Leptospira - Resistance, Antigenic properties, Pathogenesis

Resistance:

Heat labile-killed in 10 minutes at 50°C and in 10 seconds at 60°C.

Sensitive to acid, they are destroyed by gastric juice in 30 mnts- rapid destruction by bile.

Readily destroyed by chlorine and other antiseptics and disinfectants

Survive for days in moist conditions at pH 6.8-8

Survival in water/soil depends on the temperature, acidity, salinity- killed rapidly in acid urine, non-aerated sewage, saltish water.

Antigenic properties

Leptospires show considerable antigenic variability. 

A genus specific somatic antigen is present in all members of the genus.

Classification into serogroups and serotypes is based on surface antigens. Agglutination reactions, with rabbit sera or monoclonal antibodies is used to determine serotypes.

Genetic methods such as restriction endonuclease analysis or DNA pairing can be used for further classification.

Molecular diagnostic methods are increasingly being used for clinical diagnosis in endemic areas because of their sensitivity and specificity. This can be done by hybridization, restriction endonuclease digestion or DNA sequencing. PCR amplification techniques should help to characterize any Leptospira DNA sequences present.

Especially in the early stage of an outbreak, it can be extremely valuable to characterize further any diagnostic DNA sequences that have been amplified in order to confirm Leptospira.

Leptospirosis

Leptospires enter the host via small abrasions, cuts of the skin, conjunctiva, mucous membrane and genital tract. The bacteria enter blood stream or remain in the kidney tubules and be shed in the urine for a period of a few weeks to several months and even longer. 

After the number of Leptospires in the blood and tissues reaches a critical level, lesions and other symptoms appear, due to the action of  leptospiral toxin(s) or toxic cellular components .

Endotoxin activity due to Leptospiral LPS (leptospiral lipopolysaccharide) has been reported as seen in other Gram-negative bacteria. Hemolysins such as phospholipases act on erythrocytes and other cell membranes containing phospholipids, leading to cytolysis.

Pathogenesis

•      In natural reservoir hosts – infection asymptomatic. 

•      If infection is transmitted to other animals, cause clinical disease

•    Human infection- Leptospires enter the body through cuts, abrasions on the skin or through intact mucosa of mouth, nose or conjunctiva, when water is contaminated by urine of carrier animals

•      Incubation period 2-26 days (10 days)

            Symptoms

•  Mild undifferentiated pyrexia (fever) to Severe or fatal illness with hepatorenal damage (Weil’s disease)

•   In severe cases, the onset is acute, with rigor (stiffness), vomiting, headache and irritation of the eyes- retro-orbital pain (around orbit of the eyes), conjunctival redness etc.

•     The fever is irregular and subsides in about 10 days

•      Jaundice by the second or third day in 10-20 percent cases

•      Purpuric hemorrhages (small spots of blood appear on skin) - on the skin and mucosa

•      Albuminuria is common

Leptospirosis is of two clinical types- icteric (with fever) and non-icteric

•     Meningitis is common and in some, abdominal symptoms predominate. Hepatorenal failure, hemorrhage of skin and mucous membrane, jaundice, and myocarditis also seen.

•      Clinical diagnosis is impossible in majority of cases –misdiagnosis common

•      High vigilance and laboratory assistance important not to miss out leptospirosis identification

Serious cases of human leptospirosis caused by the serotype L. icterohemorrhagiae. Aseptic meningitis common in L. canicola infection. Abdominal symptoms in L. grippotyphosa infection.

But, clinical syndromes are not serotype specific- Any type of illness may be produced by any serotype.