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Taxonomic Size Site of Propagation Sample Species DiseaseViruses 20–300 nm Obligate intracellular Poliovirus Poliomyelitis Chlamydiae 200–1000 nm Obligate intracellular Chlamydia trachomatis Trachoma, urethritis Rickettsiae 300–1200 nm Obligate intracellular Rickettsia prowazekii Typhus fever Mycoplasmas 125–350 nm Extracellular Mycoplasma pneumoniae Atypical pneumonia Bacteria 0.8–15 μm Cutaneous Staphylococcus aureus Wound Mucosal Vibrio cholerae Cholera Extracellular Streptococcus pneumoniae Pneumonia Facultative intracellular Mycobacterium tuberculosis Tuberculosis Fungi 2–200 μm Cutaneous Trichophyton sp. Tinea pedis (athlete's foot) Mucosal Candida albicans Thrush Extracellular Sporothrix schenckii Sporotrichosis Facultative intracellular Histoplasma capsulatum Histoplasmosis Protozoa 1–50 μm Mucosal Giardia lamblia Giardiasis Extracellular Trypanosoma gambiense Sleeping sickness Facultative intracellular Trypanosoma cruzi Chagas disease Obligate intracellular Leishmania donovani Kala-azar Helminths 3 mm–10 m Mucosal Enterobius vermicularis Enterobiasis Extracellular Wuchereria bancrofti Filariasis Intracellular Trichinella spiralis Trichinosis Prions Prions are apparently composed of abnormal forms of a host protein, termed prion protein (PrP).[8] These agents cause transmissible spongiform encephalopathies, including kuru (associated with human cannibalism), Creutzfeldt-Jakob disease (CJD; associated with corneal transplants), bovine spongiform encephalopathy (BSE; better known as mad cow disease), and variant Creutzfeldt-Jakob disease (vCJD; likely transmitted to humans from BSE-infected cattle). [9] PrP is normally found in neurons. Diseases occur when the prion protein undergoes a conformational change that confers resistance to proteases. The protease-resistant PrP promotes conversion of the normal protease-sensitive PrP to the abnormal form, explaining the infectious nature of these diseases. Accumulation of abnormal PrP leads to neuronal damage and distinctive spongiform pathologic changes in the brain. Spontaneous or inherited mutations in PrP, which make PrP protease resistant, have been observed in the sporadic and familial forms of CJD, respectively. These diseases are discussed in detail in Chapter 28 . Viruses Viruses are obligate intracellular parasites that depend on the host cell's metabolic machinery for their replication. They consist of a nucleic acid genome surrounded by a protein coat (called a capsid) that is sometimes encased in a lipid membrane. Viruses are classified by their nucleic acid genome (DNA or RNA but not both), the shape of the capsid (icosahedral or helical), the presence or absence of a lipid TABLE 8-4-- Selected Human Viral Diseases and Their Pathogens Viral Pathogen Virus Family Genomic Type Disease Expression Respiratory Adenovirus Adenoviridae DS DNA Upper and lower respiratory tract infections, conjunctivitis, diarrhea Rhinovirus Picornaviridae SS RNA Upper respiratory tract infection Coxsackievirus Picornaviridae SS RNA Pleurodynia, herpangina, hand-foot-and-mouth disease, SARS Coronavirus Coronaviridae SS RNA Upper respiratory tract infection Influenza viruses A, B Orthomyxoviridae SS RNA Influenza Respiratory syncytial virus Paramyxoviridae SS RNA Bronchiolitis, pneumonia Digestive Mumps virus Paramyxoviridae SS RNA Mumps, pancreatitis, orchitis Rotavirus Reoviridae DS RNA Childhood diarrhea Norwalk agent Caliciviridae SS RNA Gastroenteritis Hepatitis A virus Picornaviridae SS RNA Acute viral hepatitis Hepatitis B virus Hepadnaviridae DS DNA Acute or chronic hepatitis Hepatitis D virus Viroid-like SS RNA With HBV, acute or chronic hepatitis Hepatitis C virus Flaviviridae SS RNA Acute or chronic hepatitis Hepatitis E virus Norwalk-like SS RNA Enterically transmitted hepatitis Date: 2016-04-22; view: 1830
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