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Dean Gasco

PERTUSSIS (WHOOPING COUGH) Medical Mgmt

• Immunization: Pertussis Immune Globulin
• Bordetella pertussis, B. parapertussis, B. bronchisceptica,
• Antibiotics: Erythromycin
gram (-)
• F&E replacement to prevent dehydration
• Pertussis toxin, tracheal cytotoxin, “Bordet Gengou
• Mild form of sedation: Codeine
Bacillus”
• Common in infants and young children & fatal to toddlers Diagnostic Exams
• MOT: airborne/droplet, direct contact (nose & throat • Nasopharyngeal swab
secretions); indirect contact (article) • Bordet-Gengou Test
• Infection disease characterized by repeated attacks of • Agar Plate
spasmodic coughing which consists of series of explosive • Cough plate
expirations, typically ending in a long-drawn forced • Sputum culture
inspiration which produced a crowing sound, the “whoop” • CBC (leukocytosis)
and is usually followed by vomiting.
• Also known as whooping and chin cough Treatment
• Affects children below 6 years old • Supportive therapy: F&E replacement, adequate nutrition,
• Above 6 years old has lesser risk for being infected oxygen therapy

Causative Agent: Bordetella Pertussis Nursing Mgmt

• Nonmotile, gram (-) bacillus that is easily destroyed by light,
heat and drying
• More serious when it occurs in infants
Incubation Period: 7-14 days
Source of Infection: nose and throat secretions of infected
person
Mode of Transmission: droplet & direct contact, indirect:
soiled linens & articles
Incidence
• Infants are highly susceptible
• One attack – lifetime immunity
• Second attack – due to another microorganism causing
whopping cough syndrome
Clinical Manifestations – 3 stages of Pertussis
1. Catarrhal stage (1-2 weeks)
➢ Highly contagious
➢ Stay at home
➢ S/s: presence of colds, nocturnal coughing, fever,
tiredness and listlessness
2. Spasmodic/Paroxysmal stage
➢ 5-10 successive forceful coughing ends on a prolonged
inspiratory phase or whoop
➢ Occurs on the 14th days and last from 4-6 weeks
➢ There’s production of mucus (tenacious) plugs on
airway passage
➢ Other manifestations: congested face & tongue, teary
red eyes w/ protrusion of eyeballs, distended face &
neck veins, involuntary micturition & defecation,
abdominal/inguinal hernia, deafness duet to
hemorrhage of vestibular apparatus of ear
➢ Cyanotic, nose bleeding, convulsions (intracranial
bleeding) due to paroxysmal cough
3. Convalescent stage
➢ S/s starts to disappear
➢ No longer communicable
➢ Road to recovery
• Isolation and medical asepsis
• During paroxysm, should NOT be left alone. Suctioning
equipment should be ready at all times.
• Sunshine and fresh air are important (NO AIRCON)
• Kept pt as still and quiet as possible
• Provide warm baths and keep the bed dry and free from
soiled linens
• CBR
• Vit. C to inc body resistance
• Oxygen (1-2L/min) to lessen the occurrence of paroxysm
• Proper positioning (upright) when feeding to prevent
aspiration
Preventive Measures – same as Diphtheria
Immunity: no permanent immunity but 2nd attack is rare
because child will not remain 6 yrs old forever
PULMONARY TUBERCULOSIS
• Also known as Koch’s infection, Phthisis, PTB and
Galloping consumption
• Chronic, subacute, or acute respi disease commonly
affecting the lungs characterized by the formation of
tubercles in the tissues which tend to undergo caseation,
necrosis and calcification.
Causative Agent – Acid Fast Bacilli
• Mycobacterium tuberculosis or tubercle bacilli
• Mycobacterium bovis
• Mycobacterium avium/avis
• Organism multiplies slowly & characterized as acid fast
aerobic organism which can be killed by heat, sunshine,
drying & UV light
• Sputum of persons w/ TB – most common source of
organism spread thru droplet
• Pott’s disease – thoracolumbar
• Miliary TB – kidney, lungs, liver
Incubation Period: 2-10 weeks

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Mode of Transmission – direct (droplet – sneezing & • Cough gradually becomes distressing
coughing), indirect (continuous exposure to infected • Abnormal physical signs are easily elicited
persons w/in the family) • Breath sounds increased (audible crepitant rales)
Source of Infection: sputum, blood from hemoptysis, nasal • Hemoptysis is rare
discharge and saliva 3. Chronic pulmonary TB
• Generalized systemic signs
➢ General malaise, anorexia, easy fatigability,
apathy, irritability, indigestion, general influenza-
like symptoms
➢ Physical signs are meager (tachycardia,
hypotension, dyspnea, cyanosis)
➢ Afternoon fever (38℃-39℃)
➢ Night sweat
➢ Loss of weight
• Pulmonary s/s
➢ Insidious onset of cough w/ mucopurulent sputum
Definition ➢ Fine crepitant rales over apical areas
➢ Hemoptysis & chest pain
Tubercule Brain, lymph Early ➢ Pleural pain
bacillus (sputum
smear, (+)
node, lung, Treatment - ➢ Dyspnea
infected person, spine, kidney, recovery /
airborne) joint Death Methods of PE
1. Inspection
➢ Depression of the hemothorax on one side
➢ One of both clavicles may be prominent
2. Palpation – tactile fremitus
Dissemination
Caseation, Spread Spread
necrosis, thru
Tubercule on thru brochi/
fibrosis,
calcification tissues brochioles
blood/
lymph
3. Auscultation – often advanced lesions give little or no
evidence of altered breathing
Diagnostic Exams
Etiology • Chest xray
• Overcrowded homes • Sputum smear & culture
• Malnutrition ➢ Finding the acid-fast bacilli in the sputum thru coughing
• Deficiencies in Vit. A, D, C & expectoration
• Inadequate levels of immunity ➢ Culture are helpful to determine bacterial susceptibility
• Alcoholism & smoking to anti-TB drugs
➢ Purulent material should be cultured
Risk Factors ➢ Sputum Microscopy (cheapest & confirmatory)
• Close contact w/ someone who has active TB ✓ Results take about 3 weeks to confirm
• Immunocompromised status ✓ Sputum sample should be taken 1st thing in the
• Preexisting medical conditions morning upon arising
• Living in overcrowded or substandard housing ✓ 3 specimens: 1st (on the sport – HC), 2nd (upon
• Significant reaction to tuberculin skin test arising – home), 3rd (on the spot – HC)
• Tuberculin test
Quantitative Classification of TB ➢ Tubercle bacillus & purified protein derivative
1. Minimal – slight/small lesion in the lungs ➢ Inject (ID) at the inner forearm 4 inches below the
2. Moderately advanced – one or both lungs may be elbow
involved, total diameter of cavity <4cm ➢ Results: 48-72 hrs after injection
3. Far advanced – more extensive, hemoptysis ➢ Measure diameter of induration in mm
Clinical Manifestations ➢ Interpretation of results:
1. Primary infection ✓ 0-4mm – not significant
• Change of behavior from normal to listlessness ✓ >5mm – significant to those who are at risk, due to
• Easy fatigability cross reaction to other mycobacterial infections,
due to incompletely developed sensitivity
• Alertness to apathy
✓ >10mm – significant to those who have
• From normal activity to irritability
normal/mildly impaired immunity
• Fleeting infection of respi/GIT associated w/ fever
• Crepitant rales
2. Postprimary/Progressive primary TB
• Visibly ill due to fever

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Treatment Category Type of TB patient

Prophylaxis I • New smear positive PTB
• BCG (Bacilli Calmette Guerin) – simplest, safest, most • New smear negative PTB w/ extensive
paroxysmal lesions on xray as assessed
economical & most effective measure of prevention.
II • Treatment failure
Administered during neonatal period & repeated before • Relapse
primary school • Return after default
• Primary Chemoprophylaxis – administration of Isoniazid • Other
(INH) to uninfected subjects. Administered INH instituted 8 III • New smear negative PTB w/ minimal paroxysmal
wks after BCG vaccination – high risk groups. lesions on xray as assessed by the TBDOC
Recommended daily: 5 mg/kg of body weight given in single IV • Chronic
dose
• Secondary Chemoprophylaxis – progression of primary Treatment Failure (ma-appear kuno exam)
lesions can be prevented w/ INH w/ a daily dose of 5-10 • Use of substandard dosages
mg/kg of body weight. Administered to pt w/: measles, • Irregularity in taking the drugs
pertussis, influenza, intake of steroids & • Inadequate drug regimen
immunosuppressive, after surgery under general • The premature discontinuation of therapy
anesthesia • The presence of drug resistance infections at the start of
the treatment
Specific Chemotherapy
• Rifampicin Nursing Mgmt
➢ SE: red-orange colored urine, GI upset, jaundice, renal • D – diet – small & frequent nutritious food
failure, thrombocytopenia • D – drugs – adequate drug and emphasize compliance
• Isoniazid (INH) – bacteriostatic (inhibits), bactericidal (kills) • R – rest – to conserve energy
➢ Used prophylactically to pts (+) of PPD • Contraindicated: Chest Physiotherapy – stimulate or
➢ SE: neuritis (instruct pt to eat food rich in Vit B6 aggravate hemoptysis
[beans], give vit. B6 [pyridoxine] to counteract),
hepatotoxicity (monitor liver enzymes & avoid alcoholic 1. Maintain respiratory isolation
beverages) 2. Administer medicine as ordered
• Pyrazinamide (PZA) 3. Always check sputum for blood or purulent expectoration
➢ SE: hyperuricemia 4. Encourage questions and conversation so that the pt can
➢ Mx: Inc fluid intake air his or her feelings
• Ethambutol – 15-20mg/day 5. Teach or educate the pt all about PTB
➢ SE: optic neuritis (dec visual acuity) 6. Encourage pt to stop smoking
➢ Give Vit. B6 (Pyridoxine) 7. Teach how to dispose secretion properly
• Streptomycin 8. Advised to have plenty of rest and balanced diet
➢ SE: ototoxicity, 8th cranial nerve damage – tinnitus,
Prevention
dizziness, N&V
1. Submit all babies for BCG immunization
• Fixed dose combination (FDC) – 2 or more first-line anti-TB
• After birth 0.5cc ID right deltoid area
drugs are combined in 1 tablet
• Instruct mother to not massage the area because it will
• Single drug formulation (SDF) – each drug is prepared
spill the drug.
individually, tablet: INH, ethambutol, pyrazinamide,
• Child will have fever and abscess formation on the area
capsule: rifampicin
which will develop into a scar within 2-3 months
MDT side effects (remember!!) 2. Avoid overcrowding
✓ R – orange urine 3. Improve nutritional and health status
✓ I – neuritis & hepatitis 4. Advise persons who have been exposed to receive
✓ P – hyperuricemia & liver damage tuberculin test if necessary, CXR and prophylactic INH
✓ E – impairment of vision
PNEUMONIA
✓ S – 8th cranial nerve damage
Management • Acute infection disease caused by pneumococcus
• Short course – 6-9 months associated by general toxemia and a consolidation of one
or more lobes of either one or both lungs
• Long course – 9-12 months
• Inflammation of the lung parenchyma caused by infectious
• DOTS – directly observe treatment short course
agents in which the air sacs are filled with pus or exudate
• 2 wks after medications – non-communicable
so that air is excluded and the lungs become solid
• 3 successive (-) sputum – non-communicable
(consolidation).
• Rifampicin or INH – prophylactic

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Causative Agents
• Streptococcus pneumoniae
• Staphylococcus aureus
• Hemophilus influenzae
• Klebsiella pneumoniae (Friedlander’s bacilli)
Causes of Pneumonia
• Bacteria
• Viruses
• Mycoplasma
• Other infections agents (fungi)
• Various chemicals
• Pneumonia is not a single disease. It can have over 30
different causes.
Mode of Transmission – direct contact (droplet), indirect
contact (contaminated objects)
General Classification
• Primary Pneumonia – produced as a direct result of
inhalation or aspiration of pathogen or noxious substances.
• Secondary Pneumonia – develops as a complication
• Community-acquired pneumonia (CAP) – acquired in the
course of one’s daily life. If a hospitalized pt develops
pneumonia in <36 hrs during his stay in the hosp.
Streptococcus pneumoniae – most common cause
• Nosocomial Pneumonia – while in the hospital
• Aspiration pneumonia – occurs when a foreign matter is
inhaled into the lungs, most commonly gastric contents
after vomiting.
• Pneumonia caused by opportunistic organisms –
strikes the people with compromised immune system.
Organism are not harmful for health people but can be
extremely dangerous for those w/ HIV/AIDS and other
conditions that impair the immune system.
Anatomical Classification
Bronchopneumonia – lobular or catarrhal pneumonia
• Most common type
• Infection starts from the bronchus and the bronchioles and
spread to the alveoli.
• Lobules become inflamed and consolidated.
• Onset is slow and fever is lower
Lobar Pneumonia – croupous pneumonia
• Consolidation of the entire lobe
• Manifested by chills, chest pain on breathing and cough w/
blood-streaked sputum (prune juice or rusty)
• May lead to heart failure, edema of the lungs or several
general exhaustions
Primary Atypical pneumonia – viral pneumonia
• Solidification of the lungs that comes in patches
• Cough is often delayed in appearing and greenish to whitish
secretions are often raised on coughing on the 3rd-5th day.
Pathology – 4 stages
1. Stage of Lung engorgement (congestion) – lung is
heavy, dark red in color, pits upon pressure w/ finger, and
exudes a bubbly, blood-tinged froth.
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Dean Gasco
2. Red Hepatization – lung is heavy, sinks in water and looks
like a piece of red granite
3. Gray Hepatization – red color changes to gray, looks like
an ordinary granite, softer & tears more easily and when
pressed, it exudes a purulent fluid.
4. Stage of resolution – inflammatory exudate is either
absorbed by the blood stream or expectorated.
Clinical Manifestations
Cardinal signs of Pneumonia
1. Rapid or gradual onset of fever
2. Shaking chills
3. Productive cough
4. Sputum production
• Rusty – streptococcus pneumoniae
• Creamy yellow – staphylococcus
• Currant jelly (like lychees) – Klebsiella
• Greenish – pseudomonas
• Clear – no infection (aspiration/lipid pneumonia)
5. Chest or pleuritic pain – aggravated by coughing
Diagnostic Exams
• Physical examination by: percussion, auscultation (crackles
& rhonchi), decrease breath sounds and decrease vocal
fremitus.
• Chest xray – presence of lung consolidation or patchy
infiltration that confirms pneumonia
• Sputum exam – determine specific microorganism
Treatment
Antimicrobial Therapy
• Streptococcus: macrolide (ACE) for 7-10 days, nafcillin or
oxacillin for 14 days
• Klebsiella: aminoglycosides and cephalosporins
• Pneumocystis carinii: cotrimoxazole or pentamidine
• Pen G Na is still the DOC
Supportive measures
• Humidified oxygen therapy for hypoxia
• Mechanical ventilation for respi failure
• High caloric diet and adequate fluid intake
• Absolute bed rest
Bronchodilators
Expectorants
Pain relivers – pleuritic pain
Nursing Care – similar with Diphtheria
• CBR to conserve energy
• Maintain patent airway
• Increase body resistance by adequate rest and nutrition
• Provide comfort measures
Preventive measures
• Immunization by immunovirax (pneumonia vaccine)
• Proper disposal of nasopharyngeal secretions
• Cover nose and mouth when sneezing and coughing
Immunity – no permanent immunity
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LEPROSY (HANSEN’S DISEASE)
• Chronic communicable disease of the skin & the peripheral
nerves characterized by progressive cutaneous lesions
• Contrary to popular belief, leprosy is NOT highly contagious
and actually has LOW infectivity
Causative agent: Mycobacterium leprae, acid fast bacilli
Incubation period: 5 and ½ months to 8 years
Mode of transmission: respiratory droplet, inoculation thru
skin break and mucous membrane
Types of Leprosy
Lepromatous Leprosy
• Most serious and most infectious
• Damage to the respi tract, eyes, and testes as well as the
nerves and the skin
• Lepromin test – determine what type of leprosy a person
has (same as skin test)
• (-) but skin lesion contains HANSEN’S BACILLUS
• Gradual thickening of the skin
• Lesions appear as macules and becomes nodular
(leproma)
• Slow involvement of the peripheral nerves, some degree of
anesthesia and loss of sensation and gradual destruction of
the nerves
• Atrophy of the skin and muscles and eventual melting or
absorption of small bones primarily of the hands and feet –
natural amputation
• Ulceration of the mucous membrane of the nose
• Inability to close eyelids “unblinking eyes” (lagophthalmos)
multiple lesions, loss of lateral portion of eyebrows
(madarosis), corrugated skin (leonine faces), septal
collapse (saddlenose), clawing of fingers & toes, loss of
digits, enlargement of male breasts (gynecomastia)
Tuberculoid Leprosy
• Affects the peripheral nerves and sometimes the
surrounding skin, specially the face, eyes and testes as well
as the nerves and the skin
• Lepromin test (+) but organism is rarely seen in lesions
• Anesthesia is present and involvement of the peripheral
nerves occurs more rapidly than in the lepromatous forms
• Solitary hypopigmented hypoesthetic macule, neuritic pain,
contractures of hand & foot, ulcers, eye involvement
(keratitis)
Mixed Type or Borderline or Dimorphous
• Has the characteristics of both LL and TL
• Between both LL and TL
Diagnostic Procedures
• Identification of the s/s
• Tissue biopsy
• Tissue smear
• Blood tests show increased RBC and ESR and decrease
Ca, albumin, and cholesterol level
• Skin smear (biopsy of nodule)
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Dean Gasco
Mgmt
• Domiciliary home treatment (RA 4073)
• Multi drug therapy (MDT) – use of 2 or more drugs for the
tx of leprosy. Proven effective cure & renders pts non-
infectious a wk after starting tx
• Paucibacillary – rifampicin and dapsone
• Multibacillary – rifam, dapsone, clofazimine
• Tx is from 9 mos to 18 mos
Prevention
• Report all cases and suspects of leprosy
• NB infarcts should be separated form leprous mothers
• BCG vaccine may be protective if given during the first 6
months of life
• Health educations should be given as to the MOT
ANTHRAX
• Infection caused by Bacillus anthracis that occurs primarily
in herbivores
• Aerosolized spores of B. anthracis have the potential for
use in biological warfare or bioterrorism
• Most prevalent among domestic herbivore (cattle, sheep,
horses and goats) and wild herbivores
• Humans are more resistant to anthrax that herbivorous
animals
Etiologic agent: Bacillus anthracis – large, aerobic, spore
forming, gram (+) rod shaped MO that is capsulated and no
motile. Its spores can survive for years in dry soil but can be
destroyed by boiling in 10 minutes. Most strains of the agent are
susceptible to penicillin.
Human cases are classified as:
• Agricultural cases – from contact w/ animals that have
anthrax, from bites of contaminated flies or insects and
consumption of contaminated meat.
• Industrial cases – associated w/ exposure to
contaminated hides, goat hair, wool or bones
Mode of transmission: direct (thru contact w/ infected
animals), indirect (thru animal bites and ingestion),
airborne (thru inhalation of contaminated air)
Types
• 95% are Cutaneous
• 5% are Inhalational
• GI cases are very rare
Cutaneous Anthrax
• IP ranges from 9 hours – 2 weeks (2-7days)
• 2-3 days after the entrance of the MO, a small pimple or
macule appears
• On the 4th day, a ring of vesicles develops around the
papule. Vesicular fluid may exude.
• Marked edema starts to develop
• Unless there is secondary infection, there is NO pus and
the lesion if NOT painful, although painful lymph adenitis
may occur in the inguinal area
• On the 5th-7th day, the original papules ulcerate to form the
characteristic eschar.
• Edema extends to some distance from the lesion
5

• May be accompanied w/ high fever, toxemia, regional
painful lymphadenopathy and extensive edema
• Shock and death
Inhalational Anthrax
• Woolsorter’s disease
• Presenting symptoms resembles those of several viral respi
disease
• After 1-3 days of acute phase, increasing fever, dyspnea,
stridor, hypoxia and hypotension occur usually leading to
death within 24 hours
• Organisms are directly deposited into the alveoli or into the
alveolar duct producing hemorrhagic necrosis of the nodes
associated w/ hemorrhagic mediastinitis
Gastrointestinal Anthrax
• Results from ingestion of inadequately cooked meat from
animals w/ anthrax
• Primary infection usually starts in the intestines where
lesions are formed accompanied by hemorrhagic
lymphadenitis
• Symptoms include fever, N&V, abdominal pain, bloody
diarrhea, and ascites
Complications
Anthrax Meningitis
• Intense inflammation of the meninges of the brain and
spinal cord
• Marked by elevated CSF pressure w/ bloody CSF followed
by rapid loss of consciousness and death
• CFR is almost 100%
Anthrax Sepsis
• Develops after lymphohematogenous spread of B.
anthracis from the primary infection
• Manifested by high fever, toxemia, and shock w/ death ff a
short time
Treatment – Parenteral Pen G (erythromycin, tetracycline or
chloramphenicol if sensitive to penicillin)
MENINGITIS (CS Fever)
• Inflammation of the meninges (covering of the brain and
spinal cord)
• 3 covering: dura mater, arachnoid-subarachnoid spaces
(between meninges), pia mater
• Can follow a skull fracture, penetrating head wound, lumbar
puncture or ventricular shunting procedure
Causative agents – meningococcus
• Other bacteria and viruses arising from diseases like:
pneumonia, empyema, osteomyelitis, endocarditis,
sinusitis, otitis media, mastoiditis encephalitis, myelitis or
brain abscess
• Usually caused by Neisseria meningitides, Hemophilus
influenzae, streptococcus pneumoniae and Escherichia coli
S/s
Cardinal Signs – infection (fever, chills, malaise) & ICP
(headache, vomiting, [rarely] papilledema)
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Dean Gasco
Meningeal irritation
• Nuchal rigidity, (+) Brudzinski’s and Kernig’s sign
• Opisthotonos, a spasm in which the back and extremities
arch backward, the body rests on heels and head
• Other manifestations: sinus arrythmia, irritability,
photophobia, diplopia, and other visual problems, delirium,
deep stupor, coma
Diagnostic Procedures
Lumbar Puncture – tap or aspirate CSF to evaluate
• Diagnostic purpose – to obtain specimen (CSF), take cray
of the spinal cord and canal
• Therapeutic purposes – reduce ICP, introduce medication,
inject anesthetic agents
• Color: yellowish, turbid, cloudy, clear CSF
• Lab exams: increase CHON, increase WBC, decrease
sugar
• C&S: determine causative agent & specific drug to kill
microorganism
• Counter Immuno Electrophoresis (CIE) – if CSF is clear it
tells you if microorganism is viral or protozoa
• Contraindicated for pt w/ CNS infection, pt w/ highly
increased ICP (normal ICP: 10-11)
Blood culture – done if lumbar puncture can’t be done yet
because microorganism travels to the blood stream
Gram staining
Smear & blood culture
Smear from petechiae
Urine culture
Classification – Acute Meningococcemia & Aseptic
meningitis
Treatment
Alert – meningitis if left untreated has 70-100% mortality
Antimicrobials drugs – viral (supportive tx), fungus
(antifungal), bacteria (antibiotic)
Corticosteroid – dexamethasone or solu-cortef
Mannitol – osmotic diuretic to remove excess CSF, monitor I&O
to assess effectiveness of drug, assess hydration of pt
Anticonvulsant drug – Phenytoin (Dilantin)
Nursing responsibilities
• If Phenytoin is given by IV, it should be sandwiched with
NSS because when mixed with IVF produces crystallization
causing obstruction
• If given per orem, do oral care and gum massage because
it causes gingival hyperplasia
Nursing Care – symptomatic & supportive
Nursing Diagnosis
Altered Temperature/Hyperthermia
• To lower temp: TSB, cold compress, wear light/loose
clothing, increased fluid intake, provide adequate rest, give
paracetamol
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Potential for injury due to convulsions Nursing Intervention

• Never leave pt alone 1. Prevent the occurrence of further complication
• Provide padded side rails • Maintain strict surgical aseptic technique when doing
• Put call line near pt dressings or lumbar puncture – prevent the spread of
microorganism
Altered level of consciousness • Administer O2 inhalation to prevent respi distress and
Alteration in comfort (pain) maintain a clear open airway
• 4 types of massage (petrissage [use of 2 fingers or thumb • TSB for fever to prevent convulsions
pressure], tapotement [karate style], kneading, effleurage • Observe s/s of increased ICP
[figure 8 or circular manner for back & chest]) • Change positions at least every 2 hrs to prevent
• Apply cold compress pressure sore
• Elevate head 15-20 degrees • Protect the eyes from bright lights and noise
2. Maintain normal amount of F&E balance
Risk for F&E imbalance thru projectile vomiting 3. Prevent spread of the disease, prophylaxis for close
• Assess for s/s of F&E imbalance contacts (Rifampicin)
• Monitor fluid I&O 4. Ensure the pts full comfort, prevent stress provoking factors
• Proper regulation of IVF that may retard convalescence and prevent from injury
• Provide adequate fluid 5. Maintain personal hygiene and cleanliness
6. Maintain proper elimination of waste product
Preventive measures
7. Nutritional intake
• Immunization – not a permanent immunity
• Proper disposal – place tissue paper in plastic bag and knot
before throwing
• Covering of mouth when coughing/sneezing or wear mask
MENINGOCOCCEMIA

• CA: Neisseria meningitides

• Gram (-) diplococci
• Also, be caused by H. influenzae and S. pneumoniae
• MOT: droplets (urti) to blood stream to CNS
• IP: 1-2 days (even faster), high risk – immunocompromised
S/s
1. Starts as nasopharyngitis, followed by onset of spiking
fever, chills, arthralgia. Bacteria is carried by circulation &
when it reached the meninges of the brain, bleeding occurs
into the medulla which extends to the cortex & petechial,
purpuric or ecchymotic hemorrhage is scattered in the
entire body surface appear.
2. Fulminant meningococcemia (Waterhouse
Friedrichsen) – septic shock, hypotension, tachycardia,
enlarging petechial rash, adrenal insufficiency
Clinical Manifestations
• Sudden onset of high-grade fever, rash, and rapid
deterioration of clinical condition within 24 hrs
Treatment
Antimicrobial
• Benzyl penicillin 250-400000 u/kg/day – drug of choice
• Chloramphenicol 100mg/kg/day
Symptomatic & supportive
• Fever, seizures, hydration, respi function
Chemoprophylaxis
• Rifampicin 300-600mg q 12 hrs x 4 doses
• Ofloxacin 400mg single dose
• Ceftriaxone 125-250mg IM single dose