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Cholera
Cholera is an acute infection involving the small bowel characterized by profuse watery diarrhea, vomiting, muscular cramps, dehydration, oligourea and collapse.
Etiology:
Causative organism: Vibrio Cholera sero group O1 and O139
Short curved motile aerobic rod.
Eltobir and Classic types of vibrio cholera can cause severe disease however mild or symptomatic infection is much more common with Elto bir type.
Eltobir type is subdivided into 3 serotypes
a- Inaba
b- Ogawa
c- Hikoshima
d- Bengal
Non aggulinating (NAG) Vibrio that can cause cholera-like diseases has been insolated from water and humans.
Epidemiology:
Cholera is spread by ingesting of water, sea food and other foods contaminated by excrements of person with asymptomatic or symptomatic infections.
Cholera is epidemic in portions of Asia, middle East, Africa and South and North America.
Cases transported into Europe, Australia have caused localized outbreaks.
In endemic areas outbreaks usually occur in warm months and the incidence is highest in children.
Epidemics due to direct contamination spread with soiled hands, domestic objects, because of late diagnosis.
The cause of epidemic depends on the social factor.
Elto cholera is characterized with revival of epidemic from season to season due to prolonged carrier state and unrevealed atypical cases 7 pantamines (outbreaks world wide) have occurred (due to Eltor) – most in India.
Pathogenesis:
The microbes are ingested.
Cholera Vibrio is highly sensitive to dilute HCL acid, it can survive only:
1- in an empty stomach
2- in the absence of gastric secretion
3- inside a food lump ingested with ample water
4- gastric secretion when inhibited
The vibrio multiplies in an alkaline medium intensively, mainly on the surface of intestinal mucosa and in the intestinal lumen.
As the vibrio multiplies its great qualities are accumulated together with a great amount of cholera toxins (endo and exotoxins).
The clinical symptoms of cholera develop due to general effects of cholera develop due to general effects of cholera toxins. The symptoms depend on the lesion of the central and vegetative nervous system, GIT and parenchymal organs (kidneys, adrenals, liver).
Due to effect of exotoxins or choleragens large amount of water and electrolytes especially of Na+ and K+ Chlorides are released through the membranes of epithelial cells of the small intestine.
Water is not absorbed in the large intestine and excess liquid in the intestine stimulates peristalsis to cause profuse diarrhea that is attended by vomiting (i.e. enteritis then gastroenteritis).
In severe cases (dehydration of 3th – 4th degree) a considerable amount of liquid and salts is lost. As a result exicosis (removing of water) develops along this salt depletion.
Activity of CVS become drained.
Hypothermia develops, temperature of body drops below 36°C, condition is also attended by acidosis, hyperemia, deranged gas metabolism to asphyxia.
The liver function is also upset, the mucosa and skin become icteria.
Renal function is deranged; this subsequently develops oligouria and possible anuria.
Acidosis and saline depletion cause muscular cramps.
Clinical picture:
The incubation period lasts from several hours to 5 days, more frequently 2 – 3 days.
Cholera can be mild, moderate or severe.
The onset of the disease is acute and fulminant without prodromal symptoms. The disease beginning with diarrhea-watery without pus + blood (enteritis) that develops suddenly.
Stools are watery from the very beginning of the disease.
Less frequently stools are first fecal but very soon they became waterly + profuse.
During the 1st day of the disease the stool frequently is 3 – 10 times/ day and more.
Patient is thirsty, impaired appetite and develops weakness.
Mild cholera runs its course in 2 – 3 days and the patient can completely recover. The liquid loss doesn’t exist 2 – 3% of body weight i.e. 1st degree dehydration
If the disease progresses stool frequently increases to 15 – 20 x/day.
Stools resemble rice water.
The moderate cases profuse vomiting can develop in few hours following the onset of diarrhea.
The moderate cases profuse vomiting can develop in few hours following the onset of diarrhea.
The vomitus first contains food remnants and bile but soon becomes watery.
The patient complains of vertigo, weakness, thirst and dry mouth. The skin in paled and dry, the turgor is low, lips and fingers become cyanotic, the voice is hoarse, limb muscles are attacked with short lasting cramps, twitching of masticatory muscles occurs, tachycardia, moderate HT and oligourea.
Liquid loss is 4- 6% of body weight (2nd degree dehydration).
Severe form of cholera is characterized by 3rd degree dehydration. Liquid loss 7 – 9% body weight.
The onset is acute with frequent and profuse watery stools and early repeated vomiting.
Fast and painful cramps of abdominal muscles and limb muscles.
Skin is cyanotic, its elasticity is lost, skin of hands and feet is wrinkled (washer woman hands).
The voice becomes hoarse and then in audible.
The face becomes pinched.
The lips, nose becomes cyanotic.
Heart sounds are dull, tachycardia develops, AP↓.
Body temperature can be below normal.
Active therapy can rapidly restore the metabolic equilibrium in the patient.
In adequate treat or absence of it can cause the transformation of disease to its most severe form.
For dehydration occurs.
- Liquid loss > 90% of body weight.
- Vomiting and diarrhea discontinue.
- Body temperature is low.
Further progress of disease results in hypovolumic shock.
The algid state can develop in 3 – 12 hours after disease in connection with thinking of blood the leukocyte count ↑ to 20 – 60 x 109/L.
Number of juvenile and stabs neutrophils increase to erythrocyte count ↑ to 6 – 8 x1012/L.
Asothermia ↑ with K+ and Cl- and carbonates depletions.
The decompensated acidosis develops, in the absence of active treatment the patient loses consciousness and asphyxia develops and coma.
Severe forms of cholera develop in person with achloridria, chloric enterocolitis and TB.
Ratio is: 1: 5 à 1: 10 (classic cholera)
1:25 à 1:100 (Elto cholera)
Complications:
Usually occur in hypovolemic shock due to secondary infections (pneumonia, thrombophlebitis, sepsis, etc).
Diagnosis:
Confirmed by isolation of vibrio cholera in cultures from direct recto swabs or fresh stools and its subsequent identification of serotype 01 through agglutination by specific antiserum.
Cholera must be distinguished from clinically similar disease caused by enterotoxin producing strains of escheric coli and occasionally by Salmonella or Shigella organisms.
Treatment:
Rapid correction of hypovolumic and metabolic acidosis and prevention of hypocholinemic are the main objectives.
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