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216 Cards in this Set

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Morphology
- Gram (-) bacillus with outer envelope (subject to drying)
-O antigens used for strain typing (O157:H7)
Virulence factors
1.Adhesins
2.exotoxins
3.H (flagella) and K (capsule) antigens
- Virulence factors:
i)special adhesins are sued to attach to the uroepithelium
ii)p-fimbriae
iii)hemolysin enzymes lyse RBC’s, are proinflammatory, resist C-mediated cell lysis
Signs and symptoms
i) Cystitis
- dysuria, urgency, increased frequency, incomplete voiding
ii) pyelonephritis
- same as cystitis but more severe and with fever, loin pain and (+) KI punch

Septicemia
- E. coli causes 45% of enterobacterial septicemia
lab diagnosis
pyuria, hematuria, bacteriuria
exogenous infections
from contaminated food or water
Enterotoxigenic (ETEC)
-traveler’s diarrhea (Montazuma’s revenge)
-infant diarrhea
-virulence factors
-adhesion factors
-exotoxins
-ST a / ST b  guanylyl cyclase
-LT 1 / LT 11  adenylyl cyclase
-signs and symptoms
-watery diarrhea
-vomiting (rare)
Enteroinvasive (EIEC) (compare Shigella
-signs and symptoms include scant, bloody stool that is leukocyte (+), and fever
-might progress to colonic ulceration
Enteropathogenic (EPEC
-common cause of infant diarrhea
-signs and symptoms include non-bloody stool, fever, nausea, vomiting
Enteroaggregative (EaggEC)
-persistent, watery diarrhea, low grade fever, nausea and vomiting
Enterohemorrhagic (EHEC)
S/S
V-factors
-most common strain causing disease in developed nations
-cause of “Hamburger Disease” and HUS
- low inoculation (100 bacilli) is needed
- virulence factors
- verotoxin – destroys GI cells
- ST X – stimulate cytokines to increase virulence and receptor expression
- Hemolysin – central role in disease symptomatology
-signs and symptoms
-bloody diarrhea
-NO fever
-Can progress to HUS
-Spread via undercooked beef or other meat, feces, contaminated water
-HUS
-Most common cause of acute renal failure in children
-Spread
-Person to person (importance of handwashing)
-Signs and symptoms
-Bloody diarrhea
-Acute renal failure (destruction of renal glomeruli)
-Lab diagnosis
-Stool culture (+) for E. Coli O 157:H7
-Hemolytic anemia
Diffuseaggregative (DAEC)
- bacteria imbedded in cell membrane of elongated microvilli
-watery diarrhea
neonatal meningitis
- most commonly cause by E. Coli and Group B Streptococcus
K1 capsular agonists
Epidemiology
-part of the normal GI flora
-increased risk of infection in hospitalized patients and travelers to developed nations
- public hygiene systems in developed nations play a significant role in the rarity of E. Coli infections
Treatment
-revent by good personal hygiene
-cook ground beef until the center is brown, not pink, and the juices run clear. The middle of the patty must reach at least 68°C for at least 15 s
-ABC therapy is NOT indicated
SALMONELLA (ENTEROBACTERIACEA, SALMONELLA – family, genus)
-diseases are gastroenteritis (S. enteitidis) and enteric fever (S. typhi and S. paratyphi)
MORPHOLOGY
-Gram (-) bacillus
-Outer membrane – so susceptible to drying
VIRULENCE FACTORS
1.Surface antigens
a)O Ag (on LPS)
b)V1 Ag (on capsule)
c)Species specific fimbria attach to M cells on peyers patches
2.Endotoxin
-responsible for the fevers (IL-1 signal to hypothalamus)
3.Invasiveness
-penetrate into sub-epithelia spaces with out a toxin mediated process – rearrange the host cell actin (membrane ruffling)
4.Enterotoxins
a)LT / ST-like toxins (compare E. Coli)
b)Ditto
c)Verotoxin like
5.Other
-Acid tolerance response gene
-Catalase
-SOD
S. ENTERITIDIS EPIDEMIOLOGY
-poultry / birds
-humans most commonly get salmonellosis from undercooked poultry, contaminated cutting boards, egg salad, undercooked / raw eggs
-disease incidence increases in the summer due to all the BBQ’s
-also more common in children >1 year and elderly > 60 years old
D.S. TYPHI EPIDEMIOLOGY
-humans are the only known animal host
-associated with foreign travel – spread by food or water contaminated b infected food handlers (only needs a low inoculum, compare S. enteritidis which needs a very high inoculum)
SALMONELLA CLINICAL SYNDROMES
-“salmonellosis” regardless of species
-five potential outcomes
1.no outcome
2.gastroenteritis
-S. Enteritidis – most common cause
-Occurs 6-48 hours after ingestion of contaminated food or water
-Signs and symptoms include: nausea, vomiting, fever
-Most commonly is self limiting
3.Septicemia
-most commonly due to S. typhi, and S paratyphi
-increased risk in AIDS, geriatric or pediatric patients
-symptomology of septicemia is similar to other Gram (-) septicemia (10% of patients develop arthritis, osteomyelitis, and endocarditis)
4.enteric fever
-most commonly spread by food handlers infected with S. typhi (typhoid fever) or S. paratyphoid (paratyphoid fever)
-bacteria passes directly through intestinal walls
-this is NOT typhus which is caused by Rickettsia spp.
-Signs and symptoms include: increasing, remittent fever, rose coloured spots on abdomen
5.asymptomatic carriage – 1-3%
S TYPHI PATHOGENESIS AND COMPLICATIONS
-infected foodhandlers - gall bladder - back to intestine to cause increased inflammation
-complications include
-GI lesions: hemorrhage, perforation
-Toxemia: myocarditis, liver and bone marrow damage
-Prolonged serious illness
-Other: menigitis, osteomyelitis, endocarditis
SALMONELLA TREATMENT / PREVENTION, CONTROL
-improved personal hygiene and public hygiene
-spread by the 5 F’s: food, fingers, fomites, feces, flies
-avoid antacids (also increased risk of pneumonia)
-clean cutting boards
-most commonly symptomatic treatment instead of ABC’s
-S. Typhus – oral or parenteral vaccine (70% effective, transient immunity, frequent side effects)
SHIGELLA (ENTEROBACTERIACEAE, SHIGELLA – family, genus)
-S. flexneri
-Most common cause of shigellosis in developing world
-S. sonnei
-Most common cause of shigellosis in industrialized world
-S. boydii
-S. dysenteriae
EPIDEMIOLOGY
-humans are the only carriers, transmitted via fecal-oral route
-very low inoculum (only 10-100 bacilli)
-most cases in children ages 6-10
MORPHOLOGY
- Gram (-) rod
Significant outer membrane (drying)
PATHOGENESIS
-attach an invade M cells in Peyer’s patches and cause membrane ruffling
-shiga exotoxin (S. dysenteriae) which disrupts protein synthesis
- damage glomerular epithelial cells (hemolytic uremic syndrome) (compare entero _______ E. coli)
CLINICAL SYNDROMES
-GI symptoms are caused by Shiga toxin (enterotoxic, neurotoxic, cytotoxic)
-Profuse, watery diarrhea
-Fever
-Tenesmus
-abundant blood and pus in stool
-NO VOMITING
-Shigellosis:
-Bactermia is RARE
-Infection is generally self limited
-5% of patients carry bacteria assymptomatically
TREATMENT
-same as enterobacteriaceae in general:
-proper hygiene
-proper removal, isolation, disinfection of soiled linens and diapers
-ABC are used to:
-Shorted course of disease and control spread by reducing carriage in symptomatic patients
-Resistance is likely (compare pseudomonas)
-resistant to Stomach acid (low inoculum) (contrast Salmonella)
VIBRIOACAE, VIBRIO – family, genus, species
-V. parahemolyticus
-V. vulnificus
-V. Cholera (most known)
-200 serotypes
-EI tor biotype is most common in world today
MORPHOLOGY
-Gram (-) bacillus, comma shaped (compare legionella)
-Motile – single polar flagella
-Most need salt for growth (“halophilic”) – NOT V. Cholera
VIRULENCE FACTORS (V. Cholera)
1.cholera toxin complex A-B toxin:
-structurally and functionally similar to heat – labile enterotoxin A of E. coli
-B toxin
-A toxin
-Increase cAMP
-Cause electrolyte shift - watery diarrhea
2.Adhesins
-strong attachment to intestinal epithelium despite peristalsis and flushing
3.Mucinase (hemagglutination protease)
-intestinal inflammation and degradation of tight junctions
4.Siderophores
-sequester iron
5.Neuramidase
-increase toxin receptors (compare influenza)
6.Hemolysin
-hermostable
-increase intracellular Ca -increase chloride secretion
EPIDEMIOLOGY (V. Cholera)
-ubiquitous in marine environment (contrast salmonella and campylobacter)
-even in increased salinity and temperature (10°C to 30°C)
-contaminated shellfish / seawater is most common way to transmit disease (compare Hep A)
-asymptomatic human carriers in endemic areas also transmit disease
-relatively infectious (contrast Shigella – especially if normal acidity)
-most cases seen in returning travellers(compare enterotoxogenic E. Coli)
CHOLERA S/S
-abrupt onset of watery diarrhea and vomiting
-rice water stools – colorless, odorless, no protein, speckled with mucus
-severe fluid and electrolyte loss – dehydration, metabolic acidosis, hypokalemia
-NO ABDOMINAL CRAMPS
-NO FEVER (contrast Shigella, Salmonella, Campylobacter)
-Resembles ETEC induced gastroenteritis
CHOLERA LAB DIAGNOSIS
-rarely seen in gram stained stool or wound specimens
-dark field / phase contrast microscopy – characteristic darting motility
-direct ELIZA
CHOLERA TREATMENT, PREVENTION, CONTROL
-aggressive fluid / electrolyte replacement (oral / IV) reduces mortality to less than 1%
-no long term human carriers (contrast S. typhi)
-vaccine – limited usefulness due to short lived protection
BACILLACEAE, BACILLUS – Family, genera
- Gram (+) bacillus
- Endospore forming
- 2 main species that cause disease in humans
-B. anthracis – anthrax
-B. cereus – gastroenteritis (contaminated “cereal,”rice)
B. ANTHRACIS
-biological warfare
-Gram (+) bacillus
-Clinical samples – single or paired – “jointed bamboo-rod”
-Culture – long serpentine chains “medusa head”
VIRULENCE FACTORS
a)Capsule
-anti-capsular antibodies are not protective
b)Toxin
-3 parts:
-protective Ag – binding, antiphagocytotic
-lethal factor – zinc metalloprotein, proinflammatory
-edema factor – stimulate adenylyl cyclase  fluid build up
EPIDEMIOLOGY
-domestic herbivores – sheep, goats, cattle, horses
-3 routes of transmission
-inoculation of the skin
-most common – contacting infected animals – 20% mortality
-inhalation of spores / wool – “woolsorter’s disease” – 95% mortality
-ingestion of contaminated food – rare but deadly
-endemic in developing countries
-occupational disease and biological warfare in developed countries
CUTANEOUS ANTHRAX
-transmission: break in skin exposed to spores which can survive for years
-diagnosis:
-history: mail carrier; painless, necrotic eschars
-lab diagnosis: Gram (+) bacillus in lesions, NO neutrophils
-other: internal hemorrohage
-Vs. ORF
-B. anthracis (pox virus)
-Direct contact with spore contaminated with animal products (direct contact with infected sheep or goat)
-Painless papule with necrotic eschar and gelatinous edema (painless vesicles – red weeping nodules)
-Arms, hands face, neck (hands)
-Potentially fatal – 20% (benign and self limiting)
INHALATION ANTHRAX
-carried by alveolar macrophages to mediastinal lymph nodes – prolonged latency

-initial disease
-fever / chills
-dyspnea
-cough
-head ache
-vomiting
-chest / abdominal pain


second stage
-rapidly worsening fever
-diaphoresis
-pulmonary edema
-massive enlargement of mediastinal lymph nodes
-shock - death with in 3 days
-hemorrhagic meningitis symptoms (more common than pulmonary symptoms)
INGESTION ANTHRAX
-Upper GI
-Oral / esophageal ulcers
-Edema
-Sepsis
-Regional lymphadenopathy
-dysphagia


Lower GI
-Nausea
-Vomiting
-Malaise
-Systemic S/Sx
-Bloody diarrhea
-Rare but almost 100% mortality
TREATMENT / PREVENTION
difficult due to long lived spores –
B. CEREUS
-low mortality compared to B. Anthracis
-causes two types of gasteroenteritis
1.emetic disease
-heat stable enterotoxin
2.diarrhoeal disease
-heat labile enterotoxin
-also causes panopthalmitis which is inflammation of the entire eye after a traumatic injury (also caused by S. aureus, Candida albicans, S. pneumonia, E. coli, N. meningitidis) (compare keratitis due to pseudomonas)
VIRULENCE FACTORS
-heat stable enterotoxin - emesis. Found in contaminated, improperly refrigerated rice dishes
-heat labile enterotoxin - profuse watery diarrhea. Found in contaminated meat, vegetables, and sauces (compare enterotoxin of ETEC and V. cholera)
-cerolysin - eye damage
-phosopholipase C - eye damage
-Necrotic toxin - eye damage
FOOD BORN DISEASE
a)emetic disease
-NO FEVER
-NO DIARRHEA
b)diarrheal disease
-nausea
-bloody diarrhea
-NO FEVER
PANOPTHALMITIS
-post traumatic
-rapid (<48 hours)
TREATMENT AND PREVENTION
a)Gastroenteritis
-no ABC (sickness due to toxin)
-rapid consumption of food after eating???
-Refrigerate uneaten portions
b)Panopthalmitis
-early, aggressive ABC
-multiple drug resistance
CAMPYLOBACTERACEAE (Family)
-small (0.3-0.6 um) – filterable unlike other bacteria
-Gram (-) bacillus – S or gull-wing shaped
- Motile – single bipolar flagella (compare V. cholera)
- Microaerophilic (can survive on decreased oxygen and increased carbon dioxide)
-Thermophilic (42°C)
EPIDEMIOLOGY
-number 1 bacterial cause of gastroenteritis and bacterial endocarditis in USA
-most common is C. jejuni
-carried on birds, cats
-also transmitted via raw milk and water
-peak incidence in young adults (20-29 yo)
CAMPYLOBACTER JEJUNI GASTEROENTERITIS
-need high infectious dose
-reduced with hypochloridria, TUM’s and milk
-2-11 day incubation
-foul smelling, watery diarrhea - profuse bloody diarrhea
-NO VOMITING
-Resolution in 3 days to 3 weeks
-Residual histological damage to GI mucosa (compare EIEC, enterolytictia? E. coli and shigella shiga toxin)
GUILLIAN BARRE SYNDROME
-due to many causes: C. jejuni enteritis, immunizations, pregnancy, etc…
-idiopathic, peripheral polyneuritis 1-3 weeks after the above mild condition
-progressive, symmetric pain and weakness in extremities – might ascend to trunk, face, thorax
-self limiting (few weeks to few months) with complete recovery
-autoimmune?
TREATMENT AND PREVENTION
-Gastroenteritis
-Prevent with proper preparation and storage of food
-Avoid raw milk
-Proper water treatment
-Guillan Barre syndrome
-No treatment
HELICOBACTER PYLORI
-Gram (-) bacillus – but gram stain is variable (spiral in fresh culture, coccoid in older culture)
-Motile – flagellated – “corkscrew motion”
-Urease (+) - breaks down urea to amonia and something else which increases the pH - surrounded by buffer cloud which allows it to survive in the stomach
-Temperature 30°C-38°C (contrast Compylobacter spp.)
EPIDEMIOLOGY
-found in gastric antrum and body of stomachs of humans, primates, pigs, cheetahs, dogs, cats, ferrets, mice, rats
-up to 45% in adults >50 yoa
-only <20% of people testing positive for H. pylori get peptic ulcer disease
COLONIZATION FACTORS
-survive acidity
-acid inhibitory protein
-urease
-flagella
-mucinase – breaks down mucin layer in stomach
-phospholipase
-microaerophillic
-survive in relatively anaerobic environment of stomach
VIRULENCE FACTORS
-Pro-inflammatory – platelet aggravating factor - hyper-secretion of gastric acid
DISEASES
1.Type B (infective) gastritis (type A – is autoimmune due to NSAIDS)
-30-50% of people with gastritis have H. pylori but are most commonly asymptomatic
-epigastric pain
-foul smelling breath
-lab diagnosis:
-13C urea breath test
-anti-H. pylori Abs (IgG)
-gastroscopy with biopsy
-CampyloLikeOrganism test (+)
2.Peptic ulcer disease
-especially gastric ulcers
-burning, gnawing upper GI pain 1-3 hours after meals
- < night
- >eating
- >antacids
- Lab diagnosis:
- Endoscopy
- Urea breath test
- Serology (anti H. pylori Abs)
3. Gastric adenocarcinoma
- class I carcinogen
- S/Sx (similar to other cancers)
-fatigue
-weight loss
-low grade fever
-night pain
-hemoccult (+) stools
4.Gastric mucosa-associated lymphoid type B cell lymphoma
-rare
-no evidence that eradicating H. pylori prevents progression of gastritis to carcinomas (something else must be going on)
5.Athersclerosis?
TREATMENT
-triple therapy: proton pump inhibitor, clarithromycin, metronidazole, bismuth
CLOSTRIDIUM SPP (BACILLACEAE – family)
-Gram (+) bacilli
-Most commonly anaerobic
-Spore formers
-3 general classes
-histotoxic – C. perfringen
-enterotoxigenic – C. difficile
-paralytic – C. tetani, C. botulinum
C. PERFRINGENS
-gram (+) “plump, rectangular” rod
-causes wound / soft tissue infections
-non-motile but rapid growth on sheep’s blood agar (use to distinguish)
-5 Toxins – Type A: permanent soil inhabitant, responsible for most human disease
PATHOGENICITY
-spore formation – long term survival
-alpha toxin – most tissue damage – vascular permeability increases, lyses cells
-heat kills enterotoxin
EPIDEMIOLOGY
-ubiquitous
-most commonly harmless saprophyte (live on dead tissue)
-need devitalized tissue (anaerobic)
-disease most common after trauma that causes ischemia – lowered pO2 and pH favors growth
CLINICAL SYNDROMES
-simple wound infection
-anaerobic cellulitis
-subcutaneous tissue – spares fascia and deep muscles
-superficial skin discoloration and skin necrosis
-gas forms -suppurative myositis – foul smelling discharge
-no muscle necrosis
-NO systemic S/Sx
-myonecrosis (gas gangrene)
-rapidly worsening of cellulitis
-trauma - intense pain, extensive muscle necrosis (blue black, edematous, does not bleed or contract on stimulation), toxic delirium
-much damage due to alpha toxin an gas bubbles
-diagnosis:
- debridement
-gram (+) rods in tissue specimens with no leukocytes
-food poisoning (#4 - #1 Campylobacter jejuni, #2 salmonella, #3 S. Aureus)
-from meat – refrigeration and re-heating destroys enterotoxins (compare B. cereus heat labile toxin that causes diarrhea)
-large infective dose needed
-abdominal cramps
-watery diarrhea
-NO fever
-NO nausea or vomiting
Lab DX
fast growth of culture on sheep’s blood agar
-nagler’s reaction on egg yolk agar
-gram (+) rods in tissue specimens with no leukocytes
C. DIFFICILE
-can be a normal part of GI flora without causing disease (3% will have with out disease)
-most commonly causes post ABC diarrhea and pseudomembranous colitis
VIRULENCE FACTORS
-Toxin A (enterotoxin) – hemorrhagic necrosis in pseudomembranous colitis (the key inflammatory players are IL-1, IL-6, and TNF alpha)
-Hyaluronidase – increase spread between tissues
DISEASES
-mild diarrhea to colitis to potentially life-threatening pseudomembranous colitis
-prolonged diarrhea (signs of dehydration)
- pseudomembranous colitis is confirmed by biopsy – multiple, raised white / yellow exudative plaques adhering to colonic mucosa
lab dx
in vitro cytotoxicity assay in culture cells
-immuno assay (direct ELIZA) for C. difficile toxins A and B
-sigmoidoscopy
-fecal leukocytes
TREATMENT & PREVENTION
-maintain fluid / electrolyte balance
-avoid drugs / therapies that decrease intestinal motility
-“watchful waiting” if mild
-hand washing, environmental cleansing of play areas, beds, bathrooms
-prescribe ABC w/ probiotics (but take away from each other, and taking probiotics with food, especially protein decreases stomach acidity which decreases likelihood of survival???)
-for example: saccharomyces boulardii, lactobacillus spp.
C. TETANI “extreme tension”
-gram stain variable (compare helicobacter pylori)
-classic “tennis racket”
-very sensitive to oxygen – obligate anaerobe
-relatively inactive metabolically (contrast C. perfringens)
VIRULENCE FACTORS
-spores – survive adverse conditions (3 hours of boiling, 1 hour at 160° C of dry heat, 2 weeks in 5% phenol)
-tetanospasmin
-heat labile neurotoxin – one of the three most potent toxins
-responsible for spastic paralysis
-two part toxin
-irreversibly inhibits the release of GABA and glycine in post synaptic terminals in CNS (same mechanism as strycnin poisoning)
EPIDEMIOLOGY
-ubiquitous
-spores last for years
-present in GIT of cows, horses, and some humans
- low disease incidence in developed worlds due to immunizations, herd immunity, and urbanization
- infant tetanus can be a problem in developing worlds contributing to > 50% of neonatal deaths
GENERALIZED TETANUS
-later signs: opisthotonus – back arching most common form of tetanus
-bacterium introduced by trauma to skin – animal bites
-early signs: exaggerated deep tendon reflexes, trismus (lock jaw) – masseter muscle, risus sardonicus (mock smile), drooling
OTHER FORMS OF TETANUS
-localized
-cephalic
-neonatal – from improperly cleaned umbilical stump
-firs sign: difficulty sucking 8-10 days after birth
Lab DX
-patient history
-clinical S/Sx
-gram stain and culture not that important because only 30% of people with tetanus are culture (+)
TREATMENT & PREVENTION
-Tetanospasmin binds irreversibly and therefore can only treat symptoms until nerve terminal regenerate
-Passive immunization – binds free tetanospasmin
-No natural immunity unlike many other diseases
-Active immunization – tetanus toxoids: booster every 10 years
C. BOTULINUM
-gram (+) bacillus “sausage shaped”
-produces one of the most potent exotoxins know to humans
-ubiquitous – sediments of lakes and ponds
VIRULENCE FACTORS
-spore formation – one of the most resistant from heat (hours at boiling, 10 minutes at 120°C) and cold (down to -190°C)
-botulinum toxin
-one of the most potent known neurotoxins
-binds irreversibly to cholinergic neurons
-inhibits acetylcholine release at peripheral presynaptic terminals and therefore causes a flacid paralysis (opposite of tetanospasmin)
-botox for cosmetics, migraines, other disorders
FOOD BORNE BOTULISM – INTOXICATION
-inadequate sterilization of food – home canned foods, preserved fish
-2-72 hours incubation
Signs and symptoms
-NO GI DISTRESS
-No fever
-Clear sensorium
-Dilated fixed pupils
-Dry / furry tongue
-Bilateral descending weakness of neck, face, throat
-Respiratory paralysis – 32-40% mortality
-No permanent immunity – can get repeated occurrences
INFANT BOTULISM – INFECTION, INTOXICATION
-honey contaminated with spores (pacifier)
-most common form of botulism in USA
-most common in 1-6 month olds due to bacteria growing and producing neurotoxin in infant GIT, and infant GIT doesn’t have as many competitive bowel microbes
S/Sx
-Non specific – constipation, weak cry, failure to thrive, weak suckling
-Floppy baby – acute flaccid paralysis (head, face, throat descending to extremities)
-Death from respiratory paralysis – low mortality (1-2%)
TREATMENT & PREVENTION
-acid pH (canned fruit is ok) – grow best at pH < 4.5 ??
-refrigerate (can’t survive < 4°C)
-heat for a minimum 10 minute at 80°C
-no honey to infants < 1 year old
-check cans – swollen
NEISSERIA
-gram (-) diplococci “coffee bean”
-transparent colonies on chocolate blood agar
-N. meningitidis
-Normal colonizer of nasopharynx or cause disease
-asymptomatically colonize nasopharynx or cause meningitis, meningococcemia or pneumonia
PATHOGENESIS
cells
-Phagocytosis effective?
-replicates in phagocytic vacuoles
-capsule is also anti-phagocytic
-LOS expressed?
EPIDEMIOLOGY
-most common cause of bacterial meningitis in infants through adolescence and in young adults
-epidemics
-most common when a new virulent strain is introduced into an immunologically naïve population
-transferred via close contact with respiratory droplets (et. Day cares, military barracks)
-classmates in school, hospital employees not considered close enough contact to get disease
- most common carriers are asymptomatic adults (nasopharyhgeal carriers)
-disease is most common in dry, cold months
MENINGOCOCCEMIA
– mild disease
-persistent (few days to weeks):
-arthritis
-petechial skin rashes
MENINGOCOCCEMIA
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)
-If untreated can progress to disseminated intravascular coagulation or hemorrhage into adrenal glands
-Sequelae
-none or large areas of necrosis / skin ulceration (skin grafts)
-deafness (affect CN VIII) or squint (affect CN VI)
MENINGOCOCCAL MENINGITIS
-N. meningiditis is 2nd M/C cause of adult bacterial meningitis
-Triad of rapid onset of fever, nuchal rigidity, blinding headache
-Hight number of gram (-) diplococci organisms in PMN of CSF
- inflammation of membranes covering the brain and spinal cord (M/C’ly caused by N. meningiditis, H. influenza, S. pneumonia)
-modes of control
a)proper hygiene
b)good diet (immune supporting)
c)polysaccharide vaccine
d)avoid close contact with intected person
e)ABC’s
-N. gonorrhoeae
Strict pathogen
A.N. GONORROEAE
-“the gonococcu”
-gram (-) diplococci
-fastidious growth
-2nd most common STD in USA (chlamydia is #1)
PATHOGENESIS
v-factors
-no exotoxin – host damage is from gonococcal induced inflammatory response
-anti-phagocytic – negatively charged capsule
-Pili – tissue tropism: non-ciliated epithelial cells of foreskin, vagina, fallopian tube
-LOS – classic endotoxin activity (like LPS)
-Fe++ binding proteins
-IgA protease
-Beta lactamase (degrades penicillin
EPIDEMIOLOGY
-humans are the sole natural carriers of gonorrhea
-transmission: intimate sexual contact (most commonly in 15-24 year olds)
-increased risk if female, with multiple sexual partners
-women are most commonly asymptomatic carriers
GONORRHEA IN MALES
-95% of men get acute symptoms (most commonly gonococcal urethritis)
-infection usually restricted to mucosa of penis
-2-7 day incubation – purulent urethral discharge, red / edematous urethral meatus
-can progress to peri-uretrhal abcesses, prostatitis, epididymitis
GONORRHEA IN FEMALES
- >50% of women are asymptomatic carriers or have mild symptoms (cervicitis)
-iff acute: vaginal discharge, and abnormal vaginal bleeding
-if untreated - ascending infection - major cause of infertility
DISSEMINATED GONORRHEAE
-rare but M/C in women (1-3%)
-S/Sx: fever, migratory arthralgias, tender papillary lesions / rash on the extremities
-Arthritis: M/C’ly mono-articular – knee in females
-N. gonorrhoeae is the #1 cause of purulent arthritis in young adults
LAB DIAGNOSIS
-clinical signs similar to chlamydia
-gram stain
-sensitive and specific iff men with purulent urethritis
-must confirm with culture
-gram (-) diplococci on chocolate blood agar
TREATMENT AND PREVENTION
currently no longer using penicilin due to resistance – beta lactamase, need to hight dose, damage cell surface so ABC can’t penetrate cell
- prevention: safe sex
HAEMOPHILUS SPP. (blood loving)
-small, gram (+) coccobacillus
-pleomorphic (many sizes and shapes
-fastidious growth requirements
-X factor (hematin) and V factor (NAD)
-obligate parasites on mucous membranes of humans and animals
-2 main species: H. influenzae and H. Ducreyl
A.HAEMOPHILUS DUCREYL
-small, gram (-) coccobacillus
-non-encapsulated
EPIDEMIOLOGY
- can cause STD, most common to developing world
-causes chancroid (soft chancre)
CHANCROID
H. ducreyi
Soft, purulent, painful ulcer (genitalia)
MC in uncircumcised males tropical and sub-tropical (female – carrier)
5-7 day incubation
 painful buboes (swollen inguinal lymph nodes), phimosis (can’t pull foreskin back over shaft of penis), urethral structure

dyspaerunia (painful intercourse in females)
Gram (-) coccobacillus
PRIMARY SYPHILIS
Treponema pallidum
Hard, non-purulent, non-painful ulcer
Both sexes 20-35 yoa
3 week incubation
 painless buboes
Poor gram stain – dark field microscopy (spiral rods, thin tightly coiled), non-specific tests (VRDL, RPR), specific tests (FTA-Abs, TPHA)
TREATMENT and PREVENTION
-ABC’s: ceftriaxone, erythromycin, cotrimazole
-Save sex practices
HAEMOPHILUS SPP. (blood loving)
-small, gram (+) coccobacillus
-pleomorphic (many sizes and shapes
-fastidious growth requirements
-X factor (hematin) and V factor (NAD)
-obligate parasites on mucous membranes of humans and animals
-2 main species: H. influenzae and H. Ducreyl
A.HAEMOPHILUS DUCREYL
-small, gram (-) coccobacillus
-non-encapsulated
EPIDEMIOLOGY
- can cause STD, most common to developing world
-causes chancroid (soft chancre)
CHANCROID
H. ducreyi
Soft, purulent, painful ulcer (genitalia)
MC in uncircumcised males tropical and sub-tropical (female – carrier)
5-7 day incubation
 painful buboes (swollen inguinal lymph nodes), phimosis (can’t pull foreskin back over shaft of penis), urethral structure

dyspaerunia (painful intercourse in females)
Gram (-) coccobacillus
PRIMARY SYPHILIS
Treponema pallidum
Hard, non-purulent, non-painful ulcer
Both sexes 20-35 yoa
3 week incubation
 painless buboes
Poor gram stain – dark field microscopy (spiral rods, thin tightly coiled), non-specific tests (VRDL, RPR), specific tests (FTA-Abs, TPHA)
TREATMENT and PREVENTION
-ABC’s: ceftriaxone, erythromycin, cotrimazole
-Save sex practices
HAEMOPHILUS INFLUENZAE
-non-encapsulated strains colonize both upper and lower respiratory tracts
-encapsulated strains (serotype b) can become systemic
VIRULENCE FACTORS
a)Capsule
-determines serotype, virulence and tropism – invasive disease is most commonly due to H. influenzae type b (Hib infection)
-antiphagocytotic
-presence of anti-Hib capsule Abs determines severity of disease
-transfer of maternal Abs is paramount to preventing disease
b)pili
c)LPS
-damage respiratory, ciliated epithelium
-responsible for meningitis
d)IgA protease
EPIDEMIOLOGY
-primarily a pediatric problem (don’t need to vaccinated after 5 years old, because by 6 should develop immunity)
- currently primarily a pediatric problem in developing world
-also increase risk in elderly
DISEASES
a)Meningitis
-same S/Sx as other bacterial meningitis – but more insidious onset and increased risk of neurological sequelae
b)epiglottis
-medical emergency
-most common in boys 2-4 yoa
-dysphagia, drooling, muffled voice (hot potato), minimal cough
-severe dyspnea
-“thumb sign” on lateral X-ray of neck
c)cellulitis
d)monoarticular arthritis
e)Otitius media / sinusitis
-3 most common causes are H. influenzae, S. pneumonia, Moraxella catarrhalis
-(immune acquired pneumonia and otitis media in kids is most commonly caused by dairy and sugar)
f)Pneumonia
- might be 2° to influenzae virus damage to respiratory epithelium
LAB DX, TX, CONTROL
-Gram stain of CSF (for meningitis only), blood (other diseases)
-Culture on chocolate agar
-Immunology – agglutination reaction for PRP capsule in CSF and urine
-Treatment – ampicillin, broad spectrum cephalosporins
-Control – conjugated HiB vaccine (purified PRP) – effective against encapsulated strains only – still get OM, cellulitis
-HbOC at 2, 4, 6, 15 months or
-PRP-OMC at 2, 4, 12 months
BORDETELLA SPP.
-gram (-), very small bacilli (rodlike)
-fastidious growth
-humidity, specialized media: charcoal, blood, NAD-enriched
-B. pertussis - whooping cough
VIRULENCE FACTORS
1.pertussis toxin
-A/B5 structure
-Increase adenylate cyclase - cAMP-respiratory secretions / mucus
2.adenylate cyclase toxin (cyclosin)
-increase cAMP - protects bacteria against elimination in early infection (inhibits NK cell lysis, leukocyte chmotaxis, phagocytosis, and killing)
3.tracheal cytotoxin
-part of peptidoglycan layer causing ciliostasis and then damage to epithelial cells
-cough
-increases IL-1 fever
4.dermonecrotic toxin
5.filamentous hemagglutin and other adesins
-attachment to ciliated epithelial cells and PMN’s – intracellular survival protects against clearance by humoral immunity
6.LPS
- two types (lipid A and lipid X)
EPIDEMIOLOGY
-can only cause disease in humans
-most common in developing countries in children < 1yoa
-spreads by infectious droplets
-increased incidence in older individuals
-no long term immunity
WHOOPING COUGH
-incubation – 7-10 days
-catarrhal (mucus) – 2 weeks, looks like common cold: rhinorrhea ***MOST INFECTIOUS STAGE
- paroxysmal stage – 1-2 weeks, dry non-productive, repetitive “whooping” cough
-convalescent stage – 2-4 weeks
LAB DX
-Bacteria are best isolated using nasopharyngela aspirates during catarrhal stage
-Microscopy: fluoresceine
-Culture: difficult humidity, 35°C, 7 days, specialized agar – only 50% of infective people are culture positive
-PCR
-Lymphocytosis - >18,000 WBC w/ 70-80% lymphocytes
TREATMENT / PREVENTION
-ABC’s are of limited use (disease is not recognizable until peak infectiousness has passed)
-Prevention: DPT vaccine – 2,4,6,15 months and 4-6 years
-Now use acellular B. pertussis (DtaP) (“fewer side effect”)
TREPONEMA PALLIDUM
-Treponema, Spriochaetalis (family, order)
-Small, thin, coiled spirochetes – can’t visualize via gram stain and light microscopy
- Motile – “cork screw” motility via thin fibrils at both ends
-Strict human pathogen
SUB SPECIES PALLIDUM EPIDEMIOLOGY
-humans are the only reservoir of disease
-syphilis (lover of swine) 3rd MC STD in USA (#1 Chlamydia, #2 Gonorrhea)
-very labile, susceptible to drying (can’t get from toilet seat, or dry skin)
- contagious only during primary stage and rash of secondary stage
SUB SPECIES PALLIDUM VIRULENCE FACTORS
SUB SPECIES PALLIDUM VIRULENCE FACTORS
SYPHILIS
1.Primary
-small papule – painless, hard chancre
-painless, regional lymphadenopathy – buboes
-very infectious (exudes fluid loads with spriochetes)
-heals spontaneously with in 2 months with out scarring
2.Secondary
-flu-like syndrome
-localized lymphadenopathy
-diffuse, non-pruritic maculopapular rash (includes soles, palms) – very infectious
-resolves slowly in weeks to months
3.Tertiary (Lues / leutic)
-after 3-40 years of latent syphilis
-neurosyphilis
-cardiosyphilis
-painless or deep burrowing pain
4.Congenital
-infected mother infects infants
-born appearing well then several weeks or up to 2 years later – snuffles, widespread desquamating maculopapular rash
LAB DX
-no gram stain, use silver and fluorescent stains
-non-specific tests:
-Venereal Disease Research Lab, Rapid Plasma Reagent (both look for lipids)
-Indicated current active disease
-specific tests
-Fluorescent Trepanemal Antigen-Abs and TPHA
-Indicates past infection
TX, PREVENTION, CONTROL
-hygiene (spirochetes destroyed by soap and water, temperature >42°C and drying
-safe sex practices
FAMILY CHLAMYDIA
- Very small gram (-) bacillus with virus and bacteria like properties
- Unlike other bacteria, there is no PG layer, therefore no gram stain
- Unique growth cycle within host cell – elementary bodies (extracellular survival and initiation of infection), and reticulocyte bodies (adapted for intracellular growth; metabolically active)
-Inclusion body – high amount of glycogen, therefore stain with iodine (DIAGNOSIS)
- 2 separate genera
1.Chlamydia trachomatis
2.Chlamydophila psittaci, and C. pneumonia
PATHOGENESIS, IMMUNITY (Chlamydia trachomatis)
-gains access through minute abrasion or lacerations
-limited tissue tropism: non-ciliated epithelial cells of mucous membranes of urethra, endocervix, endometrium, fallopian tubes, respiratory tract, conjuctiva
-strains causing LGV can cause systemic infections by entering lymphatic system
-clinical S/Sx due to direct destruction of cells during replication and host inflammatory response
-no long-term immunity
TRACHOMA (chronic follicular keratoconjunctivitis) EPIDEMIOLOGY
-leading cause of preventable blindness in developing countries
-MC in children
-Poor hygiene (no access to water, but they are clean people)
- Spread by droplets, hands, contaminated clothing, eye make-up, flies
TRACHOMA DISEASE
-must have specific attachment to conjunctiva-resist flushing from tears
-begins as conjunctivitis
-entropion – eyelashes chronically irritate cornea
TRACHOMA INCLUSION CONJUNCTIVITIS
1.Adult
- MC 18-30 yoa and sexually active
- Genital infection first and then unilateral mucopurulent discharge in eye
2.Neonatal
- bilateral, intense papillary conjuctivitis with lid swelling (compare nisseria)
CHLAMYDIA UROGENITAL INFECTIONS
-currently MC bacterial STD in USA
1. Women
-termed chlamydia (the drip)
-MC’ly assymptomatic
-Pain / cramping in lower abdomen, dyspaerunia, bleeding between menses
2. Men
-termed NGU (non gonococcal urethritis)
-MC symptomatic
-Yellow, clear discharge
-Pain / tenderness of genitals
-Reactive arthritis
REACTIVE ARTHRITIS
-Seronegative spondyloarthropathy
-MC in young men (20-40 yoa that are HLA-B27 positive
-C. trachomatis is MC bacterial pathogen
-S/Sx: unexplained diarrhea, superficial lesions on palms / soles / oral mucosa
LYMPHOGRANULOMA VENEREUM EPIDEMIOLOGY (LGV)
-MC in Africa, Asia, South America in male homosexuals
-STD
-Initial lesion
-Small painless (compare syphilis, contrast everything else) papule on penis, urethra, glans, scrotum, and vaginal wall
-2nd stage
-painful buboes which can rupture and drain spontaneously
-systemic
-can get proctitis (anal inflammation) in men and women
CHLAMYDIA TRACHOMATIS LAB DX
-Need adequate sample of infected cells (specimen of pus / discharge is anappropriate)
-Culture: most specific method, only infects certain cells lines; inclusion bodies
-Direct fluorescent antibody staining
CHLAMYDIA TREATMENT, PREVENTION, CONTROL
-MC also have presumptive Tx for gonorrhea
-Hygiene (hand / face washing)
-Safe sex practices
CHLAMYDOPHILA PNEUMONIA
-human pathogen that can cause atypical pneumonia (mild, persistent cough / malaise that might progress to lobar pneumonia)
-potential risk to atherosclerosis, MS, alzheimer’s?
CHLAMYDOPHILA PSITTACI
-cause psittacosis
-risk from psittacine birds (parrots, macaws, parakeets, cockatils)
inhaled dried bird excrement, urine and respiratory secretions
PSITTACOSIS DISEASE
-non-productive cough
-commonly progresses to CNS
-prevented by controlling and quarantining domestic and imported birds
MYCOBACTERIUM
-look fungal when initially growing
->70 spp. And many are associated with human disease
-M. tuberculosis, M. lepra, M. avium Complex
-Runyon classification depending on growth characteristics and pigments produced with light
-Acid fast bacillus (mycolic acid resists acid so binds strongly to stain) -DIAGNOSIS
-One of the slowest dividing microorganisms (life cycle is 18-24 hours so ABC are needed for long time)
-Mycolic acid in cell wall – acid fast, resists drying, detergents, acids / bases
-PPD for mantoux test
M. TUBERCULOSIS
EPIDEMIOLOGY
-cause of more fatalities worldwide than any other infectious disease
-MC’ly in person to person transmission via infectious aerosolized particles (which can stay in a room for 45 minutes)
- Very small inoculum needed (as little as 1-3 organisms)
- Increased risk in SE, Asia, Eastern Europe, Northern Mexico, sub-Saharan Africa in immunocomprimised patients
PATHOGENESIS
-inhaled into terminal airways and phagocytosed by alveolar macrophages
-the buggers evade humoral immunity because they grow intracellularly
-spreads to other tissues
- no known mycobacterial toxin or enzyme associated with tissue destruction which is primarily due to host response
- form tubercles (the body trying to protect itself)  caseous granulomas
-Ghon complex – initial lung lesion and locally enlarged lymph nodes
DISEASE
-“TB is the master impersonator”
-Primary infection:
-insidious onset: malaise, listelessness, night sweats, low grade fever, unexplained weight loss and progressive fatigue
-Chest X-ray shows cavitations
-Secondary TB (reactivation):
-Only 5-10% risk that active TB will develop at any time after exposure
-Hematogenous spread anywhere
-Milliary (seed like) TB w/ no pulmonary signs
LAB DIAGNOSIS
- sputum sample: acid fast bacillus w/ fastidious growth requirements, PCR
- skin test (mantoux test): delayed hypersensitivity (T cell mediated) measure induration / erythema
TREATMENT, PREVENTION, CONTROL
- Denver protocol: multi-drug cocktails for >3-6 months
-Problem: MDR-TB
-Diet/robust immune system
M.LEPRAE
EPIDEMIOLOGY
-similar structure as M. tuberculosis but can not be artificially cultured (need live mice or armadillos) and grow in Globi bundles
- rare in USA
-Armadillos are natural reservoir
-Spread via respiratory route or contact with break in skin
VIRULENCE FACTORS
-antiphagocytotic capsule
-preference for lower temperatures
-intracellular survival
-limits infection to skin and nasopharynx
-schwann cells
DISEASE
-two main types of human disease depending on the host immunity
1.Tuberculoid (Paucibacillary) – “sparce” less infectious & skin lesions
-not infectious
-< 5 cutaneous macular lesions w/ hypopigmented centres
-will react to skin test - lepromin
2.Lepromatous (Multibacillary) – “many” more infectious and more skin lesions
-highly infectious
-most destructive – disfiguring skin / bone / cartilage lesions (“leonine faces”)
->5 skin lesions
AVIUM INTRACELLULARE COMPLEX
EPIDEMIOLOGY
-opportunistic infections mostly affecting HIV / AIDS patients
-lymphadenitis
-ubiquitous in water and soil
-transmission via ingestion (raw fish / hard cheese / water) and inhalation
DISEASES
-opportunistic infection
-begins as mild pulmonary disease and spreads to local lymph nodes and then quickly to every organ
-AIDS patients show fever, sweats, weight loss, fatigue, diarrhea, SOB
-Pulmonary disease is similar to TB
-Usually GIT involvement
- Usually fatal with in months
- No person to person spread via aerosolized droplets
DIAGNOSIS / TREATMENT
-sputum cultures / smears: acid fast bacilli
-CBC w/ differential diagnosis: AIDS diagnosis, anemia, neutropenia
-Liver function tests: elevated AST / ALT
-Imaging: CT scan
-Chest: medinastinal lymphadenopathy
- Abdomen: lymphadenopathy, and hepatomegaly and splenomegaly
- ABC: clarithromycin, azithromycin, ethambutol, rifabutin
Fungal morphology
1. filamentous
-molds (mycelium)
-M/C at lower temps and free living

2. Unicellular
-yeasts
-M/C at higher temperatures and when parasitizing tissue
fungal disease classification
1.superficial
-infect outer most (dead) layers of skin
-no immune response

-eg: piedra / trichosporosis
-BLACK piedra (scalp, mustache, beard, groin)
-D/t direct or sexual contact
-Ddx: dark, hard nodules along infected hair shaft
-WHITE piedra (scalp)
-Directed contact
-Ddx: soft, pasty white growth on hair shaft

-eg: tinea (pitryiasis) versicolour
-Malasseiza furfur
-non-itchy, hypo-pigmented lesions on upper torso, arms abdomen
-ddx: “spaghetti and meatballs” organism after KOH prep and woodlamp’s positive

-eg tinea nigra
-Phaeoannuellomycose wernickii
-Well demarcated macular lesions on palms and soles
-Ddx: dark pigmented yeast cells
2.cutaneous
-infect deeper layers of epidermis, hair, nails
-invoke inflammatory immune response
-caused by 3 main genera – mistakenly termed dermatophytes
-eg: most tineas
-ddx: woods lamp (+)
3.submucotaneous
-infects the dermis and subQ tissue (fascia, muscle, bone) following tissue trauma
-rare in developed countries
-might be difficult to treat
-eg: lymphocutaneous sporotrichosis
4.systemic
-invades internal organs esp LUNG foci (respiratory tract as initial foci of infection)
-M/C’ly develop mild acute / asymptomatic lung infections
-Can also develop chronic diease or sub – clinical (latent)
-eg: histoplasmosis, blastomycosis, coccidioidomycoses
SYSTEMIC MYCOSES
-mycotic agents can cause disease in humans and are either:
-strict pathogens
-Histoplasma capsulatum
-Blastomyces dermatitides
-Coccidiodes immitis
-opportunistic pathogens
-Candida albicans
-Aspergillus flavus
-Cryptococcus neoformans
MORPHOLOGY
-can be either:
-monomorphic:
-Cryptococcus neoformans
-dimorphic:
-saprobic phase
-in envirnment
-parasitic phase – thermal dimorphism
-in human infection
HISTOPLASMA CAPSULATUM
-saprobic phase
-in N2 rich soil
-parasitic phase – thermal dimorphism
-in macrophages of Reticular Endothelial System / Mononuclear Phagocytic System
EPIDEMIOLOGY
-found in “histo” belt
-grows in soils rich in N2 – agricultural belt uses much N2 as fertilizer
-bird (starling / chicken) and bat excrement
-epidemics from:
-urbanerenewal
-campsites
-demolishing chicken coops
-spelunking
-researchers disturbing an environment rich in spores
PATHOGENESIS
-inhale ->macrophages phagocytose -> replicated in macrophages -> carried by lymphatics to rest of body
HISTOPLASMOSIS (darling’s disease, cave / spelunker’s disease)
-primary histoplasmosis (5% of people):
-10 d incubation
-acute, self limiting influenzae like illness
-residual calcified lesions in LU and lymph nodes
-not contagious
-complications
-overly aggressive immune response -> Mediastinal fibrosis
ocular histoplasmosis syndrome:
-serious retinal condition – leading cause of blindness in 20-40 yo
-“histo spots” bilaterally
-M/C’ly no visual loss but can be activated to cause visual changes like:
1.sub-retinal neovascular membrane – abnormal blood vessel growth or fluid leak into macula - severe scarring and vision loss
2.metamorphosia – wavy distorted vision due to stretching / distortion of retina
3.decreased central vision acuity – blind spot
4.others
-progressive -> disseminated via lymphatics (increased risk if impaired T-cell mediated immunity)
- TB-like: fever, night sweats, weight loss w/ destructive (caseating necrosis) lung lesions
LAB DIAGNOSIS
-microscopy: biopsy / histological exam – 10% KOH prep w/ silver or giemsa stain
-serological: skin test – too many false (+)
-cultures: selective agar – slowly growing (1-2 weeks) and spores are infections
-DNA probes
-Direct ELISA
BLASTOMYCES DERMATIDES
related to H. capsulatum
Morphology
related to H. capsulatum
epidemiology
endemic areas overlap those of histoplasmosis
-can cause disease similar to humans in dogs and horses and other animals
-unknown reservoir (unlike H. capsulatum it is rarely cultured from soil)
BLASTOMYCOSIS
gilchrists disease, chicago disease
acute
-bronchopneumonia
-***drenching sweat
-no residual calcified lesions (unlike histoplasmosis)
-not contagious
chronic
-TB or cancer like
-Skin lesions: slowly expanding ulcerative or verrucous lesions on face, nose and mouth
LAB DIAGNOSIS
-skin test and serology: too many false (+)
-microscopy: biopsy / histology of KOH prepped tissue sample
-culture: on selective sabourand agar
COCCIDIODES IMMITIS
-dimorphic
-37°C, tissue, mulitnucleated spherule “sporangia”
-new world disease – NA
-endemic in soils of hot, dry, semi-arid areas
-spread via dusty storms
-M/Cly in males 25-55 yo
COCCIDIODOMYCOSIS (
san joaquin valley fever, desert rhematism, posade-wernicke disease)
-inhalation of conidia
-M/Cly asymptomatic
-40% mild, febrile to moderately severe respiratory disease
-not contagious
-<5% - progressive pulmonary diesase
-<<1% - disseminated disease  erythema nodosum w/ arthralgia
DIAGNOSIS
-skin test antigens – 2-4 weeks after sx
-coccidiodin – cell free culture of mycelium growth
-spherulin – cell free culture of spherule phase
-complement fixation
-CXR – “egg shell lesions”
-Tissue biopsy – spherules
-Culture: CAUTION: infectious -> leading to lab acquired infections
BASIC VIRAL STRUCTURE
VIRION
whole virus particle
CAPSID
protein coat surrounding the genome – many different shapes and sizes -> involved in packaging, protection and enzymes
NUCLEOCAPSID
genome, structural proteins and capsid
VAP’s (viral adhesion protein
surface glycoproteins on capsid or envelope -> binding to specific cells, Ags for protective immunity, enzymatic, cell fusion etc (lose evelope, lose attachability)
HEMAGGLUTININS
specialized VAP that binds to RBC’s
ENVELOPED VIRUS
Fragile
Must remain wet
Labile to acids / detergents
Spread b/w cells
Pathogenesis dt hypersensitivity and inflammation
NAKED CAPSID VIRUS
Robust
Survive some drying
Resistant to acids(ST acid), detergents (bile)
Spread by lysing cells
Pathogenesis dt host cell lysis
VIRAL DISEASE
Acquisition entry – inhalation
Initiation of infection
Incubation period – amplification and spread to 2° site via blood (viremia) or lympathics
Potential outcomes include: asymptomatic, non-specific early signs (prodrome) or systemic / local damage directly (virus) or indirectly (immune system)
Covalescence
body repairs damage and develops immunity to protect self in future
VIRAL IMMUNITY
Immune system (cell mediated immunity and humoral immunity) is the best and often only means of controlling a viral infection
Interferon
-systemic symptoms (fever)
-activate immune system
-warn neighboring cells
NK cells
-kill “Ab-tagged” infected cells and tumor cells (Ab Directed Cellular Cytotoxicity)
-stimulate IFN gamma
T cells
-CD4TH – activate CTL’s
-CD8 – (CTL’s)-> kill infected cells and therefore, eliminate source of new viruses
Ab
block spread of extracellular virus to other cells
HERPESVIRIDAE FAMILY
- group of 8 DNA viruses grouped together dt their common virion morphology and mode of replication
3 sub families
-alpha – HSV-1, HSV –2, VZV
-beta – CMV, HHV-6, HHV-7, HHV-8
-gamma – EBV
replication
-adherence – interaction w/ viral glycoproteins and host cell surface receptors
-entry – envelop fuses w/ host cell plasma membrane and nucleocapsid enters cytoplasm
- transport to nucleus – nucleocapsid fuses w/ nucleus and DNA enters
- replication – virus encoded DNA polymerase
-lytic infections of fibroblasts / epithelial cells inhibit host cells of DNA and mRNA synthesis, degrade host DNA to use as substrate for its own replication (nasty buggers)
- outcomes
- latent infections – of neurons only
-persistent infections
-immortalizing infections
-TRANSMISSION: 4 M’s
Mixing & Matching of Mucus Membranes
- HSV-1: transmitted early in life via oral contact or autoinoculation (self – eg: eye to mouth)
- HSV-2: transmitted later in life
- Horizontal: person to person via sexual practices
-Vertical: mother to child via ascending in utero infection or during vaginal
INFECTION:
-Skin break
-Localized 1° infection in mucosa -> vesicular lesions ->retrograde transport ->stress (emotional, fever, direct sunlight, menstruation / hormones, immunosuppression)
ORAL HERPES (HERPES SIMPLEX, HERPES GINGIVASTOMATITIS)
-dew drop on rose petal -> pustules, shallow ulcers and then crust over w/ yellowish crust
- 2° infection is less severe, more localized and shorter duration than 1° infection
HERPES CLINICAL SYNDROMES
-HERPETIC KERATITIS (ocular herpes) –> corneal ulcers -> permanent blindness (compare pseudomonas causing blindness in contact wearers)

-HERPETIC WHITLOW – herpes infection of finger / wrists (of health professionals attending to HSV px)
HERPES SIMPLEX CNS INFECTIONS
-MENINGITIS – HSV-2: nuchal rigidity, blinding HA, nausea, photophobia

-ENCEPHALITIS – HSV-1: seizures, signs of Space Occupying Lesion -> destruction of temporal lobe (learning memory)
-Most common cause of sporadic encephalitis
GENITAL HERPES
-caused by HSV-1 (10% dt orogenital sexual practices) and HSV-2 (90% dt genital to genital contact)
-STD 3-7 days after contact
-Regional lymphadenopathy
-painful (compare chanroid ulcers, contrast syphillis ulcers), shallow ulcers
-Recurrent – prodrome of burning / tingling
FEMALE
- pruritis
- vaginal or cervical mucoid discharge
-increased risk of cervical CA in adulthood
MALE
-Dysuria
-Dyspaerunia
NEONATAL HERPES SIMPLEX INFECTION
-acquired in utero or during vaginal birth or post natally (family members or hospital personnel)
-devastating often fatal
LAB DIAGNOSIS
-tzanck smear – synctia (multinucleated giant cells from fusion of neighboring cells) – (HSV, VZV, HIV)
-cowdry type A – inclusion bodies – histological changes caused by viral components or virus-induced changes in cell structure (HSV, VZV)
-characteristic CypoPathological Effect’s – on specific cell lines
TREATMENT
-allopathic – anti virals
-naturopathic – diet, tea tree oil, geranium oil
CONTROL
-avoid contact w/ mucocutaneous lesions – infections from prodrome even to crusted lesions
-pregnant women – c-section if active genital herpes
-strengthen immune system, avoid triggers
CONTROL
-avoid contact w/ mucocutaneous lesions – infections from prodrome even to crusted lesions
- pregnant women – c-section if active genital herpes
-strengthen immune system, avoid triggers
VARICELLA ZOSTER VIRUS
-don’t confuse varicella w/ variova (small pox)
-AKA herpes virus III
-cause of chicken pox (aka varicella) and shingles (aka herpes zoster)
- like herpes simplex:
- blister-like lesions (but different sizes and stages, deeper, more painful and can cause scarring)
- latent infections
- cell mediated immune system plays a big role in controlling infections
- unlike herpes simplex:
- spreads predominantly via respiratory route
-no detectable lesions at site of entry
EPIDEMIOLOGY
-very contagious from 48 hours before symptoms until all lesions are completely dry
-peak occurrence of chicken pox is 5-10 yoa
- peak occurrence of shingles > 65 yoa
- active herpes zoster can cause chicken pox in susceptible child or adult but will not cause shingles
PATHOGENESIS
- 1° infection – 2-4 days after inhalation  lymphatics
- 2° viremia – thoracic area, vesiculopapular rah
- VZV becomes latent in DRG or cranial root ganglia -> reactivated in older adults and immunocompromised >dermatome ->shingles
CHICKEN POX
-one of the 5 childhood exanthems (eruptions) amongst rubella, roseola, 5th disease, measles / rubeola
-macuopapular rash (dew drop on rose petal)
-intense pruritis
-spread from back / chest to scalp, face and extremities – rarely on soles and palms
-successive crops of lesions
-much more harmful to adults – overzealous CMI will cause more extreme cell damage, interstitial pneumonia, CNS involved, scarring
-chicken pox rash is more severe on trunk than extremities – also on mouth, conjunctiva, vagina
CHICKEN POX COMPLICATIONS
° bacterial infection
2.reyes syndrome
-1 week after acute viral: exanthematous rash, severe vomiting
-2 days later: CNS symptoms
-can occur after chicken pox, enterovirus, EBV, influenzae B, aflatoxin, pesticide
-increased risk if < 18 yoa
-pathology unknown
ASA associated – DO NOT give ASPIRIN to a child w/ chickenpox
HERPES ZOSTER – shingles
-recurrence of latent VZV infection dt stress
-Prodrome – severe pain in localized nerve area
-3-5 days later – gradual development of small red macules, closely spaced. Most commonly in thoracic area or trigeminal nerve area – UNILATERAL
-post herpetic neuralgia – long term (months to years) severe recurring burning or itching pain, hyperesthesia
-unlike herpes simplex – lesions are various sizes
SHINGLES COMPLICATIONS
-herpes zoster opthalmicus – CN V, III
-ramsay hunt syndrome (herpes zoster oticus) – painful lesions along CN VIII (severe otalgia, hearing loss, vertigo), CN V
DIAGNOSIS
- tzanck smear – giant, multinucleate cells – synctia (compare parameso viruses, HSV, HIV, VZV)
-cowdry type A inclusion bodies – drop like masses of acidophillic material surrounded by a clear halo with in the nucleus
VZV TX and CONTROL
relatively mild disease that gives life-long immunity