Week Twelve: Bacterial Infections of Humans (Part Il)

Bacterial meningitis

Infection causing inflammation of the meninges surrounding the brain and spinal cord.

Common causes of bacterial meningitis

Streptococcus pneumoniae and Neisseria meningitidis.

Transmission of bacterial meningitis

Respiratory secretions.

Pathway of bacterial meningitis

Bacteria reach the blood or spread from a nearby infection, enter the meninges and CSF, multiply, trigger inflammation, and cause swelling and increased pressure that can impair brain function.

Meningococcal disease

A disease caused by Neisseria meningitidis that can cause meningitis, bloodstream infection, sepsis, and a nonblanching rash.

Meningitis risk factors and relevant history

Recent ear or sinus infection, close exposure, vaccination history, immunosuppression, absent spleen, CSF leak, head injury, or neurosurgery.

Classic meningitis findings

Fever, severe headache, neck stiffness, photophobia, nausea, and vomiting.

Photophobia

Sensitivity to light.

Nonblanching rash

Pinpoint spots or purple patches that do not fade when pressure is applied; may suggest meningococcal disease.

Petechial rash

Small pinpoint areas of bleeding under the skin that do not blanch with pressure.

Meningitis neurologic warning signs

Decreased alertness, seizures, or new weakness; may indicate neurologic deterioration or increased intracranial pressure.

Meningitis signs of shock or organ dysfunction

Hypotension, cool or mottled skin, rapid breathing, and oliguria.

Important meningitis assessment point

A rash may be absent, and the full symptom pattern may be absent, especially in infants and older adults.

Bacterial versus viral meningitis

Symptoms alone cannot reliably distinguish bacterial from viral meningitis.

Blood cultures in meningitis

Help identify bacteria in the bloodstream and guide treatment.

Lumbar puncture (LP)

Procedure used to collect cerebrospinal fluid for testing.

CSF testing

Cell count, glucose, protein, Gram stain, culture, and PCR help assess inflammation and identify the cause of meningitis.

Typical bacterial CSF findings

Increased white blood cells, often neutrophils; increased protein; and a lower CSF-to-blood glucose ratio.

CT before lumbar puncture

Used selectively to assess safety before LP; CT does not replace CSF testing.

Meningitis precautions

Start Standard plus Droplet Precautions while meningococcal disease is possible.

Duration of Droplet Precautions for meningococcal or Hib disease

Continue Droplet Precautions for 24 hours of effective therapy.

Meningitis mask requirements

Staff wear a surgical mask on entry; mask the patient during necessary transport.

Meningitis treatment priorities

Prompt prescribed IV antibiotics, ordered dexamethasone with or before the first antibiotic when indicated, airway and oxygenation support, prescribed fluids, and seizure safety.

Meningitis reassessment

Monitor consciousness, pupils, seizures, vital signs, and urine output; escalate new deficits, falling alertness, shock, or rapidly spreading rash.

Meningococcal contact management

Notify infection prevention and public health; identify close contacts who may need prophylaxis.

Meningitis prevention and follow-up

Review meningococcal, pneumococcal, and Hib vaccination; arrange hearing and neurologic follow-up and teach warning signs.

Hib

Haemophilus influenzae type b.

Tetanus

A toxin-mediated illness that causes muscle rigidity and painful spasms.

Causative organism of tetanus

Clostridium tetani, an anaerobic, Gram-positive, spore-forming rod.

Tetanus transmission

Environmental spores in soil or fecal contamination enter through broken skin; tetanus does not spread person to person.

Tetanus mechanism

Spores enter a wound, germinate in low-oxygen tissue, and produce toxin that blocks nerve signals normally limiting muscle contraction.

Tetanus toxin effect

The toxin acts on nerves; bacteria usually remain near the wound.

Trismus

Lockjaw; difficulty opening the mouth.

Tetanus clinical findings

Jaw stiffness, difficulty swallowing, neck stiffness, persistent muscle rigidity, and painful spasms of the trunk or limbs.

Tetanus spasm triggers

Light, noise, or touch may trigger muscle spasms.

Tetanus airway complications

Throat or chest muscle spasms can block airflow or impair breathing.

Tetanus autonomic instability

Large blood pressure or heart-rate changes, sweating, and abnormal heart rhythm.

Tetanus diagnosis

Based on clinical findings and history; no laboratory test can confirm or exclude tetanus.

Tetanus escalation findings

Suspected tetanus, breathing difficulty, severe spasms, or unstable blood pressure or cardiac rhythm.

Tetanus precautions

Standard Precautions; tetanus does not spread between people.

Tetanus nursing priorities

Monitor breathing, SpO2, secretions, and swallowing; prepare for airway support; reduce stimulation; administer ordered sedation, muscle relaxants, analgesia, TIG, and antibiotics; assist with wound cleaning or debridement.

Tetanus environmental management

Keep the room quiet and dim and minimize avoidable stimulation to reduce spasms.

TIG

Tetanus Immune Globulin.

Tetanus recovery teaching

Tetanus illness does not provide immunity; give indicated vaccination once the patient is stable.

Tetanus wound assessment

Assess the wound and verify the patient's vaccination records and date of last dose.

Tetanus prophylaxis: unknown, no doses, or incomplete primary series; clean minor wound

Give tetanus vaccine; TIG is not indicated.

Tetanus prophylaxis: unknown, no doses, or incomplete primary series; dirty or major wound

Give tetanus vaccine plus TIG.

Tetanus prophylaxis: completed primary series; clean minor wound

Give a booster if the last dose was 10 or more years ago; no TIG.

Tetanus prophylaxis: completed primary series; dirty or major wound

Give a booster if the last dose was 5 or more years ago; TIG only for HIV or severe immunodeficiency.

Botulism

A rare, life-threatening illness caused by botulinum nerve toxin; it produces weakness and flaccid paralysis.

Causative organism of botulism

Clostridium botulinum, an anaerobic, Gram-positive, spore-forming rod.

Foodborne botulism

Occurs when a person swallows toxin already present in food.

Wound botulism

Spores enter a wound, germinate into growing bacteria, and produce toxin.

Infant botulism

Swallowed spores, such as those from honey, germinate in the intestine and produce toxin.

Botulism mechanism

Toxin blocks release of acetylcholine at peripheral nerve endings, reducing muscle stimulation and causing weakness and flaccid paralysis.

Acetylcholine

A nerve messenger whose release is blocked by botulinum toxin.

Tetanus versus botulism

Tetanus causes rigidity and spasms; botulism causes weakness and flaccid paralysis.

Botulism exposure history

Ask about shared or preserved foods, wounds, injection exposures, recent botulinum-toxin injections, and whether others who ate the same food are ill.

Botulism early findings

Double or blurred vision, ptosis, slurred speech, difficulty swallowing, and descending weakness.

Ptosis

Drooping of the eyelid.

Descending weakness in botulism

Weakness usually begins in the face and neck and moves downward on both sides.

Flaccid paralysis

Paralysis characterized by reduced muscle tone.

Botulism mental status

Alertness usually remains intact.

Botulism respiratory complication

Respiratory failure from weakening respiratory muscles; a weak cough or shallow breathing is concerning.

Botulism oxygen saturation caution

SpO2 may remain normal early even when respiratory muscle weakness is developing.

Botulism aspiration risk

Difficulty swallowing or managing secretions increases aspiration risk.

Botulism diagnostic testing

Public health coordinates serum and stool toxin tests and other indicated specimens.

Botulism treatment timing

Treat on clinical suspicion with expert consultation; do not wait for laboratory confirmation.

Botulism precautions

Standard Precautions; botulism does not spread between people.

Botulism nursing priorities

Assess breathing, cough, secretions, swallowing, and respiratory strength; prepare for airway support; keep NPO until swallowing safety is assessed; promptly give prescribed antitoxin.

Botulism antitoxin

Antitoxin limits further toxin effects but does not reverse paralysis that already exists.

Botulism antitoxin monitoring

Monitor the infusion for allergic reactions.

Wound botulism treatment

May require wound debridement and antibiotics.

Botulism recovery

Recovery may take weeks to months; support communication, nutrition, eye and skin care, mobility, and rehabilitation.

Helicobacter pylori (H. pylori)

A spiral-shaped Gram-negative bacterium associated with gastritis and peptic ulcers.

Gastritis

Inflammation of the stomach lining.

Peptic ulcer

A sore in the stomach or duodenum.

H. pylori adaptations

Flagella help the organism move through gastric mucus; urease helps it survive local acidity.

H. pylori transmission

Human-to-human spread through saliva, vomit, or stool; contaminated food or water may also contribute.

H. pylori disease mechanism

H. pylori colonizes gastric mucus, survives and attaches to the lining, weakens mucosal defenses through inflammation, and may cause gastritis or ulcers.

H. pylori symptoms

May be asymptomatic; possible burning or upper abdominal discomfort, nausea, bloating, and early fullness.

Other major cause of peptic ulcers

NSAID use.

NSAIDs

Nonsteroidal anti-inflammatory drugs.

H. pylori bleeding warning signs

Blood or coffee-ground emesis, black tarry stool, dizziness, or syncope.

H. pylori perforation or obstruction warning signs

Sudden severe abdominal pain, rigid abdomen, persistent vomiting, or inability to tolerate intake.

H. pylori active infection tests

Urea breath test or stool antigen test.

H. pylori additional testing

Endoscopy and biopsy when indicated; blood counts may help assess anemia.

H. pylori nursing priorities

Standard Precautions, hand hygiene, appropriate PPE for stool or vomit, prescribed antibiotics and acid-reducing medications, medication teaching, and monitoring for bleeding or deterioration.

H. pylori eradication follow-up

Urea breath or stool antigen test at least 4 weeks after completing antibiotics.

H. pylori symptom improvement

Symptom improvement does not confirm eradication; follow-up testing is needed.

H. pylori prevention teaching

Use teach-back for medication adherence and follow-up testing; review NSAID use with the prescriber and support smoking cessation.

Bacterial gastroenteritis

Acute intestinal infection causing diarrhea, abdominal cramps, vomiting, or fever.

Bacteria associated with gastroenteritis

Nontyphoidal Salmonella, Shigella, Campylobacter, and diarrheagenic E. coli, including Shiga toxin-producing E. coli (STEC).

Gastroenteritis transmission

Fecal-oral spread through contaminated food or water, contact with infected people, or animal exposure.

Gastroenteritis mechanism

Swallowed bacteria reach the intestine, attach and multiply and sometimes invade; toxins or inflammation alter fluid movement, causing diarrhea and fluid and electrolyte loss.

Gastroenteritis history

Assess onset, stool and vomit pattern, food and water exposure, travel, animal contact, sick contacts, recent antibiotics, immune status, intake, and urine output.

Gastroenteritis findings

Watery or bloody diarrhea, cramps, nausea, vomiting, and sometimes fever.

Gastroenteritis dehydration findings

Tachycardia, hypotension, dizziness, reduced urine output, or confusion.

Gastroenteritis hydration assessment

Assess intake, thirst, mucous membranes, heart rate, blood pressure, and urine output.

STEC

Shiga toxin-producing Escherichia coli.