Infections Flashcards
Neisseria meningitides
G-ve diplococci
Transmission: resp droplets
ROS: usually just mild “flu” sx’s (carrier)
Complication: invasion of blood stream causing septicemia and meningococcemia
*meningitis in some pt’s
Meningitis Pathogenesis
Pathology: pyogenic inflamm of leptomeninges and SA space
Gross: meninges are dull, congested w/ purple to exudate
Microscopically: PMN cells, fibrin, vascular congestion (acute inflamm)
Meningitis Clinical Features
ROS: fever, HA, cloudy consciousness, nuchal rigidity
Dx: CSF w/ PMNs and increased protein, low glucose
Other causes: TB, viral or fungal
Meningitis Course Features
Complications: shock, purpura, toxemia, DIC
Epidemiology: N. meningiditis common at all stages except neonates
Waterhouse Friderichsen Syndrome
Bilateral adrenal hemorrhages
Neisseria gonorrhoeae Features (and male sx’s)
G-ve diplococci, sexually transmitted
Male ROS: urethritis, epididymitis, urethral d/c, dysuria
Homosexual male ROS: oropharyngitis and proctitis
Neisseria gonorrhoeae (female sx’s)
ROS: cervicitis, salpingitis, peritonitis, vaginal d/c, dysuria, intermenstrual bleeding, PID,
Course: chronic can cause scarring of Fallopian tubes leading to infertility
Gonorrhea Course
Rarely hematogenous - can cause tenosynovitis, arthritis, hemorrhagic skin lesion, endocarditis, rarely causes meningitis
Ophthalmia Neonatorum (Gonorrhea)
Transmission: during parturition
ROS: purple to conjunctivitis
Tx: erythromycin/silver nitrate eye drops after birth for prevention
Salmonella typhi Features
typhoid fever
G-ve bacilli
Transmission: ingestion of contaminated food/water
Mechanism: enters ileal wall, enters blood stream and causes bacteremia during (week 1)
Typhoid Fever Organ Affects
Hepatomegaly: typhoid nodules composed of Kupffer cell hyperplasia, minute fo i of hemorrhagic necrosis, collections of macrophages during (week 2)
Splenomegaly: soft spleen w/ splenetic, typhoid nodules
Typhoid Fever Course
Excretion through bile into gut, re-enter gut wall through ileum, sensitization has occurred an contact w/ the organism produces lymphoid hypertrophy and necrosis in the mucosa (week 3)
Typhoid (enteric) Fever Lesions
Ileum: lymphoid hypertrophy of Peyer’s patches, necrosis, ulceration
Features: no PMNs, only macrophages, erythrophagocytosis, mesenteric LN enlarged, hemorrhagic necrosis
Typhoid (enteric) Fever Clinical Features
ROS: fever, toxic appearance, leucopenia*, bradycardia, endotoxin produces depression of heart and bone marrow, ulcers heal w/o scarring
Complications: perforation peritonitis, bleed (week 3 and 4)
Typhoid Fever Diagnosis
Week 1: blood culture (lysis of macrophages release large # of bacilli)
Week 2: organisms can be demonstrated in feces and sometime sin urine
Week 3: demonstrate Ab’s (Widal test)
Typhoid Carrier State
Persistent/chronic infection leads to colonization of gallbladder, carrier has no sx’s but can shed the bacteria in feces/urine
Tx: need to undergo choelcystectomy
G-ve Sepsis
ROS: fever, DIC, hypotension, shock
Organisms: normally commensalism but become pathogenic in situations (immunodeficiency, break in mucous membrane)
E.g. - E. coli, h influenzae, pseudomonas aergunosa, klebsiella, proteus, serratia
Staphylococci
G+ve, normally colonize human skin
Infectious: most commonly S. aureus
Lesions: inflammatory or toxin mediated
Inflammatory Staphylococci Lesions
Skin, postpartum mastitis, bacteremia, endocarditis (tricuspid valve, common in drug addicts), osteomyelitis, pneumonia, bacteremic abscess
*MRSA
Toxin Mediated Staphylococci Lesions
Food poisoning (enterotoxin), TSS, Scalded Skin Syndrome (exfoliatintoxin)
Streptococci
G+ve cocci, present in pairs or chains, hemolytic
Lancefield grouping: Group A are beta hemolytic (e.g. - S. pyogenes), Group B are hemolytic
Streptococci Infection
Direct damage: suppurative - cellulitis, abscess, pneumonia
Exotoxins mediated: Scarlet Fever
Indirect damage: caused by immune response
Strep Pneumonia (pneumococcal pneumonia)
Causes: lobar pneumonia in healthy young adults
ROS: cough, fever, CP, hemoptysis
Early stage: exudate rich in fibrin, RBCs, few PMNs seen in lumen of alveoli
Progression: bronchioles and alveolar walls not damaged bc pt is immunocompetent
Spread: via pores of Kohn to involve the entire lobe
Course: total resolution w/in 10 days
Red Hepatization
Exudate consists of RBCs, fibrin, more PMNs
- lung loses spongy consistency and feels solid and red like liver
Grey Hepatization
Congestion and fibrin disappear, PMNs replaced by macrophages
Resolution: macrophages clear up the debris a few days later
Tx: abx accelerate the process
Complications: rare dev of abscess, fibrosis, emphysema
Rheumatic Fever Course
Initial: streptococcal ST, or skin infection
Lag: 2-3 wks after initial infection
Mechanism: Ab’s generated to M protein of the bacteria cross react w/ tissue glycoproteins in joints, heart, skin, etc.
Rheumatic Fever Sx’s
ROS: fever, poly arthritis, carditis, chorea, skin nodules, erythema (ACCNE)
Complication: carditis showing Aschoff bodies on biopsy, can become chronic and cause mitral stenosis
Tx: to prevent chronic rheumatic heart dz give pt prophylactic abx tx s/p RF
Post-Streptococcal Glomerulonephritis Course
Initial: steptococcal ST or skin infection
Lag: 1-4 wks after initial infection
Mechanism: Ab-ag immune complexes form and get deposited in BM of glomeruli, activates complement and induce acute inflammation
*type III hypersensitivity
Post-Streptococcal Glomerulonephritis Sx’s
ROS: acute malaise, fever, oliguria, hematuria, azotemia (👆🏽BUN, Creatinine and 👇🏽GFR)
Resolution: resolves spontaneously in most pt’s as immune complexes are cleared
Diphtheria
Myocarditis is the complication
Pseudomembranous Colitis (C. diff)
Clostridium difficult: G+ve bacillus
Cause: tx w/ broad spectrum abx is assoc w/ colitis bc they eliminate the normal flora of the gut that normally afford protection
C. difficile Mechanism
Exotoxin causes severe mucosal suppurative inflamation, small vascular thrombosis, necrotic mucosa forms pseudomembrane
Rickettsia Infections
Small, obligate intracellular, resemble G-ve
Epidemic Typhus
Organism: Rickettsia prowazeki
Transmission: head/body lice
ROS: hemorrhagic nodules on skin, vasculitis, thrombosis, hemorrhage
Complications: pneumonia, hepatitis, CNS involvement (typhus nodule)
Severe: necrosis of earlobes, scrotum, nose, finger
Dx: immunofluorescence and Weil Felix test (Ab’s cross react w/ Proteus ag)
Rocky Mountain Spotted Fever
Organism: Rickettsia rickettsii
Transmission: tick bite
Geography: OK, TN, AR, GA
ROS: fever, HA, myalgia followed by skin rash
Complications: vascular necrosis, hemorrhage, vasculitis, thrombosis (severe lung and CNS involvement)
Dx: immunofluorescence on biopsy
Q Fever
Organism: Cloxiella burnetti
Transmission: airborne droplets from sheep/cattle
ROS: no skin rash, pneumonia (affects liver, spleen and bone marrow)
Biopsy: ring granuloma in liver biopsy - central fat, fibrinoid material surrounded by epithelioid cells
Dx: immunofluorescence, serology
