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Final Exam Study Guide – Chapters 21-26 Your final will be a take-home exam consisting of multiple choice and case study questions. Major microbes to review have been summarized in the sections of the following overviews. Concerning conditions/diseases discussed in class, make sure that you are familiar with the following: etiology, diagnostic methodologies, means of transmission, and treatment. The expectation is that the exam is to be completed individually using textbook and notes (including this study guide); evidence of collaboration and/or plagiarism will result in a zero. Introduction to Skin & Soft Tissue Infections (Chapter 21) The resistance of skin to infection is due to the integrity of the keratinized skin, the presence of inhibitory fatty acids produced by sebaceous glands, the dryness of the skin, and the inhibitory effect of the resident normal skin flora. Skin and soft tissue infections can be caused by either direct penetration of a pathogen through the skin or hematogenous spread of the pathogen to the site. Normal skin flora includes organisms that, in the setting of a disruption in the integrity of the skin (such as the presence of a surgical suture or an insect bite), may cause infection. In the setting of severe damage to the skin, as occurs with burns, even normally innocuous organisms, including endogenous bacteria, can cause severe disease. Similarly, when the skin is no longer dry, as may occur in moist intertriginous spaces or when occlusive dressings are present, the patient is at increased risk of infection. Cutaneous manifestations of systemic disease are common. Rocky Mountain spotted fever, meningococcemia, enteroviral infection, and toxic shock syndrome can all present with fever and a diffuse erythematous macular rash. Other systemic infections that can present with a diffuse rash include scarlet fever, measles, and German measles. The characteristic rash of Lyme disease, erythema migrans, is specific enough to establish the diagnosis. The nature of the lesion (macular, papular, vesicular, pustular, or bullous) may help to narrow the differential diagnosis. For example, varicella-zoster virus infection typically results in vesicular skin lesions. The rash of secondary syphilis, on the other hand, may present clinically as macular, papular, maculopapular, or pustular skin lesions but does not present as a vesicular rash. Skin and soft tissue infections can be classified on the basis of the anatomic level at which infection occurs. The more superficial infections, such as folliculitis caused by Staphylococcus aureus or cellulitis caused by Streptococcus pyogenes, are important to treat at an early stage. Delay in treatment may result in invasion of the deeper structures, as in necrotizing fasciitis, which has a high mortality rate. Damage to the skin and soft tissues, as occurs in traumatic injuries, may allow the entry into the wound of soil organisms such as Clostridium perfringens, an anaerobic gram-positive rod. Under favorable conditions, potentially fatal soft tissue infections (myositis, gas gangrene) may occur. Skin & Soft Tissue Pathogens Organism Bacteria Bartonella henselae General Characteristics Infection Source Disease Manifestation Fastidious gram-negative bacillus Cat scratch disease, bacillary angiomatosis (in immunocompromised individuals) Borrelia burgdorferi Clostridium perfringens Spirochete Anaerobic gram-positive bacillus Clostridium tetani Anaerobic gram-positive bacillus Exogenous; cats appear to be primary host Tick bome Exogenous (wounds), endogenous (bowel flora) Exogenous (wounds) Corynebacterium diphtheriae Aerobic gram-positive bacillus Exogenous Diphtheria (pharyngeal) and wound Diphtheria Group A streptococci (Streptococcus pyogenes) Group B streptococci (Streptococcus agalactiae) Neisseria gonorrhoeae Catalase-negative, grampositive cocci Oxidase-positive, gramnegative diplpcoccus Oxidase-positive, gramnegative diplococcus Endogenous Endogenous Cellulitis, bacteremia, scarlet fever, necrotizing fasciitis, pharyngitis, pneumonia, poststreptococcal glomerulonephritis and rheumatic fever Cellulitis, sepsis, meningitis Sexually transmitted Genital tract involvement, pharyngeal infection, ocular infection, bacteremia, arthritis with dermatitis Lyme disease; rash, arthritis, nervous system and cardiac manifestations Gas gangrene, emphysematous cholecystitis, bacteremia, food poisoning Tetanus 1 Organism Neisseria meningitidis Pasteurella multocida Pseudomonas aeruginosa Staphylococcus aureus Treponema pallidum Fungi Blastomyces dermatitidis Candida albicans Candida spp., non-albicans Cryptococcus neoformans Epidermophyton floccosum Microsporum spp. General Characteristics Oxidase-positive, gramnegative diplococcus Oxidase-positive, gramnegative bacillus Infection Source Endogenous (from colonization) Zoonosis (often animal bite or scratch) Exogenous Disease Manifestation Meningitis, bacteremia Endogenous Cellulitis, bacteremia, endocarditis, septic arthritis, abscesses Direct sexual contact, vertical (mother to child) Primary (painless chancre), secondary (diffuse rash), latent, and late syphilis; can affect any organ Dimorphic mold Yeast, often germ tube positive Yeasts, germ tube negative Exogenous Endogenous Encapsulated yeast KOH-positive skin lesions; clubshaped macroconidia, absent microconidia KOH-positive skin lesions; fluoresces yellow-green under Wood's light Exogenous Anthropophilic Cutaneous infection, pneumonia, meningitis, bone infection Thrush, vaginal yeast infection, diaper rash, esophagitis, nosocomial UTI, nosocomial bloodstream infection Thrush, vaginal yeast infection, nosocomial UTI, nosocomial bloodstream infection Meningitis, pneumonia, bloodstream infection, cellulites Dermatophyte infection of keratinized tissue (rarely nails) Lactose-nonfermenting, oxidase positive, gramnegative bacillus Catalase-positive, coagulase positive, grampositive coccus Spirochete (does not Gram stain) Trichophyton spp. KOH-positive skin lesions Parasites Ancylostoma brazi/iense Ancylostoma caninum Leishmania tropica Pediculus spp. Hookworm of dog Hookworm of dog Protozoan Ectoparasite Phthirus pubis Sarcoptes scabei Viruses Erythrovirus B19 Herpes simplex virus Ectoparasite Ectoparasite Human herpesvirus type 6 Human immunodefi. ciency virus (HIV) Enveloped, dsDNA Enveloped RNA retrovirus Rubella virus (German measles) Rubeola virus (measles) Enveloped, ssRNA Papillomavirus Varicella-zoster virus Nonenveloped, dsDNA Enveloped, dsDNA Nonenveloped, ssDNA Enveloped, dsDNA Enveloped, ssRNA Endogenous Cellulitis, bacteremia, osteomyelitis, meningitis Skin infections in burn patients, community and nosocomial UTl’s, nosocomial pneumonia, nosocomial bacteremia, ecthyma gangrenosum May be zoophilic (e.g., M. canis), geophilic (e.g., M. gypseum), or anthropophilic (e.g., M. audouinil) May be zoophilic (e.g., T. mentagrophytes) or anthropophilic (e.g., T. schoenleinil) Dermatophyte infection of keratinized tissue (rarely nails) Exogenous Exogenous Exogenous Exogenous (sand fly) Exogenous Exogenous Cutaneous larva migrans Cutaneous larva migrans Ulcerative skin lesions Body lice Person to person Person to person; reactivation of latent infection; during passage of the neonate through the birth canal Person to person Bloodborne and sexual transmission Vertical, mother to child Respiratory spread Person to person Respiratory spread Erythema infectiousum; anemia Genital ulcers; oral, ocular infections; encephalitis; neonatal infection; esophagitis (immunocompromised individuals) Dermatophyte infection of keratinized tissue including nails Crab louse Scabies infestation Exanthem subitum (roseola) AIDS, mononucleosis-like syndrome with rash in primary infection Inapparent or subclinical infection in adults; birth defects in infants Measles; pneumonia, encephalomyelitis, subacute sclerosing panencephalitis Warts Chicken pox; zoster (may disseminate) Introduction to Central Nervous System Infections (Chapter 22) Infections of the central nervous system (CNS) are infrequent compared to the other infections discussed for other organ systems of 2 the human body, but they are very important because of the high mortality rates and the serious sequelae associated with them, including learning, speech, and motor skills disorders, seizures, and hearing and sight loss. The most frequent CNS infections are meningitis, encephalitis, and abscess. Intoxication with tetanus and botulinum toxins can affect the CNS, causing spastic or flaccid paralysis, but these diseases are quite rare in the developed world. There are two major forms of meningitis, septic and aseptic. Septic meningitis is typically caused by bacteria. The cerebrospinal fluid (CSF) is usually cloudy, with over 1,000 white blood cells per L with neutrophils predominating; increased protein levels due to inflammation; and decreased glucose due in part to metabolism by white blood cells. Aseptic meningitis can be caused by viruses, fungi, or Mycobacterium tuberculosis. In aseptic meningitis, the CSF is "clear" due to a cell count typically in the 100-500/l range. Except very early in the disease course, the predominant cell type is mononuclear, with lymphocytes predominating. CSF glucose levels are frequently normal, but they may be decreased in over half of patients with fungal or mycobacterial infections. CSF protein levels are frequently normal except with M. tuberculosis, where they are typically elevated. Bacterial meningitis is most common in the very young, the very old, and the immunocompromised; of these, it is seen most commonly in children 2 months to 5 years of age. Group B streptococci are the most common cause of neonatal meningitis (newborns to 2 months). Listeria monocytogenes is another organism that causes neonatal disease. It also is an important agent of meningitis in the immunosuppressed. Gram-negative enteric bacilli, including Escherichia coli, Klebsiella pneumoniae, and Citrobacter diversus, may also cause neonatal meningitis. Congenital syphilis, which may manifest itself during the neonatal period, frequently will have a CNS component, neurosyphilis. Until recently, Haemophilus influenzae type b was the most common cause of bacterial meningitis in children 2 months to 5 years of age, but the widespread use of conjugated H. influenzae type b vaccine has resulted in a dramatic decline in the incidence of this disease. Streptococcus pneumoniae and Neisseria meningitidis are now the leading causes of meningitis in this age group and the elderly. Individuals with head trauma are also at risk for developing bacterial meningitis. The organisms most frequently associated with this type of bacterial meningitis are coagulase-negative staphylococci (especially in patients with CNS shunts or who have undergone neurosurgical procedures), Staphylococcus aureus, and Pseudomonas aeruginosa. M. tuberculosis meningitis is seen primarily in children and the immunosuppressed. Viral meningitis is typically caused by enteroviruses other than poliovirus. It is seen primarily in the summer months in infants and young children. Herpes simplex virus can cause a typically benign meningitis associated with primary genital tract infections. This is not to be confused with herpes simplex encephalitis, as discussed below. Encephalitis is due primarily to viruses. Herpes simplex virus causes probably the most common form of viral encephalitis encountered in the developed world. It can occur in neonates and during reactivation of latent infection in adults. This form of herpes infection can produce necrotic lesions in the brain, resulting in long-term sequelae or death. Insect-borne viruses such as Eastern equine, Western equine, St. Louis, and La Crosse encephalitis viruses are encountered in the United States. In many states in the eastern United States, an epidemic of rabies in animals is occurring. It is only a matter of time before human cases are reported. Fungal meningitis is seen primarily but not exclusively in the immunocompromised. It is of particular importance in AIDS patients, with Cryptococcus neoformans being far and away the most important cause of CNS infection in this patient population. Parasites may also cause CNS infection. The most frequently encountered parasite causing CNS infections in the developed world is Toxoplasma gondii. These infections occur primarily in AIDS patients and represent reactivation of latent infections. In the developing world, one of the most common causes of a clinical presentation of meningitis/encephalitis is cerebral malaria. A major cause of adult onset of seizures in certain areas of the developing world where pork is a source of protein in the diet is cysticercosis. This disease occurs when eggs of the pork tapeworm Taenia solium are ingested. The parasite is unable to complete its life cycle, and cyst-like lesions occur throughout the body including the brain. An amoeba, Naegleria fowleri, causes a rare, fatal form of meningoencephalitis. It is found in individuals living in temperate regions who swim in warm fresh water during the summer months. Brain abscesses occur either through direct extension from a contiguous site, following trauma, or by hematogenous spread from another infected site. Typically, patients with abscesses due to hematogenous spread have either endocarditis or a lung abscess. Septic emboli, which are small blood clots containing infectious agents, are released from the primary infection site and enter the bloodstream. The embolus lodges in a capillary in the brain, causing a localized hemorrhage and producing a site for the initiation of infection which evolves into a brain abscess. The organisms most frequently causing abscesses in immunocompetent individuals are either S. aureus or organisms usually found in the oropharynx including the viridans group streptococci, Actinomyces spp., and 3 anaerobic bacteria. In immunocompromised individuals, Aspergillus, Mucor, Rhizopus, and Nocardia spp. can cause brain abscess. In trauma patients, S. aureus and gram-negative rods are frequently seen. In diabetic patients, rhinocerebral mucormycosis can extend from the sinuses into the brain, causing extensive necrosis. Nervous System Pathogens Organism Bacteria Actinomyces spp. Citrobacter diversus Clostridium botulinum Clostridium tetani Coagulase-negative staphylococci Escherichia coli Group B streptococci (Streptococcus agalactiae) Haemophilus influenzae type b Listeria monocytogenes Mycobacterium tuberculosis Neisseria meningitidis Nocardia spp. Oral streptococci (5. sanguis, S. mutans, etc.) Prevotella sp., Porphyromonas sp. Pseudomonas aeruginosa Staphylococcus aureus Streptococcus pneumoniae Fungi Aspergillus spp. Cryptococcus neoformans Mucor sp., Rhizopus sp. Parasites. General characteristics Patient population Disease manifestation Individuals with aspiration pneumonia Brain abscess Neonates Meningoencephalitis with abscess Infants, adults who ingest botulinum toxin Botulism, flaccid paralysis Any, often associated with deep tissue wound Tetanus, spastic paralysis Individuals with foreign bodies, e.g., shunts or bolts Meningitis Neonates Meningitis Neonates, immunocompromised adults Meningitis Unvaccinated children Meningitis Neonates, immunocompromised adults Meningitis Acid-fast bacillus Children; patients with AIDS Tuberculous Meningitis Oxidase-positive, gramnegative diplococcus Aerobic, partially acidfast branching bacilli All ages; outbreaks in college students & military Meningitis Individuals with pulmonary nocardiosis Brain abscess Individuals with aspiration pneumonia Brain abscess Individuals with aspiration pneumonia Brain abscess Branching, gram-positive bacilli, usually anaerobic Enteric gram-negative bacillus Toxin-producing, anaerobic, gram-positive bacillus Toxin-producing, anaerobic, gram-positive bacillus Catalase-positive, grampositive cocci Lactose-fermenting, gram-negative bacillus Catalase-negative, grampositive cocci Gram-negative, pleiomorphic bacillus Catalase-positive, grampositive coccobacillus Alpha-hemolytic, grampositive cocci Anaerobic, gram-negative bacilli Oxidase-positive, gramnegative bacillus Catalase-positive, grampositive cocci Catalase-negative, grampositive cocci Acute-angle, septate hyphae in tissue Encapsulated, round yeast Ribbon-like, aseptate hyphae in tissue Acanthamoeba sp Amoeba Naegleria fowleri Amoeba Individuals with head trauma or foreign bodies Individuals with head trauma or foreign bodies Meningitis Meningitis Primarily young children and elderly Meningitis Immunocompromised with invasive aspergillosis Brain abscess Immunocompromised, especially AIDS Meningitis Diabetics, immunocompromised individuals Necrotizing encephalitis, rhinocerebral mucormycosis Immunocompromised or immunocompetent Individuals with exposure to warm, fresh water Granulomatous amebic encephalitis or keratitis Fatal amebic meningoencephalitis 4 Organism Plasmodium falciparum General characteristics Delicate, ring forms in blood Patient population Individuals who visit malaria-endemic areas Taenia solium larval cyst Individuals who ingest T. solium eggs Seizures, calcified lesions in brain or muscle Toxoplasma gondii large cysts in tissue Immunocompromised, especially AIDS patients Encephalitis, abscess Viruses Echovirus/ coxsackievirus Encephalitis viruses Nonenveloped ssRNA Both enveloped and non enveloped ssRNA Herpes simplex virus Enveloped dsDNA Human immunodeficiency virus (HIV) Enveloped retrovirus Poliovirus Nonenveloped ssRNA Rabies virus Enveloped ssRNA Children and adults during summer months Children and adults bitten by viral arthropod vector Neonates, individuals with primary genital herpes, individuals with primary or recurrent herpes infections AIDS Nonvaccinated individuals; live, attenuated vaccine, especially in the immunocompromised Individuals bitten or scratched by nonvaccinated, rabid dog, cat, or other mammal Disease manifestation Cerebral malaria Aseptic meningitis Encephalitis, frequently fatal Necrotizing encephalitis; benign, aseptic meningitis; necrotizing hemorrhagic encephalitis AIDS-associated dementia; predisposes to other CNS' infections Polio paralysis Rabies Introduction to Respiratory Diseases (Chapter 24) Respiratory tract infections are a major reason why children and the elderly seek medical care. These infections are more common in cold-weather months in locales with temperate climates. Respiratory tract infections are primarily spread by inhalation of aerosolized respiratory secretions from infected hosts. Some respiratory tract pathogens such as rhinoviruses can also be spread by direct contact with mucous membranes, but this mode of transmission is much less common than inhalation. For the purpose of our discussion, we will divide these types of infection into two groups, upper tract and lower tract infection. The most common form of upper respiratory tract infection is pharyngitis. Pharyngitis is seen most frequently in children from 2 years of age through adolescence. The most common etiologic agents of pharyngitis are viruses, particularly adenoviruses, and group A streptococci. Pharyngitis due to group A streptococci predisposes individuals to the development of the poststreptococcal sequela rheumatic fever. Because this sequela can be prevented by penicillin treatment, aggressive diagnosis and treatment of group A streptococcal pharyngitis is needed. Otitis media is a common infectious problem in infants and young children. The most frequently encountered agents of this infection are bacterial, with Streptococcus pneumoniae, non-typeable Haemophilus influenzae, and Moraxella catarrhalis being most common. These organisms, along with certain viruses and anaerobic bacteria from the oral cavity, are the most important pathogens in sinusitis. S. pneumoniae, H. influenzae, Moraxella catarrhalis, and adenoviruses, as well as Chlamydia trachomtis in neonates, are the common etiologic agents of conjunctivitis. External otitis, a common problem in swimmers, is more common in warm weather months. Staphylococcus aureus and Pseudomonas aeruginosa are the most common agents of this relatively benign condition. Malignant external otitis is a serious medical condition seen primarily in diabetics, the elderly, and the immunocompromised. The infection can spread from the ear to the temporal bone, resulting in osteomyelitis and meningitis. The most common etiology of malignant otitis externa is P. aeruginosa. Two other life-threatening infections of the upper respiratory tract are rhinocerebral mucormycosis and bacterial epiglottitis. Rhinocerebral mucormycosis is most common in diabetics. In this infection of the sinuses, the fungi Mucor and Rhizopus spp. invade blood vessels, resulting in necrosis of bone and thrombosis of the cavernous sinus and internal carotid artery. Treatment of this infection requires aggressive surgical debridement of the infected tissue. Epiglottitis is almost always caused by H. influenzae type b. In this disease, the airway may become compromised due to swelling of the epiglottis, with death due to respiratory arrest. With the widespread use of H. influenzae type b vaccine, this rare disease should essentially disappear. 5 Organism General Characteristics Patient Population Disease Manifestation Bacteria Two childhood infections common in the early part of the 20th century, diphtheria and whooping cough, are now rare diseases in the developed world. This is thanks to the development and use of vaccines that are effective in children against the etiologic agents of these diseases, Cornyebacterium diphtheriae and Bordetella pertussis. Viruses play an important role in upper respiratory tract infections. The common syndrome of cough and "runny" nose is due to rhinoviruses. More severe upper respiratory infections such as the "croup" are due to respiratory syncytial virus and influenza and parainfluenza viruses. These viruses can also cause lower tract infection and are an important cause of morbidity and mortality in the very young and very old. When discussing lower respiratory tract infections, it is important to look at four different groups of patients: patients with community-acquired infections; patients with nosocomial infections; patients with underlying lung disease; and immunocompromised individuals, especially those with AIDS. Common agents of community-acquired lower respiratory tract infections include pneumoniae, especially in the elderly; Klebsiella pneumoniae, especially in alcoholics; Mycoplasma pneumoniae, especially in school-age students through young adulthood; Mycobacterium tuberculosis; respiratory syncytial virus in infants and young children; and influenza virus. Histoplasma capsulatum and Coccidioides immtis in patients residing in specific geographic locales may cause mild, self-limited diseases. S. pneumoniae, H. influenzae, S. aureus, and Moraxella catarrhalis may specifically cause bronchitis and/or pneumonia secondary to viral pneumonia in adults. Aspiration, resulting from either a seizure disorder or a semiconscious state resulting from excessive consumption of alcohol or other drugs, may lead to lung abscesses caused by organisms typically residing in the oral cavity. Nosocomial infections due to the organisms listed above certainly occur. Particular emphasis should be placed on preventing the spread of Mycobacterium tuberculosis in all patient populations and of respiratory syncytial virus in pediatric patients. Nosocomial pneumonia due to methicillin-resistant S. aureus and multi-drug-resistant gram-negative bacilli such as P. aeruginosa is a common problem in intubated patients. The potential for outbreaks of pneumonia due to Legionella spp. is a constant threat because of this bacterium's ability to survive within hospital water and air conditioning systems. Patients with chronic obstructive pulmonary disease brought on by smoking frequently develop bronchitis. S. pneumoniae, Moraxella catarrhalis, H. influenzae, and P. aeruginosa are frequent causes of this type of infection. Chronic airway infections are primarily responsible for the premature death of patients with cystic fibrosis. S. aureus and mucoid P. aeruginosa are the most important agents of such chronic airway disease. Both of these patient populations have an increased risk for developing allergic bronchopulmonary aspergillosis. Patients with cavitary lung disease, frequently due to prior Mycobacterium tuberculosis infection, are at increased risk for another type of infection, an aspergilloma or fungus ball caused by Aspergillus spp. This fungus grows in the form of a "ball" in the preformed lung cavity. The diagnosis of the etiology of lung infection in immunocompromised patients one of the most daunting in clinical microbiology and infectious disease. It has been greatly facilitated by the development of the flexible bronchoscope, which provides a relatively noninvasive means to sample the airways and alveoli. Immunocompromised patients are typically at risk for essentially all recognized respiratory tract pathogens. Certain pathogens are seen with increasing frequency in selected immunocompromised populations. In AIDS patients, Pneumocystis carinii, 5. pneumoniae, and multi-drug-resistant Mycobacterium tuberculosis are all seen more frequently than in other patient populations. Profoundly neutropenic patients have a very high risk for invasive aspergillosis and mucormycosis. Transplant patients have greatly increased risk for pneumonia with cytomegalovirus, herpes simplex virus, Legionella spp., Pneumocystis carinii, and the invasive fungi. These patients are frequently given prophylactic drugs to prevent pulmonary infection with Pneumocystis. Prophylactic therapies are not as widely used for other agents for a variety of reasons, including expense, questionable efficacy of the prophylactic measures, or the rarity with which the organism is encountered. 6 Neisseria meningitidis Nocardia spp. Nontuberculous mycobacteria (many species) Prevotella sp.; Porphyromonas spp Pseudomonas aeruginosa Oxidase-positive, gram-negative diplococcus Partially acid-fast, aerobic, branching, gram-positive bacilli Acid-fast bacilli Anaerobic gramnegative bacilli Glucosenonfermenting, gramnegative bacillus Adults Pneumonia Adults, especially with immunosuppression Pneumonia with abscess Adults with chronic lung disease; CF patients Adults with aspiration Granulomatous lung disease Adults and children; diabetic adults; nosocomial; CF patients Lung abscess Catalase-positive, gram-positive cocci in clusters Glucosenonfermenting, gramnegative bacillus Catalase-negative, gram-positive diplococcus Acid-fast bacillus Nosocomial External otitis (swimmer's ear), malignant external otitis, ventilator-associated pneumonia, chronic bronchitis with mucoid strains Pneumonia, pneumonia superinfections Nosocomial Ventilator-associated pneumonia Children and adults Otitis media, conjunctivitis, pneumonia Children and adults, especially HIV-infected Tuberculosis Acute-anglebranching, septate hyphae in tissue; mold Children and adults with chronic lung disease; adults with cavitary lung lesions; immunocompromised individuals Adults Allergic bronchopulmonary aspergillosis; aspergilloma (fungus ball); invasive pneumonia Children and adults, especially in desert southwest of US and northern Mexico Immunocompromised adults, especially with AIDS Adults, primarily with AIDS, spread through bat/bird droppings Immunocompromised individuals, especially with AIDS Flu-like illness with pneumonia Diabetics, immunocompromised individuals Rhinocerebral mucormycosis, invasive pneumonia Larvae Larvae Rhabditiform larvae Children and adults Children and adults Immunocompromised individuals Usually asymptomatic, incidental finding Usually asymptomatic, incidental finding Wheezing, cough, pneumonia Enveloped, dsDNA Children and adults Cytomegalovirus Hantavirus Herpes simplex virus Influenza virus Enveloped, dsDNA Enveloped, ssRNA Enveloped, dsDNA Enveloped, ssRNA Parainfluenza virus types I, II, III Enveloped, ssRNA Immunocompromised individuals Children and adults Immunocompromised individuals Children and adults, particularly elderly Infants and young children Pharyngitis, bronchiolitis, pneumonia, conjunctivitis Pneumonia "Shock" lung, pneumonia Pneumonia Influenza, pneumonia Staphylococcus aureus Stenotrophomonas maltophilia Streptococcus pneumoniae Mycobacterium tuberculosis Fungi Aspergillus spp. Blastomyces dermatitidis Coccidioides immitis Cryptococcus neoformans Histoplasma capsulatum Pneumocystis carinii Rhizopus sp., Mucor sp. Parasites Ascaris lumbricoides Hookworm Strongyloides stercoralis Viruses Adenovirus Broad-based budding yeast; dimorphic Spherules in tissue; mold with arthroconidia at 30.C Encapsulated, round yeast Very small, intracellular yeast; dimorphic Clusters of 4-6-l1m cysts in tissue and secretions Ribbon-like, nonseptate hyphae in tissue; rapidly growing mold Pneumonia Pneumonia, often asymptomatic preceding meningitis Pneumonia Pneumonia Croup, bronchiolitis, pneumonia 7 Respiratory syncytial virus Rhinovirus Varicella-zoster virus Enveloped, ssRNA Nonenveloped, ssRNA Enveloped, dsDNA Infants and young children Children and adults Immunocompromised individuals, pregnant women Cough, wheezing, bronchiolitis, pneumonia Common cold Pneumonia Introduction to Cardiovascular & Systemic Diseases (Chapter 23) Systemic infections can be caused by many different infectious agents: bacterial, fungal, viral, and parasitic. One common finding for all systemic infections is the need for a portal of entry. The portal of entry can be via the parenteral route (as in mosquito-borne diseases such as malaria), via the oral route (as in typhoid fever), via sexual contact (as in HIV infection), as a bloodborne pathogen (as in hepatitis B virus infection), via the respiratory tract (as in measles), and by horizontal transmission via transplacental infection (as in congenital cytomegalovirus infection). In many cases of systemic infection, colonization occurs prior to the dissemination of the infectious agent throughout the body. In some diseases (e.g., tetanus and diphtheria) the infection itself is caused by a noninvasive organism and the systemic symptoms are caused by the dissemination of a toxin that is responsible for the disease. In most cases, however, the etiologic agent is disseminated via the hematogenous route. Patients may have certain risk factors or defects in host defenses that predispose them to specific types of infections. Examples of defects in host defenses that predispose to certain specific types of infections include breaches in the integrity of the skin (patients with burns, patients with invasive medical devices), defects in cell-mediated immunity (AIDS, corticosteroids), defects in humoral immunity (hypogammaglobulinemia), decreased splenic function (splenectomy, sickle cell disease), quantitative defects in neutrophils (neutropenia following chemotherapy), qualitative defects in neutrophils (chronic granulomatous disease, Chediak-Higashi syndrome), and deficiencies in the complement system. It is important to be able to recognize these risk factors when they are present and to know to what the defect predisposes the patient. Conversely, it is important to be able to suspect a specific defect in host defenses when a patient presents with a systemic infection. Protection of the host from a systemic infection can occur as a result of a prior infection with the specific agent of infection (e.g., measles) or due to a vaccination to that agent. Unfortunately, efficacious vaccines are not available for the majority of infectious agents, and in many diseases, infection does not lead to protective immunity. Important agents of systemic infection are listed below. Please note that virtually all bacteria can potentially be isolated from the blood under circumstances of specific host defects, such as the presence of an intravenous catheter. Many of the etiologic agents listed have a particular organ tropism (such as the liver for hepatitis viruses) but may cause systemic illness. Cardiovascular & systemic Pathogens Organism Bacteria Acinetobacter spp. Bartonella henselae Borrelia burgdorferi Brucella spp. Clostridium botulinum Clostridium perfringens Clostridium tetan Coagulase-negative staphylococci Corynebacterium diphtheriae Enterobacter spp. General Characteristics Lactose-nonfermenting, gram-negative bacilli Fastidious, gram-negative bacillus Spirochete Oxidase-positive, gramnegative bacilli Anaerobic gram-positjve bacillus Anaerobic gram-positive bacillus Anaerobic gram-positive bacillus Catalase-positive, coagulase-negative, grampositive cocci Aerobic gram-positive bacillus Lactose-fermenting, gram-negative bacilli Source of Infection Exogenous Exogenous; cats appear to be primary host Tick borne Zoonosis Disease Manifestation Nosocomial UTl, nosocomial pneumonia, nosocomial and line-related bacteremia Cat scratch disease; bacillary angiomatosis (in immunocompromised) Lyme disease; rash, arthritis, nervous system and cardiac manifestations Lymphadenopathy, hepatosplenomegaly; genitourinary, bone, and CNS infection Exogenous Botulism Exogenous Gas gangrene, emphysematous cholecystitis, bacteremia, food poisoning Exogenous Tetanus Endogenous Nosocomial bacteremia Exogenous Diphtheria Endogenous Community and nosocomial UTI, bacteremia, intra-abdominal infections 8 Organism General Characteristics Catalase-negative, grampositive cocci Lactose-fermenting, gram-negative bacillus Source of Infection Francisella tularensis Gram-negative bacillus Zoonosis Group A streptococci (Streptococcus pyogenes) Catalase-negative, grampositive cocci Endogenous Group B streptococci (Streptococcus agalactiae) Catalase-negative, grampositive cocci Endogenous Sepsis, meningitis, cellulitis Klebsiella pneumoniae Lactose-fermenting, gram-negative bacillus Endogenous Community and nosocomial UTI, bacteremia, intra-abdominal infections Mycobacterium avium complex Acid-fast bacilli Exogenous Disseminated disease Mycobacterium tuberculosis Acid-fast bacillus Respiratory, may be exogenous (primary) or endogenous (reactivation) Pneumonia, extrapulmonary tuberculosis, miliary tuberculosis Endogenous (from colonization) Meningitis, bacteremia Zoonosis (often animal bite or scratch) Cellulitis, bacteremia, osteomyelitis, meningitis Community and nosocomial UTI, bacteremia Enterococcus spp. Escherichia coli Neisseria meningitidis Pasteurella multocida Proteus mirabilis Pseudomonas aeruginosa Oxidase-positive, gramnegative diplococcus Oxidase-positive, gramnegative bacillus Lactose-nonfermenting, gram-negative bacillus Lactose-nonfermenting, Oxidase-positive, gramnegative bacillus Endogenous Endogenous Endogenous Exogenous Rickettsia prowazekii Rickettsial organism Exogenous, lice to human Rickettsia rickettsii Exogenous, tick to human Viridans group streptococci Rickettsial organism Lactose-nonfermenting, gram-negative bacillus Catalase-positive, coagulase-positive, grampositive coccus Catalase-negative, grampositive coccus Spirochete (does not Gram stain) Catalase-negative, grampositive cocci Yersinia pestis Gram-negative bacillus Salmonella typhi Staphylococcus aureus Streptococcus pneumoniae Treponema pallidum Exogenous, human to human Endogenous Disease Manifestation Wound infections, nosocomial UTI, bacteremia, endocarditis Community and nosocomial UTI, bacteremia, intra-abdominal infections Ocular, lymphadenopathy, pulmonary, bacteremia Pharyngitis, cellulitis, bacteremia, scarlet fever, necrotizing fasciitis, pneumonia, poststreptococcal glomerulonephritis and rheumatic fever Community and nosocomial UTI, nosocomial pneumonia, nosocomial bacteremia Epidemic typhus causes fever and disseminated intravascular coagulation. Rocky Mountain spotted fever Typhoid fever, bacteremia, intestinal disease Skin infections, bacteremia, endocarditis, septic arthritis, abscesses Direct sexual contact, vertical (mother to child) Community-acquired pneumonia, sinusitis, meningitis, bacteremia, endocarditis Primary, secondary, latent, and late syphilis; can affect any organ Endogenous Endocarditis Zoonosis; person to person in pneumonic form Lymphadenopathy (bubonic), pneumonia, bacteremia Endogenous 9 Viruses Dengue Virus Filoviruses Parasites Babesia microti Leishmania donovani Plasmodium spp. Strongyloides stercoralis Taenia solium Toxoplasma gondii Enveloped polyhedral capsid with singlestranded RNA Enveloped helical capsid with single-stranded RNA Exogenous (Aedes aegypti mosquito) Can be seen on peripheral blood smear Amastigotes in tissue touch preparation Can be seen on peripheral blood smear Nematode Exogenous (ticks) Babesiosis Exogenous (Phlebotomus fly) Kalaazar Exogenous (Anopheles mosquito) Malaria Exogenous; endogenous (autoinfection and hyperinfection) Exogenous Gastrointestinal, pulmonary (pneumonia, wheezing), disseminated in hyperinfection Gastrointestinal infection, cysticercosis (brain, muscles, other organs) Central nervous system, ocular, hepatic, pulmonary Tapeworm Protozoan Exogenous: unknown possible animal reservoir Exogenous; endogenous (reactivation) Dengue Fever; joint pain, fever, headache, rash, muscle pain, hemorrhagic fever/shock Hemorrhagic fever with high mortality. Fungi Aspergillus spp. Molds with septate hyphae Exogenous Blastomyces dermatitidis Dimorphic mold Candida albicans Yeast, often germ tube positive Exogenous Endogenous Candida spp., non- albicans Yeasts, germ tube negative Endogenous Coccidioides immitis Dimorphic mold Exogenous Cryptococcus neoformans Encapsulated yeast Exogenous Histoplasma capsulatum Dimorphic mold Exogenous Zygomycetes Molds with aseptate hyphae Exogenous Pneumonia, sinusitis, external otitis, allergic processes, disseminated infection Pneumonia, meningitis, bone infection Thrush, vaginal yeast infection, diaper rash, esophagitis, nosocomial UTI, nosocomial bloodstream infection Thrush, vaginal yeast infection, nosocomial UTI, nosocomial bloodstream infection Pneumonia, meningitis, bone infection Meningitis, pneumonia, bloodstream infection Pneumonia, disseminated infection Pneumonia, sinusitis, invasive infection Introduction to Digestive Tract Diseases (Chapter 25) The major clinical manifestation of infections affecting the gastrointestinal tract is diarrhea. Diarrheal pathogens have two basic mechanisms by which they produce diarrhea. One is the production of toxins called enterotoxins, which cause physiologic changes in the intestinal epithelium that result in fluid and electrolyte secretion. Vibrio cholerae, which produces an enterotoxin called cholera toxin, is a classic example of a diarrheal pathogen which produces a secretory diarrhea due to the action of an enterotoxin. Microscopically, the intestinal epithelium appears normal in patients with enterotoxin-induced diarrhea. The other major mechanism of diarrheal disease is direct damage to the intestinal epithelium caused by cytotoxin or organism invasion. The protozoan Entamoeba histolytica produces such a cytotoxin. This cytotoxin is responsible for the characteristic ulcerative lesions which can be seen in individuals with amebic dysentery. A number of gastrointestinal pathogens including Salmonella spp., Shigella spp., Campylobacter spp., and Yersinia enterocolitiae are capable of invading the intestinal epithelium. Inflammation frequently occurs in response to these pathogens. Patients with diarrhea due to organisms that damage the epithelium frequently will have white blood cells visible in their feces. However, these cells may also be present in feces of patients with noninfectious inflammatory bowel disease, so results of examination of feces for white blood cells should be interpreted cautiously. Diarrheal diseases are almost always spread by the fecal-oral route. This means that individuals who become infected with diarrheal pathogens ingest either food or water which has been contaminated with human or animal feces containing the pathogens. Improper handling or preparation of food and contamination of water due to poor sanitation are major means by which diarrheal pathogens are spread. In the industrialized world, the spread of diarrheal disease is particularly problematic in day care centers for children. In addition to spread by contaminated food and water, infected children can pass the organisms directly, by placing contaminated hands in the mouths of other children, or indirectly, by using contaminated hands to handle toys which are then mouthed by other children. The infectious dose of diarrheal pathogens varies greatly, with the infectious doses of Salmonella spp. and V. cholerae in the 10 hundreds of thousands to millions, while that for Shigella spp. is less than 100 organisms. Because the major pathophysiologic effect of diarrhea is dehydration due to fluid and electrolyte loss, the most important treatment is rehydration. In recent years, simple solutions of glucose, salts, and water given orally have been developed which are proven to be highly effective in treating patients with even the most severe forms of diarrhea. The widespread use of oral rehydration in the past two decades, especially in the developing world, has been credited with saving literally millions of lives, primarily young children in whom diarrheal disease takes the greatest toll. In addition to diarrheal disease, hepatitis is an important infection in the gastrointestinal system. The epidemiology of hepatitis A virus is the same as that of diarrheal pathogens. The virus is usually obtained by ingestion of raw shellfish taken from water contaminated by human sewage or of food handled by an infected food handler who has poor personal hygiene, i.e., individuals who fail to wash their hands after a bowel movement. Hepatitis Band C viruses are spread by contaminated blood. Contracting hepatitis used to be a major concern in individuals receiving blood transfusions. With the recognition of these agents and the development of screening tests for them, the epidemiology of hepatitis due to these two viruses has changed. Hepatitis Band C virus infections (and also human immunodeficiency virus [HIV] infections) are frequent in individuals who share needles while using illicit intravenous drugs. Hepatitis B virus is also spread sexually, especially in populations which practice anal intercourse. The frequency of spread of hepatitis C virus sexually is not well understood. Unlike hepatitis A virus, which causes a relatively mild self-limited disease, hepatitis B virus can cause fulminant, sometimes fatal disease. Hepatitis Band C viruses can also cause a chronic infection culminating in liver failure. Vaccines are available for hepatitis A and B but not C virus. Other important types of gastrointestinal infection are ones in which the resident intestinal microflora or pathogens escape from the bowel and enter "sterile" tissues. One example is Entamoeba histolytica trophozoites, which enter the liver and cause an amebic abscess. Another is when there is penetrating trauma to the intestines, as might occur with a gunshot wound to the abdomen or during bowel surgery. In either situation, microbes can escape from the intestines into the peritoneum, where they can cause peritonitis or form an abscess. The organisms causing these infections are typically a mixture of both facultative and anaerobic bacteria that reside in the colon. Digestive Tract Pathogens Organism Bacteria Baeteroides (ragilis Campylobaeter spp. General characteristics Usual source of infection Disease manifestation Anaerobic, gram-negative bacillus Microaerophilic, curved, gramnegative bacilli Anaerobic, toxin-producing, grampositive bacillus Anaerobic, gram-positive bacillus Endogenous Poultry Sorbitol-nonfermenting, gramnegative bacillus Lactose-fermenting, gramnegative bacillus Lactose-nonfermenting, gramnegative bacilli Lactose-nonfermenting, gramnegative bacilli Catalase-positive, gram-positive coccus Oxidase-positive, gram-negative bacilli Lactose-nonfermenting, gramnegative bacillus Improperly cooked ground beef; apple juice/cider Fresh fruit and vegetables Abdominal abscess Invasive diarrhea, sepsis in AIDS patients Antibiotic-associated diarrhea, pseudomembranous colitis Gangrenous lesions of bowel or gall bladder; food poisoning Enterohemorrhagic colitis, hemolytic-uremic syndrome Traveler's diarrhea, watery diarrhea Invasive diarrhea, typhoid fever Parasites Ascaris lumbricoides Clostridium difficile Clostridium perfringens Enterohemorrhagic Escherichia coli Enterotoxigenic Escherichia coli Salmonella spp. Shigella spp. Staphylococcus aureus Endogenous; nosocomial Endogenous; high-protein foods Animal products; typhoid (human to human) Human to human; day care centers Invasive diarrhea, dysentery High-protein foods Food poisoning Raw fish and shellfish Large-volume watery diarrhea Meat and dairy products Watery or invasive diarrhea Roundworm Food, soil Cryptosporidium parvum Coccidian parasite Cyclospora spp. Coccidian parasite Fecally contaminated water; day care centers Water, fresh fruits and vegetables Diarrhea, abdominal discomfort, intestinal obstruction Malabsorptive diarrhea (chronic in AIDS) Malabsorptive diarrhea Vibrio spp. Yersinia enterocolitica 11 Organism Echinococcus spp. General characteristics Dog tapeworm Disease manifestation Hydatid cyst of liver Hookworm Usual source of infection Ingestion of tapeworm eggs from infected dog Water, fresh fruits and vegetables Fecally contaminated water, day care centers Skin contact with larvae in soil Entamoeba histolytica Amoeba Giardia lamblia Flagellated trophozoite Necator americanus, Ancylostoma duodenale, Viruses Enterovirus Nonenveloped RNA virus Fecal-oral Hepatitis A virus Hepatitis B virus Nonenveloped RNA virus Enveloped DNA virus Shellfish, infected food handlers Blood, direct sexual contact Hepatitis C virus RNA virus Blood Norwalk agent (calicivirus) Nonenveloped RNA virus Rotavirus Wheel-like, nonenveloped RNA virus Shellfish, common-source food outbreaks Human to human (day care center) Diarrhea, respiratory disease, aseptic meningitis, exanthems Acute, self-limited hepatitis Acute and chronic hepatitis, fulminant hepatitis, hepatic carcinoma Acute and chronic hepatitis, fulminant hepatitis, hepatic carcinoma "24-hour flu," vomiting, diarrhea Diarrhea, amebic dysentery, liver abscess Malabsorptive diarrhea (acute; chronic) Anemia, gastrointestinal discomfort Diarrhea, vomiting Introduction to Genitourinary Diseases (Chapter 26) We begin this text with a discussion of infections of the genitourinary tract for two reasons. First, the number of microorganisms which frequently cause infection in these organs is somewhat limited. Second, urinary tract infections (UTls) and sexually transmitted diseases (STDs) are two of the most common reasons why young adults, particularly women, consult a physician. UTls are examples of endogenous infections, i.e., infections which arise from the patient's own microflora. In the case of UTls, the microbes generally originate in the gastrointestinal tract and colonize the periurethral region before ascending the urethra to the bladder. STDs are exogenous infections; i.e., the infectious agent is obtained from a source outside the body. In the case of STDs, these agents are obtained by sexual contact. UTls are much more common in women than men for a number of reasons. The urethra is shorter in women than in men, making it easier for microbes to ascend to the bladder. Prostatic secretions are antibacterial, which further protects the male. The periurethral epithelium in women, especially women with recurrent UTls, is more frequently colonized with microorganisms which cause UTls. It should also be noted that the incidence of UTls is higher in sexually active women, as coitus can "force" organisms colonizing the periurethral region into the urethra. The incidence of nosocomial UTls, however, is similar in women and men. In these infections, catheterization is the major predisposing factor. The incidence of STDs is similar in both heterosexual men and women; however, the morbidity associated with these infections tends to be much greater in women. In particular, irreversible damage to reproductive organs, caused by both Chlamydia trachomatis and Neisseria gonorrhoeae, is all too common. Whereas infections with these two organisms are almost always symptomatic in males, a significant number of women may be infected asymptomatically at first. They may manifest signs and symptoms of infection only when they develop pelvic inflammatory disease, which can result in sterility. Fetal loss or severe perinatal infection may be caused by two other STD agents, herpes simplex virus and Treponema pallidum, the etiologic agent of syphilis. Important agents of genitourinary tract infections are listed in the table below. Only organisms in this table should be considered in your differential diagnosis for the cases you have been provided. You should note that not all organisms that can be spread sexually, such as hepatitis B virus and Entamoeba histolytica, are listed. This is because these infections do not have genitourinary tract manifestations. Genitourinary Tract Pathogens Organism Bacteria Actinomyces spp. Bacteroides fragilis Chlamydia trachomatis General characteristics Source of infection Disease manifestation° Anaerobic, gram-positive bacilli Anaerobic, gram-negative bacillus Obligate intracellular pathogen (does not Gram stain) Endogenous Endogenous Direct sexual contact PID associated with intrauterine device usage Pelvic abscess Urethritis, cervicitis, PID 12 Enterobacter spp. Lactose-fermenting gram-negative bacilli Catalase-negative, gram-positive cocci Lactose-fermenting gram-negative bacilli Fastidious pleiomorphic gram negative bacillus Lactose-fermenting gram-negative bacilli Lactose non-fermenting gram-negative bacillus Endogenous Community or nosocomial UTI Endogenous Nosocomial UTI Endogenous Community or Nosocomial UTI Direct sexual contact Chancroid (painful genital ulcer) Endogenous Community or nosocomial UTI Endogenous Community or nosocomial UTI Direct sexual contact Urethritis, cervicitis, PID Endogenous Community or nosocomial UTI catheterization Nosocomial UTI Catheterization, endogenous Nosocomial UTI, Community-acquired UTI, biofilm agent Catalase-positive, gram-positive coccus Endogenous Community-acquired UTI Treponema pallidum Spirochete (does not Gram stain) Direct sexual contact; vertical, from mother to child Chancre (painless genital ulcer); primary, secondary, tertiary syphilis; neonatal syphilis Fungi Candida sp. Parasites Yeast with pseudohyphae Endogenous Vaginitis, nosocomial UTI Phthirus pubis Crab lice Enterococcus spp. Escherichia coli Haemophilus ducreyi Klebsiella pneumoniae Morganella morganii Neisseria gonorrhoeae Proteus mirabilis Pseudomonas aeruginosa Staphyloccus epidermidis Staphylococcus saprophyticus Trichomonas vaginalis Viruses Gram-negative intracellular diplococcus Lactose non-fermenting, swarming gram-negative bacillus Lactose non-fermenting gram-negative bacillus Coagulase-negative, gram-positive coccus Protozoan Herpes simplex virus Enveloped DNA virus Human immunodeficiency virus (HIV) Retrovirus Human papillomavirus Nonenveloped DNA virus Direct sexual contact Direct sexual contact Direct sexual contact; vertical, from mother to child Direct sexual contact, blood; vertical, from mother to child Direct sexual contact Pubic hair infestation Vaginitis Recurrent genital ulcers, fetal/neonatal infections, encephalitis AIDS, neonatal infection, dementia Genital warts, cervical carcinoma 13