Cryptosporidiosis–Impact and Prevention

Cryptosporidium is a unicellular parasite, that infects epithelial cells of the gastroenteric and respiratory tract. In young calves it mainly appears between the first and third week of life. It is a protozoa of the phylum of apicomplexa and the class of sporozoea. Due to its similarity in life cycle, it was formally classified as part of the Coccidea. Currently it has the status of incertae sedis (temporarily taxonomic classification).

 

Worldwide common Cryptosporidium species found in cattle are C. parvum, C. bovis, C. andersoni and C. ryanae. C. parvum is a zoonotic (not host-specific) pathogen, that also infects humans. Santin et al. (2004) report that C. parvum primarily infects pre-weaned calves (between 5 days and 2 months of life) causing diarrhea. In 3 month to 2 year old dairy cattle, C. bovis species and the deer-like genotype are found predominantly (Fayer et al., 2006). Imre et al. (2011) report that C. bovis and C. ryanae are generally found in post-weaned calves and C. andersoni is generally found in yearling heifers and mature cows.

 

The life cycle of the parasite takes place in the host. The infected individual excretes a form of the parasite called oocyst. The parasites are transmitted via ingestion of oocysts from the contaminated environment (mainly water, food and feces). The oocysts have a thick “wall” and can survive for a long period in the environment. They are resistant to a lot of disinfectants. A low number of oocysts are sufficient for an infection. Cryptosporidium hosts beneath the cell membrane of the apical surfaces of gastrointestinal epithelial cells. It hosts separately from the cell cytoplasm (extracytoplamatic/intracellular) (Marcial and Madara, 1986 cited in Mair et al., 2009). Cryptosporidia destroy intestinal epithelial cells, with fusion of the villi and lengthening of the crypts, resulting in malabsorption and diarrhea.

 

In a study conducted by Sadek et al. (2014) a strong correlation between COX-2 (enzyme in the mediation of inflammation) expression and inflammation induced by pathological lesions produced by Cryptosporidium was found. This shows the potential of anti-inflammatory products in the prevention against Cryptosporidium. Specific isoquinoline alkaloids inhibit the NF-kB (transcription factor involved in the inflammation) activation (Chatuverdi et al., 1997). The inhibition of NF-kB may lead to the suppression of the expression of the enzyme COX-2 (Tunstall et al., 2006). Studies with specific isoquinoline alkaloids conducted in newborn calves have shown a reduction of problems due to diarrhea (Saltijeral et al., 2015; Wirth, 2013).

 

Two  groups  with  30  Holstein  calves  in  each  group.  The  trial  group  received  additionally  in  the  milk  5  g Sangrovit®  CS/animal/meal (2 meals/day) from the 3rd  day of live until the 23rd  day of life. Due to strong diarrhea (animal health & welfare) the control group received Halofuginone from the 6th until the 12th day of life.

 

 

Lower number of animals infected with E. coli pathogens and less days with pathogens in the Sangrovit® CS group. Rotavirus infected animals in the Sangrovit® CS group are below the level of infected calves in the positive control. With Sangrovit®  CS a clear reduction of Cryptosporidium shedding from day 19. Cryptosporidium could not be detected at day 21 in the Sangrovit® CS group in contrast to the positive control group.

 

 

Sangrovit® CS had a positive influence on the well-being and weight gain of the calves, alleviated intestinal disorders, and led to a lower persistence of diarrhea. No mortality due to diarrhea was observed in the trial group