Diagnostic Features



Condition Info

Gram-positive cocci (6%) Staphylococcus
STOIC Pustular Imepetigo Folliculitis Furuncle Carbuncle SSSS (Staph scaled skin syndrome) Bullous Impetigo TEN (Toxic Epidermal Necrosis) S. aureus Cause of most infections, coagulase +, golden colonies TSS (Toxic Shock Syndrome) Gram +, grapelike clusters. Faculatative anaerobe. Cytolytic and exfoliative exotoxins. Staphylococcal Food Poisoning Staph. Pseudomembranous Colitis Bacteremia Endocarditis transferred by physical contact, fomites, aspiration S. aureus pneumonia Staph. Mediated Septic Arthritis S. epidermidis S. saprophyticus surgery/ skin wounds UTI's Staph. Associated Osteomyelitis Coagulase negative staph disease Coagulase negative staph disease SEARS Strep Throat Seasonal variation in disease: Winter: pharyngitis, RF, PSGN. Summer: pyoderma, PSGN Might colonize oropharynx of healthy: host develops Ab to M-protein. Diseases occur before Ab or if commensal bacteria insufficient Scarlet Fever Puerperal fever "Childbed fever" Streptococcal Toxic Shock Syndrome Erythematous posterior pharynx. Culture + creamy yellow exudate. Localized lymphadenopathy. Halitosis (bad breath) Spreads via person to person contact. Resolution or abcess or Rhematic Fever (sequele) Complication of Strep Throat. Fever, H/A, malaise, anorexia, pharyngitis. Diffuse erythematous rash that blances with pressure. Strawberry tongue. 1st appeard on upper chest and then spreads to extremities. Circumoral pallor. Spares palms and soles. Septicemia following childbirth that occurs because of poor hygiene on the part of the delivering physician. Infxn from endometrium --> others and baby. Cause by different strain of S. pyogenes than one causing pharyngitis. Localized pain and inflammation. Systemic signs (feverl/chills/n/v/diarrhea). Can progress to shock and organ failure. Sudden fever. Hypotension, Rash (diffuse, blanching). Involvement of 3 or more organ systems. Acute superficial skin infection after URI. Localized erythema, bullae and pain. Clear distinction between infected and non-infected skin - well defined borders. Localized lymphadenopahy and possible systemic signs. More superfician than cellulitis. Deeper infection of the skin and subcutaneous tissue. Most commonly face and trunk. Erythema, warmth, tenderness. No clear distinction between infected and non-infected tissue. Systemic signs and symptoms are more common than with erysipelas. Peau d'orange. Caused by mutant form of S. pyogenes in susceptible people. Possibly fatal. Unexplained localized redness, swelling and pain. May have flu symptoms. Rapid spread, descruction of tissue. TSS develops if not aggresively treated. Complication of Srep A associated URI. Damage to HT valve predisposes patient to bacterial endocarditis. CHANCE: Chorea, migratory polyArthritis, subcutaneous Nodules, Carditis, Erythema marginatum Complication of Strep A disease. Cause of renal failure. Generalized edem, oligouria, dark urine, fatigue, ab pain Endogenous infection acquired in utero or in 1st 7 days of lige. Pneumonia, meningitis, bacteremia with neurological squelae. Exogenous disease within 1 week - 3 months after birth. Meningitis. A condition of the mother. Rise in temperature to greater than 38 on any 2 consecutive days after the 1st 24 hours post-partum. Fever, chills, malaise…foul smelling, yellow green/blood tinged lochia (discharge) Normal gut flora. URTI in immunocompromised. Needle stick. Lobar Pneumonia Sinusitis S. pneumoniae 85 antigenically distinct subtypes Lancet-shaped in diplococci or short chains. Otitis Media Meningitis Bacteremia S. viridans S. mutans and dental carries Bacteremia, abcess Very rapid onset. Single severe shaking chill with persistently high fever. Productive cough: hemoptysis, copious purulent "rust" colored sputum. May have URI before and immunocompromized have minimal symptoms. MC R middle lobe. Facial pain, tightness, H/A. Decreased valsalva (defection) and dependency (gravity). Tenderness. Low fever and mucopurulent discharge Otaglia (pain in ear), otorrhea, tinnitus, vertigo, nystagmus. Reduced acuity. Bulging, erythematous TM with reduced visible landmarks, gluid line and displaced COL Sudden onset of fever, nuchal rigidity (stiff neck), blinding H/A, n/v. Irritability, malaise, restlessness, delerium. Petechial rash. Seizures. S. pneumonia is 4-20x more likesly to cause neruological complications than other bacterial meningitis. Sequele : defness, blindness, mental retardation, memory loss, SIADH (syndrome of inappropriate ADH secretion) endocarditis, arthritis, or peritonitis Poor flossing/brushing --> S. mutans sticks to enamel --> acidic environment --> plaque. Carie develops if demineralization is greater than minteralization Wound or traumatic injuries Physical exam: increased fremitus (vibration), dullness on percussion, Adventitious sounds (crackles) on auscultation. CXR: dense uni-lobar consolidation with typical air bronchograms. Rapid onset of visible signs. Lab: Gram +, lancet shaped, encapsulated Many causes: Strep pneumonia, H. influenza, Moraxella catarrhalis. Increased risk with dietary sensitivites, ABC,s… Common causes: N. meingitides, H. influenza, S. pneumonia. CSF culture +, decreased CSF glucose, predominate cells are PMNs. Viral mengitis is less severe/quick and is culture -, increased CSF protein and lymphocytes in CSF Risk: inadequate salivary flow (And all the usual stuff like hygiene and high sucrose) Rapid Strep Test (+) (Direct Elisa) High Anti-ASO Ab titer Lab test - DICK test. Macule --> Papule --> Honey Crusted Lesion Superficial, raised, red, pus-filled bump Unresolved folliculitis. Painful raised nodule with underlying necrotic tissue. Unresolved furuncle. Deep into cutaneous tissue. Also have chills and fevers (could lead to sepsis) Secreted Toxin. Perioral erythema & whole body rashes. No scarring No secreted toxin. Perioral erythema. Rash primarily on fase. Scarring. Painful localized erythema. Large flaccid blisters. Epidermis peels off in sheets. Fever, chills, myalgia, malaise, n/v, H/A. Potentially fatal (fluid imbalance and organ failure) Fever, diffuse mascular erythematous rash that can deqaquamate. Potentially fatal: hypotension, septic shock, multiple organ system failure (MOSF) Intoxication. Very rapid onset of illness. Severe n.v, ab pain/cramps. No fever & watery, non-bloody diarrhea. Lasts 24 hours or less Watery diarrhea, abdominal cramps. Fever. White, ulcerated plaques on colonic mucosa. Often disseminates to HT (endocarditis) Triad: fever, murmur, anemia. Chest pain, dyspnea, clubbing fingers. Chills, rigor, night sweats. Weight loss. Arthritis. Characteristic skin lesions: 1) Janeway - flat, painless lesions on palms and soles during acute episodes. 2) Osler's Notes - painful red bumps on pads of fingers and toes. 3) Septic embolization - localized infarction in extremeties 4) Splinter hemorrhages - linear bleeding under nails Central cyanosis, dyspnea, chest pain. Sudden fever with prolonged chills. Productive cough with mucupurulent sputum. Bacterial related inflammation of joints. In children, adults with prosthetic or diseased joints, and intra-articular injection therapy. Painful, erythematous joints with purulent aspiration of fluid. Infection of osseous tissue. Children: sudden pain in metaphyseal area. Adults: intense back pain with fever. Infections associated with: catheters, surgery, CVS shunts and artificial joints. Primary cause of endocarditis in artificial HT valves Cause UTI's in sexually active women. Dysuria, pyuria, culture + urine

Ubiquitous - part of normal skin and nasopharynx flora

Nikolsky sign + (easy to separate stratum corneum) Nikolsky sign Sequelae to certain drugs. DDX from SSSS: age, history, biopsy Risk factor: hyper absorbency tampons and intravaginal contraceptive devices From contaminated food: processed meats (e.g. ham), turkey, potato salad Very similar to disease caused by Clostridium Difficile. DDX by lab dx: Stool culture + and Stool leukocyte + Most common source is iatrogenic 50% mortality. Initially looks like fly but can progress rapidly if not treated ASAP. Suspect if: congenital HT dx, IV drug use, chronic localized abcess or infection 2 types: 1) Apiration - in young/elderly. People with COPD , post-influenza. 2) Hematogenous. LAB: CXR patchy infiltrates with consolidation and abscesses. Culture + sputum with neutrophils Number one cause of this: Neiserrio Gonorrhea Lab dx: blood culture +, Brodies abcess on Xray (necrosis)


DDX Staph TSS: Strep is most commonly after deep tissue infection vs tampon usage. No single virulence factor (vs. TSST-1) No exfoliative rash.

Group A Strep - S. pyogenes

Gram + pairs/chains

Streptococcal Erysipelas "St. Anthony's Fire"

transferred by respiratory droplets or break in skin after contact with vector

Streptococcal Cellulitis Necrotizing Fasciitis Rheumatic Fever Acute Glomerulonephritis CAMP test: used to differentiate group B from group A strep. Early Onset Neonatal Disease Late Onset Neonatal disease Postpartum (peurpural) feverl UTI

Jones Criteria 1) Supporting evidence for preceding Group A strep infection (+ throat swab, rising ASO titers) 2) at least 1 major and 2 minor manifestations (see notes) Document group A strep infection. Blood: Anti DNAse B+, Urine: frank hematuria, proteinuria, RBC casts Risk factors: heavily colonized birth canal. Maternal disseminated group B Strep infection Risk factor: contact with heavily colonized persons. Breastfeeding is important!! Risk factors: Unsterile obstetric techniques!! Hand washing!

Group B Strep - S. agalactiae Group D Strep - S. Enterococcus

In the normal flora of the femail genital tract


Normal gut flora.

Resistant to bile salts. ABC resistant.

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Gram-positive endospore-forming rods (4%) Clostridium
Inhibits acetylcholine release at presynaptic terminals and therefore, flaccid paralysis (opposite tetanospasmin) Gram (+) bacillus, "sausage shaped" Botulinum toxin: one of the most potent neurotoxins. Two parts: B - protects from ST acid. A part neurotoxin specific to irreversible binding to cholinergic neurotoxins Replicated in 10 min! Food borne botulism "Intoxication" Inadequate sterilization of food: home canned foods, preserved fish. 2h-72 hour incubation. No GI distress - unlike other food poisonings, Dilated, fixed pupils; dry/ "furry" tongue. Bilateral descending weakness - of neck, face, throat. Respiratory paralysis (mortality 32-40%.) No permanent immunity - can get repeated occurances. MC complete recovery in months to years. Consumption of honey contaminated with spores. MC form of Botulism in the USA. MC in 1-6 months because infant GIT doesn't have as many competitive bowel microbes. Can resemble SIDS iff rapid onset. Non-specific signs: constipation, weak cry, failure to to thrive, weak sucking. Floppy baby: acude flaccid paralysis (head, fact, throat), descent to extremities/trunk. Death reom respiratory paralysis (low 1-2% mortality)

C. botulinum

Ubiquitous - soil, sedaments of lakes and ponds, and decaying vegetation. Homecanned foods are the MC source. Honey is the MC source of infant botulism.

Infant botulism "infection-intoxication"

Wound botulism

Very rare, little evidence of clinical infection. Limited paralysis. Same sx's of food borne botulism but long incubation (1-4 days) and no abdominal pain or constipation

Unclassified botulism Can be normal gut flora. Found in soil, air and water. C. perfringens need devitalized tissue to grow best C. perfringens Disease MC after trauma that causes ischemia: lowered pO2 and pH favors C. perfringens growth Simple wound infection Anaerobic cellulitis Gram (+) "plump, rectangular" rod Alpha toxin lecithinase

People over 1 year who have had symptoms of botulism but no documented vehicle of transmission. DDX is important. People over 1 year who have had symptoms of botulism but no documented vehicle of transmission. DDX is important. Trauma and favourable conditions. Organism spread through subQ tissue - spares fascia and deep muscles. Pain, redness, inflammation, superficial skin discoloration and skin necrosis. Gas forms develop suppurative myostitis - foul smelling discharge. No muscle necrosis, no systemic signs and symptoms. Rapid worsening of cellulitis. Trauma and 1 week incubation. Rapid onset of intense pain, extensive muscle necrosis (blue black, edematous, Fast growth of culture on sheep's blood agar. Nagler's reaction on egg yolk agar. Gram (+) rods in tissue does not bleed or contract on stimulation), toxic delerium. Progress to shock, renal failur, death within 48hrs if untreated. Much damage due to specimens with no leukocytes. alpha toxin and gas bubbles. MC in areas of poor blood supply. Need to perform debridement and examine inderlying tissue. Ingest meat (refrigerating and re-heating destroys enterotoxins) Large infective dose. Short incubation: 8-24 hrs. Abdominal cramps. Self limiting > 24 hrs. Watery diarrhea, no fever or vomiting.

C. perfringens myonecrosis "Gas gangrene" C. perfringens food poisoning

C. tetani

C. difficile

Tetanospasmin: heat labile neurotoxin (one of the most potent toxins). Causes spasdic paralysis. Spores are widespread in the 2 part toxin: B chain binds soil. Enter the body through R in neuronal membrane. penetrating injury. A chain moves to postsynaptic terminals in CNS and irriversibly long, thin bacillus with "tennis inhibits the release of raquet" morphology GABA and glycine difficult to grow: sensitivy to O2 - obligate anaerobe. Relatively inactive metabolically (unlike C. perfringens) 2 toxins: Toxin A is like cholera enterotoxin and Can be a normal part of GI Gram (+) rods causes diarrhea and flora without causing disease mucosal damge. Type B: diphtheria-like cytotoxin. MC after broat spectrum obligate anaerobes, spore- Difficult to culture, very ABCs and Proton pump forming slow growing. inhibitors (PPI's) Gram strain variable: (-) in old cultures of fresh wounds, (+) in fresh culture Primary reservoirs: domestic herbivores (sheep, goats, cattle, horses) Three routes of transmission: Inoculation of skin, inhalation of spores, ingestion of contaminated food. Developing countries: endemic, can't affort to vaccinate livestock Developed countries: occupational disease and biological warfare Ubiqutous distribution

Tetanus "lockjaw"

MC form of tetanus. Bacterium introduced by trauma to skin: rusty nail, animal bites. 3 Early signs: 3 day-2 week incubation. Muscle stiffness/ ridigity, exaggerated DTRs (deep tendon reflexes). Trismus (lockjaw), risus sardonius (rye smile), drooling, dysphagia, diaphoresis, irritabiliey. Later signs: opisthotonus (backward arching), flexion of arms, extension of lower extremitis. Complications: HTN/hypotension, tachycardia, pneumonia, dehydration, bone fractures, meningitis, Rh incompatibility. Other forms: 1) localized (to point of infection, less common than generalized), 2) Cephalic (rare but poor prognosis, from improperly cleaned umbilical stump), 3) Neonatal - first sign, difficulty sucking 8-10 days after birth.

Patient history. Clinical S's and Sx's. Gram stain culture not that important diagnostically - only 30% of people with tetanus are culture (+). Treatment: tetanospasmin binds irreversible and therefore, can only treat symptoms until nerve terminals regenerate. Either penicillin high doses or tetracycline, or passive immunization - bind free tetanospasmin and decrease progression of disease.

Pseydomembranous colitis

Range from mild diarrhea to colitis to potentially life-threatining pseudomembranous colitis. Prolonged diarrhea --> dehydration.

Pseudomem colitis confirmed by biopsy - multiple, raised white/yellow exudative plaques adhering to colonic mucosa. In vitro cytotoxicity assay in culture cells. Immunoassay for C. difficile toxins A and B. Sigmoidoscopy. Fecal leukocytes.

ABC-associated diarrhea

Bacillus species
Gram (+) bacillus. Single or paired "joined bamboo rod" Capsule - anti-capsular Abs are NOT protective Cutaneous anthrax Painless papule. Ulcer surrounded by vesicles - necrotic eschar - gelatinous edema. MC arms, hands, face, neck. Potentially fatal - 20% mortality (could spread to blood/lymph) . Internal hemorrhage, myalgia, fever, H/A, n/v. Carried by alveolar macrophages to mediastinal LN - prolonged latency. Initial disease: fever/chills, dyspnea, cough, H/A, vomiting, chest/ab pain. Second stage: rapidly worsening fever, pulmonary edema, massive enlargement of mediastinal LNs, shick/death within 3 days. Hemorrhagic meningitis Sx's MC than pulmonary Sx's. Direct contact with spore contaminated animals/producers. Look at px history: wool worker? Gm (+) bacillus in lesions, no neutrophils.

Inhalation anthrax (pulmonary) culture - "medusa head long, serpentine chains" Toxin: 3 parts that work together: Protective Ag (binding, anti-phagocytic), lethal factor, edema factor (stim adenylyl cyclase)

No person to person disease transmission. 87% mortality.

B. anthracis

"Wool sorters disease"

Ingestion anthrax

IFF upper GI: ulcers, edema, sepsis, regional lymphadenopathy - dysphagia. IFF lower GI: n/v, malaise, systemic s's and sx's, bloody diarrhea Extremely rare. 100% mortality.

Gram (+) bacillus

B. cereus

Farmers get this Low mortality compared to B. anthracis

Heat stable enterotoxin causes emesis. Found in contaminated, improperly refrigerated rice dishes Heat labile enterotoxin similar to enterotoxin of ETEC and Vibro cholera Profuse watery diarrhea. Contaminated meat and veggies.

Emetic disease

Contaminated rice, not refrigerated. 15 min-4hr incubation. Self limiting >24 hrs. Nausea, no fever or vomiting.

Diarrheal disease Bacillus cereus panopthalmitis

Contaminated meat, veggies, sauces. 8-12 hr incubation in GIT. Self limiting <24 hrs. Nausea and bloody diarrhea. No fever. Post-traumatic, penetrating eye injury or hematogenous spread. Pain, H/A, drowziness, swelling. Muddy grey iris, turbid aqueos humor, precipitate on posterior surface of cornea. Rapid <48 progressive loss of light perception. Fever.

Gram positive non-spore forming rods (2%) Cornebacterium
C. diphtheriae All species are opportunistic pathogens Ubiquitous worldwide distribution on plants and animals Disease is transmitted most commonly by areosolized nasopharyngeal secretion Normal commensals of the skin and URT Cornyebacterium diphtheriae respiratory diseases Gram + club shaped bacillus Exotoxin: Classic A-B type Form grey pseudomembrane that bleeds if forcibly removed. Malaise, sore throat, low grade fever, chills, pharyngitis. Can cause sequelae Schick test - like the razor. of myocarditis, CHF, focal neurological signs Clinical signs and symptoms are most important. Culture +, PCR for tox gene, Elek test for toxin produced. Treat with diphtheriae anti-toxin or ABC's. Screening test: Schick (like TB test)

Cornyebacterium diphtheriae cutaneous diseases papule that can progress to chronic persistent ulcer with greyish membrane. Can progress to systemic signs and symptoms if not treated Black colonies with tellurite Non-pathogenic or medium. Dark grey colonies. opportunistic infxns. May contribute to acne

Other Cornebacterium Diptheroids

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Zoonotic: disease of animals that is transmissible to small, Gram + cocobacilli humans. Animal vectors: birds, ticks, spiders… L. monocytogenes rarely affects humans but high mortality Ubiquitous: direct person to person, ingest contaminated "chinese character clumping" meat and dairy - V or L shapes. Tumbling Vertically transmitted (esp. motility. transplacentally) is the most fatal type of transmission Listeriosis

Dark red rash over trunk and legs. Endocarditis, fever malaise, septic shock, circulatory collapse and hepatosplenomegaly. Occur in 4 populations: 1) Pregnant female: causes abortion and most common in 3rd trimester with mild brief disease of chills, fever, malaise. 2) Fetus: aborted or early onset disease (granulomatosis infantiseptica) - multi organ disseminated abscesses of granulomas and high mortailty; 3) Neonate: signs of meningitis; 4) Adults: low grade fever with personality changes. Also may get meningitis/gastroenteritis

CSF culture -, motility test +, cold enrichment

Gram-negative diplococci (4%) Neisseria
Humans are sole natural carriers Gram (-) diplococci, "coffee bean" appearance Pili - enhance ability to attach to mucosal surfaces and inhibit phagocytosis IgA Protease - neutralizes secretory IgA Need intimate sexual contact. Facultative anaerobe MC in 15-24 year olds. LOS endotoxin Opthalmia neonatorum Gonorrhoeae in males 95% of men get acute symptoms. MC'ly gonococcal urethritis. Infection usually restricted to mucous of penis. 2-7 day incubation - purulent urethral discharge, red/ edematous urethral meatus, itching, burning, dysuria, urgency. Can progress to peri-urethral abcesses, prostatitis, epididymitis. Urethritis. Yellow-green discharge. >50% of women are asymptomatic or mild symtoms. Infection site MC'ly cervix (cervicitis). 2-7 day incubation. Vaginal discharge or abnormal vaginal bleeding, dysuria, urgency, swollen painful abdomen (RUQ). If untreated an ascending infection can develop. Major cause of infertility iff chronic. Secondary: Fitz Hughe Curtis syndrome: periphepatitis (affects liver - symptomatic gonorrhea). Can lead to PID. Rare but MC in women (1-3%). Systemic symptoms or complex syndrome with fever, migratory arthralgias, tender papillary lesions/ rash on extremities. Arthritis: MC'ly mono-articular - knee in females. N. gonorrhoeae is the #1 cause of purulent arthritis in young adults MC'ly caused by N. gonorrhoeae or C. trachomatis. 2-5 days after vaginal birth. Purulent conjunctivitis in newborns infected during vaginal delivery. Sticky discharge, edema/ inflammation. Can lead to scarring and blindness. Reason why newborns get eye drops of 1% sulver nitrate. Clinical signs similar to Chlamydia. Gram stain: sensitive and specific iff men with purulent urethritis. Oxidase (+), Gram (-) diplococci on chocolate blood agar - (Thayer-Martin agar) Genetic probes: PCR, ELISA.

N. gonorrhoeae

2nd most common STD in the US (chlamydia is #1)

Gonorrhoeae in females Disseminated gonorrhoeae

Can be normal flora of URT

Gram (-) diplococci, "coffee bean" appearance


Meningiococcemia - mild disease

Persistent (few days to weeks). Arthritis. Petechial skin rashes. Pharyngitis. Low grade fever.

N. meningitidis

MC cause of baterial meningitis in infants through adolescence and in transferred via close contact young adults with respiratory droplets (e.g. daycares, military barracks). Classmates in school not close enough.

Can ferment glucose and maltose (onlke N. gonorrhoeae which only ferments glucose).

Capsule - resists phagocytosis

Meningiococcemia - marked disease

URI infection then 1-3 day incubation. Small, petechial rash on trunk and lower extremities that can coalesce to form larger bullae (due to thrombosis of small blood vessels). Iff untreated can progress to DIC or hammorhage into adrenal glands (Waterhous-Friderichsen syndrome). Sequelae: none or large areas of necrosis. Deafness. Mortality 100% if untreated, 25% if treated. Occurs with or without meningitis. Rapid onset fever.

Catalase and oxidase +

IgA Protease - neutralizes secretory IgA

Meningococcal meningitis

N. mengintidis is 2nd MC cause of adult bacterial meningitis. Triad: fever, nuchal rigidity, blinding HA. Neurological sequelae (hearing deficits, arthritis, memory loss) low compared to H. influenzae or S. pneumonia

Clinical signs and symptoms and CSF analysis. High number of Gram (-) diplococci in PMNs.

Gram negative rods (14%) Escherichia
Part of the normal flora of the GIT: opportunistic pathogen 1) Adhesins: colonize GTU or GIT despite voiding or peistalsis Neonatal Meningitis Colonization of infants with E. coli is common but rarely leads to disease Most commonly caused by E. coli and group B strep. Most isolated strains from babies have K1 capsular Ags (maternal anti-K1 Abs are protective).

2) Exotoxins


Usually results from spread from GIT or GTU. Increased mortality if immunocompromised or due to complication of intestinal perforation.

E. coli is most common cause of enterobacterial septicemia (45%), then K. pnemonia

E. coli

Increased risk of disease with: hospitalization, poor personal hygiene, travel to countries with poorly developed sanitary practices, sub-optimal immune defences

Gram (-) bacillus with outer envelope


Cystitis: dysuria, urgency, increased frequency, incomplete voiding. Pyelonephritis: same as cystitis but more severe and with fever, loin pain and (+) KI punch.

Very common infection. (decrease attachment with D-mannose, blueberry & cranberry juice). Lab dx: pyuria, hematuria, bacteriuria.

3) H and K antigens relative importance/ Gastroenteritis - Enterotoxigenic (ETEC/ VTEC) presence of these factors depends on genetics of the Enteroinvasive (EIEC) - "taveler's diarrhea" strain + site of infection + condition of host Enteropathogenic (EPEC) Enteroaggregative (EAggEC) Enterohemorrhagic (EHEC) Diffuseaffregative (DAEC)

Gastroenteritis (6 types) - most common E coli infection in normally healthy persons. Exotoxins: St a/ST b: Most important cause of traveler's diarrhea and infant diarrhea (in developing countries). Symptoms take 3-4 days to resolve. Symptoms similar heat stable, stimulate guanylyl cyclase. LT1/ LT 11: heat labile, stimulate adenylyl cyclase. Induce fluid to cholera but much milder. Cramps, nausea, vomiting (Rare), low grade fever, watery diarrhea. and electrolyte loss: watery diarrhea Variable onset (1-4 days). Intense abdominal cramps. Can progress to colonic ulceration and more severe sequelae. Similar disease to Bacteria invade and destroy tissue. Shigella. Fever. Initial watery diarrhea progressing to scant, bloody stool that is leukocyte +. Bacteria adhere to plasma membrane of mucosal epithelial cells and destroy adjacent microvilli. Common Nausea. Fever. Non-bloody stool. Bottle fed infants cause of infant diarrhea. Cause persistant diarrhea in developing countries. Subset of EPEC that can form aggregates on surfaces Nausea. Low grade fever. Persistant, watery diarrhea (dehydration on risk). that they colonize. 3-4 day incubation. Severe abdominal pain. Most commonly self-limiting in 4-10 days but can progress to HUS (hemolytic uremic syndrome). Most common strain causing disease in developed nations. Cause of "Hamburger disease" and HUS Spread via: undercooked beef or other meat, feces contaminated water, unpasteurized milk, fruit juices, raw veggies/fruit. Nausea. No fever or (Walkerton). Virulence factor: hemolysin. Very low inoculation is needed (100 bacilli) just low grade. Initial non-bloody diarrhea progressing to bloody diarrhea. - E coli O157:H7 Watery diarrhea (infants 1-5) Bacteria are embedded in cell membrane of elongated microvilli.

K. pneumoniae Opportunistic pathogen Mucoid colonies Large capsule - prevents Lobar Pneumonia phagocytosis UTI's Thick jelly-like sputum that may have blood.

E. aerogenes Normal flora of the LI in humans and animals Fast-growing, shiny colonies Facultative anaerobes UTI's, nosocomial

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C. freundii Similar to salmonella, whithout Occurs in normal flora causing salmonellosis UTI's

Humans are the only known animal host. GB infxn = Gram (-) bacillus carrier state. Disease in NA primarily associated with foreign travel. Facultative anaerobe Spread by food or water contaminated by infected food handlers Humans most commonly get Salmonellosis from: undercooked poultry, contaminated cutting boards, egg salad, undercooked/ raw eggs Animals are the primary reservoirs for S. enteritides: livestock, fish, poultry/ birds, Gram (-) bacillus rodents, humans, reptiles (turtles) Requires a high infective dose - killed by gastric acid. Antacids inc risk of infxn. Salmonella induced septicemia Symptomology similar to other Gram (-) septicemia: 10% of patients develop arthritis, osteomyelitis, and endocarditis Most commonly due to S. typhi and S. paratyphi but also seen with S. enteritidis. Increased risk with AIDS, geriatrics and pediatrics.

S. Typhi

Enteric fever

MC spread is by food handlers infected with S. typhi (typhoid fever) or S. paratyphi (paratyphoid fever). Non-specific systemic symptoms (H/A, malaise, myalgias, and anorexia). Rose coloured spots on abdomen (erythematous, maculopapular, Bacteria pass directly through intestinal walls. Enter thoracic duct and then blood stream to replicated in blances with pressure, only 50% of patients). Complications: GI lesions, Toxemia, meningitis, osteomyelitis, endocarditis. 1-3% become chronic Sp, LV, bone marrow and GB. Back into the intestine to cause increased inflammation. This is NOT carries. Increasing, remittant fever. typhus.

S. enteritidis

S. enteritidis gastroenteritis

Occurs 6-48 hours after ingestion of contaminated food or water. Abdominal cramps, h/a, myalgia. Most commonly self limiting (2 days to 1 week). Low mortality but increased risk with elderly and children. Nausea, fever and non-bloody diarrhea.

Most common type of Salmonellosis

Humans are the only carriers S. dysenteriae Transmission due to fecaloral route Gram (-) rod Very low inoculum (only 10-100 baccili) Attach and invade M cells in PP Shiga toxin (only S. dysenteria) disrupts protein synthesis Shigellosis - bacillary dysentery GI symptoms are caused by Shiga toxin. Enterotoxic, neurotoxic and cytotoxic. 1-3 day incumation. Fever and diarrhea proceeds to tenesmus, Bacteremia rare. Infection self-limited. 5% can asymptomatically carry. abdundant blood and pus in stool. Profuse watery diarrhea.

S. sonnei Can be normal flora of the colon. Opportunistic - enter via catheterization Main microbe.

Bloody diarrhea

Usually produces a mild watery diarrhea in children. In more virulent strains it can progress to abdominal cramping and bloody mucoid stools.

P. mirabilis P. vulgaris Highly motile colonies, outgrow other organisms Urease + (Urea --> ammonia and CO2) UTI Once there is an infection, urease can lead to stone formation.

Get bitten by infected flea, 2-6 days later get high fever, chills. Not large but painful buboes in groin, axilla, neck. Prostration with rapid, thready pulse, delerium. Bubonic purperea: vasculitis of superficial blood vessels cause bleeding into skin - black death. Can spread to blood then to lungs. Fatal within days (75% mortality) Black plague 2 types: Urban: affects humans and can cause 3 types of plague. Rats are the main reservoir, rat flea (Xeopsylla cheopsis) is main vector. 2) Sylvatic (Woodland): disease of wild rodents found everywhere but Australia

Ubiquitous Invades through lymphatics causing them to swell (buboes). Can also cause hemorrhaging --> DIC or septic shock.

Gram (-) rod or coccobacillus

Bubonic plague

Y. pestis

Org clots in flea's stomach by enzyme coagulase then is regurgitated into the Zoonotic: most common vectors are rodents: rats, Bipolar staining: "safety pin" human at next meal. ground squirrels, rabbits, appearance mice, prairie dogs, cats, ect. Can be transmitted by: fleas or inhalation Facultative anaerobe Gram - rod that is oval in shape and larger than Y. pestis.

Pneumonic plauge

Hematogenous spread from infected buboes or aerosols from infected person. Only 2-3 day incubation. Fever, malaise, hemoptysis, dyspnea. Highly virulent, rapidly fatal form of bronchopneumonia (90% mortality)

Septicemic plague

Direct deposit of bacteria into open wound or orifice. Most common in children. Rapidly fatal meningitis before buboes form. Need a large infective dose, ingest contaminated food product. 4-6 day incubation. Right sided abdominal pain. Lasts for 1-2 weeks. Can progress to perforation of ilum and skin rash (erythema nodosum). Can get mesenteric adenitis in children (mimics acute signs of appendicitis). Fever. Watery or bloody diarrhea. - mimics appendicitis

Y. enterocolitica

Assoc with polyarthritis with diarrhea

Enterotoxin similar to E. coli ST toxin.

Yersinia entrolytica gastroenteritis/ Yersinosis

Blue-green pus: 2 pigments: pyocyanin (blue) and pyoverdin (green) Gram (-) baccilus Sweet, grape-like fruity Ubiquitous - soil, water, odor plants, hospital sinks and respiratory equipment, swimming pools, raw vegetables. Can be a part of Minimal nutritional normal flora. requirements - can grow in distilled water. Strickly aerobic. Bacterial Keratitis UTI's GIT infections Swimmer's Ear Bactermia Hot tub folliculitis Ecthyma gangernosum Contaminated central water systems, especially AC Not person to person - just inhalation Thin, flagellated, nonsporulating gram Aerobic Unilateral, acutely painful, photophobic, intensely injected eye. Decreased visual acuity. Profuse tearing, thick ropey mucopurulent discharge. Edematous cornea and eyelid 3rd leading cause of nosocomial UTIs. Prolonged indwelling catheters. Any part of the tract. Eg. Perirectal, pediatric diarrhea, gasteroenteritis, necrotizing enteritis Initial pruritis and fullness in ear. Increased pain/tenderness on palpation. Otorrhea (?), Possible hearing loss (mild erythema and edema of external auditory canal. Dull injected TM with displaced COL). No systemic signs. Primarily nosocomial. Increased risk if immunocompromised. Similar clinical presentation as other bacteremias but with higher mortality. After breakdown in skin integrity (burns, trauma, cuts, dermatitis). High moisture conditions or immunocompromised. Pathognomic Pseudomonas skin infection. Erythematous vessels become hemorrhagic, necrotic and ulcerated with a fruity odor. Can have rapid necrosis to adjacent tissue (potentially fatal) Can get chronic supporitive OM, malignant otitis externa or Swimmer's ear (acute diffuse otitis externa). Weber test: laterlize to affected side. Rinne test: AC>BC. Most common cause of bacterial keratitis and neonatal opthalmia. Increased risk iff immunocompromised, contaminated eye drops (contacts), hypoxic damage from prolonged contact wearing, corneal trauma, eye operations. Can lead to blindness. Most common bacteria is S. aureus unless contact wearer, then P. aeruginosa.

P. aeruginosa Goes to the lungs in CF patients --> pneumonia

L. pneumophila Discovered in 1976 legionnaire's conference Legionellosis, legionella pneumonia Incubation is 2-10 days. Spread through contaminated central water systems (especially AC). NOT person to person spread. Flu-like symptoms Culture, serological tests for rising serum IgM with rising fever, cough, pneumonia, diarrhea, and delerium.

Gram-negative curved rods (4%) Helicobacter
Found in stomach of humans, Microaerophillis, urease + primates, pigs, cheetas, dogs, cats, ferrets, mice, rats Only found in gastric antrum Closely resembles and body campylobacter Gram (-) bacillus: gram stain is variable. Sprial shape in Developing countries high fresh culture, coccoid in older colonization, developed culture countries low colonization Flagellated, highly motile "corkskrew motion" Type B (infective) gastritis Peptic ulcer disease (PUD) Gastric adneocarcinoma Epigastric pain, abdominal tenderness, bloating, nausea, anorxia, dyspepsia. Epigastric tenderness on percussion, foul smelling breath, hematemesis (coffee grounds) (Type A gastritis is autoimmune AKA pernicious anemia) Expecially dodenal ulcers. Burning, gnawing upper GI pain 1-3 hours after meals. < night, > eating or > antacids. Anemia, epigastric tenderness. Sequelae of untreated chronic gastritis. Classifies as a class I carcinogen. Fatigue, weight loss, low grade fever, night pain. Epigastric/abdominal mass. Hemoccult (+) stools, anemia. Chronic H. pylori infection assoc with B-cell lymphoma. No evidence that eradicating H. pylori prevents the progression of gastritis to carcinomas 30-50% of people with gastritis have H. pylori but most commonly asymptomatic. Lab Dx: 13C urea breath test, anti-H. pylori Abs (IgG), gastroscopy with biopsy, CLO test (+( Endoscopy, urea breath test, serology (anti-H. pylori Abs)

H. pylori

Gastric mucosa-associated lymphoid type (MALT) Dysphagia, dyspepsia, weight loss, GI bleeding - hematemesis. B cell lymphomas

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Transmission is recal-oral Not recognized as a pathogen route of animal-contaminated until 1973 food or water Microaerophilic Some strains can produce an enterotoxin similar to cholera. Low infectious dose. Resistant to penicillins and cephalosporins. Gastroenteritis 2-11 day incubation. Foul smelling, watery diarrhea progressing to profuse bloody diarrhea. Resolution in 3 days - 3 weeks. Residual histological damage to mucosa of jejuni, ileum and colon. Idiopathic, peripheral polyneuritis 1-3 weeks after mild above conidition. Progressive, symmetric pain and weakness in extremities - might ascend to trunk, face, thorax. Self limiting (few weeks to months) with complete recovery. Many causes. Also immunizations, pregnancy, URI, EBV, CMV, Hodgkin's lymphoma. Autoimmune link: cross reactivity with glycosphingolipids on surface of neural tissue

C. jejuni

Comma or S-shaped

Guillian Barre syndrome

Can have human carriers. V. cholerae Epidemics in SE Asia, Europe Large animal reservoir in and Africa marine shellfish Fecal-oral via contaminated food or water Comma shaped O1 antigen causes epidemics, non-O1 antigen are non pathogenic or cause mild diarrhea O1 --> entrotoxin production Need large infective dose. Simulates G protein --> cAMP --> water in intestine Food poisoning Manifests after 24-48 hr incubation. Occurs after eating contaminated seafood. Sx include painful abdominal cramps and watery diarrhea as well as, sometimes, flu-like syndrome. Self limiting. ABC not helpful. Cholera 2-3 day incubation. Abrupt onset of watery diarrhea and vomiting. Rice water stools. Severe fluid and electrolyte loss.Hypovolemic shock leads Cam resemble ETEC induced gastroenteritis. Lab Dx: rarely seen in Fram stained stool or wound to cardiac arrhythmia, renal failure, muscle cramps. 60% mortality iff untreated, self limiting within a week. No abdominal cramps or fever. specimens. Dark field/ phase contrast microscopy: characteristing darting motility.

oxidase positve Facultative anaerobic

V. parahemolyticus

Lives in salt water in costal areas globally

Gram-negative coccobacilli (4%) Haemophilus
Coccobacillus with a polysaccharide capsule H. influenzae Can be normal flora of the URT Pili - damage respiratory ciliated epithelium Menigitis Epiglottitis Cellulitis Arthritis Otitis media / Sinusitis Pneumonia H. ducreyi Indicater of dysbiosis in H. vaginalis (Gardnerella) vaginal flora. Appearance of clue cells. Common in tropical countries Non-encapsulated. Gram-variable rod. Chancroid Bacterial vaginosis Same signs and symptoms as other bacterial meningitis - but more insidious onset and increased risk of neurological sequelae. Used to be MC pediatric meningitis, before Hib vaccine Medical emergency, MC'ly in boys 2-4 yo. Dysphagia, drooling, muffled voice, minimal cough. Severe dyspnea. HIGH fever. Reddish/ blue patch on cheek or peri-orbital. Fever. Monoarticular. Large joint. Three MC causes: H. influenzae, S. pneumonia, Moraxella catarrhalis. Unexplained fever in children. Might be secondary to influenzae virus damage to respiratory epithelium. Secondary bacterial infection is more life-threatening than primary. STD, most common to developing world. Unlike primary syphilis which causes hard chancre. Soft, purulent, painful ulcer (genitalia). MC males, uncircumcised, tropical & sub-tropical (female MC asymptomatic). 5-7 day incubation. Progress to painful buboes, phimosis, urethral stricture. Positive whiff test (pungent, fishy odor with the application of 10% KOH). Trichomoniasis can also cause a positive whiff test. Gram stain of CSF. Chocolate agar culture. Agglutination reaction to PRP capsule in CSF and urine. "Thumb sign" on lateral X-ray of neck Gram stain of blood Gram stain of blood Gram stain of blood Gram stain of blood

Requires factor X (heme) and LPS - responsible for factor V (NAD) found on mengitis. Protease digests chocolate agar for growth secretory IgA.

Can only cause disease in humans - reportable disease Pertussis toxin - increase Adenylate cyclase. cAMP respiratory secretions/ mucous. Binds ciliated epithelium and kills NK cells, monocytes, macrophages, neutrophils Tracheal cytotoxin - part of the PG layer. Cause ciliostasis and then damage to ciliated epithelial cells - cough IL-1 = fever Filamentous haemagglutin and other adhesins: attachment to ciliated epithelial cells and PMNs. Intracellular survival protects against clearance by humoral immunity

Strictly aerobic

B. pertussis and parapertussis

Spread by infectious droplets.


Whooping cough

Incubation: 7-10 days, sub-clinical. Catarral phase: 2 weeks, looks like common cold: rhinorrhea, sneezing, low grade fever, anorexia, malaise Bacteria are best isolated using nasopharyngeal aspirates during catarrhal stage. Culture: difficult (most infectious stage). Paroxymal stage: 1-2 weeks, dry non-productive repetitive "whooping" cough. Cough ends in vomiting and exhaustion. humitidy, 35 C, 7 days, specialized agar (Bordet-Gengou medium) (only 50% of infected people are Convalescent stage: 2-4 weeks. Cough resolves, secondary complications: aspiration pneumonia, seizures, encephalopathy. culture (+). Throat swabs not as good - need synthetic fiber swabs. PCR. Lymphocytosis (not specific)

No long term imminity - can Encapsulated get disease more than once "protection" in developed countries due to DPT vaccine

Acid-fast rods (4%) Mycobacterium
"TB is the master impersonator." Primary infection (only 5% get active TB within 2 years): insidious onset: malaise/ listlessness, night sweats, low grade fever, unexplained weight loss and progressive fatigue. Productive purulent cough progressing to hemoptysis, dyspnea. Apical rales, cyanosis. Secondary TB (reactivation): haematogenous spread anywhere: miliaty TB (no pulmonary signs). Destroys tissues - liver, adrenals... CXR: cavitations in one or more upper lobes of lung. Sputum sample: acid fast bacillus. Fastidious growth requirements, PCR.. Skin test (Mantoux test/PPD) - intradermal injection, wait 48 hours and measure induration/ erythema (type IV hypersensitivity). Doesn't tell whether TB is active or not. False positives due to BCG vaccine.

M. tubercylosis

Causes more deaths worldwide than any other bacteria. Infects 1/3 of the population. Humans are natural reservoir. Spread via aerosolized droplets.

No toxin produced, it is phaocytosed and secretes Obligate, aerobic, acid-fast an exported protein that rod prevents fusion of the lysosome with the phagosome Produces caseous One of the slowest growers granulomas. Ghon complex on x-ray.


Armadillos are naturally Similar to M. tuberculosis but: infected and provide reservoir Can not be articicially cultured (need live mice or armadillos) Grow in globi bundles (encapsulated globs of rods in tissues) Similar to M. tuberculosis but only case opportunistic infections Also can cause lymphadenitis in children Found intracellularly in histiocytes, endothelial cells, Schwann cells

Tuberculoid (paudibacillary)

3-6 year incubation. Strong cellular response, weat humoral. Not infectious. <5 cutaneous macular lesions with hypopigmented centers. Some Will react to skin test - lepromin nerve enlargement and damage.

M. leprae Spread via respiratory route or contact with break in skin

Lepromatous (Multibacillary)

3-10 year infection. Weak cellular response, strong humoral. Relatively highly infectious. Most destructive - disfiguring skin/bone, cartilage lesions ("leonine face") Diffuse nerve involvement. Erythema nodosum present and >5 kin lesions

Not reactive to skin test

MC'ly disease in HIV/ AIDS M. avium-intracellulare patients but can cause complex disease in birds and pigs

Ubiquitous in water and soil

MAC diseases

Opportunistic infection. Begins as mild pulmonary disease: spreads to local lymph nodes and then quickly to every organ. AIDS px: fever, sweats, weight loss, fatigue, diarrhea, SOB. Pulmonary disease is similar to TB: usually GIT involvement, usually fatal within months. No person to person spread via aerosolized droplets.

Sputum cultures: acid fast bacilli. CBC with diff: AIDS diagnosis, anemia, neutropenia.

Spirochetes (4%) Treponema
Intimate contact. Vertical and Thin-walled, flexible, motile, horizontal transmission. spiral rods T. pallidum Contagious only during primary stage and rash of secondary stage - not highly contagious (only 30% chance after single sexual contact) Antibodies react with cardiolipin Syphilis Primary: small papule - painless, hard chancre. Painless, regional lymphadenopathy (buboes). Very infectious. Heals spontaneously within 2 months without scarring. Secondary: flu-like syndrome. Painless, localized lumphadenopathy. Diffuse, non-pruritic maculpapular rash, includes soles, palms. Very infecious (kissing). Tertiary (Lues/Leutic): after 3-40 years of latent syphilis. Gummas (flat rubbery tumors anywhere in body - ulcerate and heal by scarring). Affect many organ systems: neurosyphilis, cardiosyphilis. Painless or deep burrowing pain. Congenital: infected mother infects fetus. 1) Intra-uterine death; 2) Congenital abnormalities 3) Born appearing well then several weeks or up to 2 years later: snuffles, widespread desquamating maculopapular rash. (Risk if mother is in primary or secondary syphilis) Microscopy: no Gram stain, use silver stain and fluorescent stains. Non-specific tests: VDRL (veneral disease research lab) and RPR (rapid plasma reagin) (+4-6 weeks after infection - indicates current active disease but false positive). Specific tests: FTA-Abs (fluroscent treponema Ab) and MHA-TP (micro haemoglotunin for Treponema) - indicate past infection

Hyaluronidase - spreads through tissue

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vector: deer tick (Ioxdes scapularis/ Ioxdes pacificus) Larger than other spirochetes and more complex nutrition Dormant in glial cells required Microaerophilic Spirochetes release Internal flagella neurotoxins that affect pre and post-synaptic Contain cholesterol in cell membranes wall (unlike other bacteria) Unlike othr Borrelia diseases - non relapsing. Tick bite - must stay attached for >48 hrs. 7-30 day incubation. Stage 1: erythema migrans rash "bull's eye lesion". Annular rash with central clearing (40-60% don't get this!) Painless, non-infectious, H/A, myalgia, lymphadenopathy. Resolves 1-2 months. Stage 2: iff untreated develop into neurologic signs (meningitis, Bell's palsy, etc.), conjunctivitis or cardiac dysfunction. Stage 3: 2 months to 2 years after stage 1: migratory arthralgias/arthritis (knees, large joint, TMJ), encephalitis. Resolves in months, years or never. )Can manifest as popliteal cyst. ) If neurologic symptoms: neruoborelliosis. Clinical signs and symptoms and patient history. Culture and IFA stain of biopsy of initial rash (30% don't get rash and cross-reactivity with Treponema). Indirect ELISA. PCR. IgM or IgG Ab to spirochete.

B. burgdorferi

Lyme disease

Zoonotic - rodent (rat) and domestic animal (dog) reservoirs L. interrogans obligate aerobe Leptospirosis (Weil's disease) --> jaundice and aseptic meningitis Range from mild, febrile disease to LV/KI failure (Weil's disease iff icteric) No skin lesion at site of entry. Septic phase: aprupt onset fever, HA, myalgia, nausea, lasts 1 week. Immune phase - two days asymptomatic, then aseptic meningitis with severe HA, NV, myalgia. Weil's Too small for light microscope and Gram stain. Microscopic agglutination. disease (icteric) - jaundice, scleral and conjunctival hemmorhages and KI failure (MC cause of death)

Humans are accidental hosts: Survive moist, slightly MC'ly acquire disease via contact with infected urine alkaline environment for many days (up to 6 weeks in urine soaked soil). Swimming or drinking contaminated water

Wall-less bacteria (2%) Mycoplasma
Human pathogen only. Instead of a cell wall, have a 3 layer membrane (which Cause ciliostasis contains cholesterol) MILD URI/pharyngitis Acute tracheobronchitis M. pneumonia Smallest free-living organism Respiratory droplets "Fried egg" appearance Incomplete immunitiy "Walking pneumonia", "Eaton's agent" pneumona Erythema multiforme Stevens-Johnson Syndrome OM Hemolytic anemia Meningitis, pericarditis KI stones Urethritis Symptoms similar to RSV, group A strep Persistant dry cough that might become paroxysmal Prolonged, mild form of pneumonia. Initial symptoms "non specific". Increases in severity over a few days. Hypersensitivity syndrome (vasculitis). Bulls-eye lesions, associated with HSV. Severe, sometimes fatal, bullous form of erythema multiforme Common auto-immune destruction of RBCs C XRAY before symptoms felt Most difficult pathogenic organisms to grow (fastidious growth). "Fried egg colonies". Cold agglytination

U. urealyticum

Very similar to mycoplasma but urease + (breaks urea into ammonia and CO2)

Produce urease no progression to PID (non gonococcal). Might be asymptomatic

Obligate intracellular bacteria (4%) Rickettsia
Rocky Mountain Spotted Fever Painless tick bite leaves no mark (very low inoculum - <10 organisms) 1 week incubation - rapid fever, severe HA, nausea. 5 days later: rash DDX with Typhoid. (Typhus is Rickettsia). DFA stain of skin biopsy. IFA stain for LPS. Complement fixation diffuse, maculopapular rash, MC spread from trunk to extremities (inclusing palms and soles). Respiratory symptoms. Iff untreated spread to tests, (+) iff <4x increase in Ab titer. CNS (confusion), SP, GIT, LV. Encephalitis, DIC, shock, death (up to 20% mortality)

R. rickettsii

Need arthropod vectors MC in children and in summer hard ticks (dog tick or wood months tick) - Dermacentor Virus-like properties Intimate contact. Vertical and filterable and obligate horizontal transmission. intracelular parasites Bacteria-like properties Spread by droplets, hands, inner/ outer membranes, contaminated clothing, eye bacterial ribosomes, contain make-up, flies DNA, RNA and LPS

Trachoma disease Must have spscific attachment to conjuctiva - resist flushing from tears. Begins as conjunctivits. Entropian - eyelashes chronically irritate cornea causing ulceration Adult. Most common 18-30. Genital infection 1st then unilateral mucopurulent discharge in eye. Neonatal: infected mother and vaginal birth. Bilateral, intense papillary conjunctivitis with lid swelling, chemosis, and mucopurulent discharge Women: termed Chlamydia (the drip?) Most commonly asymptomatic (80%) but risk of intertility, miscarriage, ectopic pregnancy. Can cause urethritis, conjunctivits, perihepatitis (pain in RUQ). Pain/ cramping in lower abdomen, dyspaerunia, bleeding between menses. Men: NGU Currently MC bacterial STD in USA. (non gonoccocal urethritis). MC symptomatic (75%) - yellow clear discharge, pain/ tenderness of genitals. Ractive arthritis (Reiter's syndrome) can't see, can't pee, can't dance with me! Can cause cervicitis and PID. Seronegative (Rh-) spondyloarthropathy. MC in young men (20-40 years) that are HLA-B27 positiv. C. trachomatis is MC bacterial pathogen. Unexplained diarrhea, low grade fever. 2-4 weeks later conjunctivits, superficial lesions on palms/ sole/ oral mucosa, asymptomatic Clear yellow discharge (gonorrhea is yellow/purulent) polyarthritis, urethritis Also termed LGC. MC in Africa, Asia, South America (male homosexuals). Need adequeate sample of Reportable STD. Initial lesion: small painless papule on penis, urethra, glans, scrodtum, vaginal wall. 2nd stage: buboes --> painful, can infected cells (specimen of pus/ discharge is inapproptirate since they are in the cells). Culture: most rupture and drain spontaneously. Systemic. Mimics IBS. Can get proctitis in men and women. specific method, only infects certain cell lines; formation of inclusion bodies. DFA (direct fluorescent) staining. PCR. TWAR isovar. Human pathogen that can cause atypical pneumonia (mild, persistent cough/ malaise that might progress to lobar pneumonia). Difficult: PCR, Microimmunoflorescence Potential link to atherosclerosis, CAD, MS, asthma, Alzheimer's disease? MC in adults. Spread via respiratory droplets. Many cases subclinical. One of the leading causes of blindness in the world.

Trachoma inclusion conjunctivitis

C. trachmatis

MC STD in the US

Unlike other bacteria there is no PG layer, therefore no No long term immunity Gram stain Can get from toilet seat - EB is resistant to the Unique growth cell cycle environment! within host cell - EBs (elementary body) and RBs (reticylite body)

Chlamydia urogenital infections

Reactive arthritis (Reiter's syndrome)

Lymphogranuloma vererum

C. pneumoniae

Form of walking pneumonia.

Infects only humans. Spread by respiratory droplets. Infects birds and other animals. Spread by inhaling dry bird feces (parrots, parakeets, love birds and also poultry, pigeons, and canaries. Can also be respiratory droplets.

Chlamydiophilia pneumonia

C. psittaci

Chlamydophila psittace - parrot fever or Psittacosis

Cause psittacosis. Biggest risk from psittacine birds (parrots, mascaws, parakeets, cockatiels) Transmitted via inhaled dried bird excrement, urine and respiratory secretions. Non-productive cough., rales, mucous plug can block bronchi. Commonly progesses to CNS(encephalitis, convulsions, coma, death)

Rare person to person spread (non-productive cough). DX: serology: 4x increase in Ab titre. Prevention: control and quarantine domestic and imported birds.

FUNGI (8%) Superficial Funal Infections Tinea Infections
Malassezia furfur (pityriasis ovale) Phaeoannuellomycoses wernickii (Exophilia wernickii) Piedraia hortae Trichosporon beigelii Tinea, or ringworm, prefers heat and moisture Dermatophyte, it infects nails, skin and hair (never deeper structures). Presents as: Spread by direct contact with ringworm, dermatitis infected individuals Adapted to live on outermost, non-living layer of skin No immune reaction Just cosmetic Tinea (pityriasis) versicolor Tinea nigra Black piedra White piedra Lipophilic, yeast-like organism. Non-itchy hypopigmented telsions on upper torso, arms, abdomen. Dry chalky and scale easily. MC asymptomatic. Well demarcated, macular lesions on palms/soles. Hairs of scalp, mustache, beard, groin. Direct or sexual contact. Hairs of scalp. Direct contact only. "spaghetti and meatballs" organisms after KOH prep. Wood's lamp (+). DDX with vitiligo. Wood's lamp + (false negative 25% of the time) Characteristically dark pitmented yeast cells and hyphal fragments on KOH prep Dar, hard nodules along infected hair shaft Soft, pasty white growth on hair shaft.

Systemic Fungal Infections Histoplasma capsulatum
agricultural belt - N2 soil H. capsulatum Dimporphic: means it lives as MC found in "histo belt". a mold in soil and as a yeast (Ohio/ Mississippi River in tissues. valley to S. Ont/Que.) Also areas of a lot of bird (starling/ chichen) and bat excrement. Inhale hyphal fragments Primary histoplasmosis Only 5% of people get it. 10 day incubation. Acute, self limiting influenzae like illness (fever, malaise, dry cough, lymphatenopathy. Resolve Microscopy: 10% KOH prep with silver or Giemsa stain. Serological: skin test: too many false (+). Cultures: completely with some residual calcified lesions (coin lesions). Not contagious.Complications: overly aggressive immune response. Mediastinal slow growing (1-2 weeks) and spores are infectious. DNA probes. Direct ELISA. Characteristic millet fibrosis. Progressive: Disseminate via lumphatics. Increased risk if impaired CMI. TB-like iff chronic: fever, night sweats, weigh loss with seed pattern in lungs. destructive (caseating necrosis) lung lesions.

Convert to yeast form and replicate in macrophages -> travel to lymphatics

Ocular histoplasmosis syndrome.

Serious retinal condition. Leading cause of blindness in 20-40 year olds. Often misdiagnosed. "Histo spots" bilaterally. MC'ly no visual loss but can be activated to cause visual changes (4 kinds)

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Coccidioides immitis
Dimorphic - 37C, tissue, multinucleated sperule "sporangia" C. immitis New World Disease -azole drugs treat fungal infections In San Jaouquin Valley in Cali (SW US) MC in males: 25-55 Endemic in soils of hot, dry, semi-arid areas. Extensively spread via dust storms. Coccidiodomycosis (San Joaquin valley fever)

1) MC'ly asymptomatic. 2) 40% of infected people get mild, febrile to moderately severe respiratory disease. Not contagious. 3) <5% progressive pulmonary disease. 4) <<1% - disseminated disease. Erythema nodosum with arthralgia.

Skin test antigens. Skin test 2-4 weeks after symptoms. Coccidiodin. Spherulin - hypersensitivity testing. (for both phases)Complement fixation. CXR - "egg shell" lesions. Tissue Biopsy- staining and microscopy for spherules. Culture - CAUTION - infectious - leading cause of lab infections! Coin like lesions on xray.

Blastomyces dermatiditis
unknown reservoir - unlike H. Endemic areas overlap those capsulatum it is rarely of Histoplasmosis cultured from soil Dust clouds at construction sites or crop dust during farming Can cause diseases in animals Inhale conidia phargocytosed by macrophages - convert to yeast - replicate in macrophages Carried by lymphatics Acute Blastomycosis 45 day incubation. Bronchopneumonia. Drenching sweats, No residual calcified lesions (unlike Histo). Not contagious. Skin lesions are slowly expanding ulcerative or cerrucous lesions with a granulous base on face and mucocutanoues borders of nose and mouth.Ulverative granulomas of skin and bone are most recognizable signs of a disseminated infection. Skin test and serology - too many false (+). Microscopty - biopsy/ histology of KOH prepped tissue. Culture. No tuberculat macroconidia in saprobic phase (unlike H. capsulatum). CXR.

B. dermatiditis

Chronic Blastomycosis

TB or cancer like

Opportunistic Fungal Infections Candida albicans
C. albicans Seen in AIDS patients. Normal flora of URT, GI, female genital tracts. Not spread person to person. oval yeast that stains grampositive Can grow in germ tube serum Thrush (oral candidiasis) Candidal vaginitis Chronic mucocutaneous candidiasis White patches on an erythematous base that can be scraped off. Perleche is the name given to candidal infections at the corners of the mouth (related to dentures not fitting or persistant, excessive lip moisture) Manifests as vaginal erythema, white discharge, pruritis, and burning. Skin lesions are clearly defined, erythematous patches with satellite pustules on red bases. Multiple erythematous, pustular, or thick lesions appear, particularly on the face.

Aspergillus strict pathogen (unlike Candida) Extremely common. Vshaped branching and septate hyphae. no yeast-like form - only a mold form (form spore bearing hyphae) Aspergillosus flavus (on peanuts, corn and other grains) produces aflatoxin - very potent carcinogen: hepatocellular carcinoma Mycotoxicoses hypersensitivity pneumonitis (allergic bronchopulmonary aspergillosis) Aspergillus Secondary colonization Paranasal granuloma Otitis externa/sinusitis Sepsis Allergic broncophulmonary asperfillosis associated with asthma (10-20%) Aspergillus colonizes pre-existing cavity. Minimal distress, hemoptysis. Chronic sinusitus due to Aspergillus colonization of paranasal sinuses. Indistinguishable from bacterial sepsis. Skin sensitivity testing (wheal and flare reactions). IgE antibodies. Monitor with spirometry to detect development of progressive fibrosis Fungus ball on CXR - moves with dependency

Cryptococcus neoformans
Ubiquitous: soil, pigeon droppings (dessicated alkaline rich, N2 rich, hypertonic), poultry farms, eucalyptus trees Infection via inhalation NO dimorphism in pathogenesis (unlike other systemic mytotic agents) Encapsulated yeast Capsule (anti-phagocytic) Cryptococcosis (also Busse-Buschke disease or torulis) MC self-limiting mild pulmonary infection. Can lead to pulmonary nodule which mimics carcinoma or pnemonia with diffuse pulmonary infiltrates Microscopy: examine CSF after treating with 10% KOH and India ink. Serology: look for capsular Ags (mc in males) (unlike other systemic mycoses that look for Abs) MC cause of fungal meningitis. Insidious onset of HA, low grade pyrexia, focal neurological changes. Immunocompromised also get skin lesions or osteolytic bone lesions (e.g. lymphoma)

C. neoformans

Produces urease Attaches to alveolar cells inducing an inflammatory response Damages BM --> frothy exudate

Cryptococcosis meningitis

Pneumocystis carinii (P. jirovecci)
Included with fungi only because of molecular traits P. carinii Has features like protozoans Opportunistic infection common in environment Pneumonia Non-specific. Plasma cell infiltrates with "ground glass appearance" Microscopy: typical octonucleate cysts.CXR: diffuse infiltrates with ground glass appearance

also found in rodents (not reservoir for human disease) Most people exposed by age Transmission is via 4. Seen in AIDS. respiratory droplets


In AIDS - eye, ear, liver, bone marrow

Environmental Molds Stachybotris
Stachybotris Unusual black, slimy molds that grow on wet paper or wood Form large, fluffy white colonies that turn gray/brown with age Grow as variably colored colonies, depending on species Toxin produces pulmonary hemorrhage Systemic poisoning Infection may be prefaced by nose bleeds, cough or chest congestion and worsened by concomitant cigarette exposure. Small areas may be cleaned with bleach; larger infestations require professional removal.

Mucor spp
Mucor spp Allergic reactions Associated with allergy to its spores (including hypersensitivity pneumonitis) and opportunistic infections of the sinuses, skin, and lungs in immunosuppressed patients

Penicillium spp
Penicillium spp Contain mycotoxins Allergic reactions To toxins.

Aspergillus - see above Rhizopus spp
Rhizopus spp Colonies are like white cotton candy and brown with age Allergic reactions

Alternaria spp
Alternaria spp Common indoor and outdoor mold Colonies are velvety, ranging from dark green to brown. Colonies appear white-pink and blacken with age Allergic reaction and hypersensitivity pneumonitis

Pullalaria spp (Aureobasidium)
Pullalaria spp (Aureobasidium) Numerous species, possibly the most common source of spores in indoor/outdoor air Associated with wed, old buildings

Cladosporium spp
Cladosporium spp Colonies tend to be black, brown or dark green and can be powdery. Allergic reactions (rhinitis --> asthma). Opportunistic infxns.

Viruses and Prions (14%) Herpes
4M's: Mixing & Matching of Mucous Membranes (vesicle fluid, saliva, vaginal secretions) HSV-1: early on in life. Horizontal: oral contact, autoHSV-1 infects above the inoculation to eye or mouth Herpes virus DNA. Humans waist, hsv-2 infects below the are reservoirs waist HSV-2: later on in life. Horizonal: sexual practices. Vertical: ascenting in utero infection or during vaginal birth Infect and replicate in mucoepithelial cells Herpes simplex infection Skin break - localized primary infection in mucosa. Vascular lesions (damage due to viral immonopathology and apparent healing). Then retrograde transport to neuron nucleus - latent infection. Stress (emotional, fever, direct sunlight, menstruation / hormones, immunosuppresion). Lesions: "dew drop on rose petal". Secondary infection is more localized and shorter duration than primary infection. Tzanck smear: look for Syncytia (fused membrane, not specific, also for: HSV, VZV, HIV, paramyxovirus.Cowdry Type A inclusion bodies (HSV or VZV). Characteristic CPE (cyto pathological effect)

Herpetic keratitis (ocular herpes) Lytic infections at site, persistent infections in macrophages and lymphocytes, and latent infections in nerve ganglia and salivary glands Herpetic Whitlow Meningitis. Encephalitis Genital herpes Neonatal Herpes simplex infection

Unilateral, recurrent. Can lead to dendritic corneal ulcers --> permanent damage Herpes infection of finger HSV-2 - often a complication of genital herpes. Sudden onset of nuchal rigidity, blinding H/A, nausea, photophobia. Seizures, signs of SOL (space occupying lesion), cause destruction to temporal lobe. MC cause of sporadic encephalitis. Caused by HSV-1 (10& orogenital sexual practices) and HSV-2 (90%). STD 3-7 days after contact. Regional lymphadenopathy, painful shallow ulcers. Recurrent (2-3 weeks or rarely) prodrome of burning/tingling. Female: pruritis, vaginal or cervial mucoid discharge. Increased risk of cervical CA in adulthood and HIV. Male: dysuria and/or duspaerunia. Acquired in utero or during vaginal birth or post-natal (family members or hospital personnel). Devastating, often fatal. Affects CNS, lungs, liver.

Herpes simplex

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Peak occurrence of chicken pox: spring time and 5-10 years old

Like Herpes simplex: causes blister-like lesions (but different sizes and stages, deeper, more painful and can cause scarring), establish latent infections in nerves, CMI

Primary infection: 2-4 days after: to lympatics

Chicken pox

Incubates for 14-21 days. One of the 5 childhood exanthems: rubella, roseola, 5th disease, measles/rubeola. Inhalation: maculopapular rash ("dew drop on rose petal"), intense pruritus, rapid development and spread from back/chest to scalp. Within 12 hours: successive crops of lesions. Prolonged low grade fever. extremem irriability/malaise. Much more harmful to adults - scarring. More severe on trunk than extremeties, also on mouth, conjunctiva, vagina. complications: 1) secondary bacterial infections.2) Reye's syndrome, CNS symptoms.

Tzanck smear: giant, multinucleate cells - syncytia. Cowdry Type A inclusion bodies: "drop like masses of acidophilic material surrounded by a clear halo within the nucleus"

Varicella Zoster

Unlike HSV: spread via Peak occurrence of shingles: respiratory route, no Secondary viremia: adult pop esp >65 (10-20%). detectable lesions at site of DNA enveloped herpes virus thoracic fever. entry VZV becomes latent in dorsal root or cranial root ganglia Active herpes zoster can Very contagious - contagious Reactivated in older adults cause chicken pox in from 48 hrs, before and immunocompromised susceptible child or adult but symptoms until all the lesions migrates back along will NOT cause shingles. are completely dry dermatome --> shingles

Reye's syndrome

Can occur after chicken pox, enterocirus, EBV, influenzae B, aflatoxin (peanuts), pesticide. ASA associated - do NOT give aspirin to a child with chickenpox. Recurrence of latent VZV infection. Prodrome: severe pain in localized nerve area. 3-5 days later: gradual development of small red macules, closely spaced, MC'ly in thoracic area or trigeminal nerve area, unilateral. Post herpetic neuralgia: long term (months to years) severe recurring burning or itching pain, hyperesthesia. Unlike herpex simplex: lesions are various sizes.


Herpes zoster opthalmicus

CN V (facial) and CN III (ocular changes - cornal ulcers - blindness)

Ramsey Hunt syndrome (Herpes zoster oticus)

painful lesions along CN VIII (severe otalgia, hearing loss, vertigo, vesicular lesions along external ear canal) and lesions along CN V (Bell's palsy)

Very common virus

Ultimate B lymphocyte pathogen. Mitogenic and immortalizing. Viral capsid Ag helps ID it in tissues.


kissing disease - heterophile (+) mono. Symtoms: high fever, malaise, pharyngitis, tonsils with whitish exudate, lymphadenopathy, hepatosplenomegaly, fatige. Spleen rupture - avoid contact sports, hepatitis. Cyclic recurrent disease. (if lasts over 6 months) EbV induced lymphoproliferative dease(looks like leukemia)

Triad of: fever, pharyngitis and lymphadenopathy for 1-4 weeks. Downey cells. Monospot test (+) Heterophile Abs - polyclonal activation of B cells produces wide reportoire of abs that recognize "paul Bunnel" Ags on horse, sheep, cow, RBCs but not guinea pig. High IgM = acute. High IgG = past infection

Ebstein-Barr virus

Infection first in A DNA enveloped herpes Transmitted MC'ly by saliva oropharynx, shed in saliva virus. A gamma herpesvirus or from contaminated - saliva remains infectious glassware - "kissing disease" for months after clinical recovery To cause neoplasms - need other cofactors Immunity to EBV is lifelong Iiff overactive immune system --"infectious mono" iff lack of immune response --"lymphoma" e.g. burkitt's URT - lymphotropic infected cells (leukocytes, lymphocytes) spread CMV throughout the body DNA Enveloped herpes virus. Similar to Herpesviridae: 1) contains both mRNA and syncytia, 2) latent state, 3) DNA --> unlike other viruses reactivation in immunosuppressed state

African Burkitt's Lymphoma

Tumor cells are from lymphocytes and contain EBV DNA. Malaria is a co-carcinogen. Large lesions - osteolytic - on jaw

Chronic Fatigue Syndrome Nasopharyngeal carcinoma Hairy oral leukoplakia

Proposed to be one of the causitive factors of chronic fatigue Epithelial cell tumor. Co-factor: ingested nitrosamines. Opportunistic infection in HIV AIDS patients. Vertically ribbed keratinized plaques on lateral borders of the tongue

Opportunistic pathogen rarely causes disease in immuno-competent hosts Cytomegalovirus Transmitted as STD, transfusion/ transplantation, oral, congenital Can be latent in T cells, macrophages, other cells Ubiquitous. Cause life long infections

congenital - cytomegalic inclusion disease

MC viral agent of congenital disease in US. Clinical disease in 10%: microencephaly, hearing loss(SNL) rash, hepatosplenomegaly. Fetus is infected either: placenta or recurrent mother infection - ascending infection from cervix. Appearance of multinucleated giant cells with intranuclear inclusions. Infectection of fetus or newborn by any of the TORCH agents. Toxoplasmosis, other, rubella virus, cytomegalovirus, histoplasmosis. Outcome is abortion, stillbirth, or premature delivery. Fever, lethargy, poor feeding….. Through vaginal birth with infected cervix or colostrum or milk. 2 outcomes: asumptomatic or symptomatic if immunocompromised. Very common cause of failure of KI transplants. IFF immunocompromised: Retinitis: "pizza pie retina" --> scotoma, "blind spot". Esophagitis: mimic CRC esophagitis Rapid onset of high fever. Fever subsides and then get maculopapular rash. Also termed exanthum subitum. "Slapped cheeck appearance" progression time of HIV to aids. Assoc with neurological disorders: might be linked to MS, cronic fatigue.

Confirm by isolating CMV from child's urine in 1st week of life.

TORCH syndrome CMV mono, CMV hepatitis Peri-natal

Heterophile (-) mono. Clinical signs and symptoms too vague to be that useful. Biopsy: owl's eye nuclease. Cell culture: characteristic CPE in diploid fibroblastic cells

Human herpes virus-6

Lymphotropic latent infection in t cells

Roseola infantum Mononucleosis type illness Pharyngitis (acute respiratory disease) Atypical pneumonia conjunctivitis Gastroenteritis Hemorrhagic cystitis

Heterophile (-) mono. Similar to owl's eye inclusion body (in CMV). Increased CRP (unique to viruses --> similar to bacteria)

Respiratory droplets, fecal DNA non-enveloped (naked) Hemagglutinin fiber - aids oral, direct fomite inoculation virus in attachment Adenovirus 41 antigenic types Can get through birth canal Icosahedral nucleocapsid Used as a vector for gene therapy - help stimulate bone growth mild URI with fever, rhinorrhea and cough. #4 on viral respiratory diseases. #1: RSV, #2: parainfluenza #3: Rhinovirus pertussis-like illness Associated with swimming pools, dust/ debris. 2nd only to rotaviruses as cause of acute gastroenteritis in children. Serotypes 40 and 41 are thought to cause up to 15% of gastroenteritis in children. Usually occurs in epidemics

Through breaks in skin and mucosa transferred by fomites - direct contact into small breaks in Naked capsid virus skin/ mucosa Also infected birth canal (STD transmission) cause lytic, chronic, latent or transforming infections transformation occurs bc proteins bound by HPV16&18 bind tumor suppressor molecules Common flat wart (verruca plana or verucca vulgaris) Oral papillomas Laryngeal papillomas Condyloma acuminata (anogenital warts) Cervical dysplasia and cervical CA MC epithelial tumor in the larynx. Infected birth cana. Hoarseness or abnormal cry. HPV 6 & 11. HPV 6 and 11. STD, vaginal birth, or ?. Rarely regresses spontaneously. Plaque-like flesh colored lesions. Can be pre-neoplastic. 2nd MC canver in women in USA. HPV 16 & 18 & 31. Need cofactors to progress to CA MC on hands and feet. Surface is studded with black dots. Plantar is painful because it grows on pressure points

Human papilloma virus

Lesions turn white with acetic acid PAP smear - presence of Koilocytes. Topical 5% acetic acid.

Very contagious - 85% infection rate, 95% chance of disease development Measles can depress CMI for a short time, allowing bacterial Transmission by respiratory Measles virus (rubeola) RNA enveloped superinfections. It can also droplets: prodromal and first morbillovirus paramyxovirus allow reactivation of latent few days of rash diseases: shingles or TB. Hemagglutinin helps the virus penetrate cells and uncoat. Cell fusing and hemolytic properties. Infects epithelium of URT then blood and RE cells. Very infectious (but less than measles or chicken pox) infect upper respiratory tract epithelial cells. Infect parotid gland via viremia or Stenson's duct --> Parotitis Measles Prodrome: Cough, coryza, conjunctivitis, photophobia. 2 days later: Koplik's spots "grains of salt surrounded by a red halo". 1-2 days later - rash, maculopapular descending rash. MC self limiting with no complications MC clinical only - pathognomic. Microscopy: syncytia. Serology: 4x increase in measles specific IgMs suggest recent infection


Rarely occurs but is MC cause of mortality from measles

Giant cell pneumonia Post infectious encephalis Sub-acute sclerosing panencepahalitis Atypical measles Mumps

IFF T cell deficient children immunopathological - demyelinate neurons charaterized by changes in personality, behaviour, memory, movement Response to vaccine - abrupt onset of more severe symptoms. Get increased imunopathologic response. Incubation 14-21 days. Fever, malaise, anorexia. MC'ly asymptomatic (unlike measles). Bilateral parotitis. Test samples from saliva, urine or CSF. Elevated amylase (bc pancreatitis). Hemadsorption.

Only infects humans

Mumps virus paramyxovirus

Transmission is by respiratory droplets.

RNA enveloped paramyxovirus. Similar to measles.


Testicular swelling. MC unilateral, can lead to sterility if bilateral.

Oophoritis Life-long resistance to infection (like measles) Pancreatitis Meningitis. Arthritis

Unexplained abdominal pain. might be a link to juvenile onset DM H/A, stiff neck, drowsiness, unsteadiness when walking. #1 cause of aseptic meningitis in non immunized (non bacteria). Typically self-limiting Rare cause of polyarthritis in young men

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Common cold causes: 1) rhinorhea virus. 2) coronavirus 3) RSV Respiratory Syncytial Virus

Ubiquitous - virtually everyone in NA is infected by age 4 (very contagious) Epidemics in every winter in cold, temperate climate Transmitted via hands, fomites and respiratory secretions Enveloped RNA virus

No hemagglutininor neuraminidase. F glycoprotein in envelope causes cells to fuse Form syncytia

URI with marked rhinorrhea Bronchiolitis

In older children/adults OM also is common. These 2 in infants.

4x increase in anti-RSV indicates disease Respiratory secretions or detection of syncytium. Rising Ab titers.

#1 cause of severe lower respiratory tract infection in young children (Day cares, nurseries)

Parainfluenza Virus

Infection localized to upper or lower respiratory tracts. No systemic spread/ viremia No long term immunity 4 serotypes: Types 1-3: 2nd most common cause of severe respiratory Ubiquitous Enveloped RNA virus distress in infants and young children, can cause croup Initial site of infection is the upper respiratory tract Transmission is person to epithelial cells. Usually person and respiratory contained here and rarely droplets 4 serotypes. No antigen drift. becomes systemic (unlike measles/ mumps) Only partial immunity MC in infants and children <5 (unlike measles) Ingested (contaminated shellfish, clams, oysters) Naked icosahedral ssRNA genome

Severe pharyngitis

In older children and adults, croup, severe pharyngitis or URI symptoms occur



range from mild cold-like URI to bronchitis and pneumonia. Milder disease in older children and adults


Laryngeotracheobronchitis - "sound worse than they look". Seal bark - harsh brassy cough. MC self limiting - 48 hours. Xray: steeple sign. Lab DDX epiglottitis (caused by H. influenzae). "Look worse than they sound" Medical emergency, drooling. Dx: Serology >>false -. Presence of syncytia. Hamadsorb guinea pig RBCs. Xray: thumb sign.

Hepatitis viruses
Differences from HBV: HAV can not initiate a chronic Pathology due to immune extremely stable capsid infection mediated hepatocyte damage Person-to-person, fecal-oral and sewage contaminated food/water (often traceable source, can live in water for many months) Children most common. Usually from restaurants.

HAV not associated with hepatic CA Hepatitis A (HAV) rarely get immune complex related rash and polyarthritis rarely fatal (fulminant hepatitis)

slow replication, transient viremia Not stable to chlorine

Hepatitis A

Children: often asymptomatic (only 1-2% get jaundice). Adults: abrupt onset of fever/chills. Symptoms decrease in 4-6 days. Jaundice in 67%. Patient history - source of infection. Acute or recent: anti HAV igM by ELISA or RIA. IgM rises early in 99% full recovery. 1-3/1000 progress to fulminant hepatitis. disease, IgG persist for life. Serum LIV enzymes usually elevated

Hep A vaccine can prevent 1 month incubation --> abrupt infection onset of icteric symptoms fecal-oral spread differences from HAV: hepDNA vuris MC'ly in blood or blood products (serum hepatitis) Chronic carrier - test + for HbsAg 2 occasions HBsAg (surface antigen): rises in acute infection. Assoc with infectivity. HBeAg (e antigen): occurs during active infection; associated with infectivity and risk of progression to chronic liver disease. AntiInfects hepatocytes --> immune response. CD8+ T cells recognize viral particles and start attacking virus-filled hepatocytes. Ag-Ab complexes HBsAb (Anti-sruface antibody): appears weeks after recovery. Suggests past infection. Anti-HBcAb form, which probably explain arthralgias and arthritis, immune-complex glomerulonephritis, and vasculitis. Incubation is 10-12 weeks --> fever, (anti-core antibody): appears at onset of clinical symptoms. Suggests current or previous infection. Antifatigue, nausea, jaundice with hepatosplenomegaly. HBeAb (anti-e antibody): suggests low risk of infectivity and good chance of avoiding chronic liver disease.

transmitted by over 1/3 of the world is blood/needles/STD/perinatal infected Hepatitis B (HBV) longer incubation (3 months) and then insidious onset of symptoms can get chronic hepatitis carriers can cause primary hepatocellular carcinoma (PHC) not as resistant Hepatitis C (HCV) unusally stable for an enveloped virus Partially double-stranded DNA enveloped hepadnavirus Hepatitis B

IV drug users - transmitted through blood Chronic carrier state

RNA enveloped flavivirus Incomplete viral particle (Delta particle)

CMI response

Hepatitis C

Similar to hep B. Tends to not have jaundice symptoms. Chronic state usually involves low-grade, intermittent symptoms of fatigue and arthralgies. Increased rate of AI disease in carriers. Low risk of developing cirrhosis and hepatocellular carcinoma. Hepatitis, cirrhosis, liver cancer, carrier state. Coinfection with Hepatitis B needed (HBsAg required) --> acute hepatitis and also fulminant hepatitis. Increased likelihood of cirrhosis.

Hepatitis D (HDV)

Hepatitis D

over 100 serotypes - can get MC common cause (>50%) common cold more than once! of the common cold Spread via aerosolized nasal droplets, fomites, hands (#1) Rhinovirus only transient immunity Can't grow in acid of stomach (unlike enteroviruses) and also grows best at 33 C (cooler in nasal mucosa) acid and temp sensitive ssRNA bing ICAM-1 Gradual antigenic drift (like influenza A) Infection by as little as 1 infectious particle Common cold - coryza rhinorrhead (clear, waterty -> purulent/ mucoid iff secondard bacterial infection) Lab not necessary. Characteristic CPE in himan diploid fibroblast cells at 33C and acid labile

Influenza Viruses
1) Influenzae A: epidemics, pandemics, bird reservoirs (ducks, chickens) 2) Influenzae B: stomach flu Orthomyxovirus 3) Influenzae C - mild URTI Enveloped virus - wash your hands! Destroyed with soaps Epidemic --> antigenic drift. Small mutations. Will re-infect every 2-3 years ssRNA genome in 8 Pandemic --> antigenic shift. segments: facilitates Only in influenzae A, major rearrangement recombinations. Every 10 years. Also zoonoses - a new strain is formed that can be spread to humans Picornaviridae - One of the largest families: Includes enteroviruses (HAV, Coxsackie virus, polio virus, echo virus) and rhinovirus Haemagglutinin Neuramidase - allows spread through mucous membranes first strain known to cross species barrier from chicken to human - H5N1 Limited viremia - very rarely spread beyond lung Influenzae A Influenzae B Abrupt onset of fever (38-41C for 1-5 days). Non-productive cough, severe myalgia, rhinorrhea, anorexia Milder, more GI symptoms Usually symptomology and community history of outbreak is enough for diagnosis

Secondary Bacterial pneumonia Encephalopathy Reye Syndrome

In young children

Linked to ASA

Naked capsid virus Damage is direct to viral pytopathology NOT immunopathology Replicates in anterior horn of spinal cord --> death of motor neurons and paralysis Enterovirus - stable at pH3-9. Non-paralytic poliomyelitis Affects lower motor neuron Paralytic Post polio syndrome (PPS) Symptoms of abortive poliomyelitis as well as aseptic meningitis Spinal paralytic: asymmetric flaccid paralysis in one or more limbs, no sensory loss. Bulbar: affect cranial nerves or medullary respiratory center (75% mortality) Deterioration of affected muscles (or previously non-affected muscles) later in life (10-40 years later) without presence of virus. Asymptomatic Most common (90%). Limited to oropharynx and GIT.

Poliovirus IPV (salk) - inactivated polio vaccine. OPV (sabin) - live, attenuated oral polio vaccine (both stim humoral immunity)

Transmission is fecal-oral


non-specific febrile illness.

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Coxsackie A --> usually vesicular lesions Coxsackie B --> myocarditis, pleurodynia Coxsackie virus 60% of infections are subclinical Fecal oral spread RNA virus Can cause permanent nerve damage

Herpangina Hand-foot-mouth disease Acute hemorrhagic conjunctivitis Pleurodynia (Bornholm's disease) Myocarditis/ Pericarditis IDDM Aseptic meningitis Paralytic disease, Encephalitis, URTI

Coxsackie A and echovirus (not Hsv). No external skin lesions --> unlike hand-foot-mouth disease. Self limiting. White lesions inside mouth Caused by Cosdackie A16. Mild febrile disease with vesicular lesions on hands, foot, tongue Extremely contagious "devil's grip" --> severe pleuritis chest pain --> unilateral intercostal myalgia --> "stich-like pain" MC in adult males. Mistaken for MI. Children - sudden unexplained heart failure possible link if Cosxsackie B infects pancreas # 1 cause is echo virus MC cause of nonbaverial CNS infection in the US. Causes self-limiting meninigitis lasting 5-14 days or progressing to encephalitis with potentially permanent nerve damage and paralysis. Can mimic paralytic polio

Enterovirus lab dx: CPEs on monkey KI tissue culture. RT-PCR in CSF/ other fluids.

Other enteroviruses zoonoses. MC bite of rabid dog (also cats, foxes, raccoons, coyotes, skinks, bats). Body fluids Does not penetrate intact mucosal membranes


Rabies virus one of the most deadly viral diseases - 100% mortality Enveloped RNA virus Infects sensory nerve cells Rabies Long incubation phase: asymptomatic. Delay is important for treatment. Prodrome: retrograde axoplasmic flow and dorstal root ganglia. No detectable Abs. ..................Neurologic phase: travel to infect brain/encephalitis. Hydrophobia, aerophobia, hyperactivity, aggressiveness, "furius rabies" (death in 1 week). "Dumb rabies" - progress to death by cardiac ......Then back down to salivary glands (where is its spread) Once there is evidence of infection (symptoms or Abs) it is too late for effective intervention. Post mortem Negri bodies.

Live attenuated vaccine has provided immunity for up to 10 years Rubivirus (Rubella) Exterminated from the US in 2005 Alphaviruses -> arboviruses (arthropod borne), similar antigenicity Flavivirus -> Hep B, Hep C Alpha and Flavi Viruses similar pathogenesis and (Arthropod-borne viruses) epidemiology Yellow fever has a live attenuated vaccine Rubella Respiratory droplets or across placenta RNA enveloped virus with hemagglutinin to aid attachment Polyarthritis Rubella congenital TORCH agent Enveloped, linear ssRNA Mosquito control helps controlling the virus vectors -> mosquitoes Reservoirs -> "immunologically naïve" birds Humans - dead end hosts Flu-like syndromes Meningitis/ encephalitis Hepatitis, hemorrhagic fever, shock, viral arthritis Yellow Fever puddles, ditches, artificial ponds, toys, trash cans Dengue (break bone) Fever Dengue hemorrhagic shock syndrome HIV-1: 70% men. 42% homosecual men. Geveloping countries: relative increase among heterosexuals. Sexual intercourse (anal/vaginal) - HIV enters and infects Langerhands DC's in epithelium or GIT? Peri-natal - from birth HIV Virus HIV-2: mostly west africa West nile Dengue fever/yellow fever Jungle fever, Aedes aegypti mosquito. Not contagious - no person to person spread. 3-6 days incubation, then organ pathology. Jaundice, haemorrhage, encephalitis is rare.- africa and S. america Aedes aegypti mosquito. Primary infection --> bone pain. Enlarged lymph nodes, maculopapular rash, leukopenia. Seen in Middle East, Arfrica, Caribeean Hypersensitivity reactions --> weaken, rupture vasculature. No bone pain. Incubation 14-21 days. Prodrome of malaise and lymphadenopathy for 1-5 days. "3 day measles" regional lymphadenopathy (esp sub-occipital glands). Spread to skin: rash - small erythematous nodules that spread from face to trunk/limbs, gone in 3 days. Rubella disease has similar severity even if immunosuppressed. More severe in adults than children due to more vigorous immunopathology. MC in adult females. Symmetrical polyarthritis of fingers, ankles, wrists and knees Increased risk (70% babies infected) if mother infected in 1st trimester (if 4th month just sensorineural deafness). Iff no maternal Abs teratogenic effects. Classic triad: eyes, ears, heart. Also microencephaly, IDDM. Highly infectious for 1st few months of life. Difficult to diagnose clinically. Highly specific anti-rubella IgMs. NO CULTURE - no characteristic CPE. Serology: problem: false +, RT-PCR

cause lytic infections in vertebrate hosts

Delicate outer envelope hard to get! gp120 (Ag and receptor specificity leads to high amount of antigenic drift). Changes all the time! Affinity for CD4+ T cells --> loss of CMI Infects monocytes/ macrophages (Especially brain) Acute retroviral syndrome: viremia. Mono-like syndrome (heterophile -), mucocutaneous sores. Illness subsides spontaneously. 60%+ become asymptomatic. Mouth ulcers, oral candidiasis, EBV-like.

Mid stage - ACR (AIDS related complex). Insiduous onset - weight loss. Night sweats, fatigue,opportunistic infections HIV AIDS: 1) presence of anti-HIV gp120 abs, 2) decreased CD4+ t cells, 3) wasting syndrome 4) presence of opportunistic infections. Primary defence against opportunistic pathodens is progressively diminised. Diseases: hairy oral leukoplakia, oral thrush, kaposi's sarcoma, pneumocystis pneumonia, CMV retinitis AIDS related dementia: sub-acute encephalopathy. Slow, progressive deterioration of mental abilities. Can minic alzheimer's disease

Blood: IV drug users, needle stick injuries, blood transfusions RNA virus Problem: long, prodromal asymptomatic period. Infectious before identifiable symptoms.

Initial screen: indirect ELISA for gp120 or gp41 (2x to confirm). New- Ora Quick Rapid HIV-1 Ab test. Western blot: for gp120 or p24 or p31 proteins (confirmatory). Active viral replication (Recent infection or late stage) - direct ELIZA for p24, viral load in Rt or in blood via PCR. Culture - difficult, looking for syncitia

HIV gp41 and gp120 help virus enter the cell (envelope glycoproteins)

Smallpox virus Eradicated except in lab samples since 1979. Vaccine No asymptomatic carriers no longer given due to risks. Very large enveloped DNA virus Smallpox variola is inhaled (4-19 days asymptomatic and not contagious). Prodrome (2-4 days). Skin rash (most contagious) Think opaque fluid filled center with "belly button-like depression in center". Infectious until all scabs fall off. Unlike chicken pox, in smallpox all the lesions are at the same stage at the same time. 35% mortailty. MC clinical only.

Unlike other viruses - pox Molluscum contagiosum and Molluscipoxvirues. Can viruses contain all the other pox viruses are survive environment for Large enveloped DNA virus necessary information for their zoonoses - STD, fomites, years. own DNA and RNA synthesis wrestling, rugby

Ecthyma contagiousum (Orf)

Direct contact with sheep/goats, soil? Contagious pustular dermatitis.

Molluscum contagiousum Antigenic shift like Influenza A Rotavirus Rotavirus - #1 cause of infant Fecal-oral transmission diarrhea worldwide dsDNA Non-enveloped but Enveloped virus-like properties Gastroenteritis

In immunocompromised. Fleshy, pearl-like umbilicated nodules with central caseous plug.

Characteristic skin lesions. Molluscum bodies on biopsy.

48 hr incubation --> sudden onset of severe vomiting (progectile), watery diarrhea, fever, dehydration. Selt limiting. Not distinguishable from other types of gastroenteritis (Norwalk virus, bacterial) by signs and symptoms. Death by dehydration. Diagnosis via stool samples - looks like a wheel!

MC spread from respiratory droplets or close contact to blood products Smallest of Dna viruses (only binds P antigen on rbc's, 22nm) erythrocyte progenitor cells, vascular endothelium and fetal myocytes naked capsid virus very resistant to drying, acid/base, high salt etc Eating infected tissue, organ transplants, or iatrogenically Non-viral glycoproteins, 5nm filterable (size of viruses) but in diameter no DNA or RNA Erythema infectiousum - 5th disease Nonspesific URI (looks like influenza). 2-7 days later develop a "slapped cheek rash" which fades after 4 days but spreads to trunk and limbs (lacey/ reticulate appearance). Biphasic: 1) Infectious stage. 2) Immune mediated stage: recurrent rash (immune mediated) that is <sunlight, RIA or ELIsa for B19 specific Abs. IgG comes later but persists for life <exercise, <hot water, <stress. Iff seronegative mother is infected in 2nd or 3rd trimester. Hydrops fetals (dropsy) - massive edema in the fetus. Especially if SCA or thalassemia - chronic hemolytic anemia. Not developing RBC's for 5-7 days. Fever, malaise, myalgia, chills, pruritus. Symmetrical, transient polyarthritis - presents just like rubella arthritis. Increased risk in female adults. Unlike RA - no RF.

Parvovirus B19

Parvovirus B19 fetal infection Aplastic crisis Arthritis Sporatic Creutzfeld Jakob disease Creutzfeld-Jacob disease - variant form

Prions very resistant Long incubation (up to 30 years) but rapidly fatal once symptomatic (MC only 1 year). Rapidly progressing dementia. Most common after age Not cultivated in lab, no Abs producted, normal CT scan, normal MRI, abnormal EEG 70. Some genetic susceptibility. Young onset --> mean is 27 years of age. Psychiatric/ sensory symptoms. Dementia at final stage only - unlike sporatic CJD. Detect PrPSc in Strong lab and epidemiological evidence of link to BSE follicular dendritic cells (lymphoid tissue)

Parasites (6%) Amoebae
Entamoeba histolytica Cysts --> trophozoite in the ileum. Reside in cecum and Found in tropical areas with colon --> necrosis. Can enter poor sanitation. Fecal-oral portal circulation --> liver --> spread liver abscess Amebiasis/ Amebic dysentery Colitis with diarrhea and/ or many bloody stools. LV abscesses. (RUQ pain, weight loss, fever, hepatomegaly) Can have asymptomatic carriers. Failure to thrive in kids. Stool examinations - multiple stool samples (3-5). DDX UC, shigella

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Flagellated protozoa Giardia lamblia
Worldwide sylvatic (wilderness): Beavers and muskrats are local reservoirs Giardia lamblia Forms cyst in dueodenim. contaminated water: resist Trophozoites attach anywhere chlorination (unlike along the gut wall. Interferes Entamoeba but like with nutrient absorption Cryptosporidia) person to person spread via fecal-oral or oral- anal practices MC protozoal disease in Worldwide STD - can get with developed nations. infected towels as well. Urogenital protozoan ST acid induces changes to trophozoites 1) Asymptomatic carriers- 50% 2) Symptomatic: range from mild diarrhea to severe mal-absorption syndromes. 1-4 week incubation and then sudden onset of: foul smelling, watery diarrhea, abdominal cramps, flatulence and steatorrhea

Very rarely spread beyond the GIT no tissue necrosis

"beaver fever" - Gastroenteritis

DDX: Isospora belli in HIV/ AIDS. Cysts in stool. ELiSA.

Trichomonas vaginalis
Trichomonas vaginalis Monomorphic- no cyst stage Vaginitis 1) Females: M/C’ly asymptomatic or profuse frothy vaginal discharge 2) Males: M/C’ly asymptomatic Microscopic examination of urine. Culture is also possible.

Trypanosomes (T. brucei) Transmitted by tsetse flies transmitted by triatomine (reduvid, kissing, or assassin) bugs T. cruzi "Tom Cruise likes to Shag Reservoirs: dogs, cats, and Kiss" opossums, rats, other mammals Can be transmitted by transfusion or transplacentally Chagas disease (american trypanosomiases) African sleeping sickness (african trypanosomiases) 1 week after being bitten, trypomastigotes spread to the bloodstream and lymph. Cycle of replication and lysis. Found in the myocardium and CNS. Can cause death within 9 months - 2 years. Within 3-14 days, painful, indurated red nodule (trypanosoma chancre) develops and remits. Fever, HA, rigors, edema. Chronic dz can progress to meningoencephalitis. Wet mount on ir in Giemsa stained smears. Anemia, monocytosis and elevated IgM.

Kissing bug deposits feces on skin while biting and enters through mucous membranes. Parasites invade macrophages, where they transform into amastigotes, multiply and are released as trypomastigotes into blood and tissue. Infect nervous system, RE cells, myocardium, and muscle Culture of blood or lymph node. PCR. cells. Initially asymptomatic. 1-2 weeks later: fever, hepatomegaly, lymphadenopathy. Chronic: cardiomyopathy, atipcal aneuryisms, heart failure, Stokes-Adams attacks, thromboembolism, mesaesophagus, or megacolon.

L. tropica, L. mexicana, L. braziliensis, L donovani Vector: phlebotomine sandflies. Reservoir: wild mammals Hematoflagellated, unicellular, obligate, intracellular, zoonotic parasite Invade macrophages. Ab not protective - result in glomeruloN Oriental sore, chiclero ulcer Caused by L. tropica (Asia, Africa) or L. mexicana (Latin America). Papules that itch eventually, over months, ulcerate painlessly then ultimately heal (again, over months), leaving pitted scars. Lymphadenopathy accompaines initial manifestation. Semi-epidemic disease. Caused by L. donovani. Incubation is 3-12 months. Fever, hepatosplenomegaly, lymphadenopathy, diarrhea, malabsorption, gray skin discoloration "black disease", anemia, thrombocytopenia, agranulocytosis. Mortality 90% without treatment. Intracellular amastigotes and Lieshman-Donovan bodies

Visceral leishmaniasis (kala azar)

Sporozoa Plasmodium species
P. falciparum, P. vivax, P. Sickle cell trait confers ovale, P. malariae resistance female Anopheles mosquito feeds on a person with malaria and then feeds on an uninfected person Scizogony - invasion and rupture of RBC - cause symptoms Malaria Periodic episodes of high fever, shaking chills followed by profuse sweating. Other sx: anemia, hepatomegaly, splenomegaly (Brain/LU/KI damage with P falciparum). Tertian: sx every 48 hours (P. vivax and P. ovale). Quartan: sx every 72 hours (P. malariae). P. Falciparum is MC and most deadly. Black water fever - dark red or black urine. Giemsa stain. IgM and then IgG antibodies.

Toxoplasma gondii
cat feces fecal-oral spread 1) improperly cooked contaminated meat/ meat juices 2) contaminated soil 3) contaminated cat feces

•microbe present in

heterophile negative mononucleosis like syndrome chorioretinitis iff 2nd or 3rd trimester: microencephaly, chorioretinitis +/- blindness, anemia, jaundice, neurological signs (retardation, seizures, microencephaly, hearing loss). Can be asymptomatic at birth and develop disease months to years later. One of the major cause of encephalitis in AIDS. One of the TORCH agents. Can be asymptomatic.

Tosoplasma gondii

congenital disease

Microscopy of biopsy sample.

Cryptosporidium parvum
Worldwide zoonotic Cryptosporidium parvum Waterborne- resistant to usual Fecal- oral, person to person water purification (MC) Oral-anal: MSM (Flagship in highly resistant to chlorine AIDS) Transmitted by ticks MC in New England islands Cryptosporidosis Iff immunocompromised (HIV/AIDS) --> Severe diarrhea three consecutive stool samples: Un-concentrated (HIV/ AIDS) or concentrated (centrifuge, etc.). Diagnosis made by O&Px3

Babesia microti
Babesia microti Malaria-like protozoa Lives in RBC Fatigue Arthritis Prolonged fever and hemolytic anemia

Roundworms Ascaris lumbricoides (giant intestinal roundworm)
Ascaris lumbricoides (giant intestinal roundworm) Can grow up to 25cm or longer Thousands of eggs produced daily --> pass out in stool and infect soil Eggs transmitted through inhalation or ingestion Ingested infected egg develops into larval worm that penetrates duodenal wall Larvae in alveoli are coughed up and reswallowed --> malnutrition/blockage Female lives in cecum but migrates out of anus at night to lay 20,000 eggs on bedding and peri-anally every 2 weeks. Larvae migrate to lungs. Coughed up and swallowed. Slice intestinal wall and feed on blood of intestinal capillaries. Bowel obstruction/appendicitis Concentrated stool - knobby coated, bile stained, oval egg Adult worm in feces (20- 35 cm long)


Asthma-like attack. Eosinophilia and micratory pulmonary inflitrates seen on plain films help differentiate it from asthma or bronchitis.

Worms in stool/ larvae and eosinophils in sputum

Enterobius vermicularis (pinworm)
Enterobius vermicularis (pinworm) Female is 1 cm long, pin shaped, off-white worm. Perianal itching Periodic nocturnal anal itch (When eggs are laid). No intestinal damage or immune reaction. Spreads easily and rapidly Observation of eggs

Necator americanus, Ancylostoma duodenale (hookworm)
Necator americanus, "Naked american hookers Ancylostoma duodenale working barefoot at night" (hookworm) Burrow through skin and feet Hookworm clinical disease skin reaction/ rash at site of entry. If progress to LU --> pneumonitis. Iff large amount of adult worms: microcytic hypochromic anemia, fatigue, nutritional deficiencies. Characteristic eggs in stool

Trichinella spiralis (trichinosis)
Trichinella spiralis (trichinosis) Pigs are the major source. Undercooked pork. Larvae migrate to striated muscle but also cardiac and nervous tissue T. spirales clinical syndrome if many migrating --> splinter hemorrhages, persistent fever, GI distress, periorbital edema. Iff >1000 to 5000 larvae/ gm tissue - Can be lethal. encysted larvae in implicated meat Acute inflammation and myositis.

Ochocerca volvus 2-5cm long. 2000 bite from infected Reservoir is humans. Vector microfilariea daily for 15 mosquitoe: migrate to River blindness - black fly years - burrow in the eye for lymphatics 2 years. chronic symptoms are due Vector: mosquito to: physical blockage of Elephantiasis (anopheline or Culex) lymphatic vessels Transmitted by Mansonia mosquitoes Like wucheria but half has large

Wucheria bancrofti

Swelling of legs and genitals due to lymph blockage

Brugia malayi

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Flukes Schistosoma spp.
develop in intrahepatic portal system or in vesical, prostatic, rectal and uterine plexuses and veins Host response to eggs: intense, inflammatory reaction

Schistosoma spp.

Snail as intermediate host skin penetrating cercariae --> burrows through skin to liberated from snails enter bloodstream


Immediate and delayed hypersensitivity reactions. Katayama syndrome. Chronic stage: hepatosplenomegaly with portal HT and hematemesis. retained eggs cause extensive inflammation and scarring. Urinary bladder, bowel, and liver dysfunction.

Characteristic eggs in stool and urine

Tapeworms Taenia
Taenia: T. saginata, T. solium Ingestion of undercooked beef (saginatum) or pork (solium) Form cystericeri are SOL's (imp in BRAIN) . No intestinal damage except absorption problems. Malnutrition, cysticerciasis

Diphyllobothrium latum
Fish tapeworm Diphyllobothrium latum From raw, freshwater fish one of the longest tapeworms - 45cm Clinical disease low serum levels of Vitamin B12 --> megaloblastic anemia bile stained, operculated egg with knob-like projection on posterior

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