Bacteria

Typhoid fever

Etiology : Salmonella typhi MOT: Fecal-oral; food/waterborne Incubation Period:1-2 weeks

Signs and Symptoms

Involves ulceration of the Peryers patches

Cardinal signs: rose spots (erythematous maculopapules) on trunk; ladder-like fever; splenomegaly; intestinal bleeding

Other symptoms that occur include:

Abdominal tenderness Agitation Bloody stools Chills Confusion Difficulty paying attention (attention deficit) Delirium Fluctuating mood Hallucinations Nosebleeds Severe fatigue Slow, sluggish, lethargic feeling Weakness

Diagnosis
Enzyme Immunoassay (IgM/IgG) Widal test or blood serum agglutination test usually becomes (+) by the end of 2nd week (N.B. low sensitivity & specificity) Blood, urine, stool cultures for isolation CBC(anemia, leukopenia, thrombocytopenia) LFT

Complications (usually rare in children) Pneumonia (most common) Intestinal hemorrhage Cerebral thrombi and/or toxic encephalopathy

Treatment Chloramphenicol PO/IV Co-trimoxazole Ampicillin Ceftriaxone/Ciprofloxacin for resistant strains

Nursing Interventions
Administer antibiotics as ordered Bed rest F&E replacement

Pyoderma/Impetigo

Pathophysiology
Impetigo is an infection caused by group A beta-hemolytic streptococci (GABHS) or S. aureus. The organisms are thought to enter through damaged skin and are transmitted through direct contact. After infection, new lesions may be seen on the patient with no apparent break in the skin. Some individuals colonized by S. aureus experience recurrent episodes of impetigo on the nose and lip. Bacteria can spread from the nose to normal skin within 14 days, with impetigo lesions appearing 7-14 days later. Approximately 10% of individuals are colonized by S. aureus in the perineum and more uncommonly, in the axillae, pharynx, and hands.
Often these bacteria enter the body when the skin has already been irritated or injured because of other skin problems such as eczema, insect bites, chickenpox, burns, or cuts. Children may get impetigo after they have had a cold or allergies which have made the skin under the nose raw.

Etiologic agents
S. aureus Group A beta-hemolytic Streps Pyoderma/Impetigo

Epidemiology
Occurs worldwide esp. in countries with warm, humid climates

Incubation period
1-10 days

MOT
Trauma to skin (e.g. cuts, abrasions) Person to person via hands, nasal discharges, shared towels and toys Pyoderma/Impetigo

s/sx
Red spots painless, pruritic blisters on skin, around nose and mouth, b/w upper lip and nose Pyoderma/Impetigo

dx
med hx and PE (i.e. appearance of lesion)

Cx

rarely osteomyelitis, septic joints, or septicemia cellulitis in 10% of cases with strep may get lymphangitis, scarlet fever. post-streptococcal glomerulonephritis(rare) permanent skin damage and scarring Antibiotics PO (Erythromycin or Cephalexin) or topical Bacitracin,Tee tree oil (topical) Pyoderma/Impetigo

Tx

Nsg interventions
Assess the child's skin condition and document the location and appearance of lesions. Note any new lesion. Initiate and teach measures to prevent the spread of infection:
frequent hand washing, use separate towels. daily bathing with soap and water. Regular laundering of contaminated bed linens, towels and clothing. Isolate the child from direct contact with other children until 24 hours after tx has started. engage the child in diversional activities to discourage scratching. Keep lesions covered

Scarlet fever

is a disease caused by infection with the group A Streptococcus bacteria (the same bacteria that causes strep throat).

Causes, incidence, and risk factors

Scarlet fever was once a very serious childhood disease, but now is easily treatable. It is caused by the streptococcal bacteria, which produce a toxin that leads to the hallmark red rash of the illness. The main risk factor is infection with the bacteria that causes strep throat. A history of strep throat or scarlet fever in the community, neighborhood, or school may increase the risk of infection.

symptoms include:

Abdominal pain Bright red color in the creases of the underarm and groin (Pastia's lines) Chills Fever General discomfort (malaise) Headache Muscle aches Sore throat Swollen, red tongue (strawberry tongue) Vomiting

Signs and tests Physical examination Throat culture positive for group A strep Rapid antigen detection (throat swab) Treatment Antibiotics are used to kill the bacteria that causes the throat infection. This is crucial to prevent rheumatic fever, a serious complication of strep throat and scarlet fever.

DIPHTHERIA

An acute contagious disease characterized by generalized toxemia coming from a localized inflammation process known as pseudomembrane caused by Corynebacterium diphtheriae or Klebs Loffler bacillus.

Pathophysiology

The bacteria produce a powerful toxin which can spread through the body and cause serious, often life threatening complications. The toxin can damage the heart muscles and cause heart failure or paralyze the breathing muscles. The membrane that forms over the tonsils can also move deeper into the throat and block the airway.

Incubation Period 2-5 days Communicable period Variable; until bacilli are no longer present (3 negative cultures of discharge from the nose and nasopharynx, skin and other lesions); usually 2 weeks but can be as long as 4 weeks Mode of Transmission Direct (droplet) or intimate contact Indirect via contact with articles

Signs and Symptoms

Pseudomembrane grayish white, leathery consistency Serous foul odor secretion; dryness/excoriation on the upper lip/nares Dysphagia bull-neck appearance(cervical lymph nodes), neck edema Barking dry cough; sore throat

Diagnosis
Nose and throat swab Shicks test: for susceptibility to diphtheria Moloneys test: for hypersensitivity to diphtheria

Complications Due to toxemia Toxic myocarditis; neuritis; toxic nephritis Due to intercurrent infection Bronchopneumonia; respiratory failure Treatment Diphtheria antitoxin (IM or IV) + PenG (IV/IM) or Erythromycin (PO/IV)

Nursing Considerations

Ensure strict isolation for the hospitalized child, until 3 (-) cultures CBR x 2weeks Maintain F&E balance Active immunization: as DTP IM for prevention Administer diphtheria antitoxin as prescribed (after a skin test to rule out sensitivity to horse serum) AB as prescribed Provide suction and humidified oxygen as needed Provide tracheostomy care if with

Prognosis Depends on the size and location of the membrane and on early treatment with antitoxin; the longer the delay, the higher the death rate. The death rate is 10%; recovery from the illness is slow.

WHOOPING COUGH/ PERTUSSIS

Characterized by repeated attacks of spasmodic coughing with series of explosive expirations ending in long drawn forceful inspiration. Caused by Bordetella pertussis.

Signs and Symptoms

Catarrhal stage: slight fever in PM; colds; watery nasal discharge; teary eyes; nocturnal coughing(1-2 weeks) Paroxysmal/Spasmodic stage: 5-10 successive forceful coughing ending with inspiratory whoop; involuntary micturation and defecation; choking spells; cyanosis; respiratory distress and tongue protrusion Convalescence stage: 4th-6th week; diminish in frequency and severity

Diagnosis

CBC (leukocytosis & thrombocytosis) CXR Culture (Bordet Gengou agar plate) Complications bronchopneumonia; atelectasis or emphysema (secondary to mucous plugs); hemorrhage; umbilical hernia; encephalopathy; otitis media; brain damageasphyxia Treatment Erythromycin/Penicillin/Chloromycetin

Nursing Interventions

Parenteral fluids Prone position during attack Abdominal binder Isolation especially during the catarrhal stage; if child is hospitalized, institute droplet precaution Administer AB therapy as ordered Gentle aspiration of tenacious secretions Prevent exposure to smoke, dust and sudden changes in temperature which can cause coughing spasms Monitor CP status and pulse oximeter Administer Pertussis immune globulin as prescribed Active immunization: as DTP IM Note: infants do not receive maternal immunity to pertussis

Anthrax
The term anthrax means coal in Greek, and the disease is named after the appearance of its cutaneous form. Anthrax is described in the Old Testament, by the poet Virgil, and by the Egyptians. At the end of the 19th century, Robert Koch's experiments with anthrax led to the original theory of bacteria and disease. Anthrax is caused by inhalation, skin exposure, or gastrointestinal (GI) absorption. Disease caused by inhalation is usually fatal, and symptoms usually begin days after exposure. This delay makes the initial exposure to Bacillus anthracis difficult to track Can be grown in laboratories and is a potential biowarfare agent.

Pathophysiology

Virulence depends on the bacterial capsule and the toxin complex. The capsule is a poly-D-glutamic acid that protects against leukocytic phagocytosis and lysis. Anthrax toxins are composed of 3 entities: a protective antigen, a lethal factor, and an edema factor. The protective antigen is an 83-kd protein that binds to cell receptors within a target tissue. Once bound, a fragment is cleaved free to expose an additional binding site. This site can combine with edema factor to form edema toxin or with lethal factor to form lethal toxin. Edema toxin acts by converting adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP). Cellular cAMP levels are increased, leading to cellular edema within the target tissue. Lethal factor is not well understood, but recent work suggests that it may inhibit neutrophil phagocytosis, lyse macrophages, and cause release of tumor necrosis factor and interleukin 1.

Epidemiology A zoonotic disease; spores can remain viable in soil for years. Livestock can become infected and can transmit infection to humans on contact with infected animals or animal products (hides, hair, wool, meat).

Incubation Period 2-60 days Mode of Transmission Ingestion, inhalation or ingestion

Signs and Symptoms

Cutaneous: pruritic papule or vesicle which enlarges and ulcerates in 12days; a central black aschar forms (malignant pustule); lesion is painless but with surrounding edema Inhalational: fever; chills; nonproductive cough; chest pain; headache; myalgia; malaise; pleural effusion; septic shock GI: N&V; anorexia; abdominal pain; ascites; hematemesis; bloody diarrhea

Diagnosis CXR G/S and culture of blood, pleural fluid, CSF, skin discharges, tissue biopsy specimen

Treatment Penicillin Ciprofloxacin

Nursing Interventions/Considerations
Standard precaution Meds as ordered Post-exposure prophylaxis Anthrax vaccine

TETANUS

An infectious disorder characterized by increased muscle tone and spasms caused by the release of the neurotoxin tetanospasmin by Clostridium tetani following inoculation into a human host.

Pathophysiology
Tetanospasmin, a zinc metalloprotease, is released in the wound and binds to the peripheral motor neuron terminal, enters the axon, and, via retrograde intraneuronal transport, reaches the nerve cell body in the brainstem and spinal cord. The toxin migrates across the synapse to presynaptic terminals where it blocks the release of the inhibitory neurotransmitters glycine and gamma-aminobutyric acid (GABA) by cleaving proteins crucial for the proper functioning of the synaptic vesicle release apparatus. One of these important proteins is synaptobrevin. This diminished inhibition results in an increase in the resting firing rate of the motor neuron, which is responsible for the observed muscle rigidity. The lessened activity of reflexes limits the polysynaptic spread of impulses (a glycinergic activity). Agonists and antagonists may be recruited rather than inhibited, with consequent production of spasms. Loss of inhibition may also affect preganglionic sympathetic neurons in the lateral gray matter of the spinal cord and produce sympathetic hyperactivity and high levels of circulating catecholamines. Finally, tetanospasmin can block neurotransmitter release at the neuromuscular junction, causing weakness and paralysis.

Incubation Period 4-21 days Mode of Transmission Spores of bacteria are usually introduced into an area of injury of wound; disease develops only after spores are converted to vegetative forms which produce tetanospasmin under anoxic condition. In neonate, thru umbilical cord stump when cut with contaminated scissors.

Signs and Symptoms Trismus: lock jaw Risus sardonicus: sardonic grin Opisthotonus: anterior arching of spine

Complication Pneumonia; atelectasis

Treatment Tetanus Immune globulin (TIG) IM: to neutralize toxin Alternative: Tetanus antitoxin (TAT) PenG; Metronidazole; Tetracycline Diazepam(Valium): control seizure Propanolol (Inderal): Beta-adrenergic blocker

Nursing Interventions/Considerations
Dark room Aeg safety Maintain F&E, nutrition (NGT) Minimal handling Seizure precautions Oxygenation Tracheostomy if prolonged spasms of respiratory muscles, unable to cough or swallow, laryngeal obstruction, coma Active immunization: as DTP IM

LYME DISEASE

Is a multi-system infection commonly affecting the skin, CNS, heart and joints caused by the spirochete Borrelia burgdorferi. The bacterium is inoculated into the skin by a tick bite. The tick is almost always of the genus Ixodes. (ticks live in wooded areas and survive by attaching to a host)

Pathophysiology

Once in the skin, the spirochete can (1) be overwhelmed and eliminated by host defense mechanisms; (2) remain viable and localized in the skin where it produces the pathognomonic skin lesion, or erythema migrans (EM); or (3) disseminate through the lymphatics or blood. Hematogenous dissemination can occur within days to weeks of initial infection; the organism can travel to the skin, heart, joints, CNS, and other parts of the body.

Mode of Transmission Vector-borne Signs and Symptoms Bulls eye rash or Erythema Migrans (a small red pimple develops at the site of bite that spreads into a ringshaped rash) usually found in most parts of the body (133 days later; average, 7-10 days). The size varies enormously (as large as 70 cm; average, 16 cm) and depends on disease duration. EM usually is flat, round, or oval and monocyclic but non-pruritic Flu-like symptoms (HA, stiff neck, myalgia, fatigue) Arthralgia Neurological and cardiac complications Progression of arthritis

Diagnosis Aeg history Dermatologic findings: Classic EM is an erythematous papule or macule that occurs at the site of the tick. Elevated IgM

Treatment Amoxicillin Doxycycline Cefuroxime Erythromycin

Nursing Interventions

Ascertain if the aeg was exposed to deer ticks Gently remove the tick with tweezers, wash the skin with antiseptic, and dispose of the tick by flushing it down the toilet; the tick may also be placed in a sealed jar for inspection by the health care provider. Obtain a blood test 4-6 wks after a bite to detect the presence of the disease (testing before this time is not reliable) Instruct the client to avoid wooded, grassy areas, esp in summer months Instruct aeg to wear light colored, long-sleeved tops, long pants. Closed shoes and hats while outside Instruct client to use tick repellent

CHOLERA

The appellation for cholera probably derives from the Greek word for the gutter of a roof, comparing the deluge of water following a rainstorm to that of the anus of an infected person. Cholera is an ancient disease caused by Vibrio cholerae O1 or, more recently, by V cholerae O139. The hallmark for the disease is profuse secretory diarrhea. Cholera can be spread as an endemic, epidemic, or pandemic disease. Despite all the major advances in research, the condition still remains a challenge to the modern medical world.

Pathophysiology

Cholera is a toxin-mediated disease. Cholera toxin (CTX) is a potent protein enterotoxin elaborated by the organism in the small intestine. To reach the small intestine, however, the organism has to negotiate the normal defense mechanisms of the GI tract. Because the organism is not acid-resistant, it depends on its large inoculum size to bypass gastric acidity. Using its own properties, such as motility, chemotaxis, and elaboration of hemagglutinin/ protease, the organism transcends the mucous layer of the small intestine.

Epidemiology Man is the only documented source In nonendemic areas, incidence of infection is similar in all age groups, although adults are less likely to become asymptomatic than children.

Incubation Period few hours to 5 days

Mode of Transmission Fecal-oral Vomitus

Predisposing Factors Low socioeconomic stratum Age (1-4years old)

Signs and Symptoms

Rice watery stool with flecks of mucus, odorless or fishy odor No tenesmus Vomiting Oliguria

Diagnosis S/E (fecal microscopy); IF

Complications Renal failure; arrhythmia due to hypokalemia; coma/death Metabolic acidosis due to loss of large volume of bicarbonate

Treatment Tetracycline or Co-trimoxazole IVF for severe dehydration and acidosis

Nursing Interventions Antibiotics as ordered Oral rehydration salt to correct F&E imbalance Observe enteric precautions Advise careful personal hygiene, purification of water, proper prep of food

SHIGELLOSIS

Shigella organisms cause bacillary dysentery, a disease that has been described since early recorded history.

Etiologic Agents Shigella dysenteriae S. flexneri S. boydie S. sonnei

Pathophysiology Shigella species are aerobic, nonmotile, glucose-fermenting, gram-negative rods that are contagious, causing diarrhea after ingestion of as few as 180 organisms. Shigella species cause damage by 2 mechanisms, invasion of the colonic epithelium, which is dependent on a plasmid-mediated virulence factor, and production of enterotoxin, which is not essential for colitis but enhances virulence.

Epidemiology Most common cause of bloody diarrhea among infants and children 1-4years old Incubation Period 7hours-7days (average 3-4days) Mode of Transmission Fecal-oral Ingestion of contaminated food/water; fomites; mechanical vectors; swimming in polluted water; anal intercourse

Signs and Symptoms Diarrhea with profuse watery stools; fever; tenesmus; vomiting; abdominal cramps; rectal prolapse in malnourished children. Diagnosis S/E; sigmoidoscopy reveals bleeding sites; rectal swab; isolation of EA CBC: moderate to marked leukocytosis Complication Septicemia Pneumonia Colonic perforation

Treatment Co-trimoxazole Ceftriaxone or Fluoroquinolone for resistant strains Nursing Interventions Standard precautions Handwashing Chlorination; proper waste disposal

THE END