87

USMLE Step 3 (Subject) / Infectious Disease (Lesson)

This lesson was created by estoffel.

Learn lesson

back  |  next 1 / 2

• Necrotizing fascitis Pathogen: group A Streptococcus; frequently mixed infection (with aerobic and anaerobic gram-negative bacteria)- Gas gangrene is a type of necrotizing fasciitis caused by Clostridium perfringens  Clinical features:- Initially diffuse redness, swelling, initially extreme tenderness  - Later crepitus, purple skin discoloration, bullae formation, loss of sensation in the affected area - Systemic symptoms: fever, chills, acute illness- Fournier's gangrene: necrotizing fasciitis of the external genitals Diagnosis:- Laboratory analysis: leukocytosis, ↑ CRP, ↑ ESR, elevated CK levels, hyperglycemia, ketoacidosis- Imaging (X-ray, CT): detect subcutaneous accumulation of air   Treatment:- Monitoring in an intensive care unit- Immediate extensive surgical debridement with tissue culture and histopathology (confirmatory test) Complications:- Sepsis; (urosepsis in Fournier's gangrene) - Disseminated intravascular coagulation- Organ dysfunction (e.g., acute kidney injury)- Severe necrosis requiring amputation of limb- The mortality rate has been reported to range between 20% and 80%! Survivors have a shorter lifespan than the general population.
• Orbital cellulitis Definition:- An infection of the orbital contents, such as the fat and extraocular muscles- Posterior to the orbital septum- The eye globe is not affected. Etiology:- Complication of upper respiratory tract infection, most commonly due to bacterial rhinosinusitis  - Acute dacryocystitis- Infection of the teeth, middle ear (see acute otitis media), or face- Infected mucocele- Orbital trauma- Ophthalmic surgery   Epidemiology: More common in children than adults   Clinical features:- Proptosis (forward protrusion of eyeball) and ophthalmoplegia are the cardinal signs.  - Fever and malaise- Reduced vision: diplopia, afferent pupil defect, dyschromatopsia  - Ocular pain- Eyelid swelling and erythema- Chemosis- Necrotic areas in the nares and/or oral cavity in immunocompromised patients with maximally and/or ethmoid sinusitis should raise suspicion for mucormycosis. Diagnosis:- Primarily a clinical diagnosis- Laboratory tests: leukocytosis; positive blood and tissue fluid cultures- CT scan: confirm diagnosis and look for complications, e.g., orbital abscess or intracranial extension Treatment:- Empiric IV antibiotic treatment includes vancomycin PLUS one of the following: ceftriaxone, cefotaxime, ampicillin-sulbactam, piperacillin-tazobactam, or, if the patient is allergic to penicillins and cephalosporins, either ciprofloxacin or levofloxacin to cover S. aureus for 1-2 weeks- If intracranial extension is suspected, metronidazole should be added to ceftriaxone or cefotaxime to cover anaerobes Complications:- Subperiosteal or orbital abscess- Blindness due to involvement of the optic nerve  - Brain abscess- Other rare complications: cavernous sinus thrombosis and central retinal artery occlusion
• Preseptal cellulitis Definition:- An infection of the eyelid and periorbital soft tissues without involvement of the orbital contents- Anterior to the orbital septum- The eye globe is not affected. Etiology:- Complication of upper respiratory tract infection, most commonly due to bacterial rhinosinusitis- Acute dacryocystitis- Local trauma to the surrounding tissues of the face and eyelids- Insect or animal bites- Ophthalmic surgery   Epidemiology:- More common in children than adults- Much more common than orbital cellulitis Clinical features:- Ocular pain- Eyelid swelling and erythema- Less commonly, chemosis and fever Diagnostics:- Primarily a clinical diagnosis- Laboratory tests: leukocytosis; blood cultures are generally unnecessary  - CT scan: only eyelid swelling apparent   Treatment:- For mild non-systemic disease without fever, oral antibiotics and close outpatient follow-up- Oral amoxicillin-clavulanic acid- If methicillin-resistant S. aureus (MRSA) is suspected, clindamycin, trimethoprim/sulfamethoxazole, or doxycycline should be added.
• Osteomyelitis – Pathogens Staphylococcus auresus: Children and adults Staphylococcus epidermidis: - Diabetic patients with foot ulcers and pressure ulcers- Patients with prosthetics   Streptococci:- Diabetic patients with foot ulcers and pressure ulcers- Neonates and infants Pseudomonas aeruginosa- IV drug users- Plantar puncture wounds (especially if wearing rubber-soled footwear) Salmonella: Sickle cell anemia patients Klebsiella: Patients with UTIs or a history of UT instrumentation Fungal pathogens:- Immunocompromised patients- IV drug users Mycobacterium tuberculosis
• Osteomyelitis Diagnostics:- ↑ CRP, ↑ ESR, Possible leukocytosis- Blood cultures: microbiological testing  - X-ray:→ Early stages (< 2 weeks of symptoms onset): typically no pathological findings→ Later stages: bone destruction, sequestrum formation, periosteal reactions- MRI: the most sensitive diagnostic study; shows signs of inflammation ≤ 5 days after onset of infection → cortical destruction, bone marrow inflammation, soft tissue involvement- Bone biopsy: MRI/CT-guided needle or open biopsy + gram staining, culture, and histology→ Indication: should be performed whenever feasible, before administering antibiotics→ Detects both osteonecrosis and the pathogen → confirms the diagnosis and helps guide more specific therapy Treatment:- Adults: IV Vancomycin PLUS Antipseudomonal cephalosporins (ceftazidime, cefepime) OR antipseudomonal fluoroquinolones (ciprofloxacin, levofloxacin)- Methicillin-susceptible S. aureus (MSSA): IV Nafcillin/oxacillin, OR 1st or 2nd generation cephalosporin (cefazolin, cefuroxime)- MRSA or S. epidermidis: IV Vancomycin- Gram-negative pathogens (including Pseudomonas): Antipseudomonal cephalosporins (ceftazidime, cefepime) OR antipseudomonal fluoroquinolones (ciprofloxacin, levofloxacin)- Secondary osteomyelitis (e.g., prosthetic joints or foreign bodies): Rifampicin in addition to the antibiotic regimen  
• Septic arthritis Risk factors:- Prosthetic implant- Interventions (e.g., intra-articular injections)- Underlying joint disease, especially rheumatoid arthritis  - Immunosuppressed state- Diabetes mellitus- Age > 80 years- Chronic skin infections- IV drug use Clinical features:- Acute onset- Usually monoarticular  - Most commonly affected joints: knees; followed by hip, wrists, shoulders, and ankles- Classical triad of fever, joint pain, and restricted range of motion- Joint may be swollen, red, and warm Diagnostics:- Ultrasound-guided arthrocentesis: To conduct synovial fluid analysis, gram stain, and culture→ Cell count: > 50,000 WBC/μl (neutrophil predominant) points to septic arthritis (can be as low as > 10,000 in early disease).→ Fluid appears yellowish-green and turbid→ Also alleviates pain by decreasing intraarticular pressure- ↑ CRP/ESR- Blood culture: at least 2 sets of blood cultures to rule out a bacteremic origin Treatment:- Empiric antibiotic regimens→ Gram-positive cocci: Vancomycin→ Gram-negative cocci: Ceftriaxone→ Gram-negative bacilli: 3rd generation cephalosporin (e.g., ceftazidime), cefepime, piperacillin-tazobactam, or carbapenem→ Suspected pseudomonas infection (e.g., IV drug users): IV ceftazidime plus an IV aminoglycoside (e.g., gentamicin)→ No organism on gram stain but strong suspicion for bacterial septic arthritis: IV vancomycin plus either ceftazidime, cefepime, or an aminoglycoside- Start serial drainage with lavage- Continue antibiotic therapy at least ≥ 2 weeks  - Follow-up: Physiotherapy should be initiated early to prevent contracture of both the joint and its capsule
• Viral arthritis Etiology: parvovirus B19, hepatitis B virus, hepatitis C virus, rubella virus, HIV Clinical findings:- Symmetric involvement of multiple small joints- Sudden onset- Possibly accompanied by rash and fever- Usually no destruction of the joint Diagnostics:- History and clinical findings are the mainstay of establishing a diagnosis- Serology: antibodies against the suspected virus- Synovial joint analysis: very variable (can be normal or inflammatory) Therapy: supportive treatment only
• Prosthetic joint infection Etiology:- Early onset (< 3 months of placement): most commonly S. aureus- Delayed onset (3-12 months of placement): coagulase-negative staphylococci, particularly S. epidermidis- Late onset (> 12 months of placement): most commonly S. aureus Clinical findings:- Usually prolonged, low-grade course  - Minimal swelling, with or without a sinus that drains pus Diagnostic findings:- Conventional x-ray: loosening of the prosthesis, periosteal reactions Therapy:- Removal of the prosthesis (usually) and administer IV antibiotics for 6-8 weeks- Reimplantation of the prosthesis following antibiotic treatment
• Diverticulitis Modified Hinchey classification of diverticulitisStage I: Diverticulitis with a confined pericolic abscessStage II: Diverticulitis with distant abscess formationStage III: Perforated diverticulitis with generalized purulent peritonitisStage IV: Perforated diverticulitis, free communication with the peritoneum, generalized fecal peritonitis Clinical features:- Low-grade fever- Sigmoid colon most commonly affected → left lower quadrant pain  - Possibly tender, palpable mass (pericolonic inflammation)  - Change in bowel habits (∼ 50% constipation, 25-35% diarrhea)- Nausea and vomiting; caused by bowel obstruction or ileus- ↑ Urinary urgency and frequency (∼ 15%)  - Acute abdomen → indicates possible perforation and peritonitis Diagnostics:- Blood tests: Leukocytosis, ↓ Hemoglobin (in diverticular bleeding), ↑ CRP (> 5mg/100ml)- Stool test: rule out pathogens in patients with diarrhea- 1st-line: abdominal CT with oral and IV contrast  - Colonoscopy→ Not indicated during an acute episode → ↑ risk of perforation and exacerbating diverticulitis→ Performed once inflammation has subsided (after 6 weeks) to assess extent of diverticulitis and rule out malignancy Treatment:- Uncomplicated diverticulitis:→ Outpatient treatment→ Restricted, clear liquid diet and bowel rest until pain improves→ Broad-spectrum oral antibiotics for 7-10 days: Ciprofloxacin plus metronidazole / Trimethoprim/sulfamethoxazole plus metronidazolem / Amoxicillin-clavulanate- Complicated diverticulitis:→ Inpatient treatment→ IV fluids and bowel rest→ Broad-spectrum IV antibiotics: Piperacillin/tazobactam / Ampicillin/sulbactam / Imipenem, meropenem→ CT-guided percutaneous abscess drainage: in stable patient with abscess > 3 cm→ Emergency surgery: in case of peritonitis, sepsis or intestinal obstruction→ Elective surgery: recurrent disease unresponsive to antibiotics; complicated diverticulitis in young patients
• West Nile virus Reservoir: wild birds, horses, and dogsVector: mosquitoes Predominant occurrence: Asia, Africa, and the Middle East (endemic) West Nile encephalitis:- Suspect in anyone presenting with fever and altered mental status in late spring, summer, or early autumn.- Signs of viral meningitis (e.g., fever, headache, meningeal signs) and encephalitis (e.g., altered mental status)- May have extrapyramidal symptoms or flaccid paralysis suggestive transverse myelitis.- Malaise, myalgia, anorexia- Morbilliform rash on the trunk and extremities. - Symptoms typically last for 3-10 days. Diagnostics:- ELISA of serum or CSF for IgM antibody Treatment: Supportive (e.g., fluids)
• Advertisement
• Meningitis – Pathogens Newborns:- Group B Streptococcus (most common)- Gram-negative bacilli (e.g., Escherichia coli)- Listeria monocytogenes- Haemophilus influenzae- Enterobacter cloacae Infants (1 month - 2 years):- Streptococcus pneumoniae and Neisseria meningitidis (most common)- Listeria monocytogenes- Haemophilus influenzae  - Group B Streptococcus Children and teens:- Neisseria meningitidis (most common)- Streptococcus pneumoniae- Listeria monocytogenes- Enteroviruses: particularly coxsackievirus and echovirus- Herpes simplex virus (HSV-2)   Adults (18-60 years):- Streptococcus pneumoniae (most common)- Neisseria meningitidis- Listeria monocytogenes- Enteroviruses: particularly coxsackievirus and echovirus- Herpes simplex virus (HSV-2) Elderly (> 60 years):- Streptococcus pneumoniae (most common)- Gram-negative bacilli (e.g., E. coli)- Listeria monocytogenes Immunocompromised patients:- Listeria monocytogenes- Gram-negative bacilli- Streptococcus pneumoniae- Cryptococcus spp.  - CMV, VZV, HSV, JC virus- Mycobacterium tuberculosis, toxoplasma gondii Hospitalized patients:- Staphylococci (most frequently S. aureus) - Gram-negative bacilli  
• Meningitis Diagnostics:- Signs of meningeal irritation: Kernig sign and Brudzinski sign- Papilledema (< 5% of cases)- Blood cultures before antibiotic therapy is started- Blood glucose to assess CSF glucose - ↑ WBC- Coagulation studies if disseminated intravascular coagulation is suspected- Lumbar puncture: Essential in all patients with suspected meningitis, unless CNS mass effect is suspected (e.g., in case of focal neurological deficits, papilledema, altered mental status, or seizures) → Initiate empiric antibiotic treatment if bacterial meningitis is suspected (within one hour of patient admission)→ Perform cranial CT first  Post-dural puncture headache is the most probable diagnosis in patients complaining of headache, dizziness, hearing loss/tinnitus, and nausea after lumbar puncture! Treatment:1. Blood cultures2. Lumbar puncture for CSF Gram stain and culture  3. Immediate empirical treatment- < 1 month: ampicillin PLUS aminoglycoside (e.g., gentamicin) PLUS third-generation cephalosporin (e.g., cefotaxime or ceftriaxone)- > 1 month to < 50 years: vancomycin PLUS third-generation cephalosporin (e.g., cefotaxime or ceftriaxone)- > 50 years: vancomycin PLUS ampicillin PLUS third-generation cephalosporin (e.g., cefotaxime or ceftriaxone)- Immunocompromised: vancomycin PLUS ampicillin PLUS cefepime OR meropenem- Hospital-acquired: vancomycin PLUS ceftazidime OR cefepime OR meropenem- Possibly dexamethasone: only beneficial in some cases→ In adults: when pneumococcal meningitis is strongly suspected or confirmed→ In children: for suspected or confirmed HiB meningitis
• Sinusitis Pathogens:- Viral (most common): rhinovirus, coronavirus, adenovirus, influenza, and parainfluenza viruses- Bacterial: particularly S. pneumoniae, H. influenzae, M. catarrhalis, S. aureus, E. coli, and Klebsiella.  - Fungal: Aspergillus, Rhizopus oryzae   Risk factors:- Preexisting viral upper respiratory tract infection (URTI): most common- Ventilation disorders of the sinuses→ Hypertrophy of nasal turbinates, nasal polyps, deviation of nasal septum→ Impairments of ciliary function such as cystic fibrosis, primary ciliary dyskinesia, Wegener granulomatosis, allergic inflammation, and immunodeficiency→ Concha bullosa (also known as a middle turbinate pneumatization)  - Foreign body lodged in the nasal cavity (particularly seen in children).- Odontogenic infection: leads to unilateral maxillary sinusitis- Rhinitis: spread of pathogens via nasal mucosa- Bronchial asthma- Analgesic (NSAIDs, aspirin) intolerance Clinical features:- Fever (∼ 50% of cases), headaches, general malaise, myalgia- Facial pain or pressure, erythema, and swellingover the affected area due to inflammation  → Maxillary sinuses: over the cheeks (mimics dental pain)  → Frontal sinuses: lower forehead→ Ethmoidal sinuses: nasal bridge and/or between the eyes or retro-orbital pain  → Sphenoid sinuses: located in the sphenoidbones near the optic nerve and pituitary gland. These are the most posterior sinuses.- Transillumination may show opacification.   Diagnostics: Diagnosis of acute cases is usually established clinically. However, imaging or endoscopy should be considered if symptoms fail to improve within 7 days of diagnosis or worsen during the initial management of acute bacterial rhinosinusitis.- CT of sinuses (imaging modality of choice)- Nasal endoscopy   Treatment:- Viral infection: self-limiting- Bacterial infection: First-line antibiotic therapy: amoxicillin, with or without clavulanate for 5-10 days
• Acute otitis media Etiology:- Bacterial superinfection following a viral URT infection (95% of cases)  - S. pneumoniae (most common: 35% of cases)- Haemophilus influenzae (25% of cases)- Moraxella catarrhalis (15% of cases)- Group A ß-hemolytic streptococci (in older children) Risk Factors for AOM:- Bottle feeding/formula feeding, inadequate breastfeeding  - Pacifier use  - Passive cigarette smoke  - Children who attend day care centers  - Poor socioeconomic status   Clinical features:- In infants→ Irritability→ Incessant crying→ Refusal to feed (anorexia)→ Repeatedly touching the affected ear→ Fever and febrile seizures→ Tender mastoid in late stages- In older children→ Otalgia/earache, commonly with throbbing→ Hearing loss in the affected ear→ Fever→ Tender mastoid in late stages Diagnostics:- Otoscopy: tympanic membrane (TM) evaluation→ Retracted and hypomobile→ Loss of light reflex→ Late findings: Cartwheel TM, Red bulging TM with loss of landmarks, Yellow spot on TM (antero-inferior quadrant of pars tensa) which indicates site of imminent rupture→ If TM rupture → purulent/serosanguinous discharge in the external auditory canal- Tuning fork test: conductive hearing loss Treatment:- Symptomatic pain management (paracetamol, ibuprofen)- Antibiotics: Bilateral otitis media / symptoms do not improve after 48 hours / severe illness in children (very high fever, vomiting, malaise, and immunosuppression)→ First line: oral amoxicillin. Add clavulanic acid if no improvement after 48 hours.- Tympanocentesis: Aspiration of contents of middle ear using a sterile needle, indicated in patients who do not respond to initial therapy (allows for culture of bacteria contained in middle ear fluid)
• Mastoiditis Epidemiology: often occurs in children < 5 years Clinical features:- Persistence/recurrence of otalgia and fever after initial improvement- Ear discharge becomes profuse (discharge persisting > 3 weeks suggests mastoiditis).- Tender and edematous mastoid- Ear displaced laterally and forward- In advanced stages, the retroauricular sulcus is obliterated and the ear can be pushed forward. Diagnostics:- Otoscopy: The TM may be perforated.- First test: CT scan of the temporal bone Treatment:- Antibiotic treatment is always indicated→ Vancomycin alone: in patients who have not recently received antibiotics and who do not have a history of recurrent AOM→ Vancomycin + ceftazidime or cefepime or piperacillin-tazobactam: patients who recently recieved antibiotics and/or had an episode of AOM within the past 6 months- Tympanostomy (myringotomy) + tympanostomy tube insertion: for early stages of mastoiditis  - Mastoidectomy: is indicated in severe cases that do not improve with antibiotics + tympanostomy.  
• Labyrinthitis Etiology: Inflammation spreads to the inner ear (labyrinth) through the round window. Clinical features:- Severe vertigo, nausea, and vomiting- Hearing loss- Nystagmus towards healthy ear for weeks to months   Diagnostics:- Change of lateralization in Weber's test  - Audiometry: sensorineural hearing loss Treatment:- IV antibiotics + tympanostomy with insertion of tympanostomy tube + glucocorticoids- Mastoidectomy (to treat the source of infection in AOM)
• Otitis externa Pathogens- Bacterial infections (most common cause of otitis externa)→ Pseudomonas aeruginosa (∼ 40% of cases), commonly from swimming activities→ Staphylococcus aureus, Proteus mirabilis, Escherichia coli- Fungal infections (less common): Aspergillus (accounts for 90% of all fungal otitis externa), Candida- Viral infections (rare): Herpes zoster, Influenza viruses Risk factors:- Injury to the skin of the external auditory canal (e.g., cleaning, insertion of foreign objects such as hearing aids or earplugs, excessive itching)- Increased moisture in the external auditory canal (e.g., swimming, humid climate) Clinical features:- Severe ear pain, particularly at night- Otorrhea- Intense itching in the external auditory canal- The tragus is tender to touch- Pulling up and back on the auricle causes pain Diagnostics:- Otoscopic findings→ Localized OE: Furuncle→ Diffuse OE: Edematous and reddened external auditory canal- Conductive hearing loss- Check blood glucose levels to rule out diabetes- Culture and sensitivity tests are not routinely performed; they may be indicated if antibiotic treatment is not effective.Fungal otitis externa should be suspected when symptoms do not resolve with local and/or systemic antibiotic therapy(especially among immunocompromised and diabetic patients)! Treatment:- Antibiotic eardrops (typically ofloxacin, ciprofloxacin, or gentamycin) - Topical hydrocortisone to control itching and inflammation- Aural toilet: clean the external auditory canal and keep it dry using an ear wick and/or astringents (e.g., mixture of isopropyl alcohol and acetic acid)- Indications for systemic treatment with oral ciprofloxacin → Immunosuppression→ Diabetes mellitus→ Severe otitis externa with cellulitis of the face and neck
• Acute tonsillitis Epidemiology:- Viral tonsillitis: children < 5 years and young adults- Streptococcal tonsillitis: children aged 5-15 years; rare in children aged < 2 years   Etiology- Viral (50-80% of cases): adenovirus, EBV, CMV, HSV, rhinovirus, coronavirus, influenza and parainfluenza viruses, HIV- Bacterial (15-30% of cases): Streptococcus pyogenes (most common). Rarely, Neisseria gonorrhoeae, Corynebacterium diphtheriae, Mycoplasma pneumoniae. Clinical features:- Sudden onset of symptoms- Red and swollen pharynx, tonsillar exudates  - Fever, sore throat, dysphagia- Painful, swollen cervical lymph nodes- Foul breath- If viral: headache, earache, nasal congestion, and cough Trismus and changes in voice quality indicate the formation of potentially life-threatening peritonsillar abscess! Diagnostics:- Modified Centor score (A set of criteria used to estimate the probability that pharyngitis is caused by GAS)- Confirmatory tests: rapid antigen detection test and/or throat culture Treatment:- Antibiotics if infection with GAS has been confirmed → Penicillin V (or aminopenicillin) for at least 10 days. 
• Pneumonia Pathogens:- Typical pneumonia: Streptococcus pneumoniae (most common), Haemophilus influenzae  - Atypical pneumonia: Mycoplasma pneumoniae (most common in the ambulatory setting), Chlamydophila pneumoniae, Legionella pneumophila → legionellosis, Coxiella burnetii- Hospital-acquired pneumonia: Pseudomonas aeruginosa, Enterobacteriaceae, Staphylococcus aureus, Streptococcus pneumoniae- Pneumonia in newborn infants: Escherichia coli, Group B streptococcus, Streptococcus pneumoniae, Haemophilus influenzae Clinical features (Typical pneumonia):- Severe malaise- High fever and chills- Productive cough with purulent sputum (yellow-greenish)→ Crackles, bronchial, and decreased breath sounds on auscultation→ Enhanced bronchophony, egophony, and tactile fremitus→ Dullness on percussion  - Tachypnea and dyspnea (nasal flaring, thoracic retractions)- Pleuritic chest pain when breathing, often accompanying pleural effusion- Pain projecting to the abdomen and epigastric region (particularly in children) Clinical features (Atypical pneumonia):- Low-grade fever- Non-productive, dry cough- Dyspnea- Common extrapulmonary features include fatigue, headaches, sore throat, myalgias, malaise- Auscultation often unremarkable Diagnostics:- Blood: ↑ CRP, ↑ ESR, leukocytosis, ↑ procalcitonin (PCT)  - ABG to rule out respiratory failure ( ↓ PaO2, pH < 7.35, PaCO2 > 45 mm Hg)  - Blood cultures are always recommended.- Urine Legionella antigen detection and urine pneumococcal antigen test (if suspected)- PCR and antibody tests to detect Chlamydia pneumoniae  - Chest x-ray- Chest CT if inconclusive chest x-ray or recurrent pneumonia- Sputum : testing for multiresistant pathogens; severe, rapid progressive nosocomial pneumonia- Pleurocentesis: pH metry value (normally 7.60-7.64); Leukocyte count > 1000 WBCs/mm3 and protein levels (> 1-2 g/dL), Inoculation of blood cultures with the puncture fluid and subsequent analysis- Bronchoscopy: indicated to visualize and biopsy a central mass discovered on CT imaging, or if CT results are inconclusive Treatment:- CURB-65: Criteria for hospitalization- Outpatient treatment (no risk factors): Macrolide OR doxycycline- Outpatient treatment (risk factors): Fluoroquinolone OR an antipneumococcal beta-lactam- Inpatient treatment (non-ICU): Fluoroquinolone OR an antipneumococcal beta-lactam- Inpatient treatment (ICU): Antipneumococcal beta-lactam + azithromycin OR + fluoroquinolone- If Pseudomonas aeruginosa is suspected: Antipneumococcal, antipseudomonal beta-lactam (piperacillin/tazobactam, cefepime, meropenem, or imipenem) + fluoroquinolone- If MRSA is suspected: Add vancomycin or linezolid
• Pneumocystis jirovecii Risk factors:- HIV Infection: CD4 count: usually < 200/μL; Poor compliance with PCP prophylaxis or HAART- Primary immunodeficiency disorders (e.g., severe combined immunodeficiency disorder) - Malignancy (e.g., leukemia, non-Hodgkin lymphoma)- Immunosuppressive treatment (e.g., chronic glucocorticoid therapy) indicated in: → Stem cell or organ transplantation→ Connective tissue disorders (e.g., systemic lupus erythematosus)→ Vasculitides (e.g., polyarteritis nodosa)- Malnutrition Clinical features:- Symptoms typically have a gradual onset (days to weeks) and include:→ Low-grade fever and malaise→ Dyspnea and non-productive cough→ Fatigue, weight loss, chills- May progress to fulminant respiratory failure- Can be asymptomatic Diagnostics:- CD4 count: typically < 200/μL- ↑ Beta‑D‑glucan  - Confirmatory test: microscopic identification of P. jirovecii in specimen obtained via bronchoalveolar lavage or induced sputum, with methenamine silver staining and immunofluorescence  - Pulse oximetry: oxygen saturation < 90 % at rest (worsens with exertion) Treatment:- Treatment of choice: high‑dose TMP/SMX for up to 3 weeks- Glucocorticoids: add in the case of severe respiratory insufficiency (either PaO2 < 70 mmHg or arterial‑alveolar oxygen gradient ≥ 35 mmHg).  
• Tuberculosis Primary tuberculosis (primary infection):- Latent tuberculosis infection (LTBI): primary infection without any pathological findings on radiological imaging; however, screening tests indicating previous infection with M. tuberculosis are positive.  → The lifetime risk of reactivation TB for a person with LTBI is about 5–10%.  - Active primary tuberculosis (only 1-5% of cases): primary infection with radiological-pathological findings of tuberculosis  Reactivation tuberculosis (secondary infection)- Following a latent primary TB infection; 80% of secondary infections begin in the lungs (many months or years may pass between the onset of primary and secondary infection). Clinical features:- Latent infection: → Asymptomatic→ The patient is not contagious.- Active infection (either primary or reactivated)→ Constitutional symptoms: fever, weight loss, night sweats, fatigue, lymphadenopathy→ Pulmonary symptoms: dyspnea, productive cough (possibly hemoptysis) lasting > 3 weeks→ The patient is contagious→ 80% pulmonary tuberculosis→ 20% extrapulmonary tuberculosis Diagnostics:- Active TB→ Moderate to high risk: chest x-ray → if suggestive of pulmonary TB, collect three sputum samples  for culture, PCR, and microscopy → Low risk: consider testing for latent tuberculosis- Latent tuberculosis (LTBI)→ Test patients at risk for reactivation or new LTBI who would benefit from treatment of LTBI.→ If patients would benefit from treatment → TST or IGRA+ test → Evaluate for active TB- test → Repeat test after 8 week in high-risk individuals- IGRA is preferred in patients who received Bacillus Calmette-Guérin (BCG) vaccine.  - TST is preferred for children younger than 5 years of age. Treatment:- Initiation phase: 2 months of isoniazid + rifampin + pyrazinamide + ethambutol- Continuation phase: 4 months of isoniazid + rifampinThe efficacy of drugs metabolized by cytochrome P450 may be reduced because of hepatic enzyme induction by tuberculostatic drugs (especially oral diabetic treatments, calcium antagonists, statins, and oral contraceptives)! - Latent tuberculosis infection: Isoniazid monotherapy for 9 months in patients with positive interferon-γ and/or PPD test but without clinical signs of active TB- Recent contact with a person who has active TB: Perform PPD test or IGRAs and a chest x-ray
• Urinary tract infection (UTI) Pathogens- Bacteria: Escherichia coli (∼ 80% of UTIs), Proteus mirabilis (urease-producing → causes alkaline urine with an ammonia smell), Klebsiella pneumoniae, Enterobacter species, Staphylococcus saprophyticus, Enterococci (e.g. Enterococcus faecalis), Ureaplasma urealyticum- Viruses: Adenoviruses can cause hemorrhagic cystitis in children and immunocompromised patients.- Yeast: rare; usually Candida species Predisposing factors:- Female sex- Sexual intercourse- Catheter-associated urinary tract infection (CAUTI)- Structural or functional abnormalities of the urinary tract (e.g., BPH, vesicoureteral reflux, urinary bladderdiverticulum, neurogenic bladder, calculi or stones)- Pregnancy- Diabetes mellitus- Immunocompromise- Uncircumcised males- Chronic constipation in toddlers   Classification: - Asymptomatic bacteriuria: presence of significant bacteriuria without symptoms- Uncomplicated UTI: Immunocompetent, premenopausal women that are neither pregnant nor have any condition that predisposes them to an increased risk of infection or failed therapy- Complicated UTI: Male patient, Pregnant women, Children or postmenopausal women, Presence of any significant functional or anatomical abnormalities (e.g., BPH, obstruction, stricture), Diabetes mellitus, Immunocompromise (e.g., transplant recipients, HIV/AIDS), Recent history of any instrumentation (e.g., cystoscopy) Clinical features:- Dysuria, frequency, urgency  - Suprapubic pain- Gross hematuria may be present Diagnostics:- Dipstick urine test: Positive leukocyte esterase, Positive nitrites, Urine pH may be > 7 (alkaline) in Proteus mirabilis infections  - Urinalysis with microscopy: Confirmatory test  - Urine culture: ≥ 105 colony forming units (CFU)/mL confirms a UTI→ Indications: Patients with complicated UTI, Age older than 65 years, Use of a diaphragm, Recent use of antibiotics Treatment:- Uncomplicated UTI: → Trimethoprim-sulfamethoxazole (TMP-SMX) for 3 days → Nitrofurantoin for 5 days: avoid if patient has renal insufficiency or if pyelonephritis is suspected→ Fosfomycin single-dose: avoid in suspected pyelonephritis- Complicated UTI:→ Fluoroquinolones (e.g., ciprofloxacin, levofloxacin)→ Treatment is extended to 7 days in complicated cystitis.
• Pyelonephritis Pathogens:- Escherichia coli (∼ 75-90% of cases) - Pseudomonas aeruginosa- Klebsiella pneumoniae- Proteus mirabilis- Gram-positive bacteria (e.g., Enterococcus faecalis, Staphylococcus aureus)- Candida infection (esp. in immunocompromised patients) is possible Risk factors:- Most common in women because they have shorter urethras- Pregnancy- Urinary tract obstruction: Foreign bodies, anatomical abnormalities - Recent administration of antibiotics (possible antibiotic resistance)- Immunosuppression (e.g., HIV, diabetes)- Acute kidney injury Clinical features:- High fever, chills- Flank pain, costovertebral angle tenderness (usually unilateral, may be bilateral)  - Dysuria as well as other symptoms of cystitis (e.g., frequency, urgency)- Weakness, nausea, vomiting (diarrhea may also be present)- Possible abdominal or pelvic pain Diagnostics:- Urinalysis: Pyuria (→ positive esterase on dipstick test), leukocyturia, WBC casts; Bacteriuria (→ positive nitrites on dipstick test); Microhematuria- Blood: ↑ Inflammatory markers, Normal or ↑ renal function parameters  - Urine culture and blood culture  Urine and blood cultures need to be done before empiric administration of antibiotics!- Imaging: Only if: No response to therapy within 2 days; Complicated pyelonephritis (e.g., obstruction, sepsis); Unusual urinary findings present (e.g., gross hematuria); History of nephrolithiasis Treatment:- Uncomplicated pyelonephirtis: Outpatient treatment with oral fluoroquinolones (e.g., ciprofloxacin for 7 days) or oral trimethoprim-sulfamethoxazole for 14 days- Complicated pyelonephritis: IV fluoroquinolones (e.g., ciprofloxacin) for 10-14 days
• Prostatitis Epidemiology:- Very common urologic diagnosis in men < 50 years of age- 25% of men are diagnosed with prostatitis in their lifetime- Bacterial prostatitis (2-5% of cases): primarily affects men ∼20-50 years of age- Chronic pelvic pain syndrome (90-95% of cases): primarily affects men 40-60 years of age Etiology:- Bacterial prostatitis: E. coli and other Enterobacteriaceae; Enterococci and other gram-positive cocci- Chronic pelvic pain syndrome (CPPS): no detectable causative organism  Risk factors for bacterial prostatitis:- Other genitourinary tract infections (e.g., urethritis, cystitis, epididymitis)  - Genitourinary tract interventions (e.g., indwelling catheter, transurethral surgery, prostate biopsy)  - Voiding dysfunction and bladder outlet obstruction Diagnostics:- Urinalysis using midstream urine (↑ WBC), urine culture, urine Gram stain- Blood tests: ↑ inflammatory markers, ↑ PSA  - Blood cultures if sepsis is suspected- Chronic bacterial prostatitis: Fractional urine examination with four-glass test Treatment:- Bacterial prostatitis: Fluoroquinolones (e.g., ciprofloxacin) or trimethoprim-sulfamethoxazole PO  → 4-6 weeks in acute bacterial prostatitis → ≥ 6 weeks for chronic bacterial prostatitis- Chronic pelvic pain syndrome: Alpha blockers (e.g., tamsulosin, doxazosin), 5-alpha-reductase inhibitors (e.g., finasteride), Antibiotics, NSAIDs
• Syphilis Epidemiology:- Sex: ♂ > ♀ (10:1)  - Incidence: 6.3/100,000 per year in the US (The annual rate tripled between 2001 and 2014)- Peak incidence: 20-29 years   Incubation period: 10-90 days; on average 21 days Primary syphilis:- Primary lesion (chancre)  → Typically starts out as a solitary, raised papule (usually on the genitals)→ Evolves into painless, firm ulcer with indurated borders and smooth base→ Resolves spontaneously within 3-6 weeks, typically without scarring- Regional (usually inguinal) nontender lymphadenopathy Secondary syphilis: - Begins approx. 8-12 weeks after primary infection; typically lasts 2-6 weeks- Generalized nontender lymphadenopathy- Fever, fatigue, myalgia, headache- Polymorphic rash→ Typically nonpruritic macular or papular rash→ Disseminated; involves trunk and extremities, also the palms and soles→ Reddish-brown or copper-colored→ Heals within 6 months, but may recur- Condylomata lata→ Broad-based, wart-like papular erosions→ Located in the anogenital region, intertriginous folds, and on oral mucosa- Patchy alopecia (moth-eaten alopecia)- Sore throat (acute syphilitic tonsillitis) Latent syphilis:- No clinical symptoms, despite seropositivity- May last months, years, or even for the entire life of the patient- Disease may resolve, reactivate, or progress to tertiary syphilis Tertiary syphilis:- Gumma: destructive granulomatous lesions with a necrotic center that tend to ulcerate  → May affect any organ, e.g., skin, internal organs, bones  - Cardiovascular syphilis: aortitis, ascending aortic aneurysm (thoracic aortic aneurysm), syphilitic mesaortitis, aortic root dilation- Neurosyphilis  Diagnostics:1. Nontreponemal tests - Rapid Plasma Reagin (RPR): generally the test of choice- Venereal Disease Research Laboratory (VDRL)2. Treponemal tests - Treponema pallidum particle agglutination (TPPA)- Fluorescent treponemal antibody absorption test (FTA-ABS)Direct detection of the pathogen: definite tests to detect primary and secondary syphilis when a specimen can be obtained (e.g., exudative chancre, condyloma) Treatment:- First-line therapy: benzathine penicillin G  → Primary, secondary, or early latent: IM, single dose is sufficient→ Late latent, tertiary, or date of transmission unknown: weekly IM injections over a 3-week course→ Neurosyphilis: IV for 10-14 days- If penicillin allergy is confirmed with skin testing:→ Treat with doxycycline or ceftriaxone→ In neurosyphilis: desensitization and treat with penicillin→ During pregnancy: desensitize and treat with penicillin
• Cervicitis Etiology:- Infectious (most common): C. trachomatis, N. gonorrhea, herpes simplex virus, T. vaginalis- Noninfectious: localized trauma (e.g., cervical caps, diaphragms, tampons), chemical irritation (e.g., contraceptive creams, latex exposure), malignancy Risk factors: multiple partners, young age, new sexual partner within the last 6 months, unprotected intercourse Clinical features:- Often asymptomatic- Usually no fever  - Vaginal discharge: may be purulent, blood-tinged, and/or malodorous- Dyspareunia- Postcoital or intermenstrual bleeding- Lower abdominal or pelvic pain  - Symptoms of the underlying condition (e.g., genital lesions in HSV infections) Physical examination:- Abdominal palpation: tenderness/discomfort- Bimanual examination: motion tenderness of the cervix- Pelvic examination: erythematous, edematous, friable cervix; possibly visible discharge Diagnostics:- Diagnosis mainly clinical  - Assess vaginal secretions for appearance, pH, leukocyte count, and visible pathogens (e.g., protozoa in T. vaginalis infections)- Swab samples for bacterial culture Treatment:- Uncomplicated gonorrhea: single-dose ceftriaxone IM + single-dose azithromycin PO  - Complicated gonorrhea: single-dose ceftriaxone IM + doxycycline PO for 10-14 days- Chlamydia: Azithromycin or doxycycline (If gonococcal infection is suspected, combine azithromycin with ceftriaxone)
• Human immunodeficiency virus (HIV) – Diagnostics Screening tests:- Combination antigen/antibody tests: detect both HIV antigen (p24) and anti-HIV antibodies → a negative result essentially rules out HIV infection (almost 100% sensitivity)- Antibody-only tests (HIV serology):→ ELISA (enzyme-linked immunosorbent assay): standard method for detecting antibodies within approx. 1-3 hours; requires laboratory→ Rapid tests: can deliver results in ∼20 minutes and do not require a laboratory, which makes them suitable as an alternative to the more complex tests in some outpatient settings.   Confirmatory tests:- HIV-1/HIV-2 antibody differentiation immunoassay: can detect both HIV-1 and HIV-2 in ∼20 minutes and distinguish between the two types- Western blot: tests may be negative up to 2 months after infection; results are usually available after several days and HIV subtype O is not reliably detected. Detection of viral RNA: - Can detect HIV infection earlier than antibody/antigen-based tests but FDA-approved tests are limited to HIV-1- Indications: Neonatal HIV infection; Patients with indeterminate results; Patients presenting before seroconversion; Screening of blood donors
• HIV - Treatment Nucleoside reverse transcriptase inhibitors (NRTI): e.g., zidovudine, lamivudine, emtricitabine, abacavir, stavudine, didanosineSide effects:- Bone marrow suppression → neutropenia, anemia- Mitochondrial toxicity → myopathy, neuropathy, hepatic steatosis, and lactic acidosis- Abacavir-related hypersensitivity syndrome  - Didanosine/stavudine: pancreatitis- HIV-associated lipodystrophy: abnormal distribution of fat (clinical presentation varies greatly)→ Loss of subcutaneous fatty tissue (lipoatrophy) of face and extremities→ Metabolic changes: impaired glucose tolerance, hyperlipoproteinemia (elevated triglycerides, elevated total cholesterol, lowered HDL)→ Probable accumulation of fat in liver, muscles, abdomen, breasts and neck (buffalo hump)- Resistance: caused by mutations in the gene that codes for reverse transcriptase (pol gene) Non-nucleoside reverse-transcriptase inhibitors (NNRTI): e.g., nevirapine, efavirenzSide effects:- Hepatotoxicity (nevirapine)- CNS toxicity (efavirenz)- Hypersensitivity reactions (including Stevens-Johnson syndrome) Nucleotide analogs (also called nucleotide reverse-transcriptase inhibitors; NtRTI): e.g., tenofovir Protease inhibitors (PI): e.g., indinavir, ritonavir, nelfinavir, lopinavirSide effects- GI intolerance (nausea, diarrhea), lipodystrophy and fat accumulation, nephrolithiasis and crystal-induced nephropathy- Hyperglycemia: inhibition of insulin-dependent glucose transporters (GLUT 4) → peripheral insulin resistance→ impaired glucose tolerance Integrase inhibitors (INI): e.g., raltegravir, dolutegravir
• Malaria Clinical features:- Incubation: 7-42 days- Relapse in P. ovale or P. vivax infectionThe incubation period of malaria is a minimum of seven days; if a fever occurs before the seventh day following exposure in an endemic region, it is most likely not due to malaria!- Course: tertian and quartan malaria are associated with less severe symptoms, the involvement of fewer organs (rarely CNS or gastrointestinal symptoms), and a markedly lower risk of severe malaria.- Flu‑like symptoms- High fever→ Tertian malaria (P. vivax, P. ovale): periodic fever spikes every 48 hrs→ Quartan malaria (P. malariae): periodic fever spikes every 72 hrs→ Falciparum malaria (malignant tertian malaria): irregular fever spikes without a noticeable rhythm- Diaphoresis (sweating)- Weakness, paleness, dizziness  - Increased bleeding risk  → in severe cases, disseminated intravascular coagulation may occur.- Gastrointestinal: diarrhea, abdominal pain, nausea, and vomiting- Liver: hepatosplenomegaly, discrete jaundice- Severe malaria: can lead to severe organ dysfunction  → Kidneys: flank pain, oliguria, hemoglobinuria→ Cerebral: hallucinations, confusion, impaired consciousness, or even coma→ Cardiopulmonary: heart failure, pulmonary edema, shock Diagnostics:- CBC: Hemolytic anemia (↓ Hb, ↓ haptoglobin, ↑ LDH, ↑ indirect bilirubin, ↑ reticulocytes), Thrombocytopenia, Possibly leukocytopenia- Best initial test: thick blood smear (high sensitivity); detects the presence of parasites.  - Confirmatory testing: thin blood smear- Rapid diagnostic tests (RPDs): Determination of specific malaria antigens, e.g., HRP2, pLDH, and aldolaseIf symptoms persist despite negative microscopy and rapid testing, diagnostics should be repeated every eight hours for several days! Treatment:- Tertian malaria:→ Chloroquine OR hydroxychloroquine + Primaquine: to eradicate hypnozoites of P. vivax and P. ovale and prevent relapse→ P. vivax (chloroquine‑resistant): Artemether-lumefantrine- Quartan malaria→ Treatment of choice: chloroquine or hydroxychloroquine- Chloroquine-sensitive falciparum: Chloroquine OR hydroxychloroquine- Chloroquine‑resistant falciparum: Artemether-lumefantrine OR Atovaquone‑proguanil OR Quinine PLUS doxycycline OR Quinine PLUS tetracycline OR Quinine PLUS clindamycin OR Mefloquine  - Severe falciparum malaria: Artesunate followed by artemether/lumefantrine OR Quinidine PLUS doxycycline OR Quinidine PLUS tetracycline OR Quinidine PLUS clindamycin
• Side effects of antimalarial medication Chloroquine or hydroxychloroquine:- Irreversible retinopathy!- CNS: agitation, anxiety, confusion- Gastrointestinal discomfort Primaquine: Hemolytic crisis in G6PD deficiency   Mefloquine:- CNS: dizziness, confusion, nightmares, hallucinations, seizures- Rash- Gastrointestinal discomfort Atovaquone-proguanil: Gastrointestinal discomfort Quinine:- CNS: headache, mental status altered- Gastrointestinal discomfort- Fever, flushing Doxycycline or tetracycline:- Photosensitivity- Nephro- and hepatotoxicity- Damage to mucous membranes (these antibiotics should be taken with a lot of water) Artemether-lumefantrine:- Gastrointestinal discomfort- Prolonged QT interval Quinidine:- Palpitations, angina pectoris- CNS: dizziness, fatigue, headache- Rash- Gastrointestinal discomfort Artesunate: Hemolytic crisis in G6PD deficiency  
• Advertisement
• Clostridium difficile infection Pathogen: Gram-positive bacillus, obligate anaerobe- Can be toxigenic or non-toxigenic; must be toxigenic to cause the disease- Forms environmentally-resistant spores (capable of withstanding heat and acid) Risk factors:- Antibiotic treatment: Common triggers include clindamycin, cephalosporins, fluoroquinolones and, less commonly, penicillin - Gastric acid suppression (e.g., with proton pump inhibitors) Clinical features: Symptoms of C. difficile-associated diarrhea (CDAD) usually develop during antibiotic treatment or 2-10 days following its initiation; however, 25-40% of cases manifest as late as 10 weeks following treatment. - Watery diarrhea, characteristically foul-smelling- Mild disease manifests with ≥ 3 stools per day; patients with fulminant colitis may have up to 20 stools per day.- May contain traces of mucus or occult blood- Hematochezia and melena are both rare.- Cramping abdominal pain, nausea, anorexia- Fever and dehydration (especially in severe cases)- Fulminant colitis: abdominal distention and severe hypovolemia- Recurrent disease: symptom reoccurrence 2-8 weeks following the end of treatment (10-40% of cases)   Diagnostics:- Stool tests→ Indication: unexplained, new-onset, loose stool ≥ 3 times in 24 hours- Confirmatory tests of choice→ PCR for C. difficile genes alone  → Enzyme immunoassay (EIA) for C. difficile glutamate dehydrogenase antigen and EIA for C. difficile toxins A and B  - Blood tests: Leukocytosis, Elevated serum creatinine (possible kidney injury caused by dehydration), Lowered serum albumin, Electrolyte imbalance, particularly hypokalemia (caused by severe diarrhea), Elevated lactate levels- Abdominal x-ray/CT scan: detection of toxic megacolon, abscesses, perforation, or evidence of pseudomembranous colitis   Treatment:- If clinical suspicion for CDAD is high, empiric antibiotic treatment may be initiated before laboratory confirmation of C. difficile. - Nonsevere cases→ First-line: oral vancomycin or oral fidaxomicin→ Second-line: oral metronidazole- Severe cases→ First-line: oral vancomycin→ Second-line: fidaxomicin- Fulminant cases→ First-line: oral vancomycin and intravenous metronidazole→ In patients with ileus, vancomycin per rectum (enema) may be added.
• Lyme disease Stage I (early localized Lyme disease)- Symptoms develop within 7-14 days after a tick bite- Erythema chronicum migrans (EM)→ Occurs in 80% of infected individuals→ Usually a circular, slowly expanding red ring around the bite site with central clearing  → Typically warm, painless→ Self-limiting (typically subsides within 3-4 weeks)- Flu‑like symptoms Stage II (early disseminated Lyme disease):- Symptoms develop 3-10 weeks after a tick bite  - Migratory arthralgia that can progress to Lyme arthritis→ Spreads from one joint to another  → Generally in large joints (especially knee or elbow)- Early neuroborreliosis→ Cranial nerve disorders: Most commonly peripheral facial nerve palsy  → Nocturnal radicular pain, paresthesia, and paresis→ Meningitis→ Polyneuropathy (mononeuritis multiplex, asymmetrical)- Lyme carditis→ Risk of cardiac arrhythmias (e.g., AV Block) and rarely myopericarditis- Cutaneous manifestations: Multiple erythema migrans lesions- Ocular manifestations: including conjunctivitis, retinal vasculitis, optic neuropathy, and uveitis Stage III (late Lyme disease):- Symptoms develop months to years after the initial infection  - Chronic Lyme arthritis (10% of cases): Lasts over a year and may be intermittent or persistent- Late neuroborreliosis manifestations include:→ Aseptic (lymphocytic) meningitis→ Progressive encephalomyelitis→ Cognitive impairment→ Gait abnormality→ Bladder dysfunction→ Psychiatric abnormalities (e.g., depression, anxiety, bipolar disorder etc.)→ Peripheral polyneuropathy Diagnostics:- After a tick bite, observe for erythema chronicum migrans. If present → Antibiotic treatment- If symptoms of Lyme disease arise in a patient with possible exposure (especially if a history of recent travel to an area with high vector density) → conduct two-step serological testing1. Enzyme‑linked immunosorbent assay (ELISA)2. Confirmatory test: Western blotVarious diseases can lead to a false positive serology as a result of cross-reactions, including: Syphilis, Rocky Mountain spotted fever, Systemic lupus erythematosus, Rheumatoid arthritis Treatment:- First-line oral antibiotics: Doxycycline, Amoxicillin, Cefuroxime axetil- Neurological symptoms: Intravenous antibiotics with ceftriaxone (or Cefotaxime, Penicillin G) In case of a tick bite: Remove ticks immediately!  1. Grasp the tick with tweezers directly above the skin's surface.2. Carefully pull upward with even pressure.  3. Do not use nail polish remover, adhesives, oils, or similar substances to remove the tick. The tick should be removed quickly rather than waiting for it to detach slowly.4. Disinfect the site of the bite and dispose of the tick
• Babesiosis Pathogen: Babesia species (typically Babesia microti)Vector: Ixodes scapularisDistribution: midwest and northeast US Clinical features:- Incubation period: 1-6 weeks- Flu-like symptoms- Hemolytic anemia → dark urine and/or icterus- Mild splenomegaly and/or hepatomegaly- Gastrointestinal symptoms (e.g., nausea, vomiting, abdominal pain)- Typically no rash Diagnostics:- Confirmatory test: Peripheral blood smear showing intraerythrocyte rings and/or maltese crossOR- Babesia DNA detection by PCR of blood Treatment:- Mild disease: atovaquone and azithromycin- Severe disease: quinine and clindamycin
• Rocky Mountain spotted fever (RMSF) Pathogen: Rickettsia rickettsiiVector: Dermacentor variabilis/Dermacentor andersoni/Rhipicephalus sanguineusDistribution: northeast and south US   Clinical features:- Incubation period: 2-14 days- Flu-like symptoms- Blanching maculopapular rash (90% of cases): begins on wrists and ankles 2-5 days after onset of fever → spreads to trunk, palms, and soles → becomes petechial and/or hemorrhagic in 50% of cases- Ankle and/or wrist swelling- Gastrointestinal symptoms (e.g., nausea, vomiting, abdominal pain)- Meningitis, focal neurological deficits- Rapid clinical deterioration with shock and multi-organ dysfunction Diagnostics:- Confirmatory test: Detection of R. rickettsii DNA by PCR in a skin biopsy specimen or acute phase whole blood specimenOR- Serologic test: Four-fold increase in IgG-specific IFA antibody assay Treatment: Doxycycline
• Ehrlichosis Pathogen: Ehrlichia chaffeensis, Ehrlichia ewingiiVector: Amblyomma americanumDistribution: southeastern and south-central US Clinical features:- Incubation period: 1-2 weeks- Flu-like symptoms- Gastrointestinal symptoms (e.g., nausea, vomiting, abdominal pain)- Typically no rash   Diagnostics:- Peripheral blood smear shows morulae within leukocytes.  - Confirmatory test → Ehrlichia DNA detection by PCR of bloodOR→ Four-fold increase in IgG-specific IFA antibody assay between the acute and convalescent serum samples Treatment: Doxycycline
• Staphylococcal toxic shock syndrome Etiology:- ∼ 50% of cases: caused by prolonged use of tampons over several days- Postsurgical or after wound infections Pathophysiology: exotoxins  Clinical findings: - If tampon related, symptoms usually appear within five days after menstruation- Widespread exanthem with skin peeling involving palms and soles- Myalgias, vomiting, diarrhea- Symptoms of shock: hypotension, tachycardia- Fever- Altered mental status: confusion, lethargy, coma Laboratory tests: ↓ Platelets, ↑ Bilirubin, ↑ transaminases Treatment:- IV fluids- Remove focus of infection (e.g., drain surgical wounds, remove tampon)- Antibiotics→ First-line antibiotics against MSSA TSS: clindamycin + oxacillin→ First-line antibiotics against MRSA TSS: clindamycin + vancomycin
• Cryptococcosis Pathogen: Cryptococcus neoformansRisk factors: AIDS, exposure to pigeon droppingsAIDS-defining illness: IF extrapulmonary Clinical features:- Cryptococcal meningoencephalitis or brain abscess: headache, fever, signs of increased intracranial pressure, confusion, absent meningeal signs- Isolated pneumonia is possible Diagnostics:- LP: → India ink stain (clear halo), positive cryptococcal antigen (also in blood), and fungal culture (Sabouraud agar) showing ∼10-μm yeast with thick polysaccharide capsule and narrow, unequal budding→ Mucicarmine: A narrow-spectrum stain used in the diagnosis of C. neoformans. Stains the thick polysaccharide capsule bright red- Latex agglutination test: detects capsular antigen (very specific) Treatment:- IV amphotericin B and flucytosine for ≥2 weeks followed by oral fluconazole for 8 weeks- Maintenance therapy: oral fluconazole for > 1 year (until symptoms resolve and CD4 > 100/mm3)- Serial therapeutic LPs for ↑ intracranial pressure
• Histoplasmosis Pathogen: Histoplasma capsulatumRisk factors: AIDS and other immunocompromised patients, exposure to bird or bat droppings, especially in Mississippi and the Ohio river valley AIDS-defining illness if disseminated or extrapulmonary Clinical features:- Often asymptomatic- Flulike illness: fever, weight loss, erythema nodosum, hepatosplenomegaly, lymphadenopathy, nonproductive cough- The presence of ulcerative oral lesions is specific for histoplasmosis Diagnostics:- Chest x-ray: diffuse nodular densities, focal infiltrate or cavity, or lymphadenopathy- Best initial: positive urine and serum polysaccharide antigen test- Silver stain of biopsy or bronchoalveolar lavage showing macrophages filled with dimorphic fungus with septate hyphae- Culture (blood, sputum, bone marrow, lymph node, liver)- Liver biopsy: demonstrates disseminated disease with the presence of fungal organisms in the yeast-stage of development. Treatment:- Mild disease: supportive therapy- Chronic cavitation: oral itraconazole > 1 year- Severe pulmonary or disseminated disease: IV amphotericin B/liposomal then oral itraconazole  
• Coccidioidomycosis (valley fever) Pathogen: Coccidioides immitisRisk factors: travel to Southwestern United States, California  AIDS-defining illness if disseminated or extrapulmonary Clinical features:- Flu-like illness or pneumonia: fever, cough, night sweats, anorexia, chest pain, and dyspnea- Extrapulmonary: CNS (e.g., meningitis), skin (desert bumps), and joints (desert rheumatism) Diagnostics:- Serology: increased IgM (increases within 2 weeks of infection and disappears after 2 months); increased IgG at 1-3 months- Chest x-ray: normal or infiltrates/lymphadenopathy/pleural effusion- KOH or culture (sputum, wound exudate, joint effusion) showing large spherules containing endospores Treatment:- IV amphotericin B (severe infection)- Alternative: itraconazole
• Paracoccidioidomycosis Pathogen: Paracoccidioides brasiliensis, Paracoccidioides lutziiRisk factors: travel to South and Central America Clinical features:- Infected patients often asymptomatic- Acute pneumonia- Painful nasal, pharyngeal, and laryngeal mucosal ulcerations- Lymphadenopathy (usually cervical)- Can disseminate → extrapulmonary manifestations (including verrucous skin lesions) Diagnostics:- KOH/calcofluor staining on smears or silver/PAS-staining on tissue biopsy: budding yeast with “captain's wheel” formation- Cultures have a low sensitivity. Treatment:- Itraconazole- Severe or refractory cases: amphotericin B
• Blastomycosis Pathogen: Blastomyces dermatitidisRisk factors: travel to Southeastern and Central US Clinical features:- Pneumonia- Extrapulmonary: can disseminate to the skin (verrucous lesions and granulomatous nodules) and bones  Diagnostics:- KOH or culture (confirmatory) of sputum, urine, or body fluids showing → yeast form (at body temperature or > 37°C): broad-based buds→ Mold form (at room temperature): circular fungal cells with filamentous hyphae Treatment:- Local infection: fluconazole and itraconazole- Systemic infection: IV amphotericin B
• Aspergillosis Pathogen: Aspergillus fumigatus, Aspergillus flavusRisk factors: immunocompromise and chronic granulomatous infection Clinical features:- ABPA: associated with asthma and cystic fibrosis; causes bronchiectasis and eosinophilia- Pulmonary aspergilloma: chronic cough, hemoptysis- Invasive aspergillosis: fever, cough, respiratory distress- Endocarditis Diagnostics:- ABPA: eosinophilia, elevated IgE levels, pulmonary infiltrates chest x-ray or CT- Pulmonary aspergilloma: x-ray or CT shows mobile fungus ball; serology is positive Aspergillus IgG- Invasive aspergillosis: tissue biopsy showing 45° angle branching septate hyphae with fruiting bodies Treatment:- ABPA: oral prednisone for severe cases; itraconazole for recurrent episodes- Pulmonary aspergilloma: lobectomy for massive hemoptysis- Invasive aspergillosis: IV voriconazole, caspofungin, or amphotericin B
• Hookworm infections (ancylostomiasis; necatoriasis) Pathogen:- Human hookworms (Ancylostoma duodenale and Necator americanus): nematodes (roundworms)- Zoonotic hookworms, i.e., cat and dog hookworms that can also infect humans (Ancylostoma braziliense and Ancylostoma caninum) Mode of transmission: percutaneous penetration of larvae (primarily via the feet)   Clinical features:- Cutaneous entry: pruritus, erythema, maculopapular rash, occasionally with serpiginous marks representing larval tracks→ In zoonotic hookworm infections, only cutaneous symptoms are present, which is termed cutaneous larva migrans (CLM)  - Respiratory tract: dry cough, wheezing → see Löffler syndrome- Intestine: abdominal pain, weight loss, nausea, vomiting, diarrhea- Anemia   Diagnostics:- Initial test: complete blood cell (CBC) count may show eosinophilia and microcytic anemia- Confirmatory test: consecutive stool examination for eggs or worms Treatment:- For human hookworms: bendazoles or pyrantel pamoate- For CLM: bendazoles, ivermectin
• Toxocariasis Pathogen:- Toxocara canis (dog roundworm), Toxocara mystax (synonym: Toxocara cati, cat roundworm)- Toxocara are nematodes. Nematodes are a group of worms also referred to as roundworms. Mode of transmission: fecal-oral   Incubation period: 2-4 weeks Clinical features:- Visceral toxocariasis (also called visceral larva migrans): caused by larvae migrating through the organs→ Fever and flu-like symptoms→ Hepatomegaly and abdominal pain→ Respiratory symptoms: dyspnea, wheezing, cough, pneumonia (see also “Löffler syndrome”)→ Rash- Ocular toxocariasis (also called ocular larva migrans): caused by larvae migrating into the eye→ Unilateral vision loss and resulting strabismus→ Leukocoria→ Inflammation, scarring, and possible detachment of the retina Diagnostics:- Initial tests: CBC: eosinophilia, ↑ Serum total IgE- Confirmatory test: ELISA detects IgG antibodies to Toxocara excretory/secretory antigens Treatment: bendazoles
• Enterobiasis Pathogen:- Enterobius vermicularis (pinworm)- Pinworms are nematodes (roundworms). Epidemiology:- Most common helminthic infection in the U.S.- Prevalence in the US: ∼ 40 million- Primarily children 5-10 years of age   Clinical features:- Anal pruritus (especially at night)- ♀: vulvovaginitis, particularly in children- Occasionally symptoms of intestinal infection (nausea, vomiting, and abdominal pain, sometimes severe enough to mimic appendicitis)   Diagnosis: tape test   Treatment: bendazoles or pyrantel pamoate- During pregnancy: pyrantel pamoate is the drug of choice→ Should only be administered if pregnancy is compromised (e.g., weight loss, sleeplessness)→ If indicated, preferably not start until the 3rd trimester, when risk to the fetus is likely reduced 
• Trichiuriasis Pathogen:- Trichuris trichiura (whipworm)- Whipworms are nematodes. Mode of transmission: fecal-oral Life cycle: host ingests eggs → eggs hatch and release larvae in the small intestine → larvae mature into adult worms in colon → adult worms lay eggs, which are shed in feces Clinical features:- Mostly asymptomatic- In children: severe infection causes diarrhea, iron deficiency anemia, growth retardation, rectal prolapse Diagnosis:- Microscopic examination of stool for eggs  - Concentration technique can be used for light infections. Treatment: mebendazole or albendazole
• Ascariasis Pathogen:- Ascaris lumbricoides- Ascaris are nematodes (roundworms), and are also known by the synonym “giant roundworm.”   Epidemiology: most common helminth infection worldwide (mainly affecting children in tropical and developing countries) Clinical features:- Early symptoms: dry cough, blood-tinged sputum, wheezing (see also “Löffler syndrome”)- Late symptoms: anorexia, abdominal discomfort, nausea, vomiting, and diarrhea- Additional symptoms due to blockage by adult worms depend on the location of the obstruction:→ Bowel obstruction, especially at ileocecal valve→ Obstruction of the appendix → features of appendicitis→ Obstruction of biliary and pancreatic ducts → features of cholestasis, pancreatitis Diagnostics:- Initial test: complete blood cell (CBC) count showing eosinophilia- Confirmatory test: stool sample showing the presence of worms; visible eggs with a knobby appearance under microscope   Treatment: bendazoles and pyrantel pamoate  
• Trichinellosis Pathogen:- Trichinella spiralis and other Trichinella spp. - Trichinella are nematodes (roundworms). Mode of transmission: fecal-oral; consumption of undercooked meat (especially pork) containing encysted larvae Clinical features:- Intestinal phase: abdominal pain, diarrhea, nausea, and vomiting- Muscle phase: → Myositis: myalgia, muscle swelling, weakness→ Periorbital edema→ Other symptoms include: fever, rash, splinter hemorrhages, retinal and conjunctival hemorrhages, chemosis Diagnosis:- Initial test: CBC showing eosinophilia (and sometimes leukocytosis), Commonly ↑ creatinine kinase- Confirmatory test: serological detection of antibodies Treatment: bendazoles   Complications:- Cardiac: ECG changes (e.g., arrhythmias)- CNS: meningitis, encephalitis- Pulmonary: myositis involving respiratory muscles, pneumonia
• Strongyloidiasis Pathogen:- Strongyloides stercoralis- Strongyloides are nematodes (roundworms). Mode of transmission: Larvae excreted in feces penetrate the skin, e.g., while a potential host is walking barefoot.   Life cycle: penetration and migration into the skin → migration of larvae via the bloodstream to the lungs → migration via the alveoli and bronchial system to the pharynx → swallowing and autoinfection → larvae mature into adult, egg-producing worms in the intestine → eggs develop into “free-living” infectious larvae and are excreted in feces Incubation period: 1-4 weeks   Clinical features:- Cutaneous phase: swelling, erythema, maculopapular rash, and serpiginous lesions or urticarial tracts (larva currens is pathognomonic); pruritus- Pulmonary phase: dry cough and wheezing, rarely pneumonia (see also “Löffler syndrome”)- Intestinal phase: abdominal pain, diarrhea, anorexia, nausea, and vomiting   Complications: hyperinfection syndrome, possibly leading to organ dysfunction and septic shock, and occurring especially in immunosuppressed individuals (e.g., AIDS, steroid therapy)   Diagnostics:- Initial test: CBC may show eosinophilia- Confirmatory test: consecutive stool examination for mobile larvae   Treatment: ivermectin or bendazoles   Strongyloides, Ancylostoma, and Necator get into your feet from the SANd!
• Taeniasis Taeniae are tapeworms. Tapeworms are a group of worms also referred to as cestodes. Intestinal taeniasis:- Pathogen: Taenia saginata (beef tapeworm), Taenia solium (pork tapeworm)  - Mode of transmission: Ingestion of larvae (cysticerci) in raw or undercooked beef/pork - Clinical features:→ Often asymptomatic→ Symptoms caused by adult worms in the intestinal tract: abdominal pain, anorexia, weight loss, nausea, and vomiting- Diagnostics: Initial test: CBC may show eosinophilia (in only ∼ 45% of patients); Confirmatory test: stool examination → detection of eggs and/or worms- Treatment: Praziquantel Cysticercosis:- Pathogen: Taenia solium (pork tapeworm)- Mode of transmission: Fecal-oral ingestion of eggs from feces of humans with intestinal taeniasis  - Clinical features: Symptoms caused by cysticerci accumulation in subcutaneous tissue, muscles, brain, spinal cord, and eyes→ Palpable subcutaneous cysts→ Myalgia→ Neurocysticercosis: increased intracranial pressure, neurological deficits, seizures→ Ocular cysticercosis: eye pain, loss of visual acuity or vision in one eye- Diagnostics: Initial tests: CBC, stool testing→ Imaging: MRI/CT showing multiple, small (< 1 cm) cystic ring-enhancing lesions in the brain with a membranous wall→ Lumbar puncture: ↑ protein, ↓ glucose, mononuclear pleocytosis  → Confirmatory test: serum enzyme-linked immunotransfer blot (EITB) assay- Treatment: Albendazole + corticosteroids

back  |  next 1 / 2