medical surgical nursing

1. PLAGUE
PRESENTED BY;
MRS,M.JOSEPHIN,
TUTOR

2. DEFINITION
Plague is a bacterial disease, caused by Yersinia pestis, which primarily
affects wild rodents. Also known as bubonic plague, black plague, and the
Black Death.

3.  Humans bitten by an infected flea usually develop a bubonic form of
plague, which is characterized by a bubo, i.e. a swelling of the lymph
node draining the flea bite site.
 If the bacteria reach the lungs, the patient develops pneumonia
(pneumonic plague), which is then transmissible from person to person
through infected droplets spread by coughing.
 Pneumonic plague, on the other hand, is one of the most deadly
infectious diseases; patients can die 24 hours after infection

4. ETIOLOGY
 Y. pestisis a pleomorphic, non–spore-forming, gram-negative, bipolar-staining
coccobacillary member of the family Enterobacteriaceae.
 It is a nonmotile, facultative anaerobe that is able to grow aerobically on routine
microbiologic media.
 The organism can survive at room temperature in dried blood or the environment for
weeks to months.
 Y. pestisis one of the most virulent bacteria known

5. MODE OF TRANSMISSION
 Yersinia infections primarily affect rodents, pigs, and birds.
 It is spread from one rodent to another by fleas.
 Humans are accidental hosts.
 It is transmitted between animals and humans by:
 Bite of infected fleas.
 Bites or scratches from an infected animal.
 Direct contact with infected tissues or body fluids.
 Inhalation of aerosolized bacilli. • Rarely, ingestion of infective materials

6.  Male Xenopsyllacheopis (oriental rat flea) engorged with blood.
Primary vector of plague in most large plague epidemics in Asia, Africa,
and South America. Both male and female fleas can transmit the infection

7. PATHOGENESIS
 Pathogenesis Organism inoculated through the skin or mucous
membranes Invades cutaneous lymphatics Monocytes and macrophages
phagocytizeY. pestiswithout killing it, spreads infection from the
inoculation sit

8. CLINICAL MANIFESTATION
Clinical Manifestations
 Clinical plague infection manifests itself in three forms depending
on the route of infection:
• Bubonic.
• Septicaemic.
• Pneumonic

9. BUBONIC PLAGUE
Bubonic plague
 Bubonic form is the most common form of plague resulting from the bite
of an infective flea

10. CONTD..,
 The usual incubation period for bubonic plague is 2 to 3 days.
 Acute illness characterized by
 Abrupt onset of fever, chills, headache.
 Gastrointestinal symptoms.
 Local pain, followed within hours by the development of a painful, swollen mass of
lymph nodes (buboes) in the groin or axilla

11. CONTD..,

12. CONTD..,

13. SEPTICAEMIC PLAGUE
Septicaemic plague
Occurs when infection:
 Spreads directly through the bloodstream without evidence of a "bubo".
 More commonly advanced stages of bubonic plague.
 Flea bites.
 Direct contact with infective materials through cracks in the skin.

14. CONTD..,
 Buboes do not develop in patients with septicemicplague
 Patients have gastrointestinal signs and symptoms:
 Nausea & vomiting.
 Diarrhoea.
 Abdominal pain.
 There may be signs of meningitis

15. PNEUMONICPLAGUE
Pneumonic plague
 The most virulent and least common form of plague.
 Pneumonic form is due to:
 Secondary spread from advanced infection of an initial bubonic form.
 Primary pneumonic plague results from inhalation of aerosolized infective droplets
and can be transmitted from human to human without involvement of fleas or animals

16.  The usual incubation period for pneumonic plague is 2 to 3 days.
Patients usually present with:
• Tachypnea .
• Productive cough.
• Blood-tinged sputum.
• Cyanosis.
• Primary plague pneumonia is usually fatal and present as fulminant pneumonitis with
bloody, frothy sputum and sepsis

17. LABORATORY DIAGNOSIS
 TLC --»elevated 15,000 - 25,000 cells/μl, with a shift to the left
 Leukemoid reactions (> 50,000 cells/μl) can occur.
 Platelet count may be normal or mildly depressed or may be very low if DIC is
present.
 Fibrin split products is frequently elevated.
 Hepatic aminotransferases and bilirubin are often increased

18. CONFIRMATIONTEST
 Recovery and identification of Y. pestis culture from:
 Bubo aspirates.
 Blood.
 Sputum.
 The organism can be easily grown on:
 Blood agar.
 MacConkey agar.
 infusion broth

19. TREATMENT
 Plague can be a very severe disease in people, with a case-fatality ratio of 30%-60% if left untreated.
 Drug of choice:
 Streptomycin(30 mg/kg I.M. in divided doses every 12 hours) reduces mortality to approximately 5%.
 Gentamicin (more widely available than streptomycin) also appears to be effective.
 To prevent relapses, antibiotic treatment should be continued for 10 days or for at least 3 days after
deserved scence and clinical recovery.
 Most patients improve rapidly and defervesce within 72 hours of initiation of antimicrobial therapy,
although buboes can persist for weeks

20. PREVENTION ANDCONTROL
 Isolate infected animals – Limit number of people in contact
 Personal protection • Surgical mask, gloves, eye protection
 Flea control – Dogs and cats
 Spring to fall – Environment Centre for Food Security and Public Health
 Prevent roaming or hunting of pets
 Rodent control – Eliminate rodent habitat around home
 Brush, food sources, firewood, junk – Undertaken only after insecticide use
 Insect repellents for skin & clothes
 Insecticide use in epizootic areas Centre for Food Security and Public Health,

21. MALARIA
PRESENTED BY:
MRS,M.JOSEPHIN,
TUTOR,

22. INTRODUCTION
 Malaria is a life- threatening disease.
 Transmitted through the bite of infected anopheles mosquito.
 Infected mosquitoes carry the plasmodium parasite
 When this mosquitoes bite human, the parasite is released into the blood
stream

23.  Once this parasites are inside the human body, they travel to the liver,
where they mature. After several days, the mature parasites enters the
blood stream and begin to infect RBCs.
 Within 42 to 78 hours, the parasites inside the RBCs multiply, causing the
infected cells to burst open

24. DEFINITION
DEFINITION
 Malaria is a mosquito-borne disease that affects human, or Malaria is an
infection of liver and RBCs caused by parasites( that are transmitted to
people through the bite of infected female anopheles mosquitoes

25. CLINICAL MANIFESTATION
 High fever& Sweating
 Headache
 Nausea & Vomiting
 Abdominal pain
 Diarrhea
 Anemia
 Muscle pain
 Convulsions
 Coma
 Bloody stools & Weight loss

26. TYPES OF MALARIA
 PARASITE
 P. falciparum
 P. vivax
 P. malariae
 P. ovale

27. INCUBATION PERIOD
 THE PARASITE Species Incubation period
 P. Falciparum 7-14 days
 P. Vivax 12-17 days
 P. Ovale 9-18 days
 P. Malaria 13-14 days

28. RISKFACTORS

29. RISK FACTORS
 Living or traveling in a region where malaria is present
 Being outdoors, especially in rural areas
 Not taking steps to protect self from mosquitoes bites
 An infected mother can also pass the disease to her baby at birth, this is also known as
congenital malaria.
 Contaminated water storage in the environment
 Poor electricity
 Populated area

30. MALARIATRANSMISSION CYCLE
1.Mosquito
infected parasites
bite
2. Non infected
human
3.Parasite enter the
human’s
bloodstream and
migrate to liver
4. When the
parasite mature
they leave the liver
and infect RBCs
5.Mosquitoes
become infected
when they feed on
infected people

31. MALARIA TRANSMISSIONCYCLE

32. DIAGNOSISOF MALARIA
 DIAGNOSIS OF MALARIA
 Medical History
 Physical Examination
 Laboratory Diagnosis
 Blood Smear
• Thin Smear- For Species Identification,
• Thick Smear- For Quantification.
 Antigen Detection Tests
• P LDH And Aldolase- Common To All Plasmodium
• HRP2 Ag Detection- Specific For P. Falciparum

33. MALARIA

34. TREATMENT
 To treat malaria, a one must understand 2 concept
 1. the geographic pattern of susceptibility of P. falciparum to anti-
malarial drugs.
 2. the type of plasmodium species causing the infection.

35. TREATMENT
P. Falciparum
Chloroquine
resistant area
Quinine,
mefloquin
Sulfadoxine,p
yrimethamine
Chloroquine
sensitive area
chloroquine

36. TREATMENT
Chloroquine
with
primaquine
P.Malaria
P.Vivax
P.Ovale

37. PREVENTION OF MALARIA
AWARNESS
BITE PREVENTION
CHEMOPROPHYLAXIS
DIAGNOSIS
EMERGENCY

38. COMPLICATIONS
 Cerebral malaria malaria can cause a swelling of blood vessels of the brain
 Pulmonary edema- an accumulation of fluid in the lungs that causes breathing
problems.
 Organ failure of kidney, liver or spleen
 Anaemia due to the destruction of RBCs
 Low blood sugar- hypoglycaemia

39. NURSING MANAGEMENT
 Observe consciousness level
 Safety measures- bed nets, insecticides, cleaning or covering contaminated surrounding or
drainage/ pond.
 Vital signs monitor
 Hb monitoring (anaemia)
 Iron preparates (anaemia) – iron dextran, iron sorbitol citric acid complex
 Adjust fluid intake to output ( dehydration)
 Antiemetic
 Urine output to watch oliguria ( dehydration)
 Administration of anti- malarial drug, anti- pyretic drug, as prescribed by doctor at
right time, of right dose

40. HEALTHEDUCATION
 Make use of window screens,
 Wear long trousers and long sleeves shirts
 House should be sprayed with insecticides
 Indoors residual spraying is long acting (6-12 months) insecticides to the wall of the house, in order to
kill adult mosquitoes.
 Long-casting insecticidal net or bed net, can be hang over a bed to protect sleepers from insect bites.
 Recognize the sign and symptoms and when to seek appropriate treatment.
 Stay inside when it is dark.
 Keep water container covered & Filling up the pits

41. DIPHTHERIA
PRESENTED BY,
MRS,M.JOSEPHIN,
TUTOR

42. INTRODUCTION
 Diphtheria takes its name from the Greek word diphtheria meaning leather and was
named in 1826 by French physician Pierre Bretonneau.
 • This is because it refers to the leathery, sheath- like membrane that grows on the
tonsils, throat and in the nose.
 •In the past its name(general disease, killer disease )because no treatment in the past
and it was lead high mortality between children
 • It was said that the disease killed as many as 80% of the children below 10 years

43. HISTORY

History • Joseph O'Dwyer 1880 developed tubes that were inserted into the throat,
to prevented suffocating and obstructs airways.
 In 1884, Friedrich Loeffler discovered the causative organism .
 1890s, the physician Emil von Behring developed an antitoxin that did not kill the
bacterium, but neutralized the toxic poisons the bacterium releases into the body
 The first successful vaccine for diphtheria was developed in 1913 by Behring

44. DEFINITION
 Diphtheria is an acute infectious disease that typically strikes the upper respiratory
tract including the throat.
 It is caused by infection with the bacteria Corynebacterium diphtheria.
 It’s characterized by sore throat and mild fever at first. As the disease progresses, a
membranous substance forms in the throat that makes it difficult to breathe and
swallow

45. CAUSES
 Corynebacterium diphtheria causes diphtheria. Usually the bacteria multiply on or
near the surface of the mucous membranes of the throat, where they cause
inflammation.
 • The inflammation may spread to the voice box (larynx) and may make your throat
swell, narrowing your airway. Disease-causing strains of C. diphtheria release a
damaging substance (toxin), which can also involve the heart, brain and nerves

46. SIGNS ANDSYMPTOMS
 Signs and symptoms usually begin two to five days after a person becomes infected.
 A sore throat and hoarseness
 Painful swallowing
 Swollen glands (enlarged lymph nodes) in your neck

47. CONTD.,,
 A thick, gray membrane covering your throat and tonsils
 •Difficulty breathing or rapid breathing
 •Nasal discharge
 •Fever and chills

48. CONTD ..,
 Skin (cutaneous diphtheria)
 It is found in people with poor hygiene. Any break in the skin can become infected
with diphtheria.
 The infected tissue develops an ulcerated area and a diphtheria membrane may form
over the wound but is not always present. It is slow to heal and may be insensitive
when touched.

49. MODE OF TRANSMISSION
 Person-to-person transmission occurs through oral or respiratory droplets, close
physical contact

50. DIAGNOSIS
 Diphtheria can be diagnosed usually by proper clinical examination, throat culture
from the infected area and blood tests - Tests used may include:
• Gram stain or throat culture to identify Corynebacterium diphtheria .
• ECG

51. TREATMENT
 Treatment An antitoxin. After doctors confirm diphtheria, the infected child receives
an antitoxin. The antitoxin, injected into a vein or muscle, neutralizes the diphtheria
toxin already circulating in the body.
 Antibiotics. Diphtheria is also treated with antibiotics, such as penicillin or
erythromycin. Antibiotics help kill bacteria in the body, clearing up infections.

52. PREVENTION
 Prevention
• Diphtheria is easily prevented with the use of a safe and effective vaccine.
• Most people receive their first vaccination for the disease as children. This is
know as the DTP vaccine (diphtheria-tetanus- pertussis)

53. COMPLICATION
 Heart damage: The diphtheria toxin may spread through bloodstream and damage
other tissues in your body, such as heart muscle, causing inflammation of
(myocarditis). • It may be slight, showing up as minor abnormalities on an ECG, or
severe, leading sudden death.
 Nerve damage The toxin can also cause nerve damage. Typical targets are nerves to
the throat, where poor nerve conduction may cause difficulty swallowing. Nerves to
the arms and legs also may become inflamed, causing muscle weakness. Toxin may
damages the nerves that used in breathing muscles and become paralyzed. Respiration
become impossible without device