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Taxonomic Size Site of Propagation Sample Species Disease

Viruses 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 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 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


Type Disease Expression


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


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: 1482

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