Microbiology, Immunology and Public Health

Microbiology is the smallest of the six Part I domains by weight, but its questions are among the most predictable: a classic organism, a classic toxin, a classic vector or a classic lab finding. It is also the science behind everyday office decisions, from which patients need referral for a fever with back pain to how the adjusting table is cleaned between patients.

Section 1Immunology

Innate and adaptive immunity

Innate immunity is present from birth, responds within minutes to hours, is not antigen-specific and has no memory. Its components are physical and chemical barriers (skin, mucus, cilia, gastric acid, lysozyme, defensins), phagocytes (neutrophils, the first cells at an acute bacterial site, and macrophages), natural killer cells (kill virus-infected and tumor cells that have lost MHC class I), dendritic cells, mast cells, eosinophils, complement and acute-phase proteins such as CRP. Innate cells recognize conserved microbial patterns through Toll-like receptors (TLR4 binds gram-negative LPS). Activated macrophages release IL-1, IL-6 and TNF-α, which cause fever (via hypothalamic prostaglandin E2), acute-phase protein synthesis and neutrophil release.

Adaptive immunity develops over days, is highly specific, has memory and is carried by lymphocytes. Each B or T cell carries one receptor specificity created by random gene rearrangement (V(D)J recombination); antigen selects and expands the matching clone (clonal selection). Primary lymphoid organs are the bone marrow (B cell maturation) and thymus (T cell maturation); secondary organs are lymph nodes, spleen and mucosa-associated lymphoid tissue, where naive lymphocytes meet antigen. An antigen is any molecule recognized by an antibody or T cell receptor; the part recognized is the epitope. A hapten is too small to do so unless coupled to a carrier protein (the basis of penicillin allergy and of conjugate vaccines).

Antibodies

An antibody (immunoglobulin) is made of two identical heavy chains and two identical light chains (kappa or lambda) joined by disulfide bonds. The two Fab arms carry variable regions whose hypervariable loops form the antigen-binding sites. The Fc stem is the constant region that defines the class (isotype) and decides what the antibody does: binding Fc receptors on phagocytes (opsonization), mast cells (IgE) or the placenta (IgG), and fixing complement via C1q.

In a primary response there is a lag of 7 to 10 days and IgM predominates. Helper T cells then drive class switching (CD40 ligand on the T cell binding CD40 on the B cell, plus cytokines) and affinity maturation, so a secondary (anamnestic) response is faster, larger, longer and mainly high-affinity IgG. That is the logic behind booster doses.

Complement

Complement is a cascade of plasma proteins that converges on C3. The classical pathway starts when C1q binds antigen-antibody complexes (IgG or IgM: "GM makes classic cars"); the lectin pathway starts when mannose-binding lectin binds microbial sugars; the alternative pathway starts with spontaneous C3 hydrolysis stabilized on microbial surfaces. All three form a C3 convertase, then a C5 convertase. Products: C3b opsonizes; C3a and C5a are anaphylatoxins that release histamine from mast cells; C5a is a powerful neutrophil chemoattractant; C5b to C9 assemble the membrane attack complex that lyses cells, especially thin-walled Neisseria. Deficiencies: early components (C1, C2, C4) predispose to lupus-like immune complex disease; C3 to recurrent pyogenic infections; C5 to C9 to recurrent Neisseria infection; C1 esterase inhibitor to hereditary angioedema; DAF (CD55) and CD59 to paroxysmal nocturnal hemoglobinuria.

T cells, B cells and MHC

T cells mature in the thymus through positive selection (cortex: cells that recognize self-MHC survive) and negative selection (medulla: cells that bind self-antigen strongly die, aided by AIRE). T cells see only peptide presented on MHC.

CD4 helper T cells differentiate by cytokine environment: Th1 (IFN-γ, IL-2) activate macrophages against intracellular microbes such as M. tuberculosis and drive delayed (type IV) hypersensitivity; Th2 (IL-4, IL-5, IL-13) help B cells, drive IgE class switching and eosinophils against helminths and in allergy; Th17 (IL-17) recruit neutrophils against extracellular bacteria and fungi; regulatory T cells (CD25, FOXP3, IL-10, TGF-β) suppress responses and maintain tolerance. CD8 cytotoxic T cells kill virus-infected and tumor cells with perforin and granzymes and through Fas ligand. B cells (markers CD19, CD20, CD21, the EBV receptor) present antigen and become antibody-secreting plasma cells or memory cells. Most protein antigens are T-dependent; bacterial capsular polysaccharides are T-independent, giving weak IgM responses with poor memory, especially in children under 2. HLA associations worth knowing: B27 with the spondyloarthropathies, DR4 with rheumatoid arthritis, DR3 and DR4 with type 1 diabetes, DQ2 and DQ8 with celiac disease.

Classic immunodeficiencies: Bruton agammaglobulinemia (no B cells), selective IgA deficiency (most common; anaphylaxis to transfused blood), DiGeorge syndrome (absent thymus, hypocalcemia), severe combined immunodeficiency and chronic granulomatous disease (NADPH oxidase).

Vaccines and immunization

Active immunity is made by the host after infection (natural) or vaccination (artificial); it is slow to develop but lasting. Passive immunity is preformed antibody received from the mother across the placenta (IgG) or in milk (IgA) (natural), or as immune globulin or antitoxin (artificial: hepatitis B, rabies and tetanus immune globulin); it works immediately but fades in weeks to months. Herd immunity protects the unimmunized when enough of the population is immune, and the threshold rises with the infectiousness of the agent (about 95 percent for measles).

A successful hepatitis B series produces anti-HBs alone. Clinic staff with possible blood exposure should be immune to hepatitis B, MMR and varicella, with Tdap and annual influenza vaccines.

Section 2Bacteria

Structure and the Gram stain

Bacteria are prokaryotes: no nucleus, a circular chromosome, often extra plasmids, 70S ribosomes (30S plus 50S subunits, the targets of many antibiotics) and division by binary fission. Nearly all have a peptidoglycan cell wall, a mesh of sugar chains (N-acetylglucosamine and N-acetylmuramic acid) cross-linked by peptide bridges; the cross-linking transpeptidases are the penicillin-binding proteins. Staphylococci grow in clusters, streptococci in chains.

The Gram stain has four steps: crystal violet (primary stain), iodine (mordant that traps the dye), alcohol or acetone (decolorizer, the critical step) and safranin (counterstain). Gram-positive cells have a thick peptidoglycan layer, laced with teichoic and lipoteichoic acids, that holds the crystal violet and stains purple. Gram-negative cells have a thin peptidoglycan layer in a periplasmic space beneath an outer membrane containing lipopolysaccharide (LPS, endotoxin); the solvent dissolves the outer membrane, the dye washes out, and safranin stains them pink. Some organisms stain poorly and need other methods: Mycobacterium (waxy mycolic acid; acid-fast Ziehl-Neelsen stain), Treponema (too thin; dark-field microscopy), Mycoplasma (no cell wall), Chlamydia and Rickettsia (intracellular), and Legionella (silver stain).

Other structures: the capsule (usually polysaccharide) is the most important antiphagocytic factor; key encapsulated pathogens are S. pneumoniae, Haemophilus influenzae type b, N. meningitidis, Klebsiella, E. coli, Salmonella and group B streptococcus, which is why asplenic and sickle cell patients are vulnerable to them. Biofilm (slime) lets S. epidermidis colonize prosthetic joints and catheters. Pili mediate adherence, and the sex pilus mediates conjugation. Flagella give motility. Endospores, formed by Bacillus and Clostridium when nutrients run out, contain dipicolinic acid and calcium, resist heat, drying and most disinfectants, and are destroyed reliably only by sterilization such as autoclaving.

Growth and genetics

By oxygen requirement: obligate aerobes (M. tuberculosis, which favors the lung apex; Pseudomonas), obligate anaerobes (Clostridium, Bacteroides, Actinomyces; lack catalase and superoxide dismutase, produce foul-smelling abscesses and gas, and resist aminoglycosides, which need oxygen to enter the cell), facultative anaerobes (staphylococci, enterics) and microaerophiles (Campylobacter, H. pylori). Obligate intracellular bacteria (Rickettsia, Chlamydia, Coxiella) cannot make their own ATP. Blood agar shows hemolysis: alpha (partial, green: S. pneumoniae, viridans streptococci), beta (complete, clear: S. pyogenes, S. agalactiae, S. aureus), gamma (none: Enterococcus).

Bacteria exchange genes in four ways. Transformation is uptake of naked DNA from the environment (S. pneumoniae, the basis of Griffith's experiment). Conjugation is direct transfer through a sex pilus, usually of plasmids such as the F factor and resistance (R) plasmids, and is the main route by which multidrug resistance spreads among gram-negative rods. Transduction is transfer by a bacteriophage; in lysogenic conversion a phage gene gives the host a new toxin: diphtheria, botulinum, cholera, Shiga-like and streptococcal erythrogenic toxins are all phage-encoded. Transposons ("jumping genes") move between chromosome and plasmids.

Virulence factors and toxins

Beyond capsules, important virulence factors are protein A (S. aureus; binds the Fc of IgG and blocks opsonization), M protein (S. pyogenes; antiphagocytic, and molecular mimicry with cardiac myosin underlies rheumatic fever), IgA protease (S. pneumoniae, Haemophilus, Neisseria), coagulase (S. aureus), hyaluronidase and streptokinase (spread through tissue), and the cord factor and sulfatides of M. tuberculosis.

Major pathogens

Antibiotics and resistance

Resistance arises by mutation or acquired genes. Mechanisms are enzymatic inactivation (beta-lactamases, including extended-spectrum beta-lactamases and carbapenemases; aminoglycoside-modifying enzymes), altered targets (PBP2a in MRSA, D-Ala-D-Lac in vancomycin-resistant enterococci), reduced entry (porin loss) and efflux pumps (tetracyclines). Beta-lactamase inhibitors such as clavulanic acid protect amoxicillin.

Section 3Viruses and prions

Structure and replication

A virus is an obligate intracellular parasite containing DNA or RNA, never both, inside a protein capsid built of capsomeres with icosahedral or helical symmetry. Many also wear a host-derived envelope. Enveloped viruses are fragile (killed by drying, detergents, alcohol and stomach acid) and spread by respiratory droplets, blood, sex and close contact. Naked (nonenveloped) viruses survive on surfaces, resist many disinfectants and often spread by the fecal-oral route: picornaviruses (polio, coxsackie, rhinovirus, hepatitis A), norovirus, rotavirus, adenovirus and hepatitis E.

Replication proceeds in six steps. Attachment of a viral protein to a specific host receptor determines tropism (HIV gp120 to CD4 plus CCR5 or CXCR4; EBV to CD21 on B cells; influenza hemagglutinin to sialic acid; SARS-CoV-2 spike to ACE2; rabies to the acetylcholine receptor). Penetration by membrane fusion or endocytosis is followed by uncoating, then synthesis of nucleic acid and proteins, assembly, and release by budding (enveloped) or lysis (naked). DNA viruses generally replicate in the nucleus (poxviruses are the exception, carrying their own polymerase into the cytoplasm); RNA viruses generally replicate in the cytoplasm (exceptions are influenza and retroviruses). Positive-sense RNA can be translated directly as mRNA, so purified genome is infectious; negative-sense RNA must first be copied by an RNA-dependent RNA polymerase packaged in the virion; retroviruses copy RNA into DNA with reverse transcriptase and integrate it into the host genome.

Infection may be lytic, persistent, latent or transforming. Oncogenic viruses include HPV 16 and 18 (E6 and E7 inactivate p53 and Rb), EBV (Burkitt and Hodgkin lymphoma, nasopharyngeal carcinoma), hepatitis B and C (hepatocellular carcinoma), HHV-8 (Kaposi sarcoma) and HTLV-1 (adult T cell leukemia). Interferon-α and -β induce an antiviral state in neighboring cells. Influenza A changes by antigenic drift (point mutations in hemagglutinin and neuraminidase, seasonal epidemics) and antigenic shift (reassortment of its segmented genome with animal strains, pandemics).

DNA and RNA viruses

The DNA viruses (hepadna, herpes, adeno, pox, parvo, papilloma, polyoma) are double-stranded except parvovirus B19 and icosahedral except poxvirus. Rotavirus is the double-stranded RNA exception.

Viral hepatitis

Hepatitis B serology is a favorite. HBsAg means current infection (acute or chronic). Anti-HBs means immunity (alone after vaccination). HBeAg signals active replication and high infectivity. IgM anti-HBc marks acute infection and is the only marker during the window period, after HBsAg disappears and before anti-HBs appears. IgG anti-HBc indicates past or chronic infection, never vaccination. HBsAg persisting beyond 6 months defines chronic infection. Needlestick risk follows a "rule of 3s": HBV 30 percent, HCV 3 percent, HIV 0.3 percent.

HIV

HIV is a retrovirus (lentivirus) with two copies of positive-sense RNA, reverse transcriptase, integrase and protease inside a cone-shaped p24 capsid. Envelope gp120 binds CD4 and a co-receptor (CCR5 early, CXCR4 later; people homozygous for the CCR5 Δ32 deletion resist infection), and gp41 mediates fusion. It infects CD4 T cells, macrophages and microglia. Transmission is sexual, by blood and needles, and perinatal or by breast milk; it is not spread by casual contact. Infection passes through three phases.

Acute retroviral syndrome appears 2 to 4 weeks after exposure as a mononucleosis-like illness (fever, sore throat, lymphadenopathy, rash). During clinical latency the patient feels well, but replication continues in lymphoid tissue. AIDS is a CD4 count under 200 cells/µL or an AIDS-defining illness. Screening uses a fourth-generation antigen and antibody immunoassay (p24 antigen plus anti-HIV antibodies, shortening the window period) followed by a differentiation assay; viral load (RNA PCR) monitors treatment. Opportunistic infections track the CD4 count:

• Under 500: oral candidiasis (thrush), shingles, tuberculosis, oral hairy leukoplakia (EBV), Kaposi sarcoma.
• Under 200: Pneumocystis jirovecii pneumonia (prophylaxis with trimethoprim-sulfamethoxazole), HIV dementia.
• Under 100: cerebral toxoplasmosis (ring-enhancing lesions), cryptococcal meningitis, candidal esophagitis.
• Under 50: Mycobacterium avium complex, CMV retinitis, progressive multifocal leukoencephalopathy (JC virus), primary CNS lymphoma (EBV).

Combination antiretroviral therapy (nucleoside and non-nucleoside reverse transcriptase inhibitors, integrase inhibitors, protease inhibitors, entry and fusion inhibitors) suppresses the virus, restores CD4 counts and, when viral load is undetectable, prevents sexual transmission. Post-exposure prophylaxis should start as soon as possible, ideally within hours and no later than 72 hours; pre-exposure prophylaxis protects people at ongoing risk.

Respiratory viruses and latency

Rhinovirus causes most common colds. Influenza begins abruptly with high fever, myalgia and cough; complications include primary viral pneumonia and secondary bacterial pneumonia (especially S. aureus), and aspirin in children with influenza or varicella risks Reye syndrome (fatty liver and encephalopathy). Annual vaccination is the main prevention. RSV is the leading cause of bronchiolitis and pneumonia in infants. SARS-CoV-2 enters through ACE2 and ranges from mild illness with loss of smell to pneumonia and thrombosis. Latency is the hallmark of herpesviruses: HSV-1 hides in the trigeminal ganglion, HSV-2 in sacral ganglia, VZV in dorsal root and cranial nerve ganglia, EBV in memory B cells and CMV in monocytes; stress, illness, ultraviolet light and immunosuppression trigger reactivation.

Prions

Prions are infectious proteins with no nucleic acid. The abnormal isoform (PrP^Sc) is rich in β-pleated sheet, resists proteases and converts the normal α-helical cellular protein (PrP^c) into more of itself. Accumulation causes spongiform encephalopathy: vacuolated neurons and gliosis without inflammation. Creutzfeldt-Jakob disease (sporadic most common) causes rapidly progressive dementia with startle myoclonus and ataxia, periodic sharp-wave EEG complexes, CSF 14-3-3 protein and positive RT-QuIC, and death usually within a year. Variant CJD follows eating beef from cattle with bovine spongiform encephalopathy, affects younger patients and begins with psychiatric symptoms. Kuru and fatal familial insomnia are other prion diseases. Iatrogenic transmission has followed dura mater and corneal grafts, cadaveric growth hormone and reused neurosurgical instruments, because prions resist standard autoclave cycles, formaldehyde, alcohol, radiation and UV light; inactivation requires extended high-temperature autoclaving combined with sodium hydroxide, or disposal.

Section 4Fungi and parasites

Fungal biology

Fungi are eukaryotes with 80S ribosomes, a cell wall of chitin and β-glucan, and ergosterol (not cholesterol) in their cell membranes, which is why most antifungals target ergosterol. Yeasts are single round or oval cells that reproduce by budding. Molds grow as branching tubular hyphae that form a mat (mycelium); hyphae are septate (cross walls, as in Aspergillus and the dermatophytes) or nonseptate (coenocytic, as in Mucor and Rhizopus). Candida albicans forms pseudohyphae (chains of elongated buds) and true germ tubes at body temperature. Dimorphic fungi switch form with temperature: "mold in the cold, yeast in the heat," growing as mold in soil at 25 °C and as yeast in tissue at 37 °C (Coccidioides forms spherules instead). Cell-mediated immunity contains most fungal infections, so serious disease concentrates in the immunocompromised. Diagnosis uses KOH preparation, Sabouraud culture, special stains and antigen tests.

Superficial, cutaneous and subcutaneous mycoses

Superficial mycoses involve only the outer stratum corneum and provoke little inflammation. Tinea (pityriasis) versicolor, caused by Malassezia, produces hypopigmented or hyperpigmented scaly patches on the trunk and shoulders, worse in heat and humidity, with a "spaghetti and meatballs" KOH picture (short hyphae and round yeasts). Cutaneous mycoses are the dermatophytoses (Trichophyton, Microsporum, Epidermophyton), which digest keratin in skin, hair and nails and are spread by direct contact, fomites, animals and damp floors: tinea pedis (most common), corporis (ringworm with an active scaly border and central clearing), cruris, capitis and unguium (onychomycosis). Some Microsporum species fluoresce under a Wood lamp. Subcutaneous mycoses enter through puncture wounds: sporotrichosis (Sporothrix schenckii, the "rose gardener's disease") causes a nodule at the thorn prick followed by a chain of nodules along the draining lymphatics.

Systemic and opportunistic mycoses

Antifungal drugs: polyenes (amphotericin B, nephrotoxic; nystatin, topical or swish) bind ergosterol and punch pores; azoles (fluconazole, itraconazole, ketoconazole, clotrimazole) inhibit ergosterol synthesis; echinocandins (caspofungin) block β-glucan synthesis; terbinafine inhibits squalene epoxidase and is used for onychomycosis; griseofulvin binds microtubules and is used for tinea capitis.

Protozoa

Protozoa are single-celled eukaryotes; many alternate between a motile feeding trophozoite and a resistant cyst that transmits infection.

Helminths

Helminths are multicellular worms. Tissue-invading helminths drive a Th2 response with eosinophilia and high IgE; purely luminal worms often do not.

• Nematodes (roundworms): Enterobius vermicularis (pinworm; most common in the US; perianal itching at night; tape test); Ascaris lumbricoides (most common worldwide; larvae migrate through the lungs causing cough and eosinophilia, adults can obstruct the bowel or bile duct); hookworms (Necator, Ancylostoma; larvae penetrate bare feet; iron deficiency anemia); Strongyloides (skin penetration, autoinfection, fatal hyperinfection in patients on steroids); Trichinella spiralis (undercooked pork or wild game; larvae encyst in skeletal muscle causing myalgia, periorbital edema and eosinophilia); Toxocara (visceral larva migrans from dog feces); filarial worms such as Wuchereria (elephantiasis) and Onchocerca (river blindness).
• Cestodes (tapeworms): Taenia solium (eating larval cysts in pork gives intestinal tapeworm; eating eggs from human feces gives cysticercosis, and neurocysticercosis is a leading cause of acquired seizures worldwide); T. saginata (beef); Diphyllobothrium latum (raw fish; vitamin B12 deficiency); Echinococcus granulosus (dog feces, sheep; hydatid cysts in the liver; rupture risks anaphylaxis).
• Trematodes (flukes): Schistosoma (freshwater snails release cercariae that penetrate skin; S. mansoni causes portal hypertension, S. haematobium causes hematuria and squamous cell bladder cancer); Clonorchis (raw fish; cholangiocarcinoma); Paragonimus (crabs; lung disease mimicking TB).

Arthropod vectors

Section 5Epidemiology and disease control

Measuring disease

Incidence is the number of new cases in a population at risk over a stated time (for example, 12 new cases per 1,000 people per year); it measures risk. During an outbreak the incidence among those exposed is called the attack rate. Prevalence is the number of existing cases at a point in time (point prevalence) or over a period, divided by the population; it measures burden. For a stable disease, prevalence ≈ incidence × average duration. A treatment that prolongs life without curing (insulin, antiretroviral therapy) raises prevalence without changing incidence; a rapidly fatal or quickly cured disease has low prevalence even with high incidence. The mortality rate is deaths from a disease per population; the case fatality rate is deaths among those who have the disease. A disease is endemic when constantly present at a usual level, epidemic when clearly above that level, and pandemic when epidemic across several countries or continents.

Study designs

With a 2 × 2 table of exposure (rows) against disease (columns), cells a, b, c, d: relative risk = [a/(a+b)] / [c/(c+d)]; odds ratio = ad/bc; attributable risk = incidence in exposed minus incidence in unexposed. For treatments, absolute risk reduction = control event rate minus treated event rate, and the number needed to treat = 1/ARR. A relative risk or odds ratio of 1 means no association; if its 95 percent confidence interval includes 1, the result is not statistically significant. Major threats to validity are selection bias, recall bias, measurement bias, the Hawthorne effect (subjects behave differently when observed), lead-time bias (earlier diagnosis appears to prolong survival) and confounding (a third factor linked to both exposure and outcome). A type I error (α) is a false positive conclusion, a type II error (β) a false negative, and power = 1 − β.

Sensitivity, specificity and predictive values

Diagnostic and screening tests are judged against a gold standard. Sensitivity = TP / (TP + FN) is the proportion of diseased people who test positive; a highly sensitive test rarely misses disease, so a negative result rules it out ("SnNout") and such tests are used for screening. Specificity = TN / (TN + FP) is the proportion of healthy people who test negative; a highly specific test rarely labels healthy people as sick, so a positive result rules disease in ("SpPin") and such tests are used to confirm. Positive predictive value = TP / (TP + FP) and negative predictive value = TN / (TN + FN) answer the patient's question: given my result, how likely is it that I do or do not have the disease? Sensitivity and specificity are properties of the test; predictive values change with prevalence: as prevalence rises, PPV rises and NPV falls. Lowering a test's cutoff to catch more cases raises sensitivity at the cost of specificity, the trade-off traced by a ROC curve. Reliability (precision) is reproducibility between examiners or trials; validity (accuracy) is closeness to the truth.

Outbreak investigation and the chain of infection

An outbreak investigation proceeds in order: verify the diagnosis; confirm an outbreak against baseline; write a case definition; find and count cases; describe them by time, place and person with an epidemic curve; test hypotheses with an analytic study; apply control measures as early as possible; communicate and keep up surveillance. The shape of the epidemic curve is telling: a point-source outbreak (one meal) rises and falls sharply within one incubation period; a continuous common source (contaminated water supply) plateaus; a propagated outbreak (person to person, such as measles) shows successive waves one incubation period apart. Clinicians, including chiropractors in most jurisdictions, report notifiable diseases (for example measles, pertussis, tuberculosis, syphilis, hepatitis and foodborne outbreaks) to the local or state health department.

The six links: the infectious agent; its reservoir (humans, including asymptomatic carriers; animals, for zoonoses; soil or water); the portal of exit (respiratory tract, blood, skin lesions, feces); the mode of transmission; the portal of entry (mucous membranes, broken skin, needle puncture); and a susceptible host (unvaccinated, very young or old, immunosuppressed, diabetic). Modes of transmission are contact (direct skin-to-skin, or indirect via fomites such as a headrest or reflex hammer), droplet (large particles traveling about 1 to 2 meters: influenza, pertussis, N. meningitidis, mumps), airborne (small droplet nuclei that stay suspended: tuberculosis, measles, varicella; require an N95 respirator and negative-pressure room), vehicle (food, water, blood products) and vector (mechanical, such as flies, or biological, where the agent develops inside the arthropod, such as malaria in mosquitoes). Prevention is primary (prevent disease: vaccination, hand hygiene), secondary (detect early: screening) or tertiary (limit disability from established disease: rehabilitation).

Sterilization, disinfection and antisepsis

Sterilization destroys all microbial life, including bacterial spores. Methods: steam autoclave (moist heat under pressure, classically 121 °C at 15 psi for 15 to 30 minutes, or 132 to 134 °C for shorter cycles; denatures proteins and is the standard for heat-tolerant items), dry heat (about 160 to 170 °C for 1 to 2 hours), ethylene oxide gas and hydrogen peroxide plasma for heat-sensitive items, ionizing radiation for disposables, and prolonged immersion in liquid chemical sterilants such as glutaraldehyde. Steam cycles are verified with biological indicators (spores of Geobacillus stearothermophilus) and chemical indicator tape. Disinfection eliminates most pathogens on inanimate objects but not necessarily spores. Antisepsis applies an antimicrobial to living tissue (alcohol, chlorhexidine, povidone-iodine). Sanitization lowers counts to safe public health levels, and pasteurization kills milk-borne pathogens such as Listeria and Brucella but is not sterilization.

Microbes differ in resistance, from most to least: prions, bacterial spores, mycobacteria, small nonenveloped viruses (polio, norovirus), fungi, vegetative bacteria, and enveloped viruses (HIV, HBV, influenza, herpes), which are the easiest to kill. Alcohol hand rub does not kill C. difficile spores and is weak against norovirus, so soap and water are used after caring for those patients and when hands are visibly soiled, and a sporicidal agent such as diluted bleach is used on surfaces.

Standard precautions and the chiropractic office

Standard precautions treat blood and all body fluids, secretions and excretions except sweat, plus nonintact skin and mucous membranes, as potentially infectious for every patient regardless of diagnosis. They comprise hand hygiene (alcohol rub for 20 to 30 seconds, or soap and water for at least 20 seconds; before and after every patient contact, after touching surroundings, after glove removal and after body fluid exposure), personal protective equipment chosen for the anticipated exposure (gloves for blood or lesions, mask and eye protection for splashes), respiratory hygiene (masks for coughing patients, tissues, distance), safe sharps practice (never recap by hand; use puncture-resistant containers at the point of use), safe injection practices, and environmental cleaning. Transmission-based precautions are added for known or suspected infection: contact (gown and gloves: MRSA, C. difficile, scabies), droplet (surgical mask) and airborne (fit-tested N95 and an airborne isolation room). Under the occupational bloodborne pathogens standard, employers with exposed staff keep a written exposure control plan, provide annual training and PPE, and offer the hepatitis B vaccine at no cost.

In practice: change headrest paper and wipe the face cradle and any vinyl touched by skin with an EPA-registered disinfectant between patients, observing the label contact time; clean hands between patients; use single-patient or cleaned electrodes and hot pack covers; avoid direct contact with active herpes, impetigo, tinea, scabies or draining wounds; and keep staff vaccinated and home when febrile.

Words worth knowing