NON-INFECTIVE ENDOCARDITIS (marantic endocarditis): 

·       GASTROINTESTINAL TRACT INFECTION:  Esophagitis, gastritis, gastroenteritis, colitis.



GASTROENTERITIS (aka gastric flu, stomach flu although unrelated to influenza): 










·       NEUROLOGIC INFECTION:  Encephalitis and Meningitis.


MENINGITIS:  Acute aseptic meningitis, acute bacterial meningitis: 

 ·       RESPIRATORY TRACT INFECTION:  From upper to lower respiratory tract → Otitis externa, otitis media, pharyngitis, laryngotracheobronchitis (i.e. croup), bronchitis, bronchiolitis, and pneumonia.


Ø  TYPES OF STDs:  G-gay and H-heterosexuals C-contract T-these D-diseases --> G-gonorrhea, H-herpes, H-HIV, H-hemophilus ducreyi (aka chancroid), H-human papilloma virus (HPV), C-chlamydia, T-treponema pallidum, D-donovania granulomatis (aka Klebsiella granulomatis or calymmatobacterium granulomatis).

 ·       CONGENITAL INFECTIONS:  Occur at any time during pregnancy, labor, and delivery.  TORCHeS → TO-toxoplasmosis, R-rubella, C-cytomegalovirus (CMV), H-herpes, H-HIV, S-syphilis.

·       OPPORTUNISTIC INFECTIONS:  An opportunistic infection is an infection caused by pathogens that usually do not cause disease in a healthy immune system. A compromised immune system, however, presents an "opportunity" for the pathogen to infect.  T-the CHAMP à T-toxoplasmosis gondii, C-candida albicans, C-crytococcus neoformans, H-histoplasmosis encapsulatum, A-aspergillosis, M-mucor/rhizopus, P-paracoccidioidomycosis, P-pneumocystic carini. 

·       BACTERIA:




 ·       VIRUS









o   INFECTIVE ENDOCARDITIS Inflammation of the inner layer of the heart; most commonly involved the heart valves.  Endocarditis can be non-infective.

Ø  PATHOPHYSIOLOGYAltered blood flow around the valves from congenitally abnormalities, prosthetic valves, auto-immune mechanisms, rheumatic heart disease (often affect the aortic or the mitral valve), or as a consequence of old age, is a risk factor for endocarditis. The damaged valve becomes covered with a blood clot (i.e. non-bacterial thrombotic endocarditis-NBTE).  If the patient subsequently become bacteremic (often after dental procedures by S. viridans), the blood clot covered valve provides a place for bacterial proliferation.  As the valves of the heart do not receive any blood supply of their own, WBCs cannot enter, and it is difficult for the body to clear such infection.

Drawing of endocarditis

By BruceBlaus - Own work, CC BY-SA 4.0,

Ø  CLASSIFICATION: Subacute bacterial endocarditis (SBE): Progresses slowly over weeks-months and has low propensity for hematogenous spread to extracardiac sites.  Often due to low virulence bacteria (e.g. streptococci).  Acute bacterial endocarditis (ABE):  Fulminant illness over days-weeks.  Often due to highly virulence bacterial (e.g. S. aureu).  Culture-negative endocarditis may be caused by Aspergillus species, Brucella species, Coxiella burnetii, Chlamydia species, and HACEK bacteria.

Ø  PRESENTATION:  Fever, vascular phenomena (septic emboli-problems such as stroke in the parietal lobe of the brain or gangrene of fingers; Janeway lesions-painless hemorrhagic cutaneous lesions on the palms and soles, intracranial hemorrhage, conjunctival hemorrhage, splinter hemorrhages); and immunologic phenomena (glomerulonephritis, Osler's nodes-painful subcutaneous lesions in the distal fingers/toes, Roth's spots-retinal hemorrhage, positive serum rheumatoid factor).

Janeway lesion on palm of a 36 year old male with staphylococcus endocarditis

By Warfieldian - Own work, CC BY-SA 4.0,

Osler's lesions found on the hand and fingers of a 43-year-old male with subacute bacterial endocarditis

By Roberto J. Galindo - Own work, GFDL,

Splinter hemorrhage on a fingernail of the little finger.

By Splarka - Own work, Public Domain,

Ø  DIAGNOSTIC EVALUTION:  CBC. CMP.  ESR/CRP: ↑.  UA: Hematuria from renal embolic lesions.  Duke's Criteria:  Must meet 2 major or 1 major & 3 minor or 5 minor criteria

Major Criteria:  1) Positive blood cultures:  >12 hours apart 2) Positive echocardiogram: Intracardiac mass or abscess or new partial dehiscence of prosthetic valve or new valvular regurgitation

Minor Criteria:  FROM JANE:  F-fever (>38º C), R-roth’s spots, R-renal problems (e.g. glomerulonephritis), O-osler’s nodes, M-murmur, J-janeway’s lesion, A-anemia, N-nail hemorrhage, E-embolism

Vegetation on the tricuspid valve by echocardiography. Arrow denotes the vegetation.

By Daisuke Koya, Kazuyuki Shibuya, Ryuichi Kikkawa and Masakazu Haneda. - Daisuke Koya, Kazuyuki Shibuya, Ryuichi Kikkawa and Masakazu Haneda. Successful recovery of infective endocarditis-induced rapidly progressive glomerulonephritis by steroid therapy combined with antibiotics: a case report. BMC Nephrology 2004, 5:18. doi:10.1186/1471-2369-5-18, CC BY 2.0,

A mitral valve vegetation caused by bacterial endocarditis.

By, Public Domain,

v  F  _______________, _______________, _______________, _______________, _______________

v  R  _______________, _______________, _______________, _______________, _______________

v  O  _______________, _______________, _______________, _______________, _______________

v  M  _______________, _______________, _______________, _______________, _______________

v  J  _______________, _______________, _______________, _______________, _______________

v  A  _______________, _______________, _______________, _______________, _______________

v  N  _______________, _______________, _______________, _______________, _______________

v  E  _______________, _______________, _______________, _______________, _______________

Ø  TREATMENT:  High dose IV antibiotics for at least 2-6 weeks:  Allow maximize diffusion of antibiotic non-vascularized vegetation and valves.  Early empiric therapy:  Vancomycin/gentamicin for both gram- positive and gram-negative coverage.  Specific drug regimens etiologic microorganism.  SBE: Since the most common responsible organism, S. viridans, which is highly sensitive to Penicillin. High dose IV Crystalline Penicillin 20L every 4hrs for 2 weeks is recommended and still remains the drug of choice. ABC:  Requires treating for S. aureus with oxacillin or vancomycin in addition to gram-negative coverage.  Fungal endocarditis: Anti-fungal treatment (e.g. amphotericin B).  When blood culture reveals the causative organism, a combination of therapy with two bactericidal antibiotics for at least 2 weeks is a must.  Surgical removal of the valve/vegetation with placement of prosthetics:  Necessary for persistent bacteremia despite antibiotics, in patients who develop CHF from valvular destruction, and fungal endocarditis.

Ø  PROGNOSIS:  IE is associated with 25% mortality even with treatment.

o   NON-INFECTIVE ENDOCARDITIS (marantic endocarditis):  Sterile endocarditis occurring in patients with cancers, particularly mucinous adenocarcinoma, and autoimmune diseases.  These lesions are composed of fibrin and platelets but, unlike bacterial etiologies, contain no evidence microorganisms or acute inflammation.   A specific form called Libman-Sacks endocarditis (LSE) occurs more often in patients with SLE and the antiphospholipid syndrome.

·       GASTROINTESTINAL TRACT INFECTION:  Esophagitis, gastritis, gastroenteritis, colitis.

ESOPHAGITIS:  While the most common cause is GERD, other causes of esophagitis include infections, food allergies,  and physical injury (e.g. chemical injury by alkaline or acid solutions, radiation therapy, NG tubes).  Infectious esophagitis is most commonly due to candida, HSV and CMV, and is typically seen in immunocompromised people (e.g. HIV).    

Esophageal candidiasis in a patient after chemotherapy.

CC BY-SA 3.0,

Esophageal candidiasis stained by periodic acid-Schiff procedure

By KGH - Personal collection of histopathologic slides, CC BY-SA 3.0,

Endoscopic image of Herpes esophagitis

By Donald E. Mansell, MD - Own work, CC BY-SA 3.0,

Herpes eosphagitis, with the characteristic nuclear changes (nuclear moulding, chromatin clumping at the nuclear membrane (margination) and multinucleation)

By Nephron - Own work, CC BY-SA 3.0,

GASTRITIS:  Inflammation of the gastric mucosa of the stomach.

Ø  PATHOPHYSIOLOGYDepending on the cause, gastritis may persist acutely or chronically and may coincide with more serious conditions such as atrophy of the stomach.

Acute gastritis: Rapidly developing and often due to stress (e.g. burns, CNS injury, irradiation).

Chronic gastritis: Type A (~10%):  Occurs in the fundus and often due to autoantibodies to parietal cells.  Associated with autoimmune disorders such as pernicious anemia and thyroiditis.  Type B (~80%): Occurs in the antrum and may be due to NSAIDs, cigarette smoking, bacterial infection (most often by H. pylori), fungal infection (most often in people with immunodeficiency), parasitic infection (most often by Anisakis species from poorly cooked seafood), bile reflux, irradiation, and steroid therapy

Ø  PRESENTATIONAsymptomatics or complain of upper abdominal pain, N/V, anorexia, lethargy, gastric hemorrhage, and hypochlorhydria.

Ø  DIAGNOSTIC EVALUATIONCBC: Check for anemia.  Barium meal test and EGD:  Determine gastritis and related conditions such as peptic ulcers and gastric cancer. The most reliable method for determining gastritis is doing a biopsy during gastroscopy and checking for histological characteristics of gastritis and infection.  Urea breath test, stool antigen test, or blood antibody test: Detect H. pyloria.  

A peptic ulcer may accompany gastritis. Endoscopic image.

By User:Samir -, CC BY-SA 3.0,

H. pylori colonized on the surface of regenerative epithelium (Warthin-Starry silver stain)

By Yutaka Tsutsumi, M.D.Professor Department of PathologyFujita Health University School of Medicine - Yutaka Tsutsumi, M.D.Professor Department of Pathology Fujita Health University School of Medicine, Copyrighted free use,

Ø  TREATMENTEtiology dependent and usually consists of removing the irritant or the infection.  Antacids, sucralfate, H2 blocker, &/or PPIs: Help with symptoms.   Triple therapy protocol (2 antibiotics, and 1 PPI):  For H. pylori infection.  Regimens that work well include PPI, Clarithromycin, Amoxicillin or PPI, Clarithromycin, Metronidazole. Quadruple therapy:  Includes PPIs, Bismuth subsalicylates, Metronidazole, and Tetracycline and has a >90% success rate.

GASTROENTERITIS (aka gastric flu, stomach flu although unrelated to influenza):  Inflammation involving both the stomach and the small intestine and resulting in acute diarrhea.
Ø  EPIDEMIOLOGY:  Annual incidence: 1/1,000 people. Worldwide, it claims 2-5 million lives annually and is a leading cause of death among children < 5.  Most cases of gastroenteritis are seen during the winter in temperate climates and during summer in the tropics.

Ø  PATHOPHYSIOLOGY:  The inflammation is caused most often by infection with viruses (norovirus 50%, rotavirus 20%, adenovirus, astrovirus), and less often by bacteria or their toxins (e.g. C. jejuni, S. aureus), parasites, or adverse reaction to something in the diet or medication. Some sources of the infection are improperly prepared food and contaminated water. 

Ø  PRESENTATION:  Fever, diarrhea (watery suggest viral; bloody suggest bacterial or amebic infection), N/V, loss of appetite, abdominal pain/cramps, weakness, and signs of dehydration (e.g. dry mucous membranes, tachycardia, reduced skin turgor, skin color discoloration, sunken fontanelles and sunken eyeballs and darkened eye circles, poor perfusion and ultimately shock).  It usually is of acute onset, normally lasting fewer than 10 days and self-limiting.

Ø  DIAGNOSTIC EVALUATION:  CBC. CMP.  Stool Gram-stain & culture:  Positive for WBCs & bacteria/toxin/virus.

Ø  TREATMENT:  The objective of treatment is to replace lost fluids and electrolytes.  Rehydration: PO or IV as tolerated.  Dietary therapy: Usual foods and drinks should not be withheld, but consumed as the person is able to tolerate them.  However, foods high in simple sugars (sodas, juices, gelatin desserts) should be avoided because the osmotic load might worsen diarrhea.   Zinc supplement: Recommended by WHO for infants and children for up to 2 weeks after onset of gastroenteritis.  Antiemetics:  May help if the vomiting is sever; however, they are not recommended in children.  Antidiarrheal:  Antimotility agent such as loperamide may be use; however, it should be cautious with febrile dysentery or other severe colitis since it prevents the body from flushing toxins from the gut.  Empirical antimicrobial therapy (e.g. fluoroquinolone):  Usually started if symptoms are severe and a bacterial etiology is suspected.  Pseudomembranous colitis is treated by discontinuing the causative agent and starting with metronidazole or vancomycin.  Combining an antimicrobial drug and an antimotility drug, seems to be effective more rapidly.

Ø  COMPLICATION:  Most commonly is malabsorption of certain sugars, and consequent food intolerances. Bacterial gastroenteritis may lead to sepsis, anemia, renal failure, arthritis, and new onset of irritable bowel syndrome.

PSEUDOMEMBRANOUS COLITISAn infection of the colon often, but not always, caused by the bacterium Clostridium difficile.
Ø  EPIDEMIOLOGY:  Risk factors: Diabetes, increasing age and recent major surgery. 

Ø  PATHOPHYSIOLOGY:  Most cases are associated with recent use of antibiotics. Clindamycin is classically associated with this disorder, but any antibiotic can cause the condition. On the other hand, even though they are not particularly likely to cause pseudomembranous colitis, cephalosporins account for a large percentage of cases due to their very frequent use. These broad-spectrum antibiotics alter the normal bacterial flora of the bowel.  As a result, there is over-proliferation of Clostridium difficile, which elaborates a toxin that is responsible for the diarrhea.

Ø  PRESENTATION:  Fever, fatigue, anorexia, offensive-smelling non-bloody diarrhea, and abdominal pain.  In severe cases, there may be toxic megacolon or bowel perforation, resulting in peritoneal signs, sepsis or death.   

Ø  DIAGNOSTIC EVALUATIONHistory of any recent antibiotic usage:  The disease may occur as late as 1-2 months after the use of antibiotics. CBC: WBCs ↑, anemia. Serum albumin: ↓.  Colonoscopy or sigmoidoscopy: Appearance of pseudomembranes (composed of inflammatory debris, white blood cells, etc.) on the surface of the colon or rectum is diagnostic. C. difficile toxin stool test (first-line diagnostic approach):  Usually check for only Toxin A and Toxin B anemia.

Micrograph of a colonic pseudomembrane, as may be seen in Clostridium difficile colitis, a type of infectious colitis.

By Nephron - Own work, CC BY-SA 3.0,

Ø  TREATMENTAntibiotics:  Metronidazole 400 mg PO q8 hours is the usual choice. Vancomycin 125 mg PO q6 hours is an alternative reserved for relapse after a course of metronidazole. Vancomycin use should be cautioned because of the risk of the development of vancomycin-resistant enterococcus (VRE).  Adjunctive therapy:  Cholestyramine (a bile acid resin that can be used to bind C. difficile toxin) and fecal bacteriotherapy (infusion of bacterial flora acquired from the feces of a healthy donor in an attempt to repair the bacterial imbalance responsible for the recurring nature of the infection). Colectomy: If antibiotics do not control the infection.  Prevention: Probiotic drink containing Lactobacillus casei, L bulgaricus, and Streptococcus thermophilus was reported to have some efficacy.


URINARY TRACT INFECTION (UTI):  Bacterial infection of any part of the urinary tract and includes 1) Lower UTI: cystitis (most common) and urethritis 2) Upper UTIs: Pyelonephritis.
Ø  EPIDEMIOLOGY:  UTIs are most common in sexually active women and increase in people with urologic instrumentation (e.g. Foley catheter), diabetes, sickle-cell disease, anatomical malformations (e.g. BPH, VUR), immunocompromise, and pregnancy. F > M because in females, the urethra is much shorter and closer to the anus than in males, and they lack the bacteriostatic properties of prostatic secretions. Among the elderly, UTI frequency is in roughly equal proportions in women and men.

Ø  PATHOPHYSIOLOGY:  While ascending infections are generally the rule for lower UTIs (e.g. cystitis), the same may not necessarily be true for upper UTIs (e.g. pyelonephritis) which may be hematogenous in origin.  Allergies (e.g. allergies to foods can irritate the bladder wall), physical disturbances (e.g. Foley catheter), and urinary obstruction (e.g. BPH, spinal cord injury) disturb theTamm-Horsfall proteins protective lining of the urinary tract and cause urinary stasis, thus facilitating the binding of bacteria and their subsequent invasion into exposed epithelium.  Common UTI-causing bacteria: SEEKS PP --> S-S. saprophyticus (#2 cause accounting for 10% of UTIs), E-E. coli (#1 cause accounting for 80% of UTIs), E-enterobacter, S-serratia, K-klebsiella, P-proteus, P-pseudomonas

v  S  _______________, _______________, _______________, _______________, _______________

v  E  _______________, _______________, _______________, _______________, _______________

v  E  _______________, _______________, _______________, _______________, _______________

v  K  _______________, _______________, _______________, _______________, _______________

v  S  _______________, _______________, _______________, _______________, _______________

v  P  _______________, _______________, _______________, _______________, _______________

v  P  _______________, _______________, _______________, _______________, _______________

Ø  PRESENTATION:  May be asymptomatic.  Cystitis: Mild fever, frequency, urgency, dysuria, nocturia, midline suprapubic pain, cloudy and foul-smelling urine, increased confusion and associated falls (common presentations to ER for elderly patients with UTI).  Urethritis: Dysuria

DIAGNOSTIC EVALUATION: CBC: Leukocytosis. BMP: Check renal function. UA (mid-stream urine sample): Pyuria, hematuria, &/or proteinuria; nitrites, leukocytes or leukocyte esterase-positives. Urine microscopic analysis: Positive if > 5 WBC/hpf. Urine culture (confirm the diagnosis): Positive if > 105 bacteria/mL. Most cases of lower UTIs in females are benign and do not need exhaustive laboratory work-ups. However, UTI in young infants, adults males, and recurrent cases must receive further imaging study, typically a retrograde urethrogram, to ascertain the presence/absence of congenital urinary tract anomalies. Other work-ups: KUB, CT scan, &/or MRI.

Urine may contain pus (a condition known as pyuria) as seen from a person with sepsis due to a urinary tract infection.

By James Heilman, MD - Own work, CC BY-SA 3.0,

Multiple white cells seen in the urine of a person with a urinary tract infection using a microscopy

By Bobjgalindo - Own work, GFDL,

Multiple bacilli (rod-shaped bacteria, here shown as black and bean-shaped) shown between white blood cells in urinary microscopy.

By Steven Fruitsmaak - Own work, CC BY-SA 3.0,

Ø  TREATMENTSupportive: Increased water-intake, drinking unsweetened cranberry juice, taking vitamin C before bed (Vitamin C raises the acidity of the urine, which retards the growth of bacteria), and frequent voiding can shorten the time duration of the infection. Uncomplicated UTIs:  Outpatient oral antibiotics with TMP-SMX, fluoroquinolone (e.g. ciprofloxacin, levofloxacin), cephalosporins, nitrofurantoin X3 days in young adults, and X5 days in the elderly. Severe UTIs: IV antibiotics indicated with an aminoglycosides (e.g. gentamicin) used in combination with a beta-lactam (e.g. ampicillin) or ceftriaxone. These are continued for 48 hours after fever subsides, then the patient may be discharged home on oral antibiotics for a further 5 days.  If the patient makes a poor response to IV antibiotics (marked by persistent fever, worsening renal function), then imaging is indicated (e.g. CT) to rule out abscess formation either within or around the kidney, or the presence of an obstructing lesion such as a stone or tumor. Recurrent UTIs:   Prophylactic use of long courses of low dose antibiotics nightly (e.g. Bactrim, nitrofurantoin, cephalexin) help prevent unexplained cases of recurring cystitis. Other preventive measures: Cleaning the urethral meatus after intercourse, consumption of cranberry juice, and intravaginal application of topical estrogen cream in post-menopausal women can decrease the incidence of UTI.

PYELONEPHRITIS:  An ascending UTI that has reached the pyelum (pelvis) of the kidney. If the infection is severe, the term "urosepsis" is used interchangeably.
Ø  EPIDEMIOLOGY:  Annual incidence: 12-13/10,000 in women and 3-4/10,000 in men.

Ø  PATHOPHYSIOLOGY:  Acute pyelonephritis is a purulent localized inflammation of the renal parenchyma. Chronic infections can result in fibrosis and scarring.  Most cases of "community-acquired" pyelonephritis result from the same pathogens that cause lower UTIs and are predisposed by the same risk factors.

Ø  PRESENTATION:  Fever, rigors, HA, N/V, dysuria, abdominal pain radiating to the back, costovertebral angle tenderness, and in severe cases, delirium.

Ø  DIAGNOSTIC EVALUATIONCBC. CMP. UA:  Positive nitrite and leukocytes, WBC casts, hematuria.  Urine and blood cultures.   KUB X-ray: May assist in identifying radioopaque stones.  Other radiographic evaluation (e.g. US, VCUG, IVP, CT):  Indicated in cases of pregnance, recurrent UTIs, history of nephrolithiasis or GU surgery, and prepubescent age or elderly patients.   This is done to rule out perinephric abscess, renal calculi, and anatomical abnormality. 

Acute pyelonephritis with increased cortical echogenicity and blurred delineation of the upper pole

By Kristoffer Lindskov Hansen, Michael Bachmann Nielsen and Caroline Ewertsen - (2015). "Ultrasonography of the Kidney: A Pictorial Review". Diagnostics 6 (1): 2. DOI:10.3390/diagnostics6010002. ISSN 2075-4418. (CC-BY 4.0), CC BY 4.0,

Ø  TREATMENT:  Antibiotics are the mainstay of treatment.  Generally IV antibiotics are required for the initial stages of treatment. The type of antibiotic depends on local practice, and may include fluoroquinolones (e.g. ciprofloxacin), beta-lactam antibiotics (e.g. amoxicillin or a cephalosporin), TMP-SMX or nitrofurantoin.  Patient should be reevaluated in 72 hours and, if improving, may be discharged home on oral antibiotics for 14-21 days.  If the patient is unwell and septic, IVF may be administered to compensate for the reduced oral intake, insensible losses (due to the raised temperature) and vasodilation and to maximise urine output. 

·       HEMATOLOGIC INFECTION:  Bacteremia/viremia/fungemia (presence of mentioned organism in the bloodstream) and sepsis 

o   SEPSIS:  Systemic Inflammatory Response Syndrome (SIRS)  with a documented infection. 

Ø  EPIDEMIOLOGY:  Incidence:  1%-2% of all hospitalizations; ~ 25% ICU bed utilization.  According to the CDC, sepsis is the leading cause of death in non-coronary ICU patients, and the 10th most common cause of death overall.

Ø  PATHOPHYSIOLOGY:  The host's immune response to the infection (i.e. SIRS) causes most of the symptoms of sepsis.  SIRS causes widespread activation of acute phase proteins (causing fever, leukocytosis), affecting the complement system and the coagulation pathways, which then cause damage to the vasculature.  Consequently, hemodynamic compromise (tachycardia, tachypnea), metabolic derangement, and organ damage follow (potentially ending with multiple organ dysfunction syndrome-MODS). Sepsis is more common and more dangerous in the elderly, immunocompromised, and critically ill.

Ø  PRESENTATION: Symptoms/signs of infection (e.g. fever, chills, hyperventilation, tachycardia, altered mental status) and end organ damage (e.g. elevated LFTs, BUN/Cr).  The presence of petechiae or purpura suggest DIC.  Septic shock: Sepsis + hypotension (SBP < 90), which could arise from gram-positive bacteria (from exotoxins) or gram-negative bacteria (from endotoxins-LPS).

Ø  DIAGNOSTIC CRITERIA:  CBC. CMP. DIC panels: D-dimer, FDPs, fibrinogen. Sepsis is diagnosed if infection is documented (i.e. check CXR, UA, LP, abdominal XR or CT, blood gram-stain/culture) and ≥ 2 of the following SIRS criteria are met:  FOR SIRS THINK VITAL SIGNS (i.e. temperature, pulse, respiratory rate) and WBC:

1.     Temperture: < 96.8 °F or 100.4 °F (hypothermia or fever)

2.     Pulse: > 90 bpm (tachycardia)

3.     Respiratory rate: > 20 breaths per minute or PaCO2 < 32 mm Hg on ABG (tachypnea or hypocapnia due to hyperventilation)

4.     WBC: < 4 x 109 or > 12 x 109 cells/L or > 10% bands (leukopenia, leukocytosis, or bandemia)

Severe sepsis (sepsis plus signs of systemic hypoperfusion manifested as either end organ dysfunction or serum lactate > 4 mmol/dL ):  Examples of end-organ dysfunction include 1) Lungs: ARDS (PaO2/FiO2 < 200) 2) Brain (encephalopathy-agitation, confusion, coma) 3) Liver: Progressive coagulopathy (inability to synthesize clotting factors),  bilirubinemia ≥ 4 mg/dL(disruption of bilirubin metabolism) 4) Kidney: Oliguria < 0.5 ml/kg/hr /anuria, electrolyte abnormalities 5) Heart: Systolic and diastolic heart failure (cytokines depression of myocyte function).

Septic shock: Sepsis with refractory arterial hypotension (i.e. after aggressive fluid resuscitation of up to of 6 liters or 40 ml/kg of crystalloid).

Sepsis Steps. Training tool for teaching the progression of sepsis stages

By Hadroncastle - Own work, CC BY-SA 4.0,

Ø  TREATMENT:  Consider ICU admission.  Supportive therapy for organ dysfunction:  IVF, blood transfusion, vasopressors (for circulatory failure), hemodialysis (if kidney failure), mechanical ventilation (if ARDS), transfusion of blood products, and adequate nutrition.  Treat underlying infection: Antibiotics, remove infected lines or catheter, surgical drainage of infection fluid collections.  Drotrecogin alfa (activated protein C):  Considered in severe sepsis, septic shock, and DIC.  Low dose hydrocortisone:  For septic shock patients with relative adrenal insufficiency as defined by ACTH stimulation testing.

·       MUSCULOSKELETAL INFECTION:  Septic arthritis and Osteomyelitis

o   SEPTIC ARTHRITIS:  Arise from an invasion of a joint by an infectious agent (usually bacterial, but viral, mycobacterial, and fungal arthritis also).

Ø  PATHOPHYSIOLOGY:  Micro-organisms reach the synovial membrane of a joint by hematologic dissemination of from abscesses or wound infections (most common), extension from adjacent tissue (e.g. osteomyelitis focus), or via a penetrating trauma. 

Ø  PRESENTATION: From mild monoarthritis to fever + monoarthritis + REST --> R-ROM ↓, E-erythema of overlying tissue, S-swelling, T-tenderness

Ø  DIAGNOSTIC EVALUATION:  CBC: Leukocytosis. BMP.  ESR/CRP: ↑.  Arthrocentesis: Turbid, non-viscous fluid. Joint fluild Gram stain and culture.   Joint imaginging (XR, CT, MRI): Joint effusion, soft tissue swelling, periarticular osteoporosis, loss of joint space, marginal and central erosions and bone ankylosis.  Signal abnormalities in the bone marrow can indicate a concomitant osteomyelitis.

Ø  TREATMENT:  IV antibiotics, analgesia and aspiration of infected joint.

Septic arthritis as seen during arthroscopy

By Tetsuo Hagino, Masanori Wako, Satoshi Ochiai -, CC BY 2.5,

o   OSTEOMYELITIS:  Infection of bone or bone marrow, usually caused by pyogenic bacteria or mycobacteria..

Ø  ETIOLOGY: Staphylococcus aureus is the organism most commonly isolated from all forms of osteomyelitis.  Systemic mycotic infections (2 most common are Blastomyces dermatitidis and Coccidioides immitis) may also cause osteomyelitis.

Ø  PATHOPHYSIOLOGY:  Hematogenously seeded (20% of cases) osteomyelitis is seen most frequently in children, and nearly 90% of cases are caused by Staphylococcus aureus. Direct spread (80% of cases) caused by injury exposing the bone to local infection is the most common form of the disease in adults, and  Staphylococcus aureus is again the most common organism seen, but anaerobes and Gram negative organisms, including Pseudomonas aeruginosa, E. coli, and Serratia marcescens, are also common, and mixed infections are the rule rather than the exception.  Acute osteomyelitis almost invariably occurs in children. When adults are affected, it may be because of compromised host resistance due to debilitation, IVDU, infectious root-canalled teeth, other disease or drugs (e.g. immunosuppressive therapy) 

Ø  PRESENTATION:   H & P (fever and REST --> R-ROM ↓, E-erythema of overlying tissue, S-swelling, T-tenderness).  In children, the long bones are usually affected. In adults, the vertebrae and the pelvis are most commonly affected.

Ø  DIAGNOSTIC EVALUATION:  CBC (↑ WBC), ESR/CRP ↑, blood cultures.  Obtain intitial X-ray (may show periosteal elevation 10-14 days later à if this is not diagnostic, the next step is to obtain a bone scan except in the evaluation of the spine or foot then an MRI (show ↑ signal in bone marrow consistent with bone marrow edema and signs of soft tissue infection) is preferred.  Bone aspiration with Gram stain and culture (defninitive diagnosis).   

Osteomyelitis of the 1st toe

By James Heilman, MD - Own work, CC BY-SA 4.0,

Osteomyelitis in both feet as seen on bone scan

By James Heilman, MD - Own work, CC BY-SA 4.0,

Ø  TREATMENT:  Osteomyelitis often requires prolonged IV antibiotic therapy (4-6 weeks). A PICC line or central venous catheter is often placed for this purpose. Osteomyelitis also may require surgical debridement. Severe cases may require amputation. Initial first line antibiotic choice is determined by the patient's history and regional differences in common infective organisms.  Options for empiric antibiotic: S. aureus (Nafcillin, oxacillin, cephalosporin, vancomycin); Gram negative coverage (3rd generation cephalosporin and gentamicin or ciprofloxacin).

Ø  COMPLICATION: Chronic osteomyelitis, sepsis, soft tissue infection, septic arthritis, squamous cell carcinoma of the skin (Marjolin’s ulcer). 

·       NEUROLOGIC INFECTION:  Encephalitis and Meningitis.

o   ENCEPHALITIS:  Acute inflammation of the brain.

Ø  PATHOPHYSIOLOGY:  Most commonly caused by a viral infection (most often by HSV and the arboviruses, which include the bunyaviridae, togaviridae, and flaviridae).  It can be caused by HIV infection, certain parasitic infection (e.g. toxoplasmosis, malaria, or amoebic meningoencephalitis), or it may be a complication of other infectious disease (e.g. syphilis). Brain damage are caused by the brain's defense mechanisms activating to get rid of the infection and the inflamed brain pushes against the skull. 

Ø  PRESENTATION:  Fever, HA, lethargy, hallucination, confusion, stupor, and coma.  Focal neurologic signs (e.g. weakness, hyperactive DTRs), seizures, endocrinologic abnormalities (e.g. DI or SIADH), and signs of increased intracranial pressure (e.g. papilledema, CN III palsy) may also be seen.  Other symptoms/signs are possible and depend on the specific part of the brain involved. If meningeal signs (i.e. nuchal rigidity) is present, concurrent meningitis is possible.

Ø  DIAGNOSTIC EVALUTION:  CBC. CMP. Head CT:  To pave the way for lumpar puncture by excluding the presence of prominent brain swelling and an increased intracranial pressure (ICP), which could precipitate a fatal brain herniation, and may also cerebral abscess (more common with meningitis) or cerebral hemorrhage (often associated with HSV-1 encephalitis).  MRI: Temporal lobe enhancement is typically seen in HSV encephalitis. LP (only perform if prominent brain swelling is excluded):   SEE CSF PROFILES UNDER MENINGITIS.  CSF Gram stain and culture; acid-fast stain (for mycobacteria), India ink (for Cryptococcus), wet prep (for free-living amebae), &/or Giemsa stain (trypanosomes):  Perform as needed.  Molecular techniques (e.g. PCR): Confirm the diagnosis by detection of viral RNA or DNA of the virus responsible (remember HSV-1 is the most common cause of infectious encephalitis).  EEG: May show sharp waves in the temporal lobes in HSV encephalitis.

MRI scan image shows high signal in the temporal lobes and right inferior frontal gyrus in someone with HSV encephalitis.

By dr Laughlin Dawes -, CC BY 3.0,

Spinal tap on a newborn

By Bobjgalindo - Own work, GFDL,

Ø  TREATMENT:  Treatment is usually symptomatic as specific antiviral agents are available only for a few viral agents.  HSV encephalitis: Acyclovir should be initiated immediately and continue 14-21 days.  Ganciclovir and foscanet are also considered in cases where acyclovir resistace develop.

o   MENINGITIS:  Inflammation of the meninges. 

Ø  EPIDEMIOLOGY:  Risk factors:  Recent ear infection, sinusitis, neurosurgical procedures, immunodeficiencies, and sick contacts.  The "Meningitis Belt" is an area in sub-Saharan Africa which stretches from Senegal in the west to Ethiopia in the east in which large epidemics of meningococcal meningitis occur.

Ø  PATHOPHYSIOLOGY:  Meningitis can be roughly classified into 1) acute aseptic meningitis and 2) acute bacterial meningitis. 

1.     Acute aseptic meningitis (cause not apparent after initial exam & routine CSF staining): Represents the majority of the cases and are usually self-limited lasting a few days.  It can be caused by virus (# 1 cause with enteroviruses accounting for ~80% cases; other viral etiologies include HSV, mumps, measles, VZV, EBV, CMV, HIV, and LCM), tuberculosis (common in countries where tuberculosis is endemic), fungi (most often candida and cryptococcus), rickettia (i.e. RMSF), spirochetes (e.g. syphilis, leptospirosis, Lyme disease), malignancy, medication (e.g. sulfamethoxazole, NSAIDs, INH, intrathecal introduction of contrast media), and vaccine (e.g. mumps/measles).

2.     Acute bacterial meningitis

PRESENTATION: Classic triad (present in < 50% of cases) of high fever, nuchal rigidity, and altered mental status. Though not a part of the triad, severe HA is the most common presenting symptom. Other signs/symptoms: Photophobia, phonophobia, irritability, delirium, and seizures. Physical exam: Kernig's sign (patient lying supine, and both hips and knees flexed → pain is elicited when the knees are passively extended) and Brudzinski's sign (forward flexion of the neck causes involuntary knee and hip flexion) may be positive, rapidly-spreading petechiae/purpura on the trunk, lower extremities (including the palms/soles), mucous membranes, conjunctiva (may be seen in meningococcal meningitis), skin signs of hand, foot and mouth disease (coxsackie virus), and genital lesions (HSV).

Meninges of the central nervous system: dura mater, arachnoid mater, and pia mater.

By SVG by Mysid, original by SEER Development Team [1] - Vectorized in Inkscape by Mysid, based on work by SEER Development Team, Public Domain,

Neck stiffness, Texas meningitis epidemic of 1911–12

By L.A. Marty, M.D, Kansas City - Sophian, Abraham: Epidemic cerebrospinal meningitis (1913), St. Louis, C.V Mosby (Scan from, Public Domain,

Charlotte Cleverley-Bisman developed severe meningococcal meningitis as a young child; in her case, the petechial rash progressed to gangrene and required amputation of all limbs. She survived the disease and became a poster child for a meningitis vaccination campaign in New Zealand.

By, CC BY-SA 3.0,

DIAGNOSTIC EVALUATION: CBC. CMP. CXR. LP (the most important test): Must exclude a cerebral mass lesion, papilledema, focal neurologic deficits or recent head injury prior to performing an LP. If needed, perform head CT/MRI first to rule these out. During the LP procedure, the opening pressure is measured, and CSF is examined for WBCs, RBCs, protein content and glucose level, and Gram-stain and culture are done. Other tests performed on the CSF: Latex agglutination test (may be positive in both Gram-positive + Gram-negative meningitis), limulus lysates (may be positive in Gram-negative meningitis), PCR for bacterial or viral DNA, acid-fast stain, cryptococcal antigen, arbovirus antibody, fungal culture.  CT/MRI:  Rule out other diagnoses.  

Ø  TREATMENTAcute bacterial meningitis: Is a medical emergency and when suspected, high dose IV empiric antimicrobial therapy should be initiated immediately even before the results of LP and CSF analysis are known (see table in the pathophysilogy section).  Antibiotics started within 4 hours of an LP procedure will not significantly affect lab results. Adjuvant treatment with dexamethasone is recommended as it reduces mortality and neurological sequelae specifically when the causative agent is Pneumococcus.   Vaccination: Vaccines against H. influenza, N. meningitidis, and S. pneumonia are available.  Prophylaxis: Contacts of patinets with meningococcal meningitis should receive either rifampicin, ciprofloxacin or ceftriaxone. Viral meningitis:  Acyclovir is used for HSV meningitis, otherwise supportive care is given in most cases.   Fungal meningitis:  Immunosuppression must be suspected (e.g. AIDS) and patient should be placed on long courses of highly dosed antifungals. 

Ø  COMPLICATIONChildren:  Hydrocephalus, cerebral vein thrombosis, intracerebral hemorrhage, sensorineural hearing loss, epilepsy, and intellectual impairments.  Adults:  Brain infarction, brain swelling, hydrocephalus, intracerebral bleeding; systemic complications are dominated by septic shock, ARDS and DIC. 

Conducting passages of the human respiratory system


·       RESPIRATORY TRACT INFECTION:  From upper to lower respiratory tract --> Otitis externa, otitis media, pharyngitis, laryngotracheobronchitis (i.e. croup), bronchitis, bronchiolitis, and pneumonia.

OTITIS EXTERNA (aka swimmer's ear):   Inflammation of the ear canal.  
Ø  PATHOPHYSIOLOGY:  Chronic otitis externa is a low-grade disease, usually non-microbial and purely on the basis of chronic dermatitis, eczema or irritation from "cleaning" the canal (e.g. with cotton swabs). In contrast, acute otitis externa (AOE) is predominantly a microbial infection and most commonly due to P. aeruginosa (from swimming in poorly chlorinated/polluted water) and Enterobacteriaceae (especially in humid environment).  Swelling of the canal skin and purulent-blockage dampen hearing to varying degrees.   Untreated, the infection can spread to the soft tissues of the face (making chewing painful) or erode into the bone of the skull (i.e. malignant or necrotizing external otitis).  In these cases, skull base osteomyelitis can result, and the facial nerve and the vagus nerve may be affected, resulting in facial paralysis and hoarseness, respectively.

Ø  PRESENTATION:  Pain worsened when the outer ear is touched or pulled gently (unlike otitis media), purulent discharge, pruritis, conductive hearing loss (reversible if treated early), erythematous/edematous ear canal, and infra-auricular adenopathy.

A mild case of otitis externa.

By Klaus D. Peter, Gummersbach, Germany - Own work, CC BY 3.0 de,

A moderate case of otitis externa. There is narrowing of the ear channel, with a small amount of exudate and swelling of the outer ear.

A severe case of acute otitis externa. Note the narrowing of the ear channel, the large amounts of exudate, and swelling of the outer ear.

By James Heilman, MD - Own work, CC BY 3.0,

Ø  DIAGNOSTIC EVALUATION:  Otoscopic examination: Usually not done secondary to pain.  Drainage Gram-stain and culture:  Helpful to rule out fungal etiologies.  CT scan:  If patient appear toxic or failed therapy.

Ø  TREATMENT:  Ear drops with polymyxin, neomycin, and hydrocortisone: Mainstays of treatment.  Removal of debris (wax, shed skin, and pus):  Shortens recovery time. Antifungal solutions are used in the case of fungal infections. Other: Heat application, oral narcotic pain killer (often prescribed as the pain of AOE is often severe enough to interfere with sleep).  Diabetics are prone to malignant otitis externa and thus require IV antibiotics. 

OTITIS MEDIA (OM):  Inflammation of the middle ear. 
Ø  EPIDEMIOLOGY:  Most cases occur in children (peaked between 3-36 months old) owing to a shorter, more Eustachian tube. Risk factors: Bottle feeding when supine, parental smoking, CF, immunodeficienceis, day-care, cleft palate, prior OM.  Breastfeeding is associated with a reduction in the incidence of OM.

Ø  PATHOPHYSIOLOGY:  OM almost always accompanied by a viral URI, which causes swelling of the Eustachian, compromising pressure equalization and clearance of fluid from the middle ear.  This sets the stage for a bacterial infection, most commonly by S. pneumonia (33%), non-typable H. influenza (20%), or Moraxella catarrhalis (10%).  Less commonly, OM is due S. aures, P. aeruginosa, M. tuberculosis. 

Ø  PRESENTATION:  URI symptoms (stuffy nose), follow after a few days by fever (up to 102 °F), severe ear pain (ear tugging), hearing loss, irritability, feeding difficulties, N/V.  Sometimes the ear drum ruptures, which results in otorrhea and a dramatic relief of pressure and pain.  Rarely, further spread can lead to tympanosclerosis, mastoiditis, cholestatoma, meningitis, &/or brain abscess.

Otitis media.

By BruceBlaus - Own work, CC BY-SA 4.0,

Ø  DIAGNOSTIC EVALUATION:   Clinical diagnosis.  Tympanometry: Quantify degree of hearing loss in severe case.  Otoscopy:  Evaluate the tympanic membrane COMPT --> C-color (eyrthematous; not specific as condition like crying can cause vasodilation of the tympanic membrane mimicking the redness associated with AOM), O-other (e.g. bubbles, perforation, scar), M-mobility (↓ mobility with insufflation), P-position (bulging tympanic membrane), T-translucency (opague tympanic membrane with loss of the light reflex and bony landmarks).

v  C  _______________, _______________, _______________, _______________, _______________

v  O  _______________, _______________, _______________, _______________, _______________

v  M  _______________, _______________, _______________, _______________, _______________

v  P  _______________, _______________, _______________, _______________, _______________

v  T  _______________, _______________, _______________, _______________, _______________

Ø  TYPES:  Acute otitis media (AOM): The classic case as describe above.  Otitis media with effusion (OME): Collection of fluid in the middle ear, as a result of altered Eustachian tube function, without associated systemic symptoms (e.g. fever). Overtime, the fluid can thicken to a glue-like consistency, which increases the likelihood of its causing conductive hearing loss. Chronic suppurative otitis media (CSOM): Active bacterial infection within the middle ear space for several weeks or more often results in hearing loss. 

A bulging tympanic membrane which is typical in a case of acute otitis media

Acute otitis media

Chronic otitis media (otitis media chronica mesotympanalis)

By Welleschik - Own work, CC BY-SA 3.0,

Perforation of the right tympanic membrane resulting from a previous severe acute otitis media

Ø  TREATMENTAOM:  Amoxicillin PO x 7-10 days (1st line) or amoxiclin-clavulanate (2nd line for treatment failure).  Ruptured tympanic membrane usually self-heal.  CSOM or recurrent AOM (> 4 cases/year or ≥ 3 cases/6 months): Tympanostomy tube to allow air to pass through into the middle ear, and thus release any pressure buildup and help clear excess fluid within.

SINUSITIS:  Inflammation of the paranasal sinuses; most commonly the maxillary sinuses. 
Ø  PATHOPHYSIOLOGY:  Risk factors:  Allergies, structural problems (e.g deviated septum, nasal polyps), environmental (e.g. smoking, pollution), asthma, cystic fibrosis, viral infection, and decongestant overuse (due to rebound vasoconstriction).   Impaired secretion removal and damaged surface tissues enable microorganismal colonization. 

1.     Acute sinusitis (symptoms < 1 months):  Most often caused by URI viruses. Bacterial etiologies (most commonly caused by the same bacterial implicated in AOM S. pneumonia, H. influenza, and M. catarrhalis) should be considered if symptoms are severe and last > 1 week.  Others infectious etiologies: S. aureus, anaerobic bacteria, fungal invasion (considered in immunosuppressed patients such as AIDS). 

2.     Chronic sinusitis (symptoms > 3 months):  Often from obstruction of sinus drainage (e.g. nasal polyps) or bacterial formation of a protection biofilms.  These infections are more likely caused by S. aureus, anaerobes (e.g. Bacterioides) or fungal infection. In type I diabetes, ketoacidosis causes sinusitis by Mucormycosis.

Ø  PRESENTATION: Fever, cough, HA, malaise, blurred vision, sinus tenderness, nasal congestion/discharge, and an opaque sinus on transillumination test (low sensitivity).  Rarely, chronic sinusitis can lead to anosmia.  Characteristics that raise suspicion for a bacterial sinusitis include DUMB --> D-discharge purulent, U-unilateral symptoms, M-maxillary teeth pain, B-bending forward --> ↑ sinus pressure/tenderness.

Illustration depicting sinusitis

By BruceBlaus. When using this image in external sources it can be cited staff (2014). "Medical gallery of Blausen Medical 2014". WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. - Own work, CC BY 3.0,

v  D  _______________, _______________, _______________, _______________, _______________

v  U  _______________, _______________, _______________, _______________, _______________

v  M  _______________, _______________, _______________, _______________, _______________

v  B  _______________, _______________, _______________, ______________­­­_, _______________­­­­

Ø  DIAGNOSTIC EVALUATION:  Acute sinusitis is usually diagnosed clinically.  Testing is usually reserve for chronic/recurrent cases and include: 1) Sinus XR: May show air-fluid level or opacification; but is not recommended because of low sensitivity 2) Sinus CT:  Modality of choice 3) Nasal endoscopy: Allow direct visualization of the sinuses and obtainment of tissue for pathology, Gram-stain and culture.

Left-sided maxillary sinusitis marked by an arrow. Note the lack of the air transparency indicating fluid in contrast to the other side.

A computed tomograph showing infection of the ethmoid sinus

By James Heilman, MD - Own work, CC BY-SA 3.0,

MRI image showing sinusitis. Edema and mucosal thickening appears in both maxillary sinuses.

Frontal sinusitises.

Ø  TREATMENT:  Supportive therapy (e.g. systemic decongestants, saline nasal irrigations, analgesics, and a short course of topical decongestants): Considered if symptoms is mild-moderate and lasting < 1 week as most are virally-induced.  Acute bacterial sinusitis:  1st line antibiotic therapy includes amoxillin or TMP-SMX x 10 days.  2nd line: Amoxicillin-clavulanate, 2nd generation cephalosporins, and macrolides. Chronic sinusitis: Antimicrobial therapy should include anaerobic coverage and, if needed, and antifungal.  If medical therapy fails, consider endoscopic nasal surgery to remove drainage and/or fix the obstructions that predispose to sinusitis.

o   PHARYNGITIS:  Inflammation of the pharynx. 

Ø  PATHOPHYSIOLOGY:  ~ 90% of cases are caused by upper respiratory viruses (e.g. CRAP --> C-coronavirus, R-RSV, R-rhinovirus, A-adenovirus, P-parainfluenza virus), with the remainder caused by bacteria (e.g. S. pyogenes, N. gonorrhea, Corynebacterium diphtheria), and rarely, fungus (e.g. candidal oral thrush). Microorganisms usually reach the throat through inhalation of vapor or touching the mouth with contaminated hands.  The distinction of viral pharyngitis from bacterial pharyngitis is difficult clinically, and the latter carries much more dire consequences when untreated. 

Ø  PRESENTATION:  Fever, HA, sore throat, cervical lymphadenopathy, erythematous pharynx with purulent exudate, myalgia, and arthralgia.  Upper respiratory symptoms (e.g. runny nose, congestion), cough, and abdominal upset/pain is more common with viral pharyngitis.  Immune-system meditated complications may occur, especially with Group A Strep-GAS (S. pyogenes) pharyngitis, and include:

1.     Scarlet fever:  Occur in ~ 3% of streptococcal pharyngitis patients.  It is caused by GAS erythrogenic exotoxin, and characterized the symptoms/signs of streptococcal pharyngitis and a fine, erythematous, rough-textured (sandpaper) rash over the upper body or possibly the entire body.

2.     Rheumatic fever (RF):  Epidemiology:  It commonly appears in children ages 6-15 and occurs ~ 20 days after strep throat or scarlet fever.  Pathophysiology:  A Type II hypersensitivity reaction in which B cells antibodies against the M protein component of the cell wall of GAS also react against the myocardium, joints, and the brain (i.e. molecular mimicry). PresentationJONES (Jones criteria is used to make a clinical diagnosis of RF; must meet 2 major criteria, or 1 major and 2 minor criteria) --> J-joints (migratory polyarthritis usually starting in the legs and migrating upwards), O-o (carditis-imagine a round heart-endocarditis usually affects the mitral valve and results in leaflet thickening, commissural fusion and shortening and thickening of the tendinous cords, which results in mitral stenosis; myocarditis which can results in CHF; fibrinous pericarditis [bread-and-butter] which can cause a friction rub), N-nodules-subcutaneous (firm, painless nodules located on the back of the wrist, the outside elbow, and the front of the knees, and represent a collection of Aschoff bodies [eosinophilic collagen surrounded by lymphocytes and giant macrophages] and collagen fibers, E-erythema marginatum (a rash that begins on the trunk or arms as macules and spreads outward to form a snakelike ring with central clearing), S-sydenham's chorea (characteristic rapid movements without purpose of the face and arms).   Minor criteria includes: Fever, arthralgia, ↑ ESR/CRP, prolonged PR interval on EKG, and evidence of GAS infection (e.g. positive culture or elevated Antistreptolysin O titre).

v  J  _______________, _______________, _______________, _______________, _______________

v  O  _______________, _______________, _______________, _______________, _______________

v  N  _______________, _______________, _______________, _______________, _______________

v  E  _______________, _______________, _______________, _______________, _______________

v  S  _______________, _______________, _______________, _______________, _______________

3.     Post-streptococcal glomerulonephritis (PSGN):  Immune-mediated inflammation of the renal gromeruli. SEE PSGN IN NEPHROLOGY SECTION. 

A normal throat

By Lusb - Own work, CC BY 3.0,

Viral pharyngitis resulting in visible redness.

A case of strep throat

Throat swab.

Ø  DIAGNOSTIC EVALUATIONRapid Antigen Detection Test (RADT):  Identify GAS; however it is not sensitive and a negative test does not rule out streptococcal pharyngitis.  Throat culture:  May be undertaken if RADT is negative to help clarify diagnosis. EBV testing (monospot test + peripheral smear for atypical lymphocytosis) and HIV testing (ELISA):  Should be considered in selected case as EBV and HIV can lead to similar presentation.  When scarlet fever or rheumatic fever is suspected, further work up should be undertaken and include: CBC (leukocytosis with neutrophilia and eosinophilia), ESR/CRP (↑), antistreptolysin O titer (ASO ↑), CXR, EKG, and echocardiography.

Ø  TREATMENT:  Symptomatic therapy: Analgesics, warm saline gargle or Chloroseptic throat spray, and throat lozenges.  Since most cases of pharyngitis are self-limited viral infection this helps in most cases.  Antimicrobial therapy: Penicillin 500 mg PO bid x 10 days is adequate for most cases of streptococcal pharyngitis.  Historically the most important complication of strep throat was rheumatic fever, which could results in rheumatic heart disease (i.e. mitral valve stenosis).  Timely administration of antibiotics reduces the incidence rheumatic fever, and thus rheumatic heart disease.  However, it is still uncertain if antibiotics lessen the development of PSGN. 

LARYNGOTRACHEOBRONCHITIS (aka Croup): Acute inflammatory disease of the larynx, primarily within the subglottic space.  
Ø  EPIDEMIOLOGY:  Incidence: Croup affects 5% of children by 2 years of age.  The peak incidence is between 7 months -3 years.

Ø  PATHOPHYSIOLOGY:  Most often caused by parainfluenza virus (PIV) types 1.  Other etiologies include PIV-2 and 3, influenza, RSV, and adenovirus, and possibly M. pneumonia. It is most common in the fall and winter.  The respiratory distress is caused primarily by the inflammatory response to the infection, which causes laryngeal spasm as well as swelling and narrowing of the subglottic space (young children’s airways are smaller making them more susceptible).

Ø  PRESENTATION:  Prodromal URI symptoms (congestion, sneezing, sore throate) follow by fever, harsh barking (seal-like) cough, inspiratory stridor (worsened by agitation or crying), and hoarseness. More severe cases will have respiratory distress, and can be fatal if not treated.  Stridor will be provoked or worsened by agitation or crying. If stridor is also heard when the child is calm, critical narrowing of the airway may be imminent.  It is important to rule out of causes of SOB and stridor, such as foreign body aspiration, angioneurotic edema, tracheitis, and epiglottitis. 

Ø  DIAGNOSTIC EVALUATION:  Clinical diagnosis.  AP X-ray of the C-spine:  Steeple sign (i.e. subglottic/tracheal narrowing) suggests the diagnosis of croup.

Ø  TREATMENT:  Depends on the severity of symptoms.  Mild cases: Outpatient therapy with fluids and cool mist (e.g. exposing the child to steam from a hot bath or a humidifier). Moderate cases (e.g. stridor only on agitation):  A dose of inhaled, oral, or injected dexamethasone may be given. Severe cases:  Hospitalize, give nebulized racemic epinephrine and oxygen; may require intubation.

AP x-ray of the neck in a child with croup demonstrating the steeple sign; narrowing of the the trachea.

By Frank Gaillard - Own work, CC BY-SA 3.0,

EPIGLOTTITIS:  Inflammation of the epiglottis (i.e. the supraglottic structure).
Ø  EPIDEMIOLOGY:  Uncommon before age 2 y/o and after 7 y/o.  Peak incidence in between 3-7 y/o.

Ø  PATHOPHYSIOLOGY:  Prior the immunization, it is most often caused by H. influenzae type B.  Currently, the common causes include S. pneumoniae, S. pyogenes, and non-typable H. flu.

Ø  PRESENTATION: Sudden high fever, dysphagia, muffled voice, drooling, stridor, intercostal retractions, and cyanosis.  The child often appears acutely ill, anxious, and has very quiet shallow breathing, insisting on sitting up with head held forward (“sniffing dog” position).   Due to its place in the airway, swelling of the epiglottis constitutes a medical emergency as it can either obstruct or completely close off the windpipe.

Ø  DIAGNOSTIC EVALUATION:  Clinical diagnosis.  Laryngoscopy:  Can confirm the diagnosis by direct visualization of cherry-red, swollen epiglottis and arytenoids; however, when epiglottitis is suspected, do not examine the throat unless rapid instubation is available on the scenes, as it may provoke laryngospasm and airway obstruction.  Later C-spine X-ray:  Thumbprint sign (i.e. enlarged epiglottis).

Acute epiglottitis; Lateral view in X-ray imaging. The lateral soft-tissue radiograph reveals the "thumb sign" that indicates a swollen epiglottis, suggestive of epiglottitis. The diagnosis was confirmed on subsequent imaging and laryngoscopy. The patient recovered following treatment with predonine and ceftriaxone.

CT imaging showing the "halloween sign"

By Chaustanley - Own work, CC BY-SA 3.0,

Swollen epiglottis in laryngoscopy"

Ø  TREATMENT:  Urgent endotracheal intubation or tracehostomy:  Protect the airway.  Antibiotics: Ceftriaxone or cefuroxime IV ± penicillin or ampicillin for streptococcal coverage.

TRACHEITIS:  A bacterial infection of the trachea capable of producing airway obstruction.
Ø  PATHOPHYSIOLOGY:  Most commonly caused by S. aureus or S. pyogenes and often follows a recent viral URI.   It is the most serious in young children, possibly because of the relatively small size of the trachea that gets easily blocked by swelling. The most frequent sign is the rapid development of stridor. It is occasionally confused with croup.

Ø  PRESENTATION:  Follow an URI there is rapid development of inspiratory stridor, deep or barking croup cough, and sore throat.  Other possible symptoms: Fever, earache, chest pain, and intercostal retractions. In contrast to epiglottitis, usually there is no drooling or specific position of comfort (i.e. patient may lie supine.)

Ø  DIAGNOSTIC EVALUATION:  Culture and Gram stain of tracheal secretions and blood.  C-spine X-ray:  Subglottic narrowing on AP views and irregular tracheal margin on lateral view.  Laryngotracheobronchoscopy:  Definitive diagnosis by direct visualization and culture of purulent tracheal secretions; may be therapeutic by performing tracheal toilet and stripping purulent membranes

Ø  TREATMENT:  Secure the airway:  Oxygen support and, if required intubation.  IV Antibiotics: A 3rd generation cephalosporin (e.g. ceftriaxone) ± a penicillinase-resistant penicillin (e.g. oxacillin) or clindamycin (if allergic to penicillin). Vancomycin ± clindamycin should be started if MRSA is suspected or patient appears toxic or have multiorgan involvement.

BRONCHITIS (ACUTE):  Inflammation of the large bronchi.
Ø  PATHOPHYSIOLOGY:  ~95% caused by a viral pathogen (e.g. RSV, rhinovirus, influenza).  Bacterial pathogen should be suspected when symptoms are severe or prolonged ≥ 2 weeks (consider Bordetella pertussis or C. pneumonia) or when the patient has a predisposing respiratory condition.  For example:  1) COPD patients (i.e. acute exacerbation of chronic bronchitis): Suspect S. pneumonia, H. flu, and M. catarrhalis (same microorganisms as AOM and sinusitis); 2) Bronchiectatic patient: Suspect P. aeruginosa and S. aureus.  Untreated, it can lead to pneumonia.

Ø  PRESENTATION:  Fever, productive cough (e.g. yellow-green sputum), dyspnea, coarse breath sounds, wheezing, chest pains, fever, and fatigue.  The coughs due to bronchitis can continue for up to 3 weeks or more even after all other symptoms have subsided.

Ø  DIAGNOSTIC EVALUATION:  Clinical diagnosis.  Further studies are undertaken when symptoms are severe or patient has underlying chronic pulmonary disease.  CBC.  CRP. Pulse ox.  CXR:  Hyperinflation; rule out consolidations.  Sputum Gram-stain and culture: Positive for PMNs and microorganism. 

Ø  TREATMENT:  Symptomatic therapy (for most cases):  Antitussives (e.g. dextromethorphan), fluid, rest, and smoking cessation.  Antibiotics:  Macrolides (e.g. erythromycin) for documented B. pertussis cases.  COPD patients: Consider a macrolides (e.g. arythromycin), b-lactam (e.g. amoxicillin-clavulanate) or 3rd generation cephalosporin.  For hosts with sever underlying disease and compromised respiratory status (e.g. bronchiectasis), broader treatment with a flouroquinolone + aminoglycoside is indicated.    

Figure A shows the location of the lungs and bronchial tubes. Figure B is an enlarged view of a normal bronchial tube. Figure C is an enlarged view of a bronchial tube with bronchitis.

By National Heart Lung and Blood Institute - National Heart Lung and Blood Institute, Public Domain,

Mild peri hilar cuffing as seen in viral bronchitis

BRONCHIOLITIS:  Bronchiolitis is inflammation of the bronchioles, the smallest air passages of the lungs.
Ø  EPIDEMIOLOGY: Primarily affects children < 2 y/o.

Ø  PATHOPHYSIOLOGY:  Most commonly caused by RSV.  Other viral causes include: Influenza, parainfluenza, coronavirus, adenovirus, and rhinovirus.  In older children and adults, RSV causes no more than the common cold.  In infants, the viral-infected bronchioles become hyperresponsive and fill will cellular debris, which may lead to respiratory failure in extreme cases.  Recurrent bronchiolitis may predispose a child to asthma by inducing long term low-grade inflammation.

Ø  PRESENTATION:  Fever, cough, rhinorrhea, SOB, apnea, tachypnea, wheezing, crackles, and hyperresonance to percussion.  In severe cases, there can be nasal flaring, intercostals retraction, and respiratory failure.    

Ø  DIAGNOSTIC EVALUATION:  Clinical diagnosis.  CXR: Hyperinflation of the lungs, atelectasis, and interstitial infiltrates.  ELISA of nasopharyngeal aspirate for RSV.    

An X-ray of a child with RSV showing the typical bilateral perihilar fullness of bronchiolitis.

By James Heilman, MD - Own work, CC BY-SA 3.0,

Ø  TREATMENT:  Therapy is principally supportive (no effective specific treatment).  Mild disease:  Fluids, nebulize, O2, nasopharynx suction (to clear the airway).  Severe disease: Hospitalize with contact isolation and treat with IVF, O2 (may require mechanical ventilation), trial dose of bronchodilator drugs (e.g. salbutamol/albuterol or ipratropium) to clinically distinguish bronchiolitis from a viral-induced asthma, . racemic epinephrine (to distinguish bronchiolitis from croup), &/or ribavirin aerosol (may shorten symptom course and reduce viral shedding).  RSV prophylaxis: Passive immunization with Palivizumab (a monoclonal antibody against RSV), is recommended in winter for high risk patients (e.g. prematurity, age < 3 month, and underlying cardiopulmonary disease).

PNEUMONIA:  Usually described as lung parenchyma/alveolar inflammation and abnormal alveolar filling with fluid.
Ø  EPIDEMIOLOGY:  6th leading cause of death in the US.  Mortality occurs most commonly in the very young and the elderly.  Individuals with underlying illnesses such as Alzheimer's disease, CF, emphysema, tobacco smoking, alcoholism, immune system problems are at increased risk for pneumonia.

Ø  PATHOPHYSIOLOGY:  Pneumonia can be caused by microorganisms (most common), irritants, idiopathic (SEE ILD). When pneumonias are grouped this way, infectious causes are the most common type.  The microorganisms that cause pneumonia include virus, bacteria, fungi, and parasites.  In general, microorganisms enter the lung when airborne droplets are inhaled.  Once in the lungs, they cause cell death either through direct damage or apoptosis. In the subsequent immune respondse to the microorganism, leukocytes-derived cytokines inflict further damage to the pulmonary interstitium allowing fluid to leak into the alveoli.  Cell destruction and fluid-filled alveoli interrupt normal oxygen transportation.

Pneumonia fills the lung's alveoli with fluid, hindering oxygenation. The alveolus on the left is normal, whereas the one on the right is full of fluid from pneumonia.

Public Domain,

1.     VIRAL PNEUMONIA:  Usually triggers a lymphocytic immune response.  It also make the body more susceptible to bacterial infections, thus bacterial pneumonia often complicates viral pneumonia.  Common viral etiology: AIR (remember these dudes are airborne) --> A-adenovirus, I-influenze virus, R-RSV (respiratory syncitial virus).  Rare causes includes: CMV, HSV, VZV.

v  A _______________, _______________, _______________, ______________, ______________

v  I _______________, _______________, _______________, ______________, ______________

v  R _______________, _______________, _______________, ______________, ______________

2.     BACTERIAL PNEUMONIA:  Usually triggers a neutrophilic immune response.  Many bacteria live in parts of the upper respiratory tract (URT) such as the nose, mouth and sinuses, and can easily be inhaled into the alveoli. Common bacterial etiology: 

3.     FUNGAL PNEUMONIA:  Uncommon, but  may occur in immunocompromised individuals (e.g. AIDS, immunosuppresive drugs, or other medical problems).  Common fungal etiology: Histoplasma capsulatum (Mississippi River basin), Coccidioides immitis (southwestern US), Cryptococcus neoformans &  Pneumocystis jiroveci (AIDS patients), and Blastomyces.

4.     PARASITIC PNEUMONIA:  Usually an eosinophilic immune response.  These parasites typically enter the body through the skin or by being swallowed.  Common parasitic etiology:  Toxoplasma gondii, Strongyloides stercoralis, and Ascariasis lumbricoid.


1.     Pathological classification:

Lobar pneumonia: Involves a single lobe.  Most commony (95%) due to Streptococcus pneumonia.  CXR: Consolidation.  Histology:  Intra-alveolar exudate. 4 stages of progression: Congestion (predominates 1st 24 hours), Red hepatization (neutrophic infiltration with accumulation of fibrinous exudate, RBCs, and bacteria), Gray hepatization (RBCs disntegrated, while the fibrinous exudate persists), Resolution (normal structure stored).

Bronchopneumonia: Involve the bronchioles and the adjacent alveoli.  Caused by S. aureus, S. pneumonia, H. influenza, P. aeruginosa.  CXR: Diffuse, patchy infiltrate.

Interstitial pneumonia:  Involves areas in between the alveoli.  Most likely caused by virus or atypical bacteria.  CXR: Streaky interstitial infiltrates without alveolar compromise.

2.     Clinical classification

Community-Acquired Pneumonia (CAP is the most common type):  Infectious pneumonia in a person who has not recently been hospitalized.  It is usually caused by Streptococcus pneumoniae (#1), Haemophilus influenzae, and the so-called walking pneumonia (the less severe atypical bacteria and the viruses). Gram-negative bacteria cause CAP in certain at-risk populations (e.g. Klebsiella in alcoholics).

Hospital-acquired pneumonia (aka nosocomial pneumonia):  Acquired during or after hospitalization for another illness or procedure with onset at least 72 hrs after admission. Prevalence: Up to 5% of hospitalized patient. It is associated with resistant bacteria such as MRSA, and gram-negative bacteria (e.g. Pseudomonas, Enterobacter).

Ø  PRESENTATION:  History:  Fever, shaking chills, rigors, cough producing greenish or yellow sputum, SOB, pleuritic chest pain, a sharp or stabbing pain, hemoptysis, headaches, anorexia, fatigue, N/V, myalgia, and arthralgia.  Other potential symptoms:  Abdominal pain and diarrhea (occur with Legionella); weight loss and night sweats (may occur with TB, PCP).  Physical exam:  Tachypnea, tachycardia, crackles, signs of consolidation (e.g. increase tactile fremitus, bronchial breath sounds, egophony [patient says “e”, doc hears “a”), dullness to percussion), and cyanosis in severe cases.

Main symptoms of infectious pneumonia

By Mikael Häggström.When using this image in external works, it may be cited as:Häggström, Mikael (2014). "Medical gallery of Mikael Häggström 2014". WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.008. ISSN 2002-4436. Public Domain.orBy Mikael Häggström, used with permission. - All used images are in public domain., Public Domain,

Ø  DIAGNOSTIC EVALUATION:  ABG: Check for hypoxemia. CBC:  Leukocytosis. BMP:  Hyponatremia (may be due to pneumonia induced SIADH or Legionella infection) and check renal function.  UA.  Blood culture: Should be collected from those requiring hospitalization.  Serum serology:  Can check for present of Mycoplasma, Legionella and Chlamydia antigen.  Respiratory secretions:  Can check for presence of viruses (AIR --> A-adenovirus, I-influenza, R-RSV).  CXR (AP and lateral): Can reveal areas of opacity (consolidation) or streaky infiltrate, pleural effusion, and possibly masses.  Chest CT:  Sometimes used as it is more sensitive than plain x-ray.  Sputum gram-stain and cultures:  Aid in determining the exact etiologic cause and guide antibiotic therapy.   DIAGOSTIC LABS INDICATIVE OF BAD PROGNOSIS: CHOW (imagine the bacteria CHOW-ing down your Lung-lunch) à C-creatinine > 1.2 or BUN > 20, H-hematocrit < 30 or H-Hgb < 9, O-O2 < 60 (PaO2) or PaCO2 > 50, W-WBC < 4 or > 30

§  C _______________, _______________, _______________, ______________, ______________

§  H _______________, _______________, _______________, ______________, ______________

§  O _______________, _______________, _______________, ______________, ______________

§  W _______________, _______________, _______________, ______________, ______________

Chest X-ray of a pneumonia caused by influenza and Haemophilus influenzae. Right lower lobe consolidation marked by arrow.

A chest X-ray showing a very prominent wedge-shape area of airspace consolidation in the right lung characteristic of acute bacterial lobar pneumonia

Cavitating pneumonia as seen on CT. Pneumonia due to MRSA

By James Heilman, MD - Own work, CC BY-SA 4.0,

CT of the chest demonstrating right-side pneumonia (left side of the image),_demonstrating_right-sided_pneumonia.jpg

Ø  TREATMENT: Uncomplicated CAP: Outpatient oral antibiotics X 7-10 days, rest, and fluids. Complicated CAP (e.g. severe disease [unstable vitals, hypoxemia], comorbidity [alcoholism, COPD, diabetes, immunosupression], homelessness, etc.):  Hospitalize with IV antibiotics, O2 supplement.  Empiric antibiotic treatment is usually started awaiting bacterial culture and sensitivity results. 

Antibiotic choice:  Depends on the nature of the pneumonia, the most common microorganisms causing pneumonia in the local geographic area, and the immune status and underlying health of the individual. In North America, where the "atypical" are becoming more common, macrolides (azithromycin, clarithromycin) have become the first-line treatment.

Vaccination: Pneumococcal (booster q5-7 yrs): For patients >65 y/o, and those with chronic illnesses, alcoholism, CSF leaks, or asplenia. Influenzae: Given annually to the same individuals who receive the pneumococcal vaccine.

Viral pneumonia:   Treatments are available for selected virues and are beneficial only if started within 48 hours of symptoms onset. Influenza A (other the then the H5N1 strains aka bird flu):  Rimantadine or amantadine.  Influenza B: Oseltamivir or zanamivir. There are no known effective treatments for viral pneumonias caused by the SARS coronavirus, adenovirus, hantavirus, or parainfluenza virus.

Ø  COMPLICATION:  More frequently with bacterial than viral pneumonia. The most important complications include: Respiratory failure (including ARDS), Sepsis (when microorganisms enter the bloodstream and the immune system responds by secreting cytokines), Pleural effusion (including empyema), and lung A-abscess (especially with A-aspiration pneumonia).


EPIDEMIOLOGY:  Worldwide incidence: 1 million people were being infected daily with ~ 60% of these infections occur in young people < 25 y/o. 
PATHOPHYSIOLOGY:  Most STDs are transmitted through exchange of bodily fluid during sexual contact through the mucous membranes of the penis, vulva, and mouth. Less common modes of transfer include blood transfusions, sharing injection/tattoo needles, needle-stick injuries, and childbirth.
TYPES OF STDs:  G-gay and H-heterosexuals C-contract T-these D-diseases --> G-gonorrhea, H-herpes, H-HIV, H-hemophilus ducreyi (aka chancroid), H-human papilloma virus (HPV), C-chlamydia, T-treponema pallidum, D-donovania granulomatis (aka Klebsiella granulomatis or calymmatobacterium granulomatis).
Ø  G  _______________, _______________, _______________, _______________, _______________

Ø  H  _______________, _______________, _______________, _______________, ________________

Ø  C  _______________, _______________, _______________, _______________, _______________

Ø  T  _______________, _______________, _______________, _______________, _______________

Ø  D  _______________, _______________, _______________, _______________, ________________


·       CONGENITAL INFECTIONS:  Occur at any time during pregnancy, labor, and delivery.  TORCHeS --> TO-toxoplasmosis, R-rubella, C-cytomegalovirus (CMV), H-herpes, H-HIV, S-syphilis.

o   TO  _______________, _______________, _______________, _______________, _______________

o   O  _______________, _______________, _______________, _______________, _______________

o   R  _______________, _______________, _______________, _______________, _______________

o   C  _______________, _______________, _______________, _______________, _______________

o   H  _______________, _______________, _______________, _______________, _______________

o   S  _______________, _______________, _______________, _______________, _______________


·       OPPORTUNISTIC INFECTIONS:  An opportunistic infection is an infection caused by pathogens that usually do not cause disease in a healthy immune system. A compromised immune system, however, presents an "opportunity" for the pathogen to infect.  T-the CHAMP --> T-toxoplasmosis gondii, C-candida albicans, C-crytococcus neoformans, H-histoplasmosis encapsulatum, A-aspergillosis, M-mucor/rhizopus, P-paracoccidioidomycosis, P-pneumocystic carini. 

o   T  _______________, _______________, _______________, _______________, _______________

o   C  _______________, _______________, _______________, _______________, _______________

o   H  _______________, _______________, _______________, _______________, _______________

o   A  _______________, _______________, _______________, _______________, _______________

o   M  _______________, _______________, _______________, _______________, _______________

o   P  _______________, _______________, _______________, _______________, _______________


BACTERIA: Unicellular prokaryotes, which do not contain a nucleus and membrane-bound organelles.


-       Capsule: Polysaccharide (except B. anthracis, which contains D-glutamate) protects against phagocytosis.

-       Cell wall: Differences between Gram negative (Gram-) and Gram positive (Gram+).  WILL DISCUSS!

-       Plasma membrane:  Lipoprotein bilayer contains oxidative and transport enzymes.

-       Ribosomes:  70S ribosome, consists of 50S and 30S subunits, involves in protein synsthesis

-       Plasmid: Transferrable DNA contains geness for antibiotic resistance, enzymes, and toxins.

-       Flagellum: Protein complex for motility.

-       Pili: Glycoprotein meditates adhrerence to host surfaces.

Cell structure of a gram positive bacterium

By This vector image is completely made by Ali Zifan - Own work; used information from Biology 10e Textbook (chapter 4, Pg: 63) by: Peter Raven, Kenneth Mason, Jonathan Losos, Susan Singer · McGraw-Hill Education., CC BY-SA 4.0,

·       BACTERIAL CLASSIFICATION BY GRAM-STAIN:  Differentiates bacterial species into Gram+ and Gram-; based on the chemical and physical properties of their cell walls.

o   4 STEPS IN A GRAM-STAIN: CIAs (it took the CIA to investigate and understand the basis of gram-stain). 

1)    C-CRYSTAL VIOLET primary stain (1 minute):  Crystal violet cations (CV+) penetrate through the cell wall of both Gram+ and Gram- cells, interact with negatively charged components of bacterial cells and stain it PURPLE.

2)    I-IODINE (1 minute): I- interacts with CV+ and forms large CV – I complexes in the outer and inner membrane.

3)    A-ALCOHOL/A-ACETONE decolorizers (5 seconds): Interacts with the lipids of the cell membrane. A Gram- cell will lose its outer membrane along with the CV – I complexes.   In contrast, a Gram+ cell becomes dehydrated from the alcohol/acetone treatment due to the multilayered nature of its peptidoglycan, and the large CV – I complexes become trapped within the cell.

4)    S-SAFRANIN counterstain (1 minute):  Give decolorized Gram- bacteria a PINK/RED color.


-   3 layers: 1) Inner membrane 2) Thin peptidoglycan layer (10%) 3) Outer membrane with lipopolysaccharide (LPS)

-   Lipid content: HIGH --> able to block LMW substances (e.g. lysozyme, penicillins…)

-   Toxins:  Endotoxins (Lipid A lipopolysaccharides) released from lysed bacteria and induce TNF, IL-1…

-   Porin channels

-   Teichoic acid: NONE.

GRAM P-positive CELL WALL:

-   2 layers: 1) Inner membrane 2) Outer thick P-peptidoglycan layer (60-100%)

-   Lipid content: LOW

-   Toxins:  Exotoxins (heat labile protein usually with enzymatic activity); except L. monocytogenes with endotoxins. 

-   Porin channels: NONE

Teichoic acid: Provide structural support and act as antigen (induce TNF, IL-1...)

Gram stain procedure and effect on Gram-negative and Gram-positive cell walls.

o   BACTERIA THAT DO NOT GRAM STAIN WELLS-some R-rude M-microorganisms L-lacks C-colors = SRMLC --> S-spiroches (too thin to be visualized requires darkfield microscopy), R-rickettsia (intracellular bacteria), M-mycobacteria (high-lipid cell wall requires acid fast stain), M-mycoplasma (no cell wall), L-legionella (intracellular bacteria requires silver stain), C-chlamydia (intracellular bacteria).

Ø  S  _______________, _______________, _______________, _______________, _______________

Ø  R  _______________, _______________, _______________, _______________, _______________

Ø  M  _______________, _______________, _______________, _______________, _______________

Ø  L  _______________, _______________, _______________, _______________, _______________

Ø  C  _______________, _______________, _______________, _______________, _______________



"Cocci "


Form grape-like clusters "

Staphylococcus aureus

Staphylococcus epidermidis



Staphylococcus saprophyticus


2) Non-motile

3) Colonizes nasopharynx in 15-30% of adults

4) Survives drying and heat

Part of skin normal flora

Virulence factors

1) Structural:

a) Capsule or slime layer:  Anti-phagocytosis and promotes adherence to synthetic materials

b) Cell wall (peptidoglycan, teichoic acid): Stimulates immune response

c) Surface Protein A:  Binds IgG's Fc portion and inhibits antibody-mediated + complement-mediated clearance

2) Enzymatic:

a) Coagulase: Converts fibrinogen to fibrin, allows organisms to clump together, protecting them from phagocytes

b) Catalase:  Breaks H2O2 to O2 + H2O, protecting against neutrophil killing

c) Hyaluronidase: Damages connective tissue-a “spreading” factor

d) Lipase: Breaks down lipids (important for survival on skin)

e) ß-lactamases: Hydrolyse ß-lactam ring (allows resistance); carried and transmitted on plasmids

3) Toxins:

a) Cytotoxins (e.g. a, b, g, d):  Attack many host cell types causing tissue damage.  Leukocidin damages/kills WBCs

b) Exfoliative toxin: A superantigen that split epidermal intracellular bridges causing skin to slough (i.e. staphylococcal scalded skin syndrome)

c) Toxic shock syndrome toxin-1 (TSST-1): A superantigen that cause

toxic shock syndrome

d) Enterotoxins A to E: Superantigens causing food poisoning


1) Introduced via breaks in skin and mucous membranes; may disseminate systemically

2) Pyogenic (pus-producing); stimulate acute inflammatory reaction; protected by virulence factors


1) Superficial skin infection:

- Boils, sties, abscesses: Pyogenic infection of hair follicles or surgical or trauma wound. 

- Pustular impetigo: Superficial infection; pustules rupture and crust over

2) Deeper infections: Spread from local infection through lymphatics or blood

- Pulmonary:  Pneumonia from embolic spread or aspiration

- Musculoskeletal: Most common cause of osteomyelitis. Also septic arthritis, pyomyositis

- Genitourinary tract: Lower UTI, renal carbuncle,

3) Toxin-induced diseases:

- Scalded Skin Syndrome: Begins as redness around mouth that spreads to body.  Due to production of exfoliative toxin, thus, no organisms or WBC’s in blisters.  Healing occurs after antibody forms to toxin.  Mortality low, no scarring

- Toxic Shock Syndrome:  Local growth of organisms release TSST-1 into blood (not a bacteremia).  Toxins act as superantigen inducing massive cytokine release resulting in multi-organ system failure.  Death occurs in 2-5%. 

- Food Poisoning:  Enterotoxins (resistant to boiling & gut enzymes) work directly on CNS vomiting center to induce N/V and diarrhea in 2-8 hr.

Diagnostic Evaluation


1) Coagulase-positive (clots blood plasma)

2) Large creamy colonies on nutrient agar

3) Colonies may have a golden color

4) Often causes hemolysis

1) Toxic shock syndrome: IVF, IV antibiotics (must be ß-lactamase resistant e.g. oxacillin, nafcillin, clindamycin - shuts down toxin production) for 10-15 days.

2) Food poisoning: Treat dehydration, cramping and diarrhea

3) Antibiotic choice:

- Penicillin if not resistant

- b-lactamse inhibitors: Oxacillin, nafcillin, clindamycin

- For MRSA (methicillin resistance arises from alteration of  penicillin-binding proteins-PBP; most coagulase negative and 30-50% of S. aureus: Vancomycin, oxazolidinones (linezolid), streptogrammins (quinupristin-dalfopristin), daptomycin, tigecycline, clindamycin

Bind to synthetic devices by slime layer

Infections of catheters, shunts (#1 cause of CSF shunt infection), artificial heart valves (#1 infective endocarditis first 2 months following valve replacement) and artificial joints

- Hard to treat, antibiotic resistance common

#2 cause of UTI after E. coli

- Accounting for 10-15% of UTIs

- Responds to antibiotics, reinfection uncommon

1) Coagulase-negative

2) Novobiocin-sensitive

1) Coagulase-negative

2) Novobiocin-resistant

Gram stain of S. saprophyticus cells which typically occur in clusters: The cell wall readily absorbs the crystal violet stain.

S. aureus on trypticase soy agar: The strain is producing a yellow pigment staphyloxanthin.

Typical Gram-positive cocci, in clusters, from a sputum sample, Gram stain

By Bobjgalindo - Own work, CC BY-SA 3.0,

S. saprophyticus on Mueller-Hinton agar exhibiting resistance to novobiocin characteristic for species identification

By Deminorwood - Own work, CC BY-SA 4.0,




Virulence factors



Diagnostic Evaluation



- Catalase-negative

- Occur singly, in pairs or chains

Streptococcus pneumonia

Streptococcus viridans group

Nutritionally-variant streptococci

Streptococcus pyogenes

(aka Group A Strep)

Streptococcus agalactiae

(aka Group B Strep)


- Streptococcus faecalis (80-90%)

- Streptococcus faecium (5-10%)


- Streptococcus bovis

- Streptococcus equinus

1) Lancet-shaped diplococcus

2) Normal flora in URT - 25% adults

3) Transmission:  Human-to-human

1) Capsular polysaccharide (90 serotypes): Anti-phagocytic; basis for vaccines

2) Surface adhesins: Binds to epithelial cells

3) Pneumolysin: Destroys ciliated epithelial cells & leukocytes, suppresses oxidative burst

4) Phosphorylcholine:  A cell wall component that bind to endothelial cells, platelets & tissue cells allowing entry & subsequent dissemination

5) Teichoic acid: Activate complement + cytokine production (IL-1 & TNF-a) causing fever, tissue damage, inflammation

3) IgA protease: Disrupts IgA-mediated mucin clearance

2) C polysaccharide:  Precipitates CRP 

1) Pneumonia: #1 cause of bacterial pneumonia (2/3 of community-acquired pneumonia)

- Sudden and severe high fever, chills, productive blood stained "rusty" sputum, and pleurisy.  20% bacteremic

2) Otitis media (OM): #1 cause of OM

3) Sinusitis

4) Meningitis: From head trauma that causes leakage of CSF through the nose

5) Sepsis

1) α-hemolytic

2) Optochin sensitive

3) Bile soluble

4) Quellung+ (capsular swelling due to addition of type specific antibody)

5) Sputum Gram stain and culture

- Sample expectorate &/or nasotracheal suction

1) Antibiotic:

- Penicillin: Drug-of-choice if susceptible

- Alternative therapy:  Vancomycin, quinolones, clindamycin, 3rd generation cephalosporins, macrolides

2) Vaccine:

- 23-valent polysaccharide vaccine: 60-70% efficacy

- Protein conjugate vaccines: Better efficacy in children; fewer serotypes included (7-9)

1) Includes S. viridans, S. mutans, S. anginosus, intermedius, constellatus, and many others

2) Normal flora in URT, GIT, and GUT

Capsular polysaccharide

1) S. viridans:  #1 (~ 50% of cases) cause of SBE (usually on a damaged native valve & often following a dental procedure)

2) S. mutans:  Dental caries, wound infections, and toxic shock-like syndrome

3) S. anginosus, S. intermedius, and S. constellatus: Serious strep infections (10-30%); meningitis, brain + liver abscess, oral infections, appendicitis, endocarditis

1) α-hemolytic

2) Optochin resistant

3) Bile insoluble

4) Quellung-

1) Penicillin

2) Gentamicin

1) Include Granulitcatella adiacens, Abiotrophia defectiva

2) Normal flora - URT, GUT, GIT

Endocarditis (5% of cases): “Culture negative” endocarditis; greater morbidity & mortality versus other streptococcal cases

1) α-hemolytic

2) Require Vitamin B6 for growth

3) Do not grow on ordinary media - satelliting growth around staphylococci

1) Penicillin + gentamicin or

2) Vancomycin + rifampin

1) Colonize oropharynx of healthy children & adults (carriage rate 15-20%)

- Cause pharyngitis

- Person-to-person spread via respiratory droplets

2) Skin colonization followed by entry via break in skin

- Cause skin & soft tissue infections:

1) Major virulence factors:

- M-protein (> 80 serotypes):  Phagocytosis resistance; Antibody mediates type specific immunity

- Streptococcal Pyrogenic Exotoxin (SPE): Superantigens coded by bacteriophage DNA, which induce TNF (α, ß), IL (1, 2 & 6), & interferon-γ leading to fever, shock, organ failure.  Associated with Streptococcal Toxic Shock Syndrome and rashes in Scarlet Fever

2) Minor virulence factors:

- Streptolysin O (SLO): Oxygen labile hemolysin (lyses erythrocytes/leukocytes/platelets); antigenic

- Streptolysin S (SLS): Oxygen stable hemolysin (lyses erythrocytes/leukocytes/platelets); non-antigenic

- Enzymes:  Streptokinase (lyses clots, rapid spread; therapeutic use); C5a peptidase, DNase, hyaluronidase, NADase, DPNase (evasion of phagocytic cells)

- Others: Hyaluronic acid capsule, lipoteichoic acid (LTA)

1) Pharyngitis: Primarily a disease of children 5-15 years old

- History: Sore throat, HA, N/V, malaise, abdominal pain.  Exam: Fever (> 101°F), pharyngeal erythema, tender LAD, tonsillar exudat

- Complication: a) Suppurative sequelae: Peritonsillar abscess, otitis media, sinusitis, lymphadenitis, meningitis, arthritis, endocarditis, osteomyelitis, liver abscess, pneumonia

b) Non-suppurative (post-streptococcal autoimmune phenomena): Acute Rheumatic Fever (ARF), Acute Glomerulonephritis (AGN)

2) Skin & soft tissue infections

- Impetigo: Superficial epidermal thick yellow-golden crusts

- Erysipelas: Superficial cellulitis involving dermis and lymphatics.  Painful, erythematous rash with sharp border commonly involves bridge of nose and cheeks.  Fever, leukocytosis are common

- Cellulitis: Spreads below dermis to subcutaneous tissue.  Pain, erythema, edema, tenderness, vague border

- Necrotizing fasciitis (flesh eating bacteria): Deep subcutaneous tissues and fascia with rapid progression to gangrene over 24-72 hours.  Untreated case may lead to fulminant sepsis and cardiovascular collapse. 

3) Scarlet fever: GAS which elaborates SPE

- Signs/symptosm: Pharyngitis + rash (sandpaper, blanching rash appears on 2nd day and fades in 1 week followed

by desquamation) and strawberry tongue

4) Toxic Shock Syndrome

1) β-hemolytic

2) Bacitracin-sensitive

3) Direct detection: Throat swap

4) PCR: High sensitivity & specificity

5) Serology: ASO (anti-streptolysin O)

1) Penicillin

2) Alternative: Macrolides, clindamycin, cephalosporins

3) Surgical debridement:  Mainstay of therapy for necrotizing fasciitis

Normal flora - GIT, vagina, URT

- Pregnant females: 10-30% vaginal &/or rectal carriers

1) Capsule: 11 serotypes; types Ia, III & V > 80% of neonatal infections; sialic acid residues (Ia, Ib & II) prevent complement activation & opsonization

2) C5a peptidase - inactivates C5a

3) β-hemolysin - liver necrosis, hepatocyte apoptosis

Factors that ↑ vertical transmission:

- Prolonged rupture of membranes (≥ 18 hrs)

- Prematurity (< 37 wks)

- Intrapartum fever (≥ 38ºC)

- Maternal bacteriuria w/ GBS

1) Neonatal infections:

- #1 cause of neonatal pneumonia, meningitis and sepsis

2) Other diseases:  Endocarditis, sepsis, UTI, intrapartum infections, etc.

- Risk factors:  Diabetes mellitus, HIV, cancer

1) β-hemolysis

2) Bacitrin-resistant

3) Prenatal screening

1) Penicillin or ampicillin:  Antibiotic of choice (no resistance)

2) Alternatives: Cephalosporins, clindamycin, erythromycin

Normal habitat - GIT, GUT

Group D antigen on cell membrane

Diseases: UTI, bacteremia, endocarditis, wound infections, infections associated with medical hardware

- Low virulence, opportunistic, nosocomial pathogen (#2 or #3 leading cause)

1) γ-hemolytic

2) Growth in 6.5% NaCl + 40% bile

Intrinsic resistance to many antibiotics

- Ampicillin alone acceptable for UTI

- Ampicillin + aminoglycoside: Required for synergistic bactericidal activity in serious infections

- Vancomycin: Most strains susceptible

- Possible alternatives: Quinolones, chloramphenicol, imipenem

Normal flora - GIT, GUT, URT

1) S. bovis: Possesses Group D antigen

1) S. bovis: Endocarditis, wound infections, UTI

- Endocarditis/Bacteremia:  Associated with occult colon malignancy

1) γ-hemolytic (S. bovis can also be β-hemolytic)

2) Grow in 40% bile

1) Penicillin: Generally susceptible

2) Gentamicin: For synergistic killing

3) Alternative: Vancomycin, cephalosporins, quinolones

Gram-stained smear of streptococci (note the chain configuration)

By User:Graham Beards - Own work, CC BY-SA 3.0,

Alpha-hemolytic S. viridans (right) and beta-hemolytic S. pyogenes (left) streptococci growing on blood agar




Virulence factors



Diagnostic Evaluation



- Spore formers

Bacillus anthracis

1) Affects mainly herbivores (sheep, horses, cattle)

- Pastures contaminated with spores can transmit 20-30 year

3) Humans get mainly from animal sources

- Industrial- “woolsorter’s disease” from inhaling spore

- Agricultural- contact with infected animals hair or hides, insect bite or consumption of undercooked, contaminated meat

- Biological warfare

1) Edema factor

2) Protective antigen

3) Lethal factor

- Repeated subculture at 420C makes organism avirulent due to loss of plasmid encoding toxin production

1) Spores enter breaks in skin or mucous membrane

2) Spores germinate in tissue

3) Recovery from infection gives permanent immunity

- Protection results from antibody to exotoxin

1) Cutaneous disease: 2-5 day incubation followed by a "malignant pustules" usually on forearm or hand; 20% of cases are fatal if untreated

2) Pulmonary (woolsorter’s) disease: 1-5 days of mild illness followed by acute respiratory distress, massive edema of neck, chest, mediastinum and death within 24h

3) Gastrointestinal:

- Abdominal: Fever, N/V anorexia, progressive abdominal pain, hematemesis, and bloody diarrhea; time to death- 2-5 days

- Oropharyngeal: Fever, sore throat, dysphagia, cervical adenopathy with edema and tissue necrosis occur in the cervical area (posterior wall, hard palate, or tonsils); most die

1) Gram stain or direct fluorescent antibody

2) Growth on sheep blood agar or brain heart infusion

- Colony morphology: Curled extensions on colony edge (Medusa head)

- Long chains with central spores giving “bamboo” appearance in the lab

3) Specimen: Vesicle fluid, blood, CSF

1) Penicillin IV in high doses

2) Alternatives: Erythromycin, tetracycline, or chloramphenicol

3) Vaccines: Human toxoid

Photomicrograph of Bacillus anthracis (fuchsin-methylene blue spore stain)

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Bacillus cereus

Found in soil, vegetable, and water

Food poisoning

- Emetic form: 1-6h incubation followed by self-limited vomiting.  Associated with fried rice.

- Diarrheal form: 10-24h incubation followed by self-limited watery diarrhea, abdominal pain.  Associated with contaminated meat and vegetables.

Clostridium botulinum

1) Live in soil and animal intestines

2) Relatively heat-resistant spores can resist canning at lower temperatures

Neurotoxins types A-G released by germinating spores release

- Protein poisons B-block release of acetylcholine

Spores germinate and release protein toxins that cause disease

1) Classic food-borne botulism: Flaccid paralysis 12-36 h after ingestion

- Cranial nerves usually affected first (e.g. diplopia, blurred vision); dysphagia; descending paralysis with death from respiratory failure

2) Infant botulism: Rare form; seen at 3-30 weeks of age due to large intestine colonization with slow absorption of toxin

- Generalized hypotonia (“floppy baby”); weak cry and suck reflex.

3) Wound botulism: Rare form; due to spores contamination of traumatic wound

- Toxins produced at wound site and absorbed into tissues

- Disease similar to food-borne botulism

1) Classic food-borne botulism:

- Antitoxin and supportive care

- Prevention: Can and cook food properly

2) Infantile botulism: Generally favorable prognosis with or without therapy

Bacillus cereus showing hemolysis on sheep blood agar. B. cereus is a Gram-positive beta hemolytic bacteria, which may live in an environment with or without the presence of oxygen, i.e. facultative aerobe.

Clostridium botulinum stained with gentian violet.

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Clostridium tetani

1) Live in soil and animal intestines

2) Relatively heat-resistant spores can resist canning at lower temperatures


- Inhibits inhibitory neurotransmitters (GABA + glycine) release leading to generalized muscle contractions (i.e. tetanic spasm).

Spores germinate and release protein toxins that cause disease

1) Generalized tetanus (seen in 80% of cases):  Descending paralysis

- First sign is trismus (lockjaw), followed by nuchal rigidity, dysphagia, and rigidity of pectoral and calf muscles. Other symptoms:  Fever, sweating, elevated blood pressure, and episodic tachycardia. Episodes occur frequently and last several minutes. Spasms continue for 3–4 weeks, and complete recovery may take months

2) Clinical infection does not confer immunity

Spatula test:   Touching the posterior pharyngeal wall with a patula. A positive test result is the involuntary contraction of the jaw, and a negative test result would normally be a gag reflex attempting to expel the foreign object.

1) Cleaning and surgical debridement of infected tissue

2) Passive immunization: Human anti-tetanospasmin Ig or tetanus immune globulin

3) Tetanus toxoid vaccine:  All patients should be vaccinated or given booster shot.

3) Metronidazole:  ↓ bacterial load but no effect on the toxin. Penicillin:  If metronidazole is not available.

Clostridium tetani with characteristic 'tennis racket' appearance.

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Clostridium tetani, which causes the tetanus infection known for its symptoms of muscle spasms and lockjaw. This bacterium is strongly durable due to its endospores, which can carry the infection's DNA even when the bacterium is dead. Pictured is the bacterium alone, with a spore being produced, and the spore alone.

By Kholmes16 - Own work, CC BY-SA 4.0,

Clostridium perfringens

1) Enterotoxin: Acts as a superantigen

2) Lecithinase α-toxin:  Damages cell membranes causing cell death

1) Food poisoning: Meat poorly cooked, then re-warmed.  Germinating spores produce enterotoxin

2) Gas gangrene: From contamination of wound

1) Food poisoning: Symptoms usually in 7-15 hours

- Watery diarrhea (90%) and crampy abdominal pain (80%).

2) Gas gangrene: Follows trauma or surgery by 1-20 days

- Wound pain, discoloration, and crepitation. Rapid spread with myonecrosis

1) Food poisoning: Resolve without therapy in 6-24 hours

2) Gas gangrene: Emergent extensive debridement + Pen G

- Mortality 40-60%

Photomicrograph of Gram-positive Clostridium perfringens bacilli.

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Clostridium difficile colonies after 48hrs growth on a blood agar plate; Magnified 4.8X. C. difficile, an anaerobic gram-positive rod, is the most frequently identified cause of antibiotic-associated diarrhea (AAD). It accounts for approximately 15-25% of all episodes of AAD.

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Clostridium perfringens

Normal flora - GIT

1) C. difficile dormant in large bowel

2) Use of  anti-anaerobe antibiotic (e.g. clindamycin) suppresses normal GI flora causing overgrowth of resistant C. difficile

3) C. difficile releases detectable enterotoxin and cytotoxin

4) Spores transmissible to other patients

1) C. difficile diarrhea

2) Pseudomembranous colitis

1) Stop inciting antibiotic

2) Initiate metronidazole


- Non-spore formers




Virulence factors



Diagnostic Evaluation


Listeria monocytogenes

1) Facultatively anaerobic; β-hemolytic; catalase+; motile

2) Isolated from humans with disease and healthy carriers (intestinal colonization)

3) Transmission: Food a major source

- Most cases: Neonates, elderly, pregnant women

1) GI entry portal (stomach acid protects)

2) Cell invasion & intracellular division

- Internalin: Mediates engulfment by intestinal M cells, crypt cells, epithelial cells, macrophages

- Listeriolysin O:  Allows escape from vacuole

- Forms rocket-like actin tail to propel itself through the cytoplasm and into adjacent cells (avoids immune system)

3) Immunity is mainly through cell-mediated immunity (only cytokine-activated macrophages can reverse intracellular growth)

1) Meningoencephalitis:  Most common.  Usually occur in late neonatal period, the elderly, and the immunosuppressed

2) Bacteremia: Neonates or adults (mainly immunosuppressed)

3) Pregnancy-associated bacteremia (3rd trimester):  Fever, chills, back pain.  May precipitate labor

4) Granulomatosis infantiseptica (transplacental infection): Disseminated abscesses.  High mortality

1) Specimens:  CSF, blood, amniotic fluid, genital secretions

2) Culture:  Sheep’s blood.   Cold enrichment for culturing food

1) Ampicillin + gentamicin IV

2) Alternatives:  TMP-SMX

3) Therapy for meningitis may require 3-6 weeks

Colonies of typical L. monocytogenes as they appear when grown on Listeria-selective agar

By Original uploaded by James.folsom (Transfered by Syp) - Own work by James.folsom, Public Domain,

Electron micrograph of a flagellated Listeria monocytogenes bacterium, Magnified 41,250X. Listeria monocytogenes is the infectious agent responsible for the food borne illness Listeriosis. In the United States, an estimated 2,500 persons become seriously ill with listeriosis each year. Of these, 500 die.

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Corynebacterium diptheria

1) Aerobic

2) Resists drying; killed by disinfectants

3) Transmission: Person to person via respiratory droplet, contact with cutaneous infection

- Some carry for extended periods or chronically

Diphtheria toxin: Protein exotoxin encoded by a bacteriophage

- Inhibits protein synthesis/protein chain elongation in ekaryotic cells by the inactivation of EF-2 ( elongation factor-2) via ADP-ribosylation

- Antibodies to the toxin are protective.  Toxoid (i.e. formalin-inactivated toxin) is the basis of available vaccines

1) Respiratory form (e.g. nasal, facial, laryngeal, &/or tracheobronchial): Incubation 2-4 days

- Begin as pharyngitis/tonsillitis with fever

- Full syndrome: Gray-white “pseudo-membrane” from toxin effects, cervical adenitis (”bull neck” in severe cases)

- Complications: Pseudomembrane can obstruct airway and systemic toxin effects cause heart failure & neurotoxicity

2) Cutaneous form:  Tropical areas and southern US (especially the homeless)

- Begin as skin lesions at site of minor abrasions or insect bites, progressing to chronic non-healing ulcers covered by grayish membrane

- Complications: Less likely to cause cardiac or neurotoxicity

1) Gram stain: Appears like “Chinese characters”

2) Culture: Special potassium tellurite medium selectively kills normal flora (must alert lab to look) yielding black or gray colonies

- Specimen from nasopharynx, or skin

3) Direct fluorescent antibody test of specimen

1) Administer antitoxin ASAP (horse serum product):  Neutralize free toxin

2) Antibiotics: Erythromycin or penicillin

- Prophylaxis of contacts

3) Prevention: Vaccine (DPT 2, 4, 6, 15 mo & school age); Td booster every 10 yrs.

A diphtheria lesion on individual's leg

By CDC - Public Health Image Library, ID#:1941 (direct link:, Public Domain,

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Gram-positive Corynebacterium diphtheriae bacteria, which had been stained using the methylene blue technique. The specimen was taken from a Pai’s slant culture. Diphtheria is an acute bacterial disease caused by toxigenic strains of Corynebacterium diphtheriae and occasionally C. ulcerans. It is transmitted through respiratory droplets and personal contact. Diphtheria affects the mucous membranes of the respiratory tract, known as “respiratory diphtheria”, the skin, termed “cutaneous diphtheria”, and occasionally other sites including the eyes, nose, or vagina. Diphtheria remains a serious disease throughout much of the world. In particular, large outbreaks of diphtheria occurred in the 1990s throughout Russia and the other former Soviet republics. Most life-threatening cases occurred in inadequately immunized persons. Travelers to disease-endemic areas are at increased risk for exposure to toxigenic strains of C. diphtheriae.


Gram-negative cocci


Neisseria meningitidis


1) Transmission: Exchange of saliva and other respiratory secretions

- Coughing, kissing, and chewing on toys

2) Immunocompromised and asplenic patients are at particular risk of meningococcus

1) Transmission: Exchange of saliva and other respiratory secretions

- Coughing, kissing, and chewing on toys

2) Immunocompromised and asplenic patients are at particular risk of meningococcus


1) Asymptomatic carriage in the nasopharynx

2) Meningitis: Fever, HA, N/V, fatigue, petechial cutaneous rash, nuchal rigidity, and coma. Death occurs ~ 10% of cases.

3) Septicemia: Fever, altered mental status, purpuric rash (non-blanching), DIC (hypotension/shock, ischemic tissue damage).  Death occurs ~ 50% of cases

- Waterhouse-Friderichsen syndrome: Massive, usually bilateral, hemorrhagic necrosis of the adrenal glands due to fulminant meningococcemia

Diagnostic Evaluation

1) CSF anlysis

2) Blood culture: N. meningitidis will oxidize maltose, sucrose, and glucose

- Chocolate agar plate.

- Selective media: Thayer Martin VCN (V-vancomycin, C-colistin, N-nystatin)


1) Antibiotic: Treat all suspected cases ASAP

- Benzylpenicillin or Cefotaxime IV

2) Prophylaxis: Rifampin for close contacts of infected persons

3) Vaccine: Menactra and Menomune offer protection for ~ 3 years

Neisseria meningitidis colonies on New York City Medium Agar

By Xishan01 - In Microbiology lab., CC BY-SA 3.0,

Aerobic Gram-negative Neisseria meningitidis diplococcal bacteria; Mag. 1150X. Meningococcal disease is an infection caused by a bacterium called N. meningitidis or the meningococcus. The meningococcus lives in the throat of 5-10% of healthy people. Rarely, it can cause serious illness such as meningitis or blood infection.

Neisseria gonorrhea

1) Transmission: Sexually; highest risk M to F;

2) Coinfection with Chlamydia: Male (15-25%); female (30-40%)

1) Attachment factors:  Pili, Opa proteins, LOS

2) Invasion factors: Por (outer membrane pore), Opa, LOS

3) Factors that damage: LOS, peptidoglycan

4) Immune-avoidance factors: Reduction modifiable protein, IgA1 protease

Virulence factors


1) Gonococci (GC) attach to non-ciliated cells

2) GC endocytosis causing epithelial damage

3) GC transcytosis

4) GC exocytosis at base of non-ciliated cells

5) Ultimately, local inflammation (e.g. scarring and tubal blockage) +/- dissemination (e.g. arthritis)

1) Asymptomatic infection: 25-80% of women; 1-3% of men

2) Urethritis (male or female): Dysuria, purulent discharge

3) Cervicitis:  Infection of the female cervix

4) Upper genital tract infection:

- Female: PID, endometritis, salpingitis, tubo-ovarian abscess

- Male: Epididymitis, prostatitis, seminal vesiculitis

5) Disseminated gonococcal infection: Tenosynovitis &/or arthritis plus characteristic skin lesions

6) Other: Fitz-Hugh-Curtis syndrome, bartholinitis, conjunctivitis, pharyngitis, meningitis, endocarditis

1) Oxidase +

2) Ferment glucose not maltose, sucrose, or lactose

3) Gram stain and culture

- Sterile body sites- chocolate agar

- Non-sterile sites- Thayer-Martin (chocolate agar with vancomycin, colistin, trimethoprim, nystatin)

4) Rapid tests:

- ELISA, PCR or other DNA amplification test

1) Uncomplicated (cervix/urethra/rectum; 1dose)

- IM: Ceftriaxone

- PO: Cefixime, ofloxacin, levofloxacin or ciprofloxacin PLUS Rx Chlamydia

2) Complicated (upper tract)

- Treat for GC and CT, plus anaerobes, gram negative rods, and streptococci

3) Allergy: Use spectinomycin

4) Do not use quinolones in Hawaii or California due to increasing resistance; get travel history

Thayer-Martin Agar is selective for growth of Neisseria species. Further testing (oxidase, gram stain, carbohydrate utilization) is needed to differentiate N. gonorrhoeae from meningitidis

Public Domain,

Carbohydrate utilization of Neisseria gonorrhoeae. N. gonorrhoeae will oxidise glucose, not maltose, sucrose, or lactose; N. meningitidis ferments glucose and maltose.

This illustration depicts a Gram-stain of a urethral exudate showing typical intracellular gram-negative diplococci, and pleomorphic extracellular gram-negative organisms, which is diagnostic for gonococcal urethritis.

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- Respiratory GNR

This low-resolution photomicrograph reveals the histopathology in an acute case of gonococcal urethritis using Gram-stain technique. This slide is used to demonstrate the non-random distribution of gonococci among polymorphonuclear neutrophils. Note that there are both intracellular and extracellular bacteria in the field of view. (CDC) Higher resolution image (25.71 MB) available at PHIL.

The growth of Neisseria gonorrhoeae colonies on New York City medium agar, a specialised and selective media for Gonococci

By Xishan01 - In the Microbiology Lab., CC BY-SA 3.0,

Gram-negative cocci



Hemophilus influenza


1) Facultatively anaerobic

2) Normal flora - Nasopharynx, conjunctiva, genital tract (rare)

3) Transmission: Person-to-person via airborne droplets

Virulence factors



Diagnostic Evaluation


1) Type b: Meningitis, sepsis, cellulitis, septic arthritis, epiglottitis, pneumonia, empyema

2) Nontypeable & other types: Sinusitis, otitis media, conjunctivitis, exacerbation of COPD, community-acquired pneumonia, neonatal & maternal sepsis, bacteremia, other invasive infections

3) Biogroup aegyptius: Conjunctivitis & Brazilian purpuric fever

1) Gram stain/culture:

- Nutritionally fastidious: Requires hemin (X factor) & NAD (V factor)

2) Oxidase positive

1) Life-threatening infections: IV 3rd generation cephalosporins, chloramphenicol, ampicillin

3) Other infections: PO Augmentin, 2nd generation cephalosporins, quinolones, new macrolides, TMP-SMX

4) Chemoprophylaxis (for unimmunized < 4 y/o with close contact to index case of type b meningitis): Rifampin

5) Conjugate vaccine:  97-99% effective in prevention of type b disease in children ≤ 5 y/o

H. influenzae on a blood agar plate.

Haemophilus influenzae satelliting colonies (pin point) near Staphylococcus aureus (yellow) on blood agar plate.

By Deminorwood - Own work, CC BY-SA 4.0,

Haemophilus influenzae requires X and V factors for growth. In this culture haemophilus has only grown around the paper disc that has been impregnated with X and V factors. There is no bacterial growth around the discs that only contain either X or V factor.

H. influenzae, in a Gram stain of a sputum sample, appear as Gram-negative coccobacilli.

Chest X-ray of a case of Haemophilus influenzae, presumably as a secondary infection from influenza.

By Mikael Häggström - Own work, CC0,

ActHIB (Hib-vaccine)




- Respiratory GNR



Virulence factors



Diagnostic Evaluation


Hemophilus parainfluenza

Normal flora - URT

Endocarditis, otitis media, epiglottitis, conjunctivitis, pneumonia, various other infections

1) Gram stain & culture:

- Requires V factor only

Antibiotics: Similar to H. influenzae; β-lactamase production less common




- Respiratory GNR


Hemophilus ducreyi


1) Transmission: Sexual contact

2) Found primarily in developing countries, associated with prostitution

Virulence factors



Chancroid (soft chancre) - STD

- Incubation 5‑7 days

- Painful, shallow, circular ulcers with necrotic erythematous border and a yellow-gray base, which heals in about 7 days.  Tender inguinal lymphadenopathy that may rupture through the skine, forming suppurative buboes

Diagnostic Evaluation

1) Gram stain: Clusters of GNR

2) Culture: Difficult; if positive is definitive

- On enriched chocolate agar.  Requires X factor only. Also requires CO2


1) Erythromycin or azithro-mycin

2) Alternatives: Ceftriaxone, TMP-SXZ, ciprofloxacin

3) Treat for 7 days

Photomicrograph of H. ducreyi the causative agent of chancroid

Public Domain,




Virulence factors



Diagnostic Evaluation




- Respiratory GNR

Bordetella pertussis

1) Transmission: Respiratory droplets

2) Reservoir: Human adolescents + adults

1) Whooping cough: 3 stages

- Catarrhal stage (1-2 wks): Maximum communicability

- Paroxysmal cough stage  (1-6 wks):

- Convalescence stage (weeks-months):

2) Secondary attack rate up to 80%

3) Complications: Pneumonia, seizures, encephalopathy, death

1) Calcium alginate swab of nasopharyngeal specimen

2) Polymerase chain reaction (PCR)

3) DFA (direct fluorescent antibody)

4) Culture

Antibiotic: Erythromycin, other macrolides

Prevention: Vaccine (acellular pertussis -dtap)

Gram stain of the bacteria Bordetella pertussis

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