus

Back 42

Diseases: mumps (orchitis, oophoritis possible in adults)
Transmission: respiratory droplets
Pathogenesis: replication in upper respiratory tract → spread to local lymph nodes → viremia → spread to various organs (especially parotid glands)

Front 43

Norovirus (Norwalk Virus)

Back 43

Diseases: gastroenteritis
Transmission: fecal-oral route
Pathogenesis: infection limited to mucosal cells of GI tract

Front 44

Parvovirus B19

Back 44

Diseases: erythema infectiosum (fifth disease), arthritis (in adults), aplastic anemia, hydrops fetalis
Transmission: respiratory droplets, transplacental
Pathogenesis: replication in upper respiratory epithelium → viremia → bone marrow → lytic infection of erythrocyte precursor cells → transient anemia

Front 45

Rotavirus

Back 45

Diseases: gastroenteritis (especially in small children)
Transmission: fecal-oral route
Pathogenesis: replication in columnar epithelial cells small-intestinal villi; viral NSP4 protein → influx of Ca++ into enterocytes, stimulates release of neuronal activators & neuronal alteration of water absorption

Front 46

Rubella Virus

Back 46

Diseases: German measles, congenital rubella syndrome
Transmission: droplet infection, transplacental infection of fetus
Pathogenesis: replication in upper respiratory epithelium → migration to local lymph nodes → viremia → various tissues (especially skin) → skin rash

Front 47

Rubeola Virus

Back 47

Diseases: measles
Transmission: respiratory droplets
Pathogenesis: replication in upper respiratory epithelium → viremia → infection of endothelial cells; skin rash caused by immune T cells targeted against virus-infected endothelial cells in small blood vessels under skin

Front 48

Varicella-Zoster Virus (VZV, HHV3)

Back 48

Diseases: varicella (chicken pox), zoster (shingles)
Transmission: droplet infection
Pathogenesis: replication in upper respiratory epithelium → viremia → cells of reticuloendothelial system & lymphatic system → secondary amplification → secondary viremia → skin → chicken pox lesions; latent infection in dorsal root or cranial nerve ganglia; reactivation of virus → migration down neural pathway → skin → lesions in single dermatome, damage to nerve endings

Front 49

Varioloa Virus

Back 49

Diseases: smallpox
Transmission: droplet infection; direct contact with skin lesions
Pathogenesis: initial infection in oropharynx → regional lymph nodes → viremia → mononuclear phagocyte system (spleen, bone marrow, lymph nodes) → secondary viremia → dermal & oropharyngeal vasculature → smallpox lesions

Front 50

Candida albicans

Back 50

Diseases: fungal vulvovaginitis; wide range of opportunistic infections in compromised hosts (thrush, disseminated infections, etc.)
Transmission: N/A, member of normal flora (endogenous infections)
Pathogenesis: opportunistic pathogen; growth of fungus → direct tissue damage

Front 51

Dermatophyte Fungi

Back 51

Diseases: tinea infections (“ringworm”)
Transmission: direct contact with lesions; exposure from environment
Pathogenesis: growth of fungus in keratinized layer of skin → inflammatory response

Front 52

Malassezia furfur

Back 52

Diseases: pityriasis (tinea) versicolor
Transmission: direct contact with lesions; exposure from environment
Pathogenesis: growth of fungus only causes very superficial infections

Front 53

Pneumocystis jiroveci

Back 53

Diseases: Pneumocystis carinii pneumonia (PCP), various types of extrapul-monary infections – only in immunocompromised hosts
Transmission: droplet infection (immunocompetent hosts are asymptomatic carriers)
Pathogenesis: growth in alveoli provokes inflammatory response

Front 54

Zygomycetes (Mucor, Rhizopus)

Back 54

Diseases: zygomycoses (various forms)
Transmission: inhalation of spores from environment
Pathogenesis: direct damage to infected tissues; opportunistic pathogens that cause disease primarily in ketoacidotic diabetic and leukemic patients

Front 55

Ascaris lumbricoides

Back 55

Diseases: ascariasis
Transmission: via food contaminated with soil containing eggs; humans are only hosts
Pathogenesis: eggs hatch in small intestine; larvae then penetrate intestinal mucosa, enter bloodstream, rupture into alveoli of lungs (cause pulmonary symptoms), coughed up, swallowed; in small intestine, swallowed larvae → adult worms (females lay eggs passed in stool)

Front 56

Cryptosporidium parvum

Back 56

Diseases: cryptosporidiosis (especially diarrhea)
Transmission: fecal-oral route (cysts); human and animal reservoirs
Pathogenesis: trophozoites attach to intestinal mucosa but do not invade; pathogenic mechanism unknown

Front 57

Entamoeba histolytica

Back 57

Diseases: amebic dysentery (amebiasis); liver abscess possible complication
Transmission: fecal-oral route (cysts); humans only reservoir
Pathogenesis: trophozoites invade colonic epithelium and produce flask-shaped ulcers; can spread to liver by invading veins & traveling to portal venous system; necrosis of hepatocytes in liver

Front 58

Enterobius vermicularis (Pinworm)

Back 58

Diseases: pinworm infection
Transmission: ingestion of eggs (often via fecal-oral route); humans are only hosts
Pathogenesis: worms and eggs cause perianal irritation and pruritus

Front 59

Fasciola hepatica (Sheep Liver Fluke)

Back 59

Diseases: fascioliasis (liver fluke disease)
Transmission: ingestion of aquatic plants, water, or food contaminated with infective metacercariae; ingestion of raw sheep liver (from infected sheep)
Pathogenesis: metacercariae → larvae in GI tract, larvae → duodenal wall → peritoneal cavity → liver → bile ducts (mature into adult worms); may migrate back to liver (liver rot)

Front 60

Giardia lamblia

Back 60

Diseases: giardiasis (gastroenteritis)
Transmission: fecal-oral route (cysts); human and animal reservoirs
Pathogenesis: trophozoites attach to intestinal wall (but do not invade) and interfere with absorption of fat and protein

Front 61

Necator americanus (Hookworm)

Back 61

Diseases: hookworm
Transmission: filariform larvae in soil penetrate skin of feet; humans only hosts
Pathogenesis: larvae → bloodstream → lungs (pulmonary symptoms) → trachea (swallowed) → small intestine (attach to walls, produce eggs that are passed in feces and → filariform larvae

Front 62

Strongyloides stercoralis

Back 62

Diseases: strongyloidiasis
Transmission: penetration of skin by filariform larvae; humans only host
Pathogenesis: filariform larvae → bloodstream → lungs (pulmonary symp-toms) → trachea (swallowed) → small intestine (mature into adults); auto-infection cycle kept in check by immune response; loss of immunity allows autoinfection cycle to → superinfection

Front 63

Taenia solium (Pork Tapeworm)

Back 63

Diseases: taeniasis (tapeworm infection), cysticercosis
Transmission: ingestion of larval stage of T. solium (cysticercus), usually in raw or uncooked pork (taeniasis); ingestion of eggs in fecally contaminated food or water (cysticercosis); humans and pigs are reservoirs
Pathogenesis: taeniasis: scolex attaches to small intestinal wall, develops into adult by producing proglottids (often asymptomatic or mild); cysticer-cosis: eggs → oncospheres → penetrate intestinal wall → bloodstream → various tissues & develop into cysticerci

Front 64

Toxoplasma gondii

Back 64

Diseases: toxoplasmosis (including congenital toxoplasmosis)
Transmission: ingestion of oocysts from environmental source; ingestion of infected animal tissues (felines are primary reservoir hosts); transplacental infection of fetus
Pathogenesis: opportunistic pathogen that infects immunocompromised hosts; tachyzoites → bloodstream → various tissues → tissue cysts; loss of immune response allows cysts to germinate & tachyzoites replicate in and kill tissue cells