Killing of metacestodes by normal or post-infection macrophages and the regulation of this activity by cytokines were studied in vitro. The protoscolecidal activity of normal macrophages against Echinococcus granulosus was inhibited by a product of naive T-enriched lymphocytes co-cultured with protoscoleces (PSC). By contrast, supernates from co-cultures of Mesocestoides corti tetrathyridia (MCT) and T-enriched or B-enriched normal lymphocytes increased killing of MCT by normal macrophages. Larvicidal activity (against both PSC and MCT) was enhanced by high concentrations of macrophage-activating factors produced by Con A-stimulated rat lymphocytes (Con A-LK), but was reduced by low concentrations of these factors. Activation by synergism between Con A-LK and recombinant interferon-gamma(r. IFN-gamma) was demonstrated in macrophage-mediated killing of MCT at high effector to target ratio. Cytokine-activation of normal or post-MCT infection macrophages was compared. Macrophages from both 8 and 20 week post-infection mice were refractory to lymphokines from lymphocyte-MCT cultures and displayed greatly reduced killing of MCT. Macrophage activation by Con A-LK and r.IFN-gamma was also impaired, implying a general defect in the ability of these post-infection macrophages to respond to macrophage activating signals. The data indicate that two different mechanisms may exist by which metacestodes regulate potentially larvicidal effector mechanisms. E. granulosus can elicit the production of lymphokines suppressive for PSC killing, whereas M. corti appears directly to induce a refractory state in effector macrophages.

Summary :Taenia multiceps secretions modify accessory cell activity in macrophages. The present experiments were designed to elucidate the cellular mechanisms involved. W hile normal, murine peritoneal macrophages amplified mitogen-activated T-cell proliferation, macrophages modified by exposure to parasite secretions inhibited this proliferation. The modified behaviour w as shown by glutaraldehyde-fixed as well as living macrophages, and modification w as inducible by FPLC fraction 2 4 of coenurus fluid and w as associated with an expanded population of la -macrophages. Secretory products of parasite-activated macrophages also inhibited T-cell proliferation, and secretion was prevented by indomethacin. The measurement of modified accessory activity w as not influenced by the concentration of tritiated thymidine in lymphocyte proliferation assays. Consequently there is no evidence that the reported events are affected by macrophage-derived, cold thymidine secretion. It is concluded that T. multiceps is able to manipulate macrophage accessory function by mechanisms which involve altered histocompatibility antigen expression and the secretion of prostaglandin. KEY WORDS : IN TR O D U C TIO N E x p o s u r e t o s o l u b l e f a c t o r s f r o m T aen ia m ulti ceps im p a ir s t h e a c c e s s o r y f u n c t i o n o f m a c r o p h a g e s in p r e s e n t i n g m i t o g e n i c s ig n a ls t o ly m p h o c y t e s ( R a k h a e t a l ., 1 9 9 1 a ). T h e p a r a s i t e c o m p o n e n t s w h i c h m e d i a t e t h is m o d i f i c a t i o n c a n b e s e p a r a t e d c h r o m a t o g r a p h i c a l l y f r o m o t h e r im m u n o log ic a ll y a c t i v e c o m p o n e n t s o f T. multiceps, s u c h a s t h e T -c e l l m i t o g e n i c f a c t o r . T h e m a c r o p h a g e m o d if y in g f r a c t i o n o f T. m ulticeps h a s b e e n s h o w n t o im p a ir t h er o s e t t e f o r m in g r e s p o n s e o f m u r in e ly m p h -n o d e c e lls t o s h e e p e r y t h r o c y t e s ( R a k h a et al., 1 9 9 1 b), b u t t h e s a m e f r a c t i o n is a l s o a n a n t ig e n w h i c h i n d u c e s a n t i b o d y r e s p o n s e in t h e n a t u r a l o v i n e i n f e c t i o n ( R a k h a is a p o t e n t ia l m e a n s f o r t h e p a r a s it e t o r e g u la t e t h e h o s t 's p r im a r y a n d s e c o n d a r y r e s p o n s e t o a n t ig e n , it a p p e a r s im p o r t a n t t o id e n t if y c h a n g e s in m a c r o p h a g e m e m b r a n e s t r u c t u r e o r s e c r e t o r y b e h a v i o u r w h i c h a r e c h a r a c t e r i s t i c o f t h e m o d if ie d s t a t e . T h e p r e s e n t r e p o r t d e s c r i b e s i n c r e a s e d f r e q u e n c y o f l a -c e l l s in m o d if ie d m u r in e m a c r o p h a g e p o p u la t io n s , a n d t h e s e c r e t i o n , b y a n i n d o m e t h a c i n -s e n s i t i v e m e c h a n i s m , o f a s o l u b l e s u p p r e s s o r o f l y m p h o p r o lif e r a t iv e r e s p o n s e t o T -c e l l m it o g e n s . ...

Fowl typhoid caused by Salmonella enterica serovar Gallinarum is one of the most important bacterial diseases of poultry. The present study was undertaken to ascertain the epidemiological status of fowl typhoid in broilers in Haryana for the past four years (2005)(2006)(2007)(2008) and to establish the role of hatcheries in spreading the Salmonella infection. A total of 227 outbreaks of fowl typhoid were recorded in chickens during the period from January 2005 to December 2008. The maximum number of outbreaks (96) was recorded in the age group of 7-9 days during the past four years. Maximum mortality and case fatality rate were found in chickens of 1-2 weeks of age. Temporal distribution of the disease indicates more outbreaks in extreme weather conditions. From spatial distribution of the disease, it was evident that the disease was prevalent in nine districts of Haryana out of 20. By analysing the data regarding the prevalence of Salmonella infection in hatcheries, more than one third (37.8%) of hatcheries were found to be infected with Salmonella, which is an alarming situation for the region.

Many liver-invasive parasites cause extensive liver damage which may result in an impaired ability to catabolize endotoxin. The influence of endogenous endotoxin on the progress of liver-invasive parasitic diseases has been investigated in murine Mesocestoides corti infection. Invasion of liver tissue by tetrathyridia resulted in extensive parenchymal destruction with fibrosis. In association with this, undetoxified endotoxin, in potentially biologically active concentration, was found on peritoneal macrophages, 5 months post-M, corti infection. Host susceptibility was influenced by the Lps gene for responsiveness to lipopolysaccharide (LPS). The parasite burden of LPS-responsive (C3H/HeN) mice was significantly increased in the livers of these mice when compared to LPS-resistant (C3H/HeJ) mice. LPS reduced the ability of normal peritoneal macrophages to kill tetrathyridia, when co-cultured in vitro. LPS also abrogated the ability of recombinant interferon-gamma (r.IFN-gamma) to enhance macrophage larvicidal activity. These in vitro findings were confirmed in vivo. Daily intraperitoneal administration of LPS, at low concentration, caused a 4-fold increase in parasite burden in the liver, while r.IFN-gamma at optimal concentration reduced parasite burden by 57%. Post-infection macrophages have previously been shown to be refractory to cytokine-activation for larval killing. In this report, we conclude that (1) this refractoriness may be due to the presence of undetoxified endotoxin on post-infection macrophages and (2) endotoxin may reduce host resistance by abrogating effector macrophage response to IFN-gamma.

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