Table-1.

Brief summary of published papers on the effects of parasites coinfection with other pathogens on host immunity in different animal species.

Title	Type of study and animal species	Brief summary	Reference
Effect of preexisting FeLV infection or FeLV and feline immunodeficiency virus coinfection on pathogenicity of the small variant of H. felis in cats	- Experimental - Cats	- Cats coinfected with FeLV and H. felis develop more critical anemia than cats infected with H. felis alone - Conclusion: H. felis induce myeloproliferative disease in cats infected with FeLV	[11]
Association of F. gigantica coinfection with bovine tuberculosis infection and diagnosis in a naturally infected cattle population in Africa	- Natural outbreak investigation - Cattle	- Coinfected cattle with F. gigantic and TB had a higher risk of developing TB lesions - Fasciola gigantica infection with bovine tuberculosis had lower IFN-γ levels - Conclusion: Breed-dependent differences in responses to coinfections with F. gigantic and TB were observed	[12]
Severity of bovine tuberculosis is associated with coinfection with common pathogens in wild boar	- Natural outbreak investigation - Wild boars	- Infection with PCV2, ADV, and Metastrongylus spp. positively correlated to tuberculosis severity in wild boars - Conclusion: Control measures such as vaccination against PCV2 and ADV and deworming of wild boars is recommended as part of tuberculosis control program in the wild boar	[13]
Trematode infections in pregnant ewes can predispose to mastitis during the subsequent lactation period	- Experimental - Sheep	- Sheep that have infection of liver flukes (Dicrocoelium dendriticum or F. hepatica) are more susceptible to mastitis in the immediate postpartum period - Conclusion: Trematode infection predisposes ewes to mastitis through increased blood concentrations of β-hydroxybutyrate which may adversely affect mammary cellular defenses	[14]
Chronic intestinal nematode infection exacerbates experimental S. mansoni infection	- Experimental - Mice	- Mice coinfected with Trichuris muris and S. mansoni showed significantly higher S. mansoni worm burdens and higher egg burden in the liver - Conclusion: T. muris induced alterations in lung cytokine expression and inflammatory foci surrounding lung stage schistosomula	[15]
Coinfection with the intestinal nematode H. polygyrus markedly reduces hepatic egg-induced immunopathology and pro-inflammatory cytokines in mouse models of severe schistosomiasis	- Experimental - Mice	- Mice infected with H. polygyrus have a marked reduction in schistosome egg-induced hepatic pathology - Conclusion: Intestinal nematodes prevent Th1- and Th17cell-mediated inflammation by promoting a strong Th2-polarized environment associated with increases in the levels of alternatively activated macrophages and T regulatory cells, which result in significant amelioration of schistosome-induced immunopathology	[16]
Coinfection with S. mansoni reactivates viremia in rhesus macaques with chronic simian-human immunodeficiency virus clade C infection	- Experimental - Rhesus macaques	- Coinfected monkeys with S. mansoni and chronic simian-human immunodeficiency virus clade C had significantly more fecal shedding of parasite eggs, eosinophilia, and increased viral replication - Conclusion: S. mansoni coinfection resulted in elevated mRNA expression of T-helper type 2 cytokine (Il-4) and induced T-cell subset alterations	[17]
Coinfection with P. berghei and T. brucei increases severity of malaria and trypanosomiasis in mice	- Experimental - Mice	- The severity of malaria increased when mice were coinfected with P. berghei and T. brucei. Mice with coinfection had lower survival rates, greater parasitemia loads, and more severe anemia	[18]
Trypanosoma infection favors Brucella elimination through IL-12/IFN-γ-dependent pathways	- Experimental - Mice	- Mice chronically infected with B. melitensis, B. abortus, or B. suis had lower bacterial loads in their spleen if they were coinfected with T. brucei - Conclusion: Strong pro-inflammatory IFN-γ-mediated response induced by T. brucei protects coinfected animals against Brucella	[19]
Schistosoma mansoni-T. cruzi coinfection modulates arginase-1/iNOS expression, liver and heart disease in mice	- Experimental - Mice	- Mice coinfected with S. mansoni and T. cruzi were unable to control T. cruzi infection with tremendous inflammation in their livers due to increased parasitemia. - Conclusion: S. mansoni reduced protection against T. cruzi due to reduced production of IFN-γ and NO	[20]
Experimental T. gondii and E. tenella coinfection in chickens	- Experimental - Chicken	- Coinfection of chickens with T. gondii and E. tenella did not show any detrimental effects on disease development or pathology	[21]
Toxoplasma gondii coinfection with diseases and parasites in wild rabbits in Scotland	- Natural outbreak investigation - Wild rabbits	- Wild rabbits coinfected with T. gondii and E. stiedae had higher burdens of E. stiedae	[22]
Toxoplasma coinfection prevents Th2 differentiation and leads to a helminth-specific Th1 response	- Experimental - Mice	- Coinfected mice with H. polygyrus and T. gondii displayed significantly higher worm fecundity - Conclusion: T. gondii infection limits a helminth-specific Th2 immune response while promoting a shift toward a Th1-type immune response	[23]
Enteric helminths promote Salmonella coinfection by altering the intestinal metabolome	- Experimental - Mice	- Mice coinfected with H. polygyrus and Salmonella showed enhanced pathogenesis of S. enterica serovar Typhimurium independently of actions of Th2 cells or regulatory T-cells - Conclusion: Infection with H. polygyrus disrupted the metabolic profile in the small intestine, thereby affecting the invasive capacity of S. Typhimurium	[24]
Generating super-shedders: Coinfection increases bacterial load and egg production of a gastrointestinal helminth	- Experimental - Mice	- Co-infected mice with H. polygyrus and B. bronchiseptica shed significantly more parasite eggs in their feces and had higher bacterial loads - Conclusion: Coinfection can be regarded as a mechanism that explains the often observed high variance in parasite load and shedding rates	[25]
Interactions between gastrointestinal parasitism and pneumonia in Nigerian goats	- Natural outbreak investigation - Goats	- Coinfected goats had pulmonary edema - Conclusion: Coinfection reduced the immunity in the lung, thereby allowing other pathogens (viruses and or bacteria) to create infection and facilitate the later development of pneumonia	[26]
Virus helminth coinfection reveals a microbiota-independent mechanism of immunomodulation	- Experimental - Mice	- Mice coinfected with T. spiralis or H. polygyrus and with mouse Norovirus (MNV) had increased viral loads and reduced amounts of specific CD4+ T cells expressing IFN-γ and TNF-alpha when compared to the mice infected with Norovirus alone - Conclusion: Parasite infection alters the immune response creating favorable environment for the parasite at the expense of antiviral immunity	[27]
Amelioration of influenza-induced pathology in mice by coinfection with T. spiralis	- Experimental - Mice	- Coinfection of mice during the enteric phase of trichinosis results in reduced lung pathology and accelerated recovery of weight - Conclusion: Infection with T. spiralis resulted in lower levels of tumor necrosis factor in bronchoalveolar lavage fluid and inhibited cellular recruitment into the airways of mice coinfected with influenza A virus	[28]
Nematode parasites and scrapie: Experiments in sheep and mice	- Experimental - Lambs, mice	- Lambs: Nematode infection shortened the development of scrapie with a significantly younger age at which first symptoms appeared - Mice: Parasitized mice demonstrated significant longer survival period - Conclusion: Nematodes modified the host susceptibility to scrapie	[29]
Coinfection with F. hepatica may increase the risk of E. coli O157 shedding in British cattle destined for the food chain	- Natural outbreak investigation - Cattle	- Coinfection with F. hepatica increases the risk of E. coli O157 fecal shedding. - Conclusion: Control of F. hepatica infection may have an impact on the shedding of E. coli O157 in cattle destined for the human food chain	[30]
Evaluation of the link between gyrodactylosis and streptococcosis of Nile tilapia, O. niloticus (L.)	- Experimental - Tilapia fish	- Co-infected fish with S. iniae and G. niloticus had increased mortality rates (42.2%) when compared to fish only infected with S. iniae (6.7%) - Conclusion: Gyrodactylus parasites carried viable bacterial cells, damaged fish epithelium, and allowed entry of the bacteria into the tissues	[31]
Enhanced mortality in Nile tilapia O. niloticus following coinfections with ichthyophthiriasis and streptococcosis	- Experimental - Tilapia fish	- Coinfected fish with I. multifiliis and S. iniae resulted in a negative impact on developmental size and an increase in mortality and parasite loads - Parasite load and trophont size increased susceptibility and mortality of tilapia to S. iniae infection - Conclusion: Coinfection permitted extra time for I. multifiliis to produce large, well-developed trophonts that allowed for more damage to epithelium of fish and thus more facilitated bacterial invasion, leading to higher mortality rates	[32]
Dactylogyrus intermedius parasitism enhances F. columnare invasion and alters immune-related gene expression in C. auratus	- Experimental - Goldfish	- Goldfish (C. auratus) infected with D. intermedius demonstrated increased susceptibility to F. columnare. - Confection resulted in higher mortality rates, and higher bacterial loads. - Conclusion: D. intermedius resulted in immunosuppression which enhanced bacterial invasion	[33]
Effect of I. multifiliis parasitism on the survival, hematology, and bacterial load in channel catfish previously exposed to E. ictaluri	- Experimental - Catfish	- Coinfection of catfish with I. multifiliis and E. ictaluri resulted in increased mortality rates and increased bacterial loads in different organs (71.1%) when compared to single infection groups - Conclusion: Coinfected catfish exhibited significant lymphopenia, suggesting that lymphocytes were actively involved in the immune response	[34]
Ichthyophthirius multifiliis as a potential vector of E. ictaluri in channel catfish	- Experimental - Catfish	- The study concluded that I. multifiliis could be a vector to E. ictaluri	[35]
Parasitism by protozoan I. multifiliis enhanced invasion of Aeromonas hydrophila in tissues of channel catfish	- Experimental - Catfish	- Coinfected catfish with I. multifiliis and A. hydrophila had increased mortality rate (80%), and higher amounts of A. hydrophila in their internal organs Conclusion: I. multifiliis infection leads to higher levels of cortisol in the channel catfish, leading to immune suppression	[36]
Flavobacterium columnare/M. tilapiae concurrent infection in the Earthen Pond Reared Nile Tilapia (O. niloticus) during the early summer	- Natural outbreak investigation - Nile tilapia	- Coinfection of tilapia fish with F. columnare and M. tilapiae resulted in high mortality rate - F. columnare and M. tilapiae exhibited a synergistic effect to induce severe pathology resulting in fish mass mortalities - Conclusion: Damage to the fish skin by M. tilapiae may have allowed for more F. columnare invasion in tissues	[37]
Immunomodulation and disease resistance in post-yearling rainbow trout infected with M. cerebralis, the causative agent of whirling disease	- Experimental - Rainbow trouts	- Rainbow trouts were chronically infected with M. cerebralis and challenged with Y. ruckeri - Coinfected rainbow trouts had higher mortality rates and faster onset of death than in rainbow trout without M. cerebralis infection - Conclusion: M. cerebralis modulate the immune response by inducing leukocyte suppression	[38]

H. felis=Haemobartonella felis, F. gigantica=Fasciola gigantica, S. mansoni=Schistosoma mansoni, H. polygyrus= Heligmosomoides polygyrus, S. Typhimurium=Salmonella Typhimurium, S. enterica=Salmonella enterica, P. berghei=Plasmodium berghei, T. brucei=Trypanosoma brucei, M. cerebralis=Myxobolus cerebralis, B. melitensis=Brucella melitensis, B. abortus=Brucella abortus, or B. suis=Brucella suis, O. niloticus=Oreochromis niloticus, F. columnare=Flavobacterium columnare, M. tilapiae=Myxobolus tilapiae, I. multifiliis=Ichthyophthirius multifiliis, E. ictaluri=Edwardsiella ictaluri, T. cruzi=Trypanosoma cruzi, T. gondii=Toxoplasma gondii, E. tenella=Eimeria tenella, T. spiralis=Trichinella spiralis, F. hepatica=Fasciola hepatica, E. coli=Escherichia coli, D. intermedius=Dyschirius intermedius, C. auratus=Carassius auratus, PCV2=Porcine circovirus type 2, ADV=Aujeszky’s disease virus, FeLV=Feline leukemia virus, IFN-γ=Interferon-gamma, IL-12=Interleukin-12, NO=Nitrous oxide