Acne: not contagious, overgrowth, overproduction of sebum stimulated by hormones
CC: Propionibacterium acnes (NF in small amounts)
VF: Lipase
Treatment: cleansing, topical antibiotics sometimes
Boil: painful, purulent lesions (common for MRSA)
CC: Staphylococcus aureus, VF: enzymes & toxins
Dx: appearance & gram stain, Tx: topical/oral antibio.
*MRSA: S.aureus gained meth. resist. via plasmid - use VANC!!
Impetigo: scabs are picked, land, and spread
CC: S. aureus or Streptococcus Pyogenes (GAS)
VF: exoenzymes - break down skin
* not huge bloodstream concern b/c superficial
Dx: Gram stain, Tx: topical antibiotics
Abscess: purulent, swelling, (result from boil/cellulitis)
CC: S.aureus (~MRSA), GAS, VRE (vanc resistant)
VF: exoenzymes & toxins, PVL toxin, Hemolysin (VRE) - kills WBCs, Dx: gram stain (VRE cocci short)
Tx: antibiotics + open & drain
Cellulitis: tight, hot, tender, pain, lymphangitis(track)
CC: S.aureus, GAS, Pasteurella multocida, Bartonella henselae(rods) (ellas come from pet NF)
VF: deeper tissue enzymes & toxins (MRSA&blood risk)
Dx: Gram stain, Tx: antibiotics (oral or IV)
SSSS: skin peeling, babies, bullous lesions
CC: S.aureus, spread by adults who have S.a. in NF
VF: exfoliative toxins (ET-A, ET-B) cause detachment within keratinized layers
Tx: handwashing & antibiotics to prevent 2nd infect.
Scarlet Fever: strawberry, pastia lines (creases), rash missing @mouth, rash - tiny red bumps
CC: GAS (starts as strep throat) - your GAS must be able to produce SpeA toxin to cause scarlet fever
VF: SpeA (erythrogenic toxin causes red. + inflam.)
Dx: culture/gram stain, Tx: antibiotics
Chickenpox: macule-papule-vesicle-scab (POX)
Spread by aerosol (respiratory) or fluid (from spots)
Shingles: virus enters nerves & becomes latent, banded, crust, more spots = higher chance of shingles
CC: Varicella Zoster (VZV) > herpes virus
VF: latency, Dx: appearance, Tx: vaccine
Reye’s Syndrome: swelling in liver and brain
Viral infection + aspirin = Reye’s, rare but serious
S&S: encephalopathy, confusion, seizures, hypoglyc.
Fifth Disease: slap cheek, lacy, low fever
CC: Parvovirus B19, no VF, Dx: appearance, No Tx
* concern for 5th & rubella is if spread to pregnant mother can & passed across placenta can cause birth defects or death
Rubella: macular & mild, respiratory or urine, fever
Teratogenic virus: transmitted in utero, persistent!
CC: Rubella virus (Rubivirus, RNA), no VF, Dx: appearance, no treatment, covered in MMR vaccine
Roseola: high fever, blanching, aerosol spread
CC: Human Herpesvirus 6&7, no VF, Dx: fever & rash
Measles: rubeola, dry cough, conjunctivitis, koplik’s spots, angry red rash, highly aerosol contagious
CC: Measles Virus (helical RNA, Morbilliviridae)
VF: cause syncytia, high risk of 2nd infection, treat symptoms, ~Vitamin A injections, MMR vaccine
Hand, Foot, Mouth: blister rash, nail loss
CC: Coxsackievirus A16, VF: viral, Tx: OTC
Warts: benign squamous epithelial growths, plantar, seed, genital, contagious (not highly)
CC: human papillomavirus (HPV 1,2,3,4)
VF: cause unregulated cell growth
Dx: appearance, Tx: cosmetic removal, biopsy?
Molluscum contagiosum: pearly, plug, cheesy, waxy, can spread into “crops”
CC: MCV (poxvirus family) VF: same as warts
Tx: cosmetic removal *deeper than warts
Ringworm (cutaneous mycoses (fungal)): scaly patches, circle, many diff. types
CC: Dermatophytes - multiple funguses
VF: eukaryotic, skin breakdown enzymes
Dx: appearance or KOH test (will be mixed bag), Tx: antifungal antibiotic, hygiene
Tinea Versicolor: discolored patches
CC: Malassezia furfur (fungal)
VF: eukaryotic, Dx: appearance, KOH test (will be one organism, not mixed bag)
Tx: topical antifungals
Leishmaniasis: eukaryotic w/ nucleus
Cutaneous: infects capillaries-open,wet sore
Mucocutaneous: nasal systems, oral/pharyngeal symptoms, can progress to ulcerative destruction of naso-oropharyngeal mucosa (perforation of the nasal septum)
Systemic (visceral): affects organs & marrow, fever, weight loss, pancytopenia, discoloration
CC: [Parasite] Leishmania spp. (L.donovani for systemic/visceral)
VF: spread by sand flies, hides in host immune cells, endemic in tropical/equatorial
Dx: culturing for parasite, Tx: antiparasitics
Gas Gangrene: necrosis, anaerobic, crunchy
“Anaerobic cellulitis” - so deep it has no O2
CC: Clostridium perfringens (rods)
VF: multiple toxins, anaerobic growth, spores (post surgery)
Dx: smell, appearance, gram stain
Tx: aggressive antibiotics & HBO2
Anthrax: spores, black eschar, animal hide
Lesion that is black w raised red outer ring
Can be from contact with and animal hide
CC: bacillus anthracis, G+ spore former & toxin producer, big risk is entering blood
VF: glutamate capsule & 3-part toxin Dx: gram stain (G+ bamboo rods +/- spores) and medusa head colonies
Tx: immediate antibiotics
(PA-EF-LF)
protective antigen: binder unit latches onto cell
edema factor: cells push nutrients & fluid out & fluid builds up in outer tissue (edema)
lethal factor: kills cells, shuts down protein synthesis & cell signaling = cell death (black)
Styes: skin/eye, sebaceous/lacrimal glands
Painful inflammation, purulent
CC: S.aureus, VF: enzymes, Dx: gram stain
Tx: antibiotics (often erythromycin), ~drainage
Conjunctivitis: pink-eye, discharge, ~bloodshot
Bacterial: milky, yellow discharge
Viral: clear, liquid discharge
CC: S.aureus, GAS, babies & adults = N.gonorrhoeae, Chlamydias (Gram N/A)
Viral causes also, including adenovirus (newborn)
Dx: appearance & discharge, gram stain
Tx: varies based on type
Keratitis: cornea, coldsore, gritty, dendrite
Clear, tear-like discharge, pain & light sensitive
CC: herpes simplex virus virus (type 1)
VF: viral, latency, spread, Dx: appearance & discharge type (clear = viral), Tx: aggressive corticosteroids + antivirals
Trachoma: not in US, scarring, scraping, blind
Spread by fomites (towel, bucket of water)
CC: Chlamydia trachomatis (type A,B,C)
VF: intracellular bacterium, evades immune
Dx: lash position, Tx: antibiotics
Meningitis Overview: inflamation of meninges
Headache, painful, stiff neck, ^# WBC in CSF
Petechiae, intracranial pressure, necrosis
Lumbar puncture = CSF, hard diagnoses infants
Treatment: 3rd gen cephs! (for PPG), steroids
- Ceftriaxone (Rocephin), Cefotaxime (Claforan)
Sequelae: brain damage post meng - cognitive dysfunction, hearing loss, seizures, death
Neisseria Meningitidis: letters, LPS, bacterial
Most dangerous, kidney bean diplococci,
VF: pili, capsule, LPS (leads to sepsis and DIC)
Sudden high fever & flu-like
Meningococcemia: systemic N.meng of blood = LPS, fever, rash, joint pain, diffuse intravascular coagulation (DIC), Waterhouse Friderichsen Syndrome = N.meng of adrenal glands
Capsular type B = worst! Menactra MCV4 doesn't cover, Trumenba for type B
Ceftriaxone for exposed
Streptococcus pneumoniae: most common
Bacterial lancet shaped diplococci
Community-acquired, pneumonia, OM, sinusitis
VF: capsule, NO LPS, no rash, Stereotype 3 is worse, developing resist to 3rd gen cephs
Vaccine: Prevnar/Pneumovax, NUMBERS
Haemophilus Influenzae: ear infection
Bacterial tiny pleomorphic rods, VF: capsule
Has LPS, not enough for rash, opportunistic(NF)
Capsular type B was main but now HiB (vax)
Listeria monocytogenes: food, diarrhea
Affect elderly, immunocompromised, infants
VF: invasion, listeriolysin (LLO), motility
Enters host cells in gut, LLO to break & duplic.
Neonatal Bacterial Meningitis: rapid deterior.
Streptococcus agalactiae (GBS) - vaginal NF
RDS, puerperal sepsis (childbed fever) in mom (purple spotted rash), skipped neo. visits
Escherichia coli - fecal flora (ExPEC or NMEC)
“KI” capsule type, endotoxin
Cryptococcus neoformans: fungal meningitis
S/S gradual onset, birds, decayed plant matter
VF: large capsule, capsule stain on india ink
Slow, chronic meng., respiratory, gummy rash
Coccidioides Immitis: fungus > 2ndary meng.
Pulmonary infection, soil, San Joaquin Valley
VF: none (fungal), bag of coins, blocky spores
Viral meningitis: common in kids
Aseptic, rarely fatal w/ good immune
Respiratory, mumps, EBV, HSV, VZV
CC: enteroviruses = GI viruses
VF: none (virus)
CC: enterovirus-D68 = acute flaccid myelitis
Naegleria fowleri: meningoenceph.
Brain eating amoeba, water, head ache, fever, vomiting, confusion, coma, stupor
Olfactory nerve > BBB > destroy frontal lobe, massive swelling, no cure or known treatments
Generalized Acute Encephalitis: behavior
Viral infections, VF: viral replication & immune response - immune influx, inclusions, no bacteria, NOT contagious
Fever, behavior change, vision loss, confusion, seizures, paralysis, stiff neck
Mild S/S: NSS fever, skin rash, swollen LN
No symptoms in most, Tx: aggressive antivirals & treat symptoms immediately
Arbovirus family: insects, mosquitoes
WNV: most common, little or no flu-like S/S
SLE: mosquitoes ^, midwest & south
LaCrosse/Cali. Enceph: children, non-fatal
Jamestown Canyon (JCV): deer/moose
Powassan Enceph.: ticks/rodents
Western & Eastern Equine: (WEE/EEE) = large hoofed animals (horse, cattle, ranches)
*Tx: unresponsive to acyclovir but in case it is actually HSV, treat symptoms: monitor fever, reduce pain, identify source
Other virus families: (no bite, think herpes)
Herpesvirus: severe, aggressive enceph.
Tx: acyclovir, cigarette burn baby possible
JC Virus: “Progressive multifocal leuko- encephalopathy (PML), HIV/AIDS, twitching
Demyelinizes cerebrum, bad if immunocomp
Measles: two different forms
PIE (post infection/immunization enceph): part of immune response, not virus related
SSPE (subacute sclerosing panencephalitis):
years post-measles from persistent virus
Toxoplasma gondii: subacute encephalitis
Flagellated parasite, severe in fetus or immunocompromised, CAT FECES, pregnant
VF: eukaryotic. Teratogenic, birth defects
Rabies: slow, progressive, zoonotic, fatal
“Furious”: agitation, disorientation, seizures, twitching, foaming at mouth, spasms in neck and pharyngeal muscles = hydrophobia
“Dumb”: paralyzed, disorientation, stupor
CC: rabies virus (rhabdoviridae)
VF: viral, enveloped, Tx: immediately administer antibodies then boost w vaccine
NON-cellular neuro infectious agents:
Prions: converting proteins, normal = PrPc, mutant = PrPp > refold normal into pathologic
Bad prion enters, turns good to bad, buildup & deposits, cells die, holes in tissue (spongi.)
Prion diseases: BSE (mad cow), Creutzfeldt-Jakob disease, Kuru, Scrapie
Prion TSE’s: transmissible spongiform encephalopathies
Neurodivergent, apoptosis, holes in brain
Human TSE’s: mad cow - consumed/ exogenous prion, CJD - mutated normal prion
VF: convert normal to PrPp
Tetanus: lockjaw, toxin based, puncture
Rigid paralysis disease: extreme clenching & contraction (Risus Sardonicus)
CC: Clostridium tetani, spore forming, toxin gets to neurotract, VF: powerful neurotoxin called tetanospasmin, targets inhibitory motor neurons, blocks inhibition of muscle contraction, Dx: symptoms & lollipop
Tx: antitoxin, then antibiotics, “tetanus shots”, vaccine (DaPT) & 10 year booster
Botulism: flaccid paralysis, poorly preserved foods, double vision, difficulty swallowing, dizziness, descending (flaccid) muscular paralysis, respiratory compromise
Food-borne botulism: ingestion of preformed toxin
Infant botulism (floppy baby syndrome): entrance of botulinum toxin into blood, honey as major source of spores
CC: Clostridium botulinum, spore forming anaerobe, VF: exotoxin that attacks acetylcholine neurotransmitter
Dx: gram stain & appearance, Guillain- Barre, Tx: antitoxin, monitor for respiratory distress
Urinary Tract Infections: *if virus, NOT UTI
Bacterial VF: urease (breakdown urea into nitrites (G-) & CO2), flagella, pili
Urinalysis: WBC, bacteria epithelial cells, nitrites, leukocyte esterase (= had WBC) - all bad to have
Dx: colony counts in clean-catch sample (mid-flow)
Start as urethritis: painful, burning urination
Cystitis: bacteria in bladder - pubic pain, frequent urge to urinate, burning pain, cloudy urine, red/pink/orange, fever, nausea
Pyelonephritis: kidneys - back pain @CVA
E.coli UTI: most common, fecal strains, anal sex
S/S: dysuria, increased frequency & urgency
Reinfection/persistent UTI possible
CC: Uropathogenic E.coli (UPEC) - bacillus (rods)
VF: P-pili, flagella, Tx: Bactrim (can't use in pregnant women, & resistance is growing), Ciprofloxacin
Proteus species UTI: kidney stone, catheter, sex
CC: Proteus mirabilis or Proteus vulgaris
VF: highly motile, potent urease, Dx: indole test to determine strain - P.m. = no ring, P.v. = red ring
Tx P.m.: broad spec b-lactams or cephs, removal of stones
Tx P.v.: resistant to b-lactams & cephs, use imipenem, 4th gen cephs, bactrim, or AGs
Staphylococcus saprophyticus UTI:
Frequently seen in younger (12-25) sex active females
CC: Staphylococcus saprophyticus, VF: none known
Dx: novobiocin, S.sapro = resistant to novo
Tx: 1st/3rd gen cephs, Vanc if necessary (not first option), gaining resistance to Bactrim
Vaginitis: itching, burning, white discharge
CC: Candida albicans (fungus) - opportunistic
Dimorphic (yeast & hyphae forms) yeast = budding fungus
Dx: Sabouraud-Dextrose agar, egg-shaped, germ tubes
Tx: Antifungal (fluconazole), (C.a. also = oral thrush, diaper rash)
Vaginosis = overgrowth:
CC: Gardnerella vaginalis - itching, fishy, gray/yellow
VF: none, Dx: clue cells, Tx: broad spec antiribosomals (metronidazole)
Multiple sex partners & frequent washing
CC: Trichomonas vaginalis - green/white, frothy, foul smelling, strawberry cervix - can be asymptomatic
VF: none, Dx: parasite w/ one eyespot & whiskers
Tx: Flagyl (trichomonas is parasite), metronidazole
~ tight clothing
Prostatitis: pain in pelvis/low back/genitals, hematuria, painful ejaculation, frequent urination, acute or chronic
CC: unknown likely GI flora into urinary tract
Homosexual men, anal sex, diapers for elderly
Low testosterone, prostate damage/carcinoma
Tx: mixed causes so very broad spec antibiotics for longer courses (often tetracycline 21-28 days)
Gonorrhea: urethritis, purulent discharge, mucopurulent or bloody discharge, PID
CC: Neisseria gonorrhoeae (diplococci), VF: pili w/ antigenic variation - always changing so not self limiting
Dx: grows on Thayer-Martin, uses glucose only G=G
*Ophthalmia Neonatorum: newborn eyes from birth
*Can move to joints and cause arthritis
Tx: 3rd gen ceph (ceftriaxone)
NGU-2: burning but no gon. or chlamydia (mimics Chl.)
CC: Mycoplasma species - Ureaplasma urealyticum
VF: urease enzyme, Dx: NO CELL WALL
Tx: erythromycin & tetracycline, azithromycin
Chlamydia: most common, asymptomatic
Urethra inflammation, watery discharge, epididymitis
Watery discharge, cervicitis, salpingitis, can lead PID
CC: Chlamydia trachomatis, stereotypes D-K (genital)
VF: intracellular, Dx: bi-phasic life cycle = infectious form (elementary body evade), replication form (reticulate body replicate)
*Stereotypes A,B,C = pinkeye, common in infants
Lymphogranuloma venereum: L1, L2, L3 - ulcer on genitals > groin lymph nodes > buboes, painful, may rupture - mostly homosexual men
Tx: Tetracycline & erythromycin (antiribosomals), azithromycin, doxycycline
Syphilis: enters thru small abrasions & replicates
CC: Treponema pallidum (spirochete) - no gram type
VF: very smooth - antibodies cant stick (Teflon pathogen), motile, Dx: darkfield microscopy - appears white, won't gram stain so Giesma stain - pale pink
Tx: penicillin (long-acting doses - Benzathine)
Primary: small, hard chancre - painless, serous exudate – highly infectious *congenital syphilis starts as 2nd or 3rd
Secondary: Spreading skin rash (palms & soles), mucous patches in/around mouth, condyloma lata (warts near chancre)
Tertiary: due to immune response, gummas, necrotic soft palate, CNS involvement (dementia, ataxia, etc)
Genital Herpes: malaise, anorexia, recurrent episodes
CC: Herpes Simplex Virus (mostly HSV type 2)
VF: viral, can be latent, can be transferred between oral and genital, Tx: Acyclovir or Valacyclovir (Valtrex)
Genital Warts: most common, but not reported
CC: Human papillomavirus (HPV) - papovaviridae family, icosahedral non enveloped, circular dsDNA
VF: viral, HPV 6,11 = warts, HPV 16,18 = carcinoma, HPV 1-4 = skin and plantar warts, best prevention is to avoid contact, Vaccine: Gardasil = 6,11,16,18
No Tx, just cosmetic removal
Oral Infections:
Gingivitis: swelling, loss of color, redness, bleeding
Necrotizing Ulcerative Gingivitis (NUG): severe pain, bleeding, necrosis (no oral hygiene)
CC: Streptococcus mutans, VF: biofilms
* trench mouth
Mumps: fever, nasal discharge, muscle pain, malaise, AEROSOL risk, cheek swelling (parotitis)
Virus multiplication in salivary glands - can spread to other organs, swelling of testes, ovaries, breasts
CC: Mumps virus (orthomyxoviridae family)
VF: forms syncytia to allow cell-cell spread
Self limiting w/ normal tissue & hormone levels
MMR vaccine, but can still get it (85/15)
Gastritis: burning abdomen pain
Gastric Ulcers: lesions in stomach mucosa (bloody stools, vomiting coffee grounds, upper GI bleed
Can cause Gastric carcinoma from cell damage/repair
CC: Helicobacter pylori (spirochete)
VF: urease enzyme – urea + urease enzyme = ammonia + CO2, changes pH allowing survival
Dx: ammonia breath test (urease detection)
Tx: AMOX/TET/Flagyl/Clarithromycin + proton pump
Intestinal Mucosa: absorb water & nutrients for body
Enterocytes: cells w/villi, primary cells for adsorption
Crypt cells: secrete hormones and Cl- for digestion, produce new enterocytes (renewal & maintenance)
Goblet cells: secrete mucus
M-cells & Peyer’s patches: intestinal immune lineages & outposts for immune cells
Intestinal Mucosa: absorb water & nutrients for body
Enterocytes: cells w/villi, primary cells for adsorption
Crypt cells: secrete hormones and Cl- for digestion, produce new enterocytes (renewal & maintenance)
Goblet cells: secrete mucus
M-cells & Peyer’s patches: intestinal immune lineages & outposts for immune cells
Foodborne Infections: live cells delivered by food, multiply in host once consumed, longer duration
Food intoxications (food poisoning): food looks, tastes, smells normal, NOT from spoiled food
Contains organism-produced molecules, but may not have live organisms, produced toxins, shorter duration
Acute Diarrhea: 3+ loose stools in one day
Bacterial, viral, & parasitic causes
Characterize by: 1) type/description, 2) downstream consequences, most are self limiting w/ no Tx
Rapid dehydration G(-) > multiple organ failure
Reiter’s syndrome: urethritis, conjunctivitis, arthritis (can’t see/pee/climb tree) - from LPS
Guillain-Barre syndrome: peripheral neuropathy (paralysis) - from LPS
Typhoid fever: salmonella complication (S.typhi)
Invasion of spleen and/or liver where large numbers of bacteria get to bloodstream – high fever, chills, abdominal rash, neurological symptoms
Treat systemic = Ampicillin or Bactrim
Salmonella: 2nd common, fecal-oral spread
Linked to dairy or raw poultry products (milk, eggs, meat)
CC: Salmonella spp. VF: invasive – enters/hides in cells after “membrane ruffling”, can enter bloodstream to cause shock, can invade bones (osteomyelitis) or liver, mostly self-limiting, hydrate/fluid replacement
Shigella: highly contagious, DYSENTERY
CC: Shigella sonnei, S.flexneri, Shigella dysenteriae
VF: Shiga toxin: inhibits protein synthesis (cell death)
VF: Invasive: replicates inside intestinal cells
Tx: Ampicillin, Bactrim Azithro
Complication: hemolytic uremic syndrome:
Enterohemorrhagic (EHEC): O157:H7, O104:H4 STEC
Complication: hemolytic uremic syndrome ^
Undercooked meat, spinach, apple juice, lettuce, etc
VF: shiga toxin & effacing lesions
Dx: can't use sorbitol for metabolism, grows on lactose
Tx: supportive care & rehydrate, no antibiotics!
Enteroinvasive (EIEC): significant fever
Invades gut mucosa > cell destruction > diarrhea
VF: I = invasive, Dx: grows on sorbitol, not lactose
Self-limiting, fecal-oral spread, supportive treatment
Enterotoxigenic (ETEC): travelers, water/ice
Watery diarrhea, fever, nausea, vomiting
Transmitted by fomites - dirty glasses, water, ice
VF: 2 toxins - Heat stable toxin (ST) & heat labile toxin (LT), self-limiting
Enteropathogenic (EPEC): infants & toddlers
VF: causes intestinal cell membrane rearrangements by depolymerizing actin into “pedestal formations”
Monitor patient, especially if young, rehydrate & supportive care
Enteroaggregative (EAEC): chronic watery diarrhea in children & AIDS patients, associated w/ malnutrition
VF: biofilm/clustering attachment to cell surface
Supportive therapies & look for underlying issues
Campylobacter jejuni: watery, yellow-green stools
Most common bacterial diarrhea, symptoms can subside & recur, cooked poultry products
VF: 2 toxins = enterotoxin (cAMP) & cytotoxin (PS)
Microaerophilic spirochete organism, can cause Guillain-Barre syndrome from LPS, usually self-limiting
Tx: rehydrate & electrolytes, erythromycin for severe
Clostridium difficile: NF, nosocomial diarrhea
VF: 2 enterotoxins (toxins A and B, not A-B!)
Toxins > apoptosis/necrosis of tissues, sloughing
Complication: pseudomembranous colitis
VF: produce spores, Tx: discontinue ABX, use Flagyl, replacement therapy (yeasts/yogurt, FFRT, probiotics)
Vibrio cholerae: comma-shaped bacterium
Lives in water (halophilic > salt), replicates in humans
Transmission = fecal-oral via water (fish, drinking, etc)
Debilitating PROFUSE watery (Rice water) diarrhea
VF: Cholera toxin – classic A/B cAMP regulator
DEHYDRATION > MOF from lack of fluids!!
Tx: REHYDRATE, Trimethoprim or ribosomal inhibitors for children, clean water supply
> Vibrio parahaemolyticus: extreme watery diarrhea, linked to shellfish, invasive w low power enterotoxin
Bacterial Food Poisoning: gut symptoms caused by preformed toxin, if symptoms are violent w/ very short incubation period intoxication rather than infection
Staphylococcus aureus Exotoxin: unrefrigerated white foods (mayo, cream, meat, X salad)
VF: Staph enterotoxin A (SEA) (can’t taste or smell toxin)
Cramping, nausea, vomiting, diarrhea, rapid recovery
Bacillus cereus: fried rice, cookmats, reheated foods
Two exotoxins: cause diarrheal-type or emetic disease
Parasitic Diarrhea:
Cryptosporidium parvum: waterborne (fecal-oral)
Ruminant wastes (sheep, cows, goats), also snakes and geese, in water – causes intense diarrhea
Headache, sweating, vomiting, severe abdominal pain
Immunocompetent: mild, self-limiting
Immunocompromised: 50+ stools/day, extreme dehydration, nausea, vomiting, fatigue - may last years
Dx: stains as “Acid-fast” & find oocysts in samples
Giardia lamblia: flatulence, greasy/malodorous stools
Fecal-oral transmission via water, backpackers, boy scout, beaver fever, parasite w/ 2 eyespots (monkey) + flagella, Tx: flagyl
Entamoeba histolytica: Bloody diarrhea, weight loss
“Non-bacillary dysentery”, hemorrhage, perforation, appendicitis, leaves erosive ulcerations
VF: secretes enzymes that dissolve tissues
Can spread from intestines to liver/spleen - Amoebic hepatitis (chocolate pus), fecal-oral transmission of cysts (found in pt samples) Tx: flagyl
Cyclosporiasis: watery diarrhea, cramping, bloating
Fresh produce, & water w fecal contamination
CC: Cyclospora cayetanensis (protozoan)
VF: parasitic, invasive; Dx: O&P (acid-fast staining)
Tx: Bactrim
Rotavirus: watery diarrhea, sudden onset/short incubation
Infects & kills enterocytes > loss of microvilli
Vaccine: RotaTeq
Norovirus: vomit + diarrhea, self limiting
Oysters, clams, seafood, highly contagious (airborne)
CC: Norovirus (+) ssRNA, Caliciviridae family
VF: CPE seen in both intestinal cell types
Astrovirus: similar to norovirus, fecal-oral, (+)ssRNA
Adenovirus: fecal-oral, longer incubation period
Complications: respiratory symptoms, develop lactose intolerance
CC: Adenovirus dsDNA w/ complex structural proteins
“Sputnik virus” icosahedral virus w/ attachment spikes
Gastroenteritis – serotypes 40,41,42
“Pharyngoconjunctival fever” – 3,7
VF: viral capsid spikes to attach, infects intestinal lining cells, (replication inhibits protein synthesis)
Hepatitis: inflammation of liver, jaundice, dark urine, clay stool, antibodies are key to diagnosis
Hep A/E: mild, Hep B/C: chronic, potentially carcinogenic
Hep A: transmitted fecal-orally (usually by food) – contaminated water, milk, seafood, fruits/veggies
CC: ssRNA genome, Picornaviridae family
WHO: children, military, crowded living, homosexual
Tx: Ribavirin
Hep B: may cause chronic hepatitis leading to cirrhosis/cancer, transmitted thru body fluid exchange
CC: partially dsDNA virus, Hepadnaviridae family
“Balls & Sticks” appearance
VF: hepatitis protein antigens (Ag) “Australia antigens”
- HBsAg = [surface] forms a complex in liver leading to complexed deposits
- HBcAg = [core] unknown fcn
- HBeAg = unknown fcn
VF: encodes an “RT”/RDDP enzyme > episomal latency (not integrated)
WHO: IV drug users, healthcare workers, sexually promiscuity, TX: with IFN (interferon) and often combinations of valacyclovir or lamivudine
Hep C: transmitted thru body fluids, primarily blood
CC: (+)ssRNA, Flaviviridae family, multiple types
VF: Hepatitis core protein (HCcAg) - immune suppression - HCV antibody
Tx: Harvoni (2 antivirals in one pill), WHO: IV drug users, transfusion & organ transplant recipients
Helminthic Intestinal Infections: Worms
Mechanical blockage & tissue damage, Dx: discover eggs, larvae, or adult worms in stool/other tissues
Tx: minimize human contact, physical removal, antihelminthic drugs
Enterobius vermicularis (Pinworm): butthole worm
Scotch tape test, lay eggs in anal folds
Ascaris lumbricoides (Roundworms): intestinal, eggs consumed from environment (fecal-oral), hatch in large intestine, migrate thru liver & intestine to lungs, cough larvae/eggs to reswallow, causes distended belly, intestinal blockage, nutrient depletion, death. Affects humans & animals
Necator americanus (Hookworm): tissue worm, uses teeth to burrow into skin from soil, “ground itch”, “larvae migrans” rash via circulation to lungs, coughing to swallow to intestines, direct infection leads to cyst in muscle/intestine/etc, nutrient depletion, failure to thrive, “blood sucking worm”, poor communities and developing countries
Trichinella spiralis (Hunter’s worm): tissue worm, consumption of larvae in contaminated meat, likes wild game: bear/boar/deer/etc, nausea, vomiting, diarrhea, painful lesions, inflammatory response, migrates to other tissues, forms cysts in muscle or brain, characteristic lesions
Neurocysticercosis: seizures, chronic headache, nausea, vomiting, impaired vision, mental status changes
Taenia saginata (beef tapeworm): intestinal worm, consumption of eggs/cysts in contaminated meat, from undercooked BEEF, nausea, vomiting, painful bowels, intestinal blockage, inflammatory response, recognized by scolex with suckers only
Taenia solium (pork tapeworm): intestinal worm, undercooked PORK, more dangerous due to auto-infectious cycle, cysticercosis: causes cysts (brain & muscle), same S&S as beef, recognized by scolex with suckers AND teeth
Mechanism 1 - Cell wall level (narrow spec)
Fam 1: Beta-Lactam antibiotics (cillin compounds) inhibit PPG synthesis, NAM/NAG subunite destabilize & lyse cell, Cillins: best effective against G(+), Penicillin=basic, amoxicillin & ampicillin=extended spectra, used in many infections, ox/clox/meth/naf= anti-staphylococcal, carbeni/pipera/ticar/mezlo= anti pseudomonas/resistant G+, carbepenem= good B-lac for G-, imipenem=similar to PEN, resistant to B-lactamase
Fam 2: Non-B-lac Class, Vancomycin=against almost all G+, but not G-, last line, Red man syndrome - activates immune system (VANC IV pushed too fast), SJS/TEN - allergic reaction, Isoniazid & ethambutol= Gram NA, disrupts formation of mycolic acid, mycobacterium TB, Pretomanid= inhibitory actions on bacteria cell wall mycolic acid biosynthesis, killing of active replicating M.tuberculosis bacteria, Fosfomycin =inhibits MurA enzyme, precursor step in PPG synthesis, single dose oral therapy for uncomplicated UTIs, G- enteroba
Fam 3: Cephalosporins (better targeted than B-lactams) “2 R groups+house+garage”
HEN PEcK (Haemophilus influenzae, enterobacter SPP, Neisseria SPP, Proteus, E.coli, Klebsiella) + Pseudomonas, 1st gen=Cephalexin(Keflex) - minor G- & HEN, 2nd gen=Cefuroxime(Zinacef)=fewer G+ & HEN PEcK=G-, 3rd gen=Ceftazidime(Fortaz), Ceftriaxone(Rocephin)=3G & up can cross BBB, fewer G+ & HEN PEcK, aggressive G-, 4th gen=Cefepime (Maxipime), rare G+, strong G- Bacitracin+ Polymyxin B(simple G+/-)=pore formers, Nephrotoxic (topical use only), Daptomycin=G+ effective vs staph
Mechanism 2 (Protein synthesis) good to treat G N/A
CLEAn TAG: Chloramphenicol= very broad spec, high side effects, only used when NO alternatives, Lincomycin & derivative CLindamycin(Cleocin)=used for anaerobic & severe aerobic infections (streptococcal TSS) adverse effect: pseudo colitis (C.diff), Erythromycin=G+,N/A, good for PEN allergies, chlamydia, syphilis, disrupts normal GI flora, diarrhea Azithromycin (Zithromax, Z-Pak), Tetracycline (Doxycycline, Minocycline) broad spec G+/-/NA - TERATOGENIC! Aminoglycoside=serious G-, IV use, must have oxygen, effects: nephrotoxicity (kidney failure), hearing loss, will cross placenta
New Antiribosomals: Synercid= inhibits 50S ribosome, effective against Staphylococcus, Enterococcus, & resistant strains of streptococcus G-/+ secret last line
Oxazolidones=Zyvox & Linezolid treat MRSA & Vanc Resistant Enterococcus, last line for G+, no G- activity
Mechanism 3 (Metabolic Synthesis) mimics a natural compound, competitive inhibition, shuts down natural process (stops folic acid, folic acid is necessary for DNA replication), Sulfonamides(Sulfamethoxazole) & silver Sulfadiazine=G-, enteric bacteria, Shigellosis, acute UTI, Trimethoprim= otitis media, UTI, Brand names: Bactrim, Cotrim, Septra, NO PREGNANCY!!
Sulf & Trim work better together = SYNERGISTIC, NEW Bedaquiline= antimycobacterial drug that inhibits the proton pump in M.tuberculosis Mechanism 4 (Nucleic Acid Str/Fcn: stops workers (Fluoro)Quinolones (-flox antibiotics)=stop replication(unwinding DNA) Ciprofloxacin= prophylaxis, anthrax (weakest) Norfloxacin= G+/-, pseudomonas, UTI Levofloxacin= many STD organisms, skin/systemic infection (strongest)
Nalidixic acid=UTIs (especially G+ for pregnant women, doesn’t stop VF or protein synthesis, just stops duplication) Rifampin= inhibit action of bacterial RNA polymerase during transcription (G+/-, mycobacterium tuberculosis) treats pneumonia, UTI, gastroenteritis, can cause tendon rupture
Antivirals: DNA polymerase synthesis inhibitors: Cyclovir compounds=mimic nucleotides to chain terminate, Foscarnet may be added when resistance to cyclovirs occurs, Trifluridine=virus infection of eye
RNA polymerase synthesis inhibitors: Ribavirin=tries to stop RDRP, doesnt stop every RDRP, limited usagem useless against common cold, flu, polio, measles Remdesivir= NEW, attacks RDRP, Covid19 polymerase version. Nucleoside Reverse Transcriptase Inhibitors: NRTIs= competitive inhibition of RT, need host phosphorylation pathways to work (going after RDDP) -vudine compounds (zidovudine- AZT, stavudine, lamivudine) Retro/RDDP -avir compounds (abacavir, entecavir) competitive inhibitors, get across BBB
Non-Nucleoside Reverse Transcriptase Inhibitors= non-competitive inhibitors of RT (bind away from active site) Unconventional namings (efavirenz/nevirapine) taken less frequently & does not inhibit human DNA polymerase, can be teratogenic
Fungal Infections: Synthetic Azoles (-azole) broad spec antifungal agents (ringworm) Clotrimazole/Miconazole=mainly topical ointments for infections in skin/mouth/vagina (monistat) Ketoconazole =oral & topically for cutaneous mycoses, vaginal/oral candidiasis, & some systemic mycoses (higher power) Fluconazole=used in selected patients for AIDS-related mycoses, get CSF (brain fluid)(highest power!) good choice for yeast infection Amphotericin B=attack fungal membranes by binding fungal sterols (ergosterol) & form pores, can react w/ human cholesterol if overdosed, high toxicity Terbinafine (Lamisil)=topical ointments for skin (used for nails) Nystatin= oral thrush
Antiparasitic compounds: Quinine & Artemisinin as anitmalarials(keeps parasite contained) Chloroquine & Primaquine=less toxic to humans, both slow parasitic growth, commonly used as combo therapy (include Bactrim) Metronidazole(Flagyl)=-dazole works best on parasites, usually for protozoan infections, causes DNA & protein damage Amoebicide/Giardia Lamblia/ Trichomonas Vaginalis=good for anaerobic
Antihelminth compounds: energy drainers for worm infections, leads to paralysis or death or worm expulsion from body, ion channel blockers/membrane permeabilizing/cytoskeletal depolarizers/nicotinic acid inhibitors Pyrantel Pamoate (Pinworms), Mebendazole & Thiabendazole=good for pinworm & hookworm, and flat (tape) worms Ivermectin=good on other worms such as lice, scabies, and rosacea
Immunity 1 & 2: 1st line defense, no memory, always same
Cytokines IL: cell communication, interleukins (IL) & interferons (IFN)
Actions: “Come” =chemotaxis, “Do”=activation, “Become”=differentiate, “Go”=amplification
IL-1: recruits cells to site - chemotaxis, fever & inflammation, “GET HERE NOW”
IFN-a/B: Antiviral response (defense/alert), activate NK cells, increase antigen presentation, signals neighboring cells, slows metabolic activity & therefore viral replication
IFN-y: innate cell activation, signaling, turn B-cells to T-cells
IL-2: T-cell growth Innate& replication, stimulates T-cell survival & growth(especially CD4+ & CD8+)
IL-4,5,6: signals class switching from IgM to IgG/IgA (4=maybe IgE)
IL-10: Anti-inflammatory, reduces cytokine production, T-reg cells, “STOP”
IL-17,22: Produced by CD4 TH17, recruit neutrophils, promote inflammation, bouncer
BAFF: B-cell activation factor, survival, differentiation, & maturation, involved in autoimmune when dysregulated (lupus), tells 4/5/6 to class switch
TNF-a: pro-inflammatory cytokine, activates macrophages & T-cells, rheumatoid arthritis
TNF-B: immune regulation & inflammation, redundancy in activation signals (only a few)
1st line defense: physical barriers - skin, mucous, body temp, pH, microflora
2nd line defense: antigen (Ag)=foreign & causes immune response, epitope=part of antigen that immune response recognizes, PAMPS (molecular patterns), APC=antigen present. Cells
C1:Granulocytes (BOMB): large granule, PYOgenic=pus-forming, PYROgenic=fever forming
- Neutrophils=first responders, most common wbc, trap (NETs) & bomb (granules), short life
- Basophils=blue/purple staining granules, B=blue=barbell, MAST cells w/ allergies
- Eosinophils= red/pink staining granules, fights worms & parasites
C2:Agranulocytes (EAT): APCs, monocytes, single nucleus
- Macrophages=big cell eaters, APC
- Dendritic cells=octopus shape, best APC b/c of superior antigen capture
C3:Lymphocyte: rbc, B-cells, T-cells
Seek & destroy: (MØ/DC mechanism) 1)binding, 2)recognition by PRR (engulf), 3)fusion (phagosome+lysosome=phagolysosome), 4)digestion, T-cell development: presentation, B-cell activation: poop
Agranulocytes: primary phagocytic or specialized functions
Monocytes: become MØ or DC (phagocytes & APCs)
PAMP: short fragments that aren’t “self” shared among antigens, non-clonal distribution (multiple recognitions on each cell), multifunctional, activate MØ, NØ, DC
PRR: pattern recognition receptor, common type = toll-like receptor (TLR)
TLR2: LTA/PPG in G+, G- proteins; TLR4: LPS, cover cell surface & scans impact shaping of immune response, guides & produces only needed cells
Complement cascade: set of soluble serum proteins (C1-C9), assemble stepwise (1 thru 9) on antigen surface similar to bomb, forms membrane attack complex (MAC)
C3a: inflammation & recruit, C3b: opsonization/phagocytosis
Inflammation: second line response/defense, redness(vasodilation), swelling(edema), heat (fever), pain(damage & mediators) - arrival of neutrophils, macrophages, dendrites, recognition of antigen by innate cells, activation
- trapping antigen, eliminate antigen, amplification specialization of response, win or death
B-cells: made & trained in bone marrow, makes antibodies, specific response, memory cells, secrete antibodies, best against EXTRAcellular
Good-Naive cell: immune cell ready to be used, never encountered antigen before, “less than perfect response”, Better-Activated effector cell: immune cell that has encountered antigen, now react to cause an effect, Best-Memory cell: veteran cell that responds as effector faster/more efficiently to previously encountered antigen
Positive selection: “do you have a receptor & work”, Negative selection: “do you hurt self”
Adaptive cell responses: 1) find specific epitope, 2) bind antigen & activate adaptive cell, 3)do effector function & duplicate, 4) specialize response based on affinity & performance, 5)either memory cells form or apoptosis, WIN!
Activated B-cells = plasma cell (clock face nuclei) make & secrete antibodies
Humoral immunity - each B-cell produces ONE antibody that recognizes ONE epitope
T independent antigen (Ti-Ag): acute, antigen that stimulate B-cells w/out co-stimulation by helper T-cells, IgM only, cross link antigen receptors on surface
T dependent antigen (Td-Ag): response to protein & most antigens, interaction of B-cells & helper T-cells, CD40 & CD40L (need T) humoral
Y shaped arrangement: variable antigen binding sites on top ends
Class Switch: convert antibody from IgM to IgG or IgA, requires help from T-cells, IL-4,5,6
B-cell memory: memory B-cells reverted to inactive no Ig release, carry IgG
IgG= Great, crosses placenta, blood responses (monomer)
IgA= Mucosal responses (dimer), breast milk, GI
IgM= Meh, initial naive response, switches to G/A as response narrows, rookie
IgE= Parasitic response & allergies, binds & activates mast cells, T1 HB reaction
IgD= Don't care, naive response, B-cell receptor, surface bound
T-cells: made in thymus, coordination & killing cells, INTRAcellular, virus
T-cell receptor (TCR): on surface exposed to antigen, +/- selections till used
CD4 with MHC-2: Helper or protein marker, MHC-2 binds/shows extracellular antigen for helper T-cell response, release IL-4,5,6 - class switching!
TH1= help innate & killer T-cells to improve responses, release IFN-y
TH2= help B-cells differentiate/class switch, release IL-4,5,6, BAFF, & CD20
TH17= promotes/regulates, inflammation, BOUNCER, IL-17,22
CD8 with MHC-1: KILLER, only needs signal 2 once, professional, MHC-1 binds/shows intracellular antigen for killer T-cell response, lyse cells, DESTROY
Cytotoxic T lymphocytes(CTL): apoptotic(cell suicide), granules(bomb),
1) Perforin: granule, stabs tiny holes in cell, gets granzyme inside
2) Granzyme: granule/apo, activate target caspases > apoptosis(guts)
3) Fas-FasL: apoptosis, death receptor that doubles caspase action/no ls > release IFN-y for innate to clean up the mess, collateral damage possible
T-cell Activation: APC presents to T-cell using MHC, move MHC+antigen to surface to interact with T-cell and CD4/CD8, co-stimulation
Signal 1: TCR>MHC+antigen // CD4/8>MHC2/1, recognition
Signal 2: CD28>B7 - ½ full activation, CD8 only once/4 every time
Activated T-cell function: 1)produces IL02 (CLONE) & others to give orders, 2)TOUCH: only after signal 1+2, CD40(ear) molecule on the surface of immune cells, CD40L(hook) molecule on the surface of T-cell = pass signals
Treg cells: (CD4), IL-10, hippies, reduce inflammation, slow response, CD25 or FOXp3 surface markers, autoimmunity, CTLA-4 contact regulation
Natural Killers (NK): recognize like MØ, kill like CD8 CTL T-cell, cancer
- Lazy T-cells>tolerance/anergy
Hypersensitivity: response to foreign antigen hurts self antigens, damage host
Type 1: “immediate” or “allergic” rxn, allergies, wrong antibody type
Intolerance vs allergy: intolerance is host can’t use or process a compound bc of genetic mutation, allergy: immune system is directly targeting something
Localized or systemic rxns from release of inflammatory molecules, FAST!
1. Atopic: chronic local allergy (hay fever, asthma, etc)
2. Anaphylaxis: systemic, sometimes fatal reaction, low bp, & airway constriction, BAD, anaphylactic shock, mast cells everywhere
Formation of IgE antibody type, IgE binds & activates mast cells/basophils, mast cells= granulocytes, granules=HISTAMINE
Empty IgE coats mast cell=SENSITIZATION, immediate release after bind
Dx: wheal/flare rxn, skin testing=patients skin injected with allergen, look for wheel response in skin, common/fast, in vitro: IgE blood levels
Tx: antihistamines, epinephrine (EpiPen), cromolyn new, homeopathic
Asthma: severe bronchoconstriction, antigen unknown nut histamine releases
Tx=steroids(Flovent), bronchodilators(Albuterol), combo drugs(Advair)
Atopic Dermatitis: Eczema, intensely itchy inflammatory on skin,
Food/Drug Allergies: peanuts, fish, cows milk, eggs, shellfish, soybeans
* mucosal/intestinal absorption, vomiting, diarrhea, abdominal pain, hives
Red Man Syndrome: VANC, pruritus itch, red rash, antihistamines tx no vanc, side effect not allergy
Type 2 (cytotoxic): “antibody-mediated” rxn, B-cell misrecognition of self vs foreign, should be treated as self, but targeted for destruction, IgG
Binding of antibody to “self” antigen patterns that are confused, antibody binds & activates innate/complement, MAC & innate responses = destruction
Transfusion Rxn: binding of antibody to RBC, hemolysis, + has RH
Hemolytic Disease of Newborn: administer Rhogam to RH- pregnant women, only RH- mothers with RH+ fathers, mom could attack baby RH+ if no Rhogam
Drug-Induced Rxn: PEN(cillins) act as haptens, appears foreign w/ self-protein contact, can produce autoimmune diseases - ITCP
Immune Thrombocytopenic Purpura: destruction of platelets & decreased # of circulating platelets, easy bruising (purpura), caused by quinidine/quinine
Autoimmune Hemolytic Anemia(AIHA): destruction of RBCs, two variants (immune & idiopathic) “sore tongue”, blue sclera, fever, headaches
* Warm: autoantibody IgG attacks RBC, 50+ age, corticosteroids
* Cold: IgM & C3d coat RBC triggering hemolysis, 50+ age, avoid cold
Type 3: “Complexing” rxn, wrong clearance (too much trash left over), autoimmune diseases, complexes accumulate & cause new reactions
Systemic: Systemic Lupus Erythematosus (SLE), rheumatoid arthritis (RA), serum sickness rxn to vaccine after exposure (baby rash), blotchy/veiny pruritus red rash
Localized: HS pneumonitis, kidney failure, arthus rxn to vaccine after exposure, hot/tight/knotted red tissue, painful to touch, can become necrotic
Type 2/3 Tx: limit inflammation by corticosteroids, plasmapheresis: replace anti (specific), biologics: anti-CD40 or anti-CD19 or 20 (B-cell surface marker)
Type 4: Delayed or cell-mediated or CMI rxn, T-cell, wrong response, didn't need T-cells but they came and caused damage
Antigens attach to cells, targets for intracellular (CMI) responses, T-cells!
Typically chronic, progressive disease, T+MØ cycles = epitope spread
Tx: corticosteroids, anti-B7 (Costim), anti-IL-2, TNF antagonists, cyclosporin (prevent organ rejection) and limit inflammation
Allergic Contact Dermatitis: intense irritating skin rash, foreign haptens, poison ivy, PPD serum, formaldehyde, used for TB testing, blisters develop
Graft Rejection: when CTLs recognize foreign MHC-1 on graft, slow rejections, ends in graft death, graft vs host disease - 30% of grafts, slow
* Hyperacute rejection: takes minutes, type 2, Ab-related
1. Autograft: tissue transplanted from one site on body to another site
2. Allografts: (common), cadaver grafting, tissue exchange between people
3. Xenograft: tissue exchange between different species, pig heart valve
Stevens Johnsons Syndrome (SJS): serious, painful red or purplish rash that spreads & blisters causing top layer of skiing to die/shed, B-lactams cause, NSAIDS, not true allergy
Autoimmunity: immune response mistargeted against self, attacks self antigen
Adaptive process, recognizes self vs foreign, DAMP vs PAMP, type 2 or 3
Failures in self tolerance, inheritable genes/errors environmental stimuli
Tx: immune suppression (corticosteroids, NSAIDs, TNF-inhibitor, biologics
* Personalized immunotherapy: infusions of needed molecules, short-term
* Immune replacements: bone marrow, costly, risk of rejection
T-cell: TCR/Antigen/MHC+Costim vs TCR/Antigen?=/MHC only, different presentation = different response, tolerance major way to control immunity and keep safe
* Responses: productive response, tolerance (ignore), ignorance(no response)
B-cell: autoantibody production, antibodies mark self & response follows
* Negative selection primary for B-cell tolerance, receptor editing, 2nd recombination of light chain variable rxns, control by BAFF/CD20 protein
Primary IA: self antigen is recognized during generative lymph process, (BM/Thymus)
* Most likely, MHC haplotypes may be more likely to present as a self antigen
Negative Selection development: AIRE gene mutation, lack/failure of control mechanisms, tolerance errors, bad signal 2 (CD28/B97), wrong # of Tregs
Peripheral: previously controlled mature lymphocytes mis-activated
1. Molecular mimicry: PAMP patterns mimic self patterns, confusion
2. Bystander activation: bad orders given, wrong MHC, superantigens
3. Epitope spreading: frees self antigen not normally seen > foreign & destroy
Type 1 Diabetes (Mellitus): immune cells (B) vs insulin-producing cells, genetic
Multiple Sclerosis: CD8 & CD4 T-cells attack myelin sheath insulating brain and spinal cord neurons, deficits in speech, vision, muscle function
Myasthenia Gravis: Autoantibodies target ACh receptors, Ddx for Guillain-Barre, botulism, weakening/paralysis of muscles as synapses fail
Hashimoto’s Thyroiditis: target thyroid hormones, T3/4, puffy face, tongue enlargement, Tx: anti-inflammatory + thyroid replace (levothyroxine)
SLE: Produce antibodies against DNA fragmentation, T3, rash, arthritis, kidney failure, butterfly rash, spring break disease
Rheumatoid arthritis: attacks joints/cartilage or uncleared Ig+Ag in joints, related to TNF amounts in synovial, anti-inflammatories (TNF-inhibitors), advi
Celiac Disease: spure, autoantibodies against gluten, NOT allergy, IgA, damage to intestines (shag vs tile), tense vesicles, mouth ulcers
Immunodeficiency: reduced or no functional immune response
* Increased susceptibility to infectious diseases, reduced immune potency
1. Primary: resulting from a genetic defect
2. Secondary: acquired resulting from an environmental cause, cancer, HIV
Congenital: primary, naturally occurring genetic errors/defects, 3 types
* TLR defects, no PRR recognition, complement defects (C2-C5), slow innate
Chronic Granulomatosis Disease: MØ form granulomas, staphylococci, skin infections, fungal, pneumonia, diarrhea, Tx = antibiotics & IFN-y
Hyper IgE Syndrome (Job’s): lack of fever, lots of histamine, bone fragments, cuts behind ear, eczema, dental abnormalities, Tx = antibiotics & immunosuppressives
Lymphocyte Maturation: defects in B, T, or both maturation 3rd line
SCID (severe combined immunodeficiency): bubble boy, no B or T cells, no + selection, mutations in RAG recombinase
Bruton’s Agammaglobulinemia: No B cell maturation, lack of Ig, extracellular, BM transplant, not fatal
DiGeorge’s Syndrome: thymus no function, no T cell maturation, cardiac, abnormal face, thymic aplasia, cleft palate, hypocalcemia, chromosome 22 (Catch 22)
Lymphocyte Activation: normal maturation, bad effectors (can't do job)
X-linked Hyper IgM syndrome: No B class switching, defects in contact molecules/T-cells, only produces IgM, extracellular infections like bacteria/fungus
Common variable immunodeficiency: environmental cause, design/intended as therapy (corticosteroids), cancer/treatments, HIV
Designed Immunodeficiency: corticosteroids = compounds that reduce immune function, works through multiple methods
Cancer: Tx=destruction on tissue via chemo drugs/radiation, anti-inflammatory (corticosteroids), protein calorie malnutrition (replication blocks, terminal illness)
HIV: retrovirus, uses RDDP to get to host, stage 3=AIDS, integrate to host
* Infects T-cells, uses MØ & DCs as reservoirs, CD4 for entry, then turn on & clone & kill
* GP41 & GPI20 (capsid molecules), results in SLOW T-cell death
Stage 1: vague, flu-like symptoms, T-cell count 500+, asymptomatic
Stage 2: chronic HIV infection, more numerous mild opportunistic infections, lasts 2-15 years, T-cell count 200-500, low HIV in blood
Stage 3: AIDS, rare infections, neoplasms, gateway to other infections like cancer or meningitis, T-cell count below 200
Kaposi’s Sarcoma: papular rash from HHV-8, tumors in endothelial cells
B-cell Lymphoma: tumors form B-cells from EBV
HIV/AIDS Tx: start antiretroviral therapy ASAP if expected, life-long treatment, maintain T-cells, Atripla or PrEP/PEP, inhibit RT/integrase/protease
Serology (Vaccines): immunology that deals with in vitro diagnostic testing of the serum, presence/absence of antibodies and type/tiered, TITER detection
Sensitivity: how well does the test detect people with the condition vs Specificity: how does the test determine people that do NOT have the condition
Agglutination: binding whole cells together, clumping
Precipitation: binding epitope molecules in solution
* Positive: clumping, precipitate, color change, etc
* Negative: milky or uniform, both by immunoassay tests (ELISA used for HIV testing & can see multiple antigens at a time and changes color
Antigen Testing: must have detectable amount of antigen, need universally good antibody that binds antigen, detects infectious agents, no info on immune response, known antibody given, covid or pregnancy test
Antibody testing: needs immunocompetent patient, recent analysis, detects immune response to antigen, but not directly detect the antigen (unknown antibody)
* E.coli on plate, if sample binds than yes E.coli antigen
Hybridomas: generate designer B-cells to recognize antigens for research/tests
Anti-toxin: inject specific antibodies, protection needed NOW, neutralizing
Immune Serum Globulin: Ig extracted from pooled blood, lab-made, polyclonal Ig, hyperimmune people, replacing antibodies immunodeficiency, lots of cloning, nurse-saver, not a long term solution for immunodeficiency
Biologics: lab made monoclonal Ig, bind to specific antigen & block it, mAbs, targeted immunotherapy, antibodies block one process, CD28, turns cell quiet
NO LIVE VACCINE: pregnant, immunodeficient, cancer, can’t make memory cells
Herd immunity: collective immunity through mass immunization makes indirect protection on the non immune members(umbrella) one protects lots
Types of immunity:
Active immunity: person is challenged with antigen that stimulates, production of antibodies, creates memory, takes time, lasting
Passive immunity: molecules are donated to an individual, no memory, acts immediately, short-term
Natural immunity: through normal life experiences (chickenpox)
Artificial immunity: through a medical procedure/protection (vaccine)
Combinations:
Active natural immunity: disease & develop natural protection/memory
Active artificial Immunity: vaccination & experience “practice” antigen to develop memory from known set of antigens
Passive natural immunity: molecules are donated to provide protection until system(breastfeed)
Passive artificial immunity: you get a shot to neutralize an antigen, develop no memory (gamma globulin, antitoxins)
Live vaccine: M(mumps), Y(yellow fever), R(rubella), O(oral polio & oral typhoid) M(measles), E(endemic typhus), T(TB=BCG), I(nasal influenza=LAIV), P(plague)
Live attenuated vaccines: uses living pathogens with reduced virulence (harm) - stronger immune potential but less safe for immunocompromised
Subunit vaccines: antigen/epitope fragments, safest vaccine class, (B)TH2 response, no live or whole organism, weak, booster/conjugate good
Genetic engineered recombinant vaccines: DNA/RNA/plasmid from infectious agent, expressed foreign antigen inside cells, adaptive response, MRNA makes protein ans body makes epitopes, uses BOTH B & T cells
Sign: measurable (102 fever) vs Symptom: subjective to patient (pain scale)
Disease stages: incubation=time w/out S&S, prodromal=generic S&S & lots of spread, illness=specific S&S, convalescent=recovery
Infection classification:
Common source=from shared source, propagated=person-person
Acute=rapid onset/short duration, persistent=chronic/latent/slow
Focal=infectious agent left and turned into something else (i.e. sore throat to heart problem), mixed=more than one pathogen/infection
Primary=starting infection, secondary=occurs after primary
Infectious dose=# of organisms needed to infect (lower ID=more virulent)
Mortality rate: total # of deaths in population due to disease
Morbidity rate: # of persons afflicted with infectious disease
Reservoir: water sources, soil, Vector: drinking, fleas/ticks/mosquitos
Sporadic: occasionally or irregular from contact w reservoir
Endemic: native to a region at constant % from related organism
Outbreak: sudden unexpected occurrence (often from travel)
Epidemic: outbreak affecting multiple populations, above expected levels
Pandemic: world-wide, linkages across continents
Identification methods: staining(gram=PPG/acid fast=lipid) based on pathogen structure, growth/colony morphology colony size/odor/color, slow physiological/biochemical traits traditional, metabolic/chemical analysis (sorbitol/indole), serology & genetic detection faster, better, more accurate
Mutations: point mutant=single base change, silent=base change that does not change AA codon, nonsense=stop codon, ends protein early, missense= changes codon to different AA, frameshift=disrupts normal triplet reading by insert or delete
Bacterial DNA movement: transformation=free acquisition & recombination transduction=phage shuttling, conjugation=pilus-mediated transfer of plasmids, transposons=jumping genes, + all mutations/natural changes
PCR: best for genetic diagnosis, very sensitive, 16S RNA(if protein is made, there is 16S), no growth needed, form sample to DNA in 4-6 hours
1. Pick a DNA sequence that is unique(16S RNA) to what you want to detect
2. Take sample and harvest DNA out of it (@30min)
3. RUn PCR rxn to detect that unique thing (@3hrs)
4. Evaluate PCR result (if +(has a band), the sequence is there
RFLP: restriction, fragment, length, pattern - compare (paternity testing)
Gene therapy: replacing bad gene with a good copy, gene inserted in viruses for infection, delivery into host tissues, expression of new copy
RESPIRATORY TRACT: most common place for infectious agent access
URT: mouth, nose, nasal cavity, sinuses, pharynx, epiglottis, larynx
LRT: trachea, bronchi, bronchioles, lungs, alveoli (U&L divided at voicebox)
Defenses: cilia, mucus(catch&trap), coughing, sneezing, swallowing
Rhinitis(common cold): sneezing, scratchy throat, runny nose(rhinorrhea)
CC: rhinoviruses, coronaviruses (can be RSV/pertussis/EBV/ED68,hMPV,etc)
VF: penetrate mucus&attach to cells, use sialic acid - specific bind molecule, no IL1, highly mutable, Dx: appearance, Tx: droplet control, “chicken soup & rest”
Enterovirus D68: summer cold, pre-flu, CCS, low grade fever
CC: Enterovirus strains(primarily ED68), VF: viral, 100 serotypes
Dx: appearance, Tx: CCTx, warn abt respiratory collapse, supportive care
*AFM:acute flaccid myelitis=slow, likely reversible paralysis, can cause encephalitis if crosses BBB
Sinusitis(sinus infection): congestion, pressure, head/toothache, swelling, following CC, opaque discharge=bacterial, clear=viral
CC: mixed bacterial/fungal/viral agents, likely NF (explains recurrence)
VF: biofilms, persistence, mixed infections, Dx:appearance, can use radiology
Tx: broad spec ABX, alternate ABX to prevent resistance
Otitis Media(ear infection): URT infection reaches eustachian tubes, CCS, fullness/pain in ear, hearing loss, pus/inflammatory fluid in middle ear
AOM (acute otitis media)=bulge, loss of landmarks, CC: streptococcus pneumoniae, Haemophilus influenzae
OM w/ effusion=retraction of eardrum, CC: viruses (rhinovirus, RSV, etc)
VF: capsule for bacteria, variance(mutations), Dx: appearance, screaming, Tx: 72hr watchful waiting, B-lactams(not preferred bc increasing resistance), vax(HiB, pneumovax/Prevnar) *severe infx can eardrum rupture(tubes), meng
Pharyngitis(strep throat-sometimes): inflammation, pain/swelling, reddened mucosa, bad breath, white packets/pus, may affect speech & swallowing
*can be non infectious-yelling/vocal cord strain, post-nasal drip
CC1: often viral caused, less severe, rhinovirus, RSV, influenza, EBV, ED68...
CC2: Streptococcus pyogenes(GAS)(true strep throat), causes ⅓, some NF
VF: surface antigens: lipoteichoic acid(LTA), M protein, hyaluronic acid (HA)
*M protein=adhesin&WBC evasion, type (1,5,etc) tell what VFs are coming
Linked to strain serotype&sequelae determinate(scarlet fever, AGN & RA, rheumatic fever, etc), true strep give PEN
extracellular toxins: streptolysins (SLO&SLS) for hemolysis, erythrogenic toxin responsible for rash/fever typical of scarlet fever, superantigens: SpeA, SpeC activate Tcells & induce tumor necrosis factor(TNF) cytokine damage
CC3: fusobacterium necrophorum, rare, identical to GAS, can lead to Lemierre’s syndrome: bacteria spreads from throat to jugular vein, clumps of bacteria travel thru bloodstream
S.pyogenes complications: scarlet fever(sandpaper-like rash,high fever), rheumatic fever(damage to heart valves, arthritis in multiple joints), glomerulonephritis(kidney function/failure), TSS & necrotizing fasciitis
Diphtheria: sore throat, lack of appetite, low-grade fever, pseudomembrane forms on tonsils/pharynx, asphyxiation, systemic diphtheria=toxin attacks CNS & cardiac tissue - extreme fatigue, dementia, death that looks like MI
CC: corynebacterium diphtheriae(rods), gram stain “chinese character” or “XY” VF: toxin(no invasion) A/B toxin attacks protein synthesis, ELEK test, tinsdale agar(black colonies), Dx: appearance, rapid strep testing(serological), Tx: antitoxin + PEN or ERY, vax (DPT)
Pertussis(whooping cough)(U/LRT): CCS, paroxysmal(comes&goes), severe cough with “whoop” sound, burst blood vessels in eyes, vomiting, cracked ribs
Long recovery(convalescent) phase of weeks/months, secondary infections
CC: bordetella pertussis, VF: tracheal toxin(CT) - AB toxin, kills ciliated nasopharynx cells, pertussis toxin(PT) - upregulate cAMP (EXPORT) in cells
*toxins enter cells, kill cells, dead cells slough off=airway full of dead cells & debris, @ same time PT enters cell & turns on cAMP, causes cell export(mucus), now mucus & dead cells fill airway, Dx: sound, throat culture, Tx: erythromycin, vax(DPT) - 5x boosters *highly contagious, aerosol transmis.
Croup(U/LRT): CCS, inflamed voice box & windpipe, can spread to bronchi, barking cough, stridor w/ inhalation, worse at night, CC: parainfluenza virus, VF: viral, Dx: sounds, CXR steeple sign, Tx: cool mist, outdoors, monitor
RSV(U/LRT): fever, rhinitis, pharyngitis, otitis, can lead to wheezing, rales, etc, blueing from airway inflammation(LRT involvement-pneumonia)
CC: respiratory syncytial virus (RNA virus), VF: syncytia, triple RSV: syncytial (no O2 transfer)+inflammation+remodeling, Dx: bronchial or nasal wash to find syncytial cells, Tx: self-limiting, severe=O2, IV fluids, ventilation, Ribavirin
Influenza(U/LRT): rapid onset, headache, chills, dry cough, body ache, fever (but H1N1 variable), extreme fatigue can last days/weeks, cytokine storm responsible for systemic symptoms, largest cause of death - second bacterial infections(pneumonia), epidemic CC: influenza virus(orthomyxovirus) types A&B, “subclasses”=HxNx typing differences but still usually A strain
VF: mutability, Hemagglutinin(HA) & Neuraminidase(NA) capsid proteins bind to host cell, spikes for attachment&entry to host cells, Dx: symptomatic, rapid testing, Tx: self limiting, severe=may give antivirals(relenza, Tamiflu-placebo at this point), “best guess” vaccine yearly for anyone +6mo (inactive), or LAIV(live attenuated)(FluMist, 5yr+) for mucosal protection
Best prevention: hygiene+vaccine, Other antivirals: entry/exit blockers- Zanamivir(Relenza), SpOA=influenza virus(HxNx)
Influenza variation: segmented genome of 8 RNA strands-allows for reassortment&mutations, yearly strain mutations=antigenic DRIFT, epidemic strain changes(reassortment)=antigenic SHIFT
Coronaviruses(U//LRT): CCS, swift severe acute respiratory collapse, fever, cough, SOB, progression to pneumonia, zoonotic
SARS(sudden acute respiratory syndrome),MERS(middle east resp. syndrome)
CC: coronaviruses - 1. SARS(not seen since 2005), 2. Novel coronavirus (nCov) or MERS-CoV, VF: unknown, super spreaders, rapid transmission
Dx: lab tests(PCR) for MERS-CoV, Tx: supportive to relieve symptoms
Metapneumovirus(hMPV)(U/LRT): influenza symptoms, found as influenza & RSV negative, CC: metapneumovirus(paramyxovirus), VF: unknown
Dx: DFA, PCR, Tx: treat symptoms not virus, self-limiting
Tuberculosis: mycobacterium tuberculosis (#1 cause) or mycobacterium avium intracellulare (MAC) + *NEW* mycobacterium bovis, organism w/ heavy lipid content, need acid-fast staining - shows slim red-snapper rods w/ segments
Positive ID typically requires culture, (M.tb vs MAC) very slow growing(weeks), produces breadcrumb colonies, VF: cord factor & proton pump=allow intracellular growth, very low infectious dose (ID= ~10)
M∅ ingest M.tb(eaten but not killed), killing by CD8+ Tcells needed, leaves cell debris, need for more M∅, leads to stalemate, formation of granulomas/tubercules & M.tb(dormancy/latency)=Primary TB
Reactivation/escape causes large immune response by Tcells, Secondary TB= destructive pneumonia(consumption), CTLs & cytokine release from Tcells results in caseous necrosis(cottage cheese lung)
Primary=infection>trap>latency, Secondary=death
Tuberculosis Dx: tuberculin testing(PPD)=T4HS(delayed rxn)-inject very small amount that doesn't get large rxn but if you had TB before, memory Tcells will cause rxn, if + PPD test then: CXR, AFB, culture isolation
Quant-iFeron GOLD=new TB blood test(take Tcells out & stimulate w/ epitope to see if they produce IFN-y)
Primary TB: goes dormant, flu-like, + PPD, - infiltrates, not highly contagious
Secondary TB: active, contagious, fever, blood tinged sputum, night sweat, weight loss, caseous necrosis, + PPD & infiltrates
Miliary(disseminated/Potts)TB: spread out of lungs to other tissues
High level of ABX resistance due to long tx & pt noncompliance, MDR-TB= multidrug-resistant TB, XDR-TB= extensively drug-resistant TB, TDR-TB= totally drug-resistant TB
Tx: heat & UV sensitive(sun&outdoors), cocktail tx=long term(mo-yrs) ABX, RIPESAg= Rifampin, Isoniazid, Pyrazinamide, Ethambutol, Streptomycin, & Aminoglycosides, Prevention: education & detection, monitor primary TB
Vaccine: BCG - ineffective & not used in U.S., NEW XDR-TB Tx= NixTB
Bronchitis: extreme cough, congestion, chest pain, fever, fatigue, as inflammation of bronchial tubes progressive=excessive mucus, chest pains, SOB
Chronic if >3mo, watch for pneumonia, CC: virus(influenza,RSV,hMPV), bacterial(S.pneumoniae,H.influenzae,Mycoplasma,Klebsiella), environmental/ immunological(smoke,allergens,pollutants), Dx: bronchial wash to find agent, CXR, Tx: self-limiting, may need O2,IV,vent., treat symptoms(inhaler, albuterol)
Pneumonia: fluid in alveoli of lung, begin w URT symptoms, then chest pain, fever, cough, discolored sputum, hypoxia, SOB, tachypnea, hyponatremia(loss of sodium) common bc of fluid imbalances w Na/K pump, possible septic spread
Dx: CXR & physical exam w auscultation-crackles, rales, 99 speech, egophony
CC: wide variety, almost any bacteria, but fungal/viral/parasitic forms exist too
Classifiers: lobar=lower lobes,unilateral
CAP-community-acquired(walking): most common CC: streptococcus pneumoniae(lancet shaped diplococci) VF:capsule, string test, rust sputum, Tx: cephalosporins, Other CC: H.influenzae,Neisseria spp,viral pneumonia
HAP-hospital acquired(nosocomial): S.pneumoniae stays at top, then S.aureus/MRSA(common VAP-ventilator associated),P.aeruginosa(common VAP),
Klebsiella pneumoniae(CRKP)-gut surgery,catheter, bacillus NF of gut & feces
Atypical(interstitial)pneumonia: walking pneumonia, infection of interstitial space & alveolar walls, bi-lateral, wispy fluid, young&college-age, CC: chlamydia pneumoniae(intra) or mycoplasma pneumoniae(extracellular fried egg colonies), Tx: macrolides or tetracyclines
Fungal: Aspergillus fumigatus “black mold” can be NF or opportunistic, breathe in over time=SLOW, AIDS patients, black lesions, “lightning/broccoli”
Pneumocystis jirovecii (PCP): cold-like, lower septum, HIV/AIDS patients, AIDS-defining illness, “ping pong balls” on a methenamine silver stain, Tx: Bactrim(only immunocompetent!)
Histoplasma capsulatum: bird dropping, bat caves, soil locations, endemic in MO rural populations & midwest, small oval budding yeasts in M∅, snowstorm, slow progress fungus
Legionella pneumophila: water, A/C cooling towers, chlorine resistant, cough, chest pain, vomiting, delirium, diarrhea, shock, MOF, death
Pontiac fever: breathing weak or dead L.pneumo bacteria, Tx: immediate ABX, environmental H2O control/sourcing, grow on CYBE agar
Hantavirus: environmental virus, rodents poop>dry up>air currents>inhaled, starts w/ flu-like symptoms+pneumonia, recovery begins then SUDDEN, MASSIVE, UNEXPLAINABLE inflammation, bleeding into lungs, often fatal
CARDIOVASCULAR & LYMPHATIC SYSTEMS:
SIRS(systemic inflammatory respiratory syndrome): pre-sepsis, defined as two or more of: fever(>100.4), heart rate(>90bpm), resp rate(>20), abnormal WBC count, main issue: MOF, highly dangerous, may need both suppression (corticosteroids) & ABX (ABX cant stop toxins&VFS)
>SEPSIS: 2 SIRS+confirmed/suspected infection >SEVERE SEPSIS: sepsis + signs of end organ damage, hypotension >SEPTIC SHOCK: severe sepsis w/ persistent hypotension, signs of end organ damage, lactate >4mmol
Endocarditis: endocardium inflammation, infection of heart valves, microbe attachment & growth(“vegetations”), fever, anemia, abnormal heartbeat, petechiae rash, Osler’s nodes/Janeway lesions, splinter hemorrhage
CC: staphylococcus epidermidis (coag-negative Staph-won’t clump w/ antibodies), skin NF, cocci in clusters
CC2: oral streptococci (S.mutans or S.oralis)
CC3: high power pathogens like S.aureus, GAS, etc
VF: biofilm formation - has to stick & stay to form vegetation
Negative for coagulase enzyme, may follow infection of prosthetic devices or IV drug use, Tx: complete removal of prosthetic, long-term ABX, possibly VANC
Toxic Shock Syndrome: sudden high fever & low bp (hypotension), vomiting/ diarrhea, confusion, seizures, head/muscle aches, rash resembling sunburn on palms & soles, peeling of hands/feet, boiled lobster rash, can lead to MOF
CC: almost any bacteria, Staph aureus(toxemia)-staph can release TSST-1(superantigen) w/out entering bloodstream, tampon usage, Strep pyogenes(bacteria+toxemia)-often introduced w/ puncture wounds, SpeA & SpeC toxins(superantigens), Gram(-) bacteria from LPS release (septic shock) endotoxin
Necrotizing Fasciitis (NF): flesh eating disease, use bloodstream to move, death & necrosis of tissue requires debridement, often after trauma
CC: streptococcus pyogenes or staphylococcus aureus, toxin mediated
Tx: debridement>removal of tissue(cutting margins, possible amputation)
NEW emerging causes= Vibrio vulnificus(waterborne), Aeromonas hydrophila(waterborne)
Septicemias: organisms actively replicating in blood, fever & hypotension, very ill, altered mental state, shaking, chills, GI symptoms, increased respiratory
Many different bacteria & a few fungi can cause this - NOT viruses
Favorites: GAS & pseudomonas aeruginosa - NF, grows anywhere w/ O2, grows on almost any media, greenish color, fruity/grape-like odor, identify by fluorescence (+) and oxidase testing (+)(purple color), ENDOTOXIN (LPS), lots of adhesion molecules, alginate capsule, elastase destroys connective tissues, Exotoxin A & Exoenzyme S for direct tissue damage(protein synthesis inhibitors, highly multi-drug resistant, prefers wet/moist, hot tub bug, burn wounds, cystic fibrosis, swimmers ear
Plague: bubonic plague, black death, flea bite, causes necrosis of lymph nodes, swollen bubo in groin/axilla, fever, chills, nausea, headache, DIC, subcutaneous hemorrhage/purpura, tissue necrosis, HIGH mortality
Septicemic plague form:progresses to massive bacterial growth(blood&lymph)
Pneumonic plague form: respiratory disease- attacks lungs
CC: Yersinia pestis, VF: low ID(3-50), Yop T3SS(stabs immune cells, injects toxins), ENDEMIC to West/SW US, from fleas, contact w wild animals
Tx: aminoglycoside ABX, vax available for high risk individuals
Tularemia: lawn mower fever, rabbit fever, headache, fever, chills, malaise, progresses to ulcerative lesions, swollen LN, sore throat, intestinal disrupt, debilitating, fatal if inhalation exposure, vector=tick(open sore @tick bite)
CC: Francisella tularensis, VF: intracellular, highly infectious (ID=1-10)
Tularemia cont. Potential bioweapon CatA, Tx: Aminoglycosides (Gent, Kan)
Lyme Disease: rash spread by tick,mimics neuromuscular&rheumatoid condit.
“Post lyme disease syndrome”=headache, fatigue, arthralgias 6mo to 1 year
CC: Borrelia burgdorferii (spirochete), VF: motility, adhesion, antigen shifting
Tx: doxycycline or b-lactams(1st), cefotaxime or ceftriaxone(2nd), over 3-4 weeks, corticosteroids for inflammatory
Early localized (EM): bullseye rash, not painful
Early disseminated: acute neurologic or cardiac involvement usually weeks to months after bite, meningitis, cranial neuropathy, motor/sensory radiculo- neuropathy- facial nerve is most often affected cranial nerve, Lyme can cause bilateral cranial nerve palsies, occasional conjunctivitis
Late disease: months to years later, arthritis, mild neurologic syndrome Lyme encephalopathy
Rock Mountain Spotted Fever(RMSF): tick, fever, chills, headache, muscle pain, spotted rash from extremities to trunk, CV disruption, restlessness, delirium, convulsion, tremor, coma
CC: Rickettsia rickettsii, VF: obligate intracellular pathogen, replicates in endothelial cells, these are killed, blood system compromised, kidney failure, GI problems, heart complications, Tx: Tetracycline, limit tick exposure
Ehrlichiosis: RMSF w/ no rash, tick, no rash bc infects WBC
CC: E.chaffiensis(HME)-Human Monocytic Ehrlichia(M∅, DC) or E.equi (HGE)- Human Granulocytic Ehrlichia(N∅, Masts, etc) both are identical infections but infect different immune cell types, VF: intracellular pathogen, Tx: Tetracycline, limit tick exposure
CSF & CBC: animal wound, start as classic cellulitis, moves to capillaries or lymphatics-LN swell & become pus-filled, track lines, CC: CSF= Bartonella henselae(intracellular bacterium), CBC= Pasteurella multocida(safety pin stain, capsule, P.multocida toxin(PMT) destroys connective tissue & allows invasion
Tx: self-limiting, possible ABX, immunocompromised=aggressive therapy
Ebola: hemorrhagic fever, headache, weakness, vomiting, zoonotic, chest pain, impaired kidney/liver function, rash, red eyes, CC: ebola virus, Marburg virus, VF: aggressive viremia, clotting leading to internal/external bleeding, Tx: unknown, treat symptoms if possible, spread by blood and close contact
Vax: rVSV-ZEBOV, hemorrhagic fever variants, 6/U shape, bud from host cells
Infectious Mononucleosis: mono, kissing disease, sore throat, grey/white color, swelling, CC: Epstein-Barr virus(EBV human herpesvirus 4), infects bcells, can be latent, no Tx, could lead to spleen rupture-internal bleeding
Dengue Fever: mosquito, sudden high fever(104-5), flat red rash w second rash on top, bonebreak fever, CC: dengue virus, puerto rico, VF: viremia
Zika Virus: mosquito, similar to dengue, fever, rash, conjunctivitis, joint pain, treat symptoms-no aspirin, not deadly, Guillain-Barre, if pregnant risk of microcephaly during 1st trimester=lack of brain development, small head
Malaria: mosquitos, cyclic fevers, anemia, fatigue, neurological damage, abnormal posturing, CC: plasmodium falciparum(parasite), circles/rings, Dx: thick & thin blood smears, Tx: quinine ABX, mosquito repellent & water source cleanup
HIV: retrovirus, uses RDDP to get to host, 1: flu-like, Tcell 500+, asymptomatic, 2: chronic, 2-15yrs, Tcell 200-500, 3: AIDS, gateway to infection(cancer/meng), Tcell <200, Tx: antiretroviral therapy ASAP, life-long, Atripla or PrEP/PEP, HAART:highly active antiretroviral therapy, cART, combination antiretroviral therapy, cocktail therapy for life
COVID: zoonotic RNA virus, spikes as main epitope, frequent mutations, COHABITATION is our goal, ARDS as main killer event>immune based response fills alveoli & leads to fibrosis(non-elastic), Tx as RDRP inhibitors (remdesivir), combo of B&T responses, long covid: microvascular clot issues, taste/smell, SOB/scarring, neuropathy, cardiac damage, stroke, seizure, Guillain-Barre, spike glycoprotein(S) binds ACE2, TMPRSS cleaves S & starts membrane fusion & virus entry, infection of T2 pneumocytes/surfactant, cytokine storm, PCR, antigen/antibody serology testing, herd immunity
Antigenic Original Sin(AOS): responses based on memory(as opposed to modifying ABX)work fastest, so Bcells get to work pumping out antibodies of shapes they’ve seen before=imprinting, neither good nor bad, simply reflects that a person’s first exposure to a virus can have a noticeable effect on their later responses to variants of that same virus. In AOS, prior memory can interfere or even prevent you from generating antibodies against new variants. Not currently seen in COVID, but carefully watching “you can’t teach an old dog new tricks” old dog is your immune memory.
Extra Notes:
Rapid strep test: serology of Ig’s against outer Lancefield group antigens of GAS
Streptococcal Pharyngitis Tx: b-lactams
Diphtheria cases increasing bc less children receiving DPT vax